neurosurgicaloperativeatlas- V2

NEUROSURGICALOPERATIVE ATLAS

Volume 2

The American Association of Neurological Surgeons

AANS Publications Committee

Editors

SETTI S. RENGACHARYROBERT H. WILKINS

C o n t e n t sVolume I

Optic Gliomas. Edgar M. Housepian / 1-13F i b rous Dysplasia Involving the Craniofacial Skeleton.

James T. Goodrich, Craig D. Hall / 14-22D e p ressed Skull Fracture in Adults. F red H. Geisler / 23-33

Cervical Hemilaminectomy for Excision of a Herniated Disc. Robert H. Wilkins, Sarah J. Gaskill / 34-38

Lateral Sphenoid Wing Meningioma. Joseph Ransohoff / 39-45Selective Micro s u rgical Vestibular Nerve Section for Intractable Ménière’s Syndro m e .

E d w a rd Tarlov / 46-53Chiari Malformations and Syringohydromyelia in Children. W. Jerry Oakes / 54-60

C a rotid Body Tumors. F redric B. Meyer, Thoralf M. Sundt, Jr. / 61-69Olfactory Groove Meningiomas. Joshua B. Bederson, Charles B. Wilson / 70-78

C e rebral Aneurysms at the Bifurcation of the Internal Carotid Artery.Eugene S. Flamm / 79-88

Treatment of Unilateral or Bilateral Coronal Synostosis. John A. Persing, John A. Jane / 89-98Convexity Meningioma. Sarah J. Gaskill, Robert H. Wilkins / 99-105

Occipital Lobectomy. Milam E. Leavens / 106-112Spinal Meningiomas. Michael N. Bucci, Julian T. Hoff / 113-116

P e rcutaneous Trigeminal Glycerol Rhizotomy. Ronald F. Young / 117-123Lumbar Hemilaminectomy for Excision of a Herniated Disc.

Patrick W. Hitchon, Vincent C. Traynelis / 124-129Transoral Surgery for Craniovertebral Junction Anomalies. A rnold H. Menezes / 130-135

A n t e rolateral Cervical Approach to the Craniovertebral Junction. Dennis E. McDonnell / 136-153

C o r rection of Malposition of the Orbits. John A. Persing / 154-163Removal of Cervical Ossified Posterior Longitudinal Ligament at Single and Multiple Levels.

Ralph B. Cloward / 164-170Technique of Ventriculostomy. Joseph H. Piatt, Jr., Kim J. Burchiel / 171-175

C e rebellar Medulloblastoma. Arthur E. Marlin, Sarah J. Gaskill / 176-183Shunting of a Posttraumatic Syrinx. David J. Gower / 184-190

D i rect Surgical Treatment of Vein of Galen Malformations. H a rold J. Hoffman / 191-200Spinal Nerve Schwannoma. Phyo Kim, Burton M. Onofrio / 201-206Combined Craniofacial Resection for Anterior Skull Base Tumors.

Ehud Arbit, Jatin Shah / 207-217Diagnostic Open Brain and Meningeal Biopsy.

R i c h a rd P. Anderson, Howard H. Kaufman, Sydney S. Schochet / 218-222Ventriculoperitoneal Shunting. David C. McCullough / 223-230

Ventriculoatrial Shunting. Paul J. Camarata, Stephen J. Haines / 231-239Excision of Acoustic Neuromas by the Middle Fossa Approach. Derald E. Brackmann / 240-248

Upper Thoracic Sympathectomy by a Posterior Midline Approach. P rem K. Pillay, Issam A. Awad, Donald F. Dohn / 249-255

C a rotid Endarterectomy. Daniel L. Barrow, Christopher E. Clare / 256-266Transsphenoidal Excision of Macroadenomas of the Pituitary Gland.

NEUROSURGICAL OPERATIVE ATLAS: TABLE OF CONTENTS

G e o rge T. Tindall, Eric J. Wo o d a rd, Daniel L. Barrow / 267-278C o m p u t e r-D i rected Stereotactic Resection of Brain Tumors. Patrick J. Kelly / 279-293

Sagittal Synostosis. A. Leland Albright / 294-300Glossopharyngeal Rhizotomy. Burton M. Onofrio / 301-304

Occipitocervical and High Cervical Stabilization. Volker K.H. Sonntag, Curtis A. Dickman / 305-315

P e t roclival Meningiomas. Ossama Al-Mefty, Michael P. Schenk, Robert R. Smith / 316-326Facial Reanimation without the Facial Nerve. Mark May, Steven M. Sobol / 327-336

Omental and Musculocutaneous Free Flaps for Coverage of Complicated Neuro s u rg i c a lWounds. Daniel L. Barrow, Foad Nahai / 337-348

Repair of “Growing” Skull Fracture. Tadanori Tomita / 349-354Occipital Encephaloceles. William O. Bell / 355-362

Foramen Magnum Meningiomas and Schwannomas: Posterior Approach. Chad D. Abernathey, Burton M. Onofrio / 363-371

Penetrating Wounds of the Spine. E d w a rd C. Benzel / 372-378P e rcutaneous Radiofrequency Rhizolysis for Trigeminal Neuralgia.

James Fick, John M. Tew, Jr. / 379-390Extended Costotransversectomy. Eddy Garrido / 391-396

S u rgical Resection of Posterior Fossa Epidermoid and Dermoid Cysts. Lee Kesterson / 397-406Luque Rod Segmental Spinal Instrumentation. E d w a rd C. Benzel, / 407-412

En Bloc Anterior Temporal Lobectomy for Te m p o rolimbic Epilepsy. Michel F. Levesque / 413-422

Cingulotomy for Intractable Pain Using Stereotaxis Guided by Magnetic Resonance Imaging.Samuel J. Hassenbusch, Prem K. Pillay / 423-432

C e rebellar Astrocytomas. A. Leland Albright / 433-439E x t reme Lateral Lumbar Disc Herniation. Robert S. Hood / 440-444

Tentorial Meningiomas. Laligam N. Sekhar, Atul Goel / 445-455

Volume II

S u rgical Repair of Trigonocephaly. Ken R. Winston, Michael J. Burke / 1-8Dorsal Root Entry Zone (DREZ) Lesioning. Blaine S. Nashold, Jr., Amr O. Ei-Naggar / 9-24

Ophthalmic Segment Aneurysms. Arthur L. Day / 25-41C h ronic Subdural Hematoma. James E. Wi l b e rg e r, Jr. / 42-48

Ta i l o red Temporal Lobectomy Using Subdural Electrode Grids. Issam A. Awad, Joseph F. Hahn / 49-55

Gunshot Wounds of the Brain. Suzie C. Tindall, Ali Krisht / 56-59Tr a n s t o rcular Occlusion of Vein of Galen Malformations. J. Parker Mickle, Ronald G. Quisling, Keith Peters / 60-66

Detection of an Epileptic Focus and Cortical Mapping Using a Subdural Grid.Sumio Uematsu / 67-78

A n t e romesial Temporal Lobectomy for Epilepsy. Issam A. Awad, Prem K. Pillay / 79-87Anastomosis of the Facial Nerve After Resection of an Acoustic Neuroma.

Charles M. Luetje / 88-90An Extended Subfrontal Approach to the Skull Base.

Chandranath Sen, Laligam N. Sekhar / 91-100


Pansynostosis: Surgical Management of Multiple Pre m a t u re Suture Closure. James T. Goodrich, Craig D. Hall / 101-112

Distal Anterior Cerebral Artery Aneurysms. H. Hunt Batjer, Duke Samson / 113-126Te t h e red Spinal Cord, Intramedullary Spinal Lipoma, and Lipomyelomeningocele.

W. Jerry Oakes / 127-135Interstitial Brachytherapy. J e ff rey D. McDonald, Philip H. Gutin / 136-144

Lateral Extracavitary Approach to the Thoracic and Lumbar Spine. Dennis J. Maiman, Sanford J. Larson / 145-153

An Extreme Lateral Transcondylar Approach to the Foramen Magnum and Cervical Spine.Chandranath Sen, Laligam N. Sekhar / 154-162

R e t rolabyrinthine Presigmoid Approach for Sectioning of the Vestibular Nerve for Ménière ’ sDisease. Charles M. Luetje / 163-166

S t e reotactic Surgical Ablation for Pain Relief. Ronald F. Young / 167-177Anterior Screw Fixation of Odontoid Fractures. Ronald I. Apfelbaum / 178-188

Carpal Tunnel Syndrome. Setti S. Rengachary / 189-199Transantral Ethmoidal Orbital Decompression For Graves’ Ophthalmopathy.

L a w rence W. DeSanto / 200-206Middle Fossa Approaches for Invasive Tumors Involving the Skull Base.

Laligam N. Sekhar, Atul Goel, Chandranath Sen / 207-218Transthoracic Excision of a Spinal Metastasis with Vertebral Body Reconstruction.

G regory J. Bennett / 219-228Anterior Cervical Discectomy and Fusion-the Cloward Technique. Ralph B. Cloward / 229-240

Cubital Tunnel Syndrome. Setti S. Rengachary / 241-245Caspar Plating of the Cervical Spine.

H. Louis Harkey, Wo l f h a rd Caspar, Yaghoub Tarassoli / 246-256S u rgical Management of Anterior Communicating Artery Aneurysms.

Timothy C. Ryken, Chistopher M. Loftus / 257-265Basilar Bifurcation Aneurysm: Pterional (Transsylvian) Approach.

H. Hunt Batjer, Duke S. Samson / 266-281Thalamotomy for Tre m o r. Roy A. E. Bakay, Jerrold L. Vitek, Mahlon R. Delong / 282-295

Endovascular Treatment of Carotid Cavernous Fistulas. Arvind Ahuja, Lee R. Guterman, Kimberly Livingston, Leo N. Hopkins / 296-304

Combined Transsylvian and Middle Fossa Approach to Interpeduncular Fossa Lesions.Chandranath Sen, Laligam N. Sekhar / 305-311

Aneurysms of the Ophthalmic Segment of the Internal Carotid Artery. Daniel L. Barrow / 312-322

L u m b a r-Peritoneal Shunting. Setti S. Rengachary / 323-333S u rgery of the Cavernous Sinus.

Harry van Loveren, Magdy El-Kalliny, Jeff rey Keller, John M. Tew, Jr. / 334-344Encephaloceles of the Anterior Cranial Base. Alan R. Cohen / 345-353

C o t re l-Dubousset Instrumentation: Internal Fixation for Thoracolumbar Fractures and Tumors. Bruce E. van Dam / 354-358

P o s t e r i o r-Lateral Lumbar Spinal Fusion. E d w a rd S. Connolly / 359-366C o r rection of Exorbitism.

Constance M. Barone, Ravelo V. Argamaso, David F. Jimenez, James T. Goodrich / 367-372Meralgia Paresthetica. Setti S. Rengachary / 373-379

D e p ressed Skull Fracture in Infants. Lyn C. Wright, Marion L. Walker / 380-383Combined Pre s i g m o i d-Transtransversarium Intradural Approach to the Entire Clivus and


Anterior Craniospinal Region. Mario Ammirati, Melvin Cheatham / 384-395Partial Median Corpectomy with Fibular Grafting for Cervical Spondylotic Myelopathy.

Setti S. Rengachary / 396-409C o r rection of Orbital Hypertelorism and Orbital Dystopia.

Constance M. Barone, David F. Jimenez, Ravelo V. Argamaso, James T. Goodrich / 410-416P e rcutaneous Radiofrequency Rhizotomy for the Treatment of Paraplegic Spasms.

Sumio Uematsu / 417-427E n d o c r i n e-Inactive Pituitary Adenomas. Charles B. Wilson / 428-437

Posterior Decompression and Fusion for Cervical Spondylotic Myelopathy. Paul Kurt Maure r, Charles Nussbaum / 438-447

S u rgical Correction of Swan Neck Deformity. Peter M. Klara, Kevin T. Foley / 448-461

Volume III

Tu b e rculum Sellae Meningiomas. Ossama Al-Mefty / 1-11Craniofacial Techniques Used in Resection of Anterior Skull Base Tumors.

James T. Goodrich, Ravelo V. Argamaso / 12-20Occipital Transtentorial Approach to Pineal Region Neoplasms.

James I. Ausman, Balaji Sadasivan / 21-26Meningioma of the Lateral Ventricle. E d w a rd Tarlov / 27-30

P re a u r i c u l a r-Infratemporal Fossa Approach to Tumors that Involve the Lateral Cranial Base.Robert L. Grubb, Peter G. Smith / 31-37

Repair of the Myelomeningocele. David G. McLone / 38-44Anterior Clinoidal Meningiomas. Franco DeMonte, Ossama Al-Mefty / 45-57

D a n d y - Walker Malformation. Arthur E. Marlin, Sarah J. Gaskill / 58-65Acoustic Neuromas: Surgical Anatomy of the Suboccipital Approach.

Martin B. Camins, Jeff rey S. Oppenheim / 66-75E x p o s u re of the Skull Base via the Midface.

James T. Goodrich, Sidney Eisig, George J. Cisneros, Allen B. Kantrowitz / 76-83E x p o s u re of the Skull Base by Transoral, Translabial, and Transmandibular Routes.

James T. Goodrich, Sidney Eisig, Joseph G. Feghali, Allen B. Kantrowitz / 84-93S u rgical Management of Chiari I Malformations and Syringomyelia.

R i c h a rd B. Morawetz / 94-102Open-Door Maxillotomy Approach for Lesions of the Clivus.

H. Louis Harkey, Vinod K. Anand, H. Alan Cro c k a rd, Michael P. Schenk / 103-112Peripheral Nerve Repair. Allan J. Belzberg, James N. Campbell / 113-128

S u rgical Management of Split Cord Malformations. Dachling Pang / 129-143Te t h e red Cord Syndrome Secondary to Previous Repair of a Myelomeningocele.

Timothy A. Strait / 144-150Craniofacial Techniques for Managing Orbital Trauma.

James T. Goodrich, Simeon A. Lauer, Ravelo V. A rgamaso / 151-158Tr a n s o r a l - Transclival Approach to Basilar Artery Aneurysms.

R. A. de los Reyes, Paul W. Detwiler / 159-166F rontal Lobectomy. Setti S. Rengachary / 167-175

Thoracic Outlet Syndrome: Supraclavicular First Rib Resection and Brachial PlexusD e c o m p ression. Susan E. Mackinnon, G. A. Patterson / 176-182

Transfacial Approaches to the Clivus and Upper Cervical Spine. Ivo P. Janecka / 183-192S u rgical Management of Prolactinomas. A n d rew D. Parent / 193-202


Sectioning of the Filum Te rminale. F rederick A. Boop, William M. Chadduck / 203-209Repair of Diastematomyelia. F rederick A. Boop, William M. Chadduck / 210-214

Repair of a Lipomyelomeningocele. F rederick A. Boop, William M. Chadduck / 215-219Untethering of the Spinal Cord After a Previous Myelomeningocele Repair.

F rederick A. Boop, William M. Chadduck / 220-224Secondary Carpal Tunnel Syndrome. Susan E. Mackinnon / 225-234

Spheno-Orbital Craniotomy for Meningioma. Joseph C. Maroon, John S. Kennerdell, Danko V. Vidovich / 235-243

S u rgical Treatment of Anterior Sacral Meningocele. K. Stuart Lee / 244-251Acrylic Cranioplasty. Setti S. Rengachary / 252-259

P reauricular Transzygomatic Infratemporal Craniotomy for Skull Base Tumors. Stephen L. Ondra, Michael G. Donovan / 260-269

Medial Sphenoid Ridge Meningiomas. Vallo Benjamin, Jules M. Nazzaro / 270-282S u rgical Treatment of Arteriovenous Malformations of the Cerebral Convexity.

Wink S. Fisher III / 283-291Lumbar Microdiscectomy. Peter M. Klara, Kevin T. Foley / 292-301

M i c rovascular Decompression of the Facial Nerve. Robert H. Wilkins / 302-311Craniofacial Resection of Neoplasms of the Anterior Skull Base.

Vincent C. Traynelis, Timothy M. McCulloch, Henry T. Hoffman / 312-323Postlaminectomy Instability: Posterior Pro c e d u res.

Seth M. Zeidman, Thomas B. Ducker / 324-336Vertebral Artery and Posterior Inferior Cerebellar Artery Aneurysms: Surgical Management.

F e rnando G. Diaz, Richard D. Fessler / 337-343Anterior Cervical Discectomy and Fusion: Smith-Robinson Technique.

Philip R. Weinstein / 344-358Management of Basilar and Posterior Cerebral Artery Aneurysms by

Subtemporal Approaches. Robert M. Crowell, Christopher S. Ogilvy / 359-374Subcutaneous Transposition of the Ulnar Nerve for Ta rdy Ulnar Palsy.

Melvin L. Cheatham, Fredric L. Edelman, Martin Holland / 375-381Image-Guided Neuro s u rgery: Frame-Based and Frameless Approaches.

Lucia Zamorano, Lutz Nolte, Charlie Jiang, Majeed Kadi / 482-401Anterior Stabilization of the Cervical Spine Using a Locking Plate System.

Setti S. Rengachary / 402-413Endoscopic Neuro s u rg e r y . Alan R. Cohen / 414-426

S u rgical Management of Brain Abscess. Timothy C. Ryken, Christopher M. Loftus / 427-435Submuscular Transposition of the Ulnar Nerve at the Elbow: Musculofascial Lengthening

Technique. A. Lee Dellon / 436-443S u p e rficial Temporal Artery to Middle Cerebral Artery Bypass Grafting.

Issam A. Awad / 444-456

Volume IV

Spinal Vascular Malformations. E d w a rd H. Oldfield / 1-18Posterior C1-2 Screw Fixation for Atlantoaxial Instability. Ronald I. Apfelbaum / 19-28

S u p r a c e rebellar Infratentorial Approaches to the Pineal Region. Michael L. Levy, Michael L. J. Apuzzo / 29-36

T h i rd-Ventricle Exposure by the Interhemispheric Corridor. Peter Gruen, Michael L. J. Apuzzo / 37-42


Arteriovenous Malformations of the Basal Ganglia, Thalamus, and Adjacent Ventricles. Ghaus M. Malik, Fady T. Charbel / 43-58

Selective Denervation for Spasmodic Torticollis. Antonio A. F. DeSalles / 59-66Unilateral Coronal Synostosis. James T. Goodrich, Ravelo Argamaso / 67-74

N e u ro s u rgical Approaches to the Orbit. Part 1: Orbital Anatomy and Lateral Orbitotomy.Johnny B. Delashaw, Jr. / 75-84

N e u ro s u rgical Aproaches to the Orbit. Part 2: Craniotomy for Surgical Exposure of the Orbit.Johnny B. Delashaw, Jr. / 85-94

Fourth Ventricular Ependymoma. J. Gordon McComb, John H. Schneider / 95-106Sectioning of the Corpus Callosum for Epilepsy. Issam A. Awad / 107-116

S u rgical Treatment of Intracranial Glomus Tumors. Vinod K. Anand, Michael P. Schenk, John P. Leonetti, Ossama Al-Mefty / 117-130

Technique of Temporal Lobectomy. Allen R. Wyler / 131-138Treatment of Moyamoya Syndrome in Children with Pial Synangiosis.

R i c h a rd G. Ellenbogen, R. Michael Scott / 139-146Isthmic Spondylolysis and Spondylolisthesis: Treatment by Reduction, Interbody Fusion,

and Lateral Stabilization. Timothy C. Wirt / 147-158Translabyrinthine Removal of Acoustic Neuromas. John T. McElveen, Jr. / 159-164

Transsphenoidal Surgical Treatment of Cushing’s Disease. William F. Chandler / 165-172Upper Thoracic Spinal Exposure Through a Lateral Parascapular Extrapleural Appro a c h .

R i c h a rd G. Fessler, Donald Dietze, David Peace / 173-182Selective Dorsal Rhizotomy for the Spasticity of Cerebral Palsy. T. S. Park / 183-190

S u rgical Treatment of the Subclavian Steal Syndrome. G e o rge E. Pierce / 191-198S u rgery for Tumors Affecting the Cavernous Sinus.

Franco DeMonte, Vinod K. Anand, Ossama Al-Mefty / 199-208Lambdoidal Synostosis.

David F. Jimenez, Constance M. Barone, Ravelo V. Argamaso, James T. Goodrich / 209-214Gamma Knife Radiosurgery of Intracranial Lesions. Robert J. Coffey / 215-224

Submuscular Transposition of the Ulnar Nerve at the Elbow. Susan E. Mackinnon / 225-234Ulnar Nerve Entrapment at the Wrist. V. Leroy Young, Jill M. Young / 235-249

Volume V

Endoscopic Pituitary Surgery. H a e-Dong Jho, Ricardo L. Carrau, Yong Ko / 1-12To rcular and Peritorcular Meningiomas. G r i ffith R. Harsh IV / 13-22

S u rgical Resection of Lower Clivus-Anterior Foramen Magnum Meningioma.Vallo Benjamin, Ramesh P. Babu / 23-32

Basilar Bifurcation Aneurysms: Transsylvian Transclinoidal Tr a n s c a v e rnous Appro a c h .Murali Guthikonda, Fernando G. Diaz / 33-42

S u rgical Management of Posterior Plagiocephaly. R i c h a rd G. Ellenbogen, Michael H. Mayer / 43-56

Acute Subdural Hematoma. F red H. Geisler / 57-64Intracranial Pre s s u re Monitoring. A n d rew D. Firlik, Donald W. Marion / 65-74

Temporal Lobectomy Under General Anesthesia. Diana L. Abson Kraemer, Dennis D. Spencer / 75-84

F a r-Lateral Disc Herniation Treated by Microscopic Fragment Excision. Bruce V. Darden II, J. Robinson Hicks / 85-90

Stabilization of the Cervical Spine (C3-7) with Articular Mass (Lateral Mass) Plate and


S c re w s . T. Glenn Pait, Luis A. B. Borba / 91-100Stabilization of the Cervical Spine with the Orion Anterior Cervical Plate System.

Gary L. Lowery / 101-108Texas Scottish Rite Hospital System for Internal Stabilization of Thoracolumbar Fracture s .

B r a d f o rd M. Mullin, Gary L. Rea / 109-120Application of Frameless Stereotaxy in the Management of Intracranial Lesions.

Dennis A. Tu rn e r, Paul B. Johnson / 121-128A Modified Transfacial Approach to the Clivus.

B rooke Swearingen, Michael P. Joseph, Matthew Cheney, Robert G. Ojemann / 129-134Management of the Vertebral Artery During Excision of Extradural Tumors of the Cervical

Spine. Chandranath Sen, Mark Eisenberg / 135-142P o s t e roventral Pallidotomy for Patients with Parkinson’s Disease.

Robert P. Iacono, Shokei Yamada / 143-154Functional Hemispherectomy. Joseph R. Smith, Mark R. Lee / 155-164

M i c ro s u rgical Decompresson of the Root Entry Zone for Trigeminal Neuralgia.Chandranath Sen / 165-170

The Anterior Cervical Approach to the Cervicothoracic Junction. Julian K. Wu / 171-176Management of Extradural Non-Neoplastic Lesions of the Craniovertebral Junction via theTranscondylar Appro a c h . Luis A. B. Borba, Ossama Al-Mefty, T. Glenn Pait, Ronald Tribell /

1 7 7 - 1 8 4Far Lateral Lumbar Disc Herniation. Nancy E. Epstein, Joseph A. Epstein / 185-198

Repair and Reconstruction of Scalp and Calvarial Defects. Wa r ren Schubert, Jeff rey Aldridge / 199-218

Sagittal Synostosis. Larry A. Sargent, Timothy A. Strait / 219-226M i c ro s u rgical Lumbar Decompression Using Pro g ressive Local Anesthesia.

Stephen D. Kuslich / 227-232Banked Fibula, the Locking Anterior Cervical Plate, and Allogeneic Bone Matrix in Anterior

Cervical Fusions Following Cervical Discectomy. Scott Shapiro / 233-240Endoscopic Third Ventriculostomy for Obstructive Hydrocephalus.

Jonathan J. Baskin, Kim H. Manwaring / 241-246

Volume VI

Treatment of Caro t i d-C a v e rnous Sinus Fistulas Using a Superior Ophthalmic Vein Appro a c h .Neil R. Miller, Lee H. Monsein, Rafael J. Ta m a rgo / 1-4

The Separation of Craniopagus Twins. H a rold J. Hoffman, James T. Rutka / 5-12P o s t e roventral Pallidotomy for Parkinson’s Disease Patients.

Kim J. Burchiel, Jamal M. Taha, Jacques Favre / 13-26M i c ro e l e c t ro d e-Guided Pallidotomy. A n d res M. Lozano, William D. Hutchison / 27-34

A n t e rolateral Transforaminal Approach for a Large Dumbbell-Shaped Cervical Neurinoma.Isao Yamamoto / 35-42

Bridge Bypass Coaptation for Cervical Nerve Root Avulsion. Shokei Yamada, Russell R. Lonser, Robert P. Iacono / 43-50

Sinus Skeletonization Technique: A Treatment for Dural Arteriovenous Malformations atthe Tentorial Apex. E v a n d ro De Oliveira, Helder Tedeschi / 51-56

M i c ro s u rgical Carotid Endarterectomy. Julian E. Bailes, Patrick P. Flannagan / 57-64Endoscopic Approaches to the Ventricular System. David F. Jimenez / 65-74

S u rgical Management of Cranial Dural Arteriovenous Fistulas. Lokesh S. Tantuwaya, Julian E. Bailes / 75-84


Intraventricular Endoscopy: Diagnostic Ventriculoscopy, Tissue Biopsy, Cyst Fenestration,and Shunting. Jonathan J. Baskin, Kim H. Manwaring / 85-98

Endoscopic Carpal Tunnel Release Through a Monoportal Approach. Jay Menon / 99-108Endoscopic Excision of Colloid Cysts. Jonathan J. Baskin, Kim H. Manwaring / 109-114

S u rgical Anatomy of the Temporal Lobe. Steven N. Roper / 115-124Multiple Subpial Transection. Walter W. Whisler / 125-130

S t e reotactic Depth Electrode Implantation in the Evaluation of Candidates for AblativeEpilepsy Surgery. Joseph R. Smith, Mark R. Lee / 131-146

Tr a n s-Sulcal Approach to Mesiotemporal Lesions. Isabelle M. Germano / 147-156Anterior Cervical Spine Stabilization with the Codman Locking Plate System.

R. John Hurlbert, Volker K. H. Sonntag / 157-166Posterior Cervical Fusion with Tension Band Wiring. Thomas J. Lovely / 167-172

Primary Anterior Treatment of Thoracolumbar Burst Fractures. David W. Polly, Jr., Richard G. Ellenbogen / 173-182

Technique for Reduction of Spondylolisthesis Using Custom Texas Scottish Rite HospitalF o rceps. Gary L. Lowery, David A. Fernandez, Atul L. Bhat, A. Eugene Pennisi / 183-192

S u rgical Management of Infected Ventriculoperitoneal Shunt. Timothy M. George, Sohaib A. Kureshi / 193-200

Combined Fro n t o-Orbital and Occipital Advancement for Total Calvarial Reconstruction. Ian F. Pollack, H. Wolfgang Losken / 201-212

Repair of Meningoceles. Timothy M. George, Eric M. Gabriel / 213-220Installation of a Dorsal Column Stimulator for Pain Relief. John P. Gorecki / 221-236

Implantation of Drug Infusion Pumps. John P. Gorecki / 237-250S t e reotactic Micro s u rgical Craniotomy for the Treatment of Third Ventricular Colloid Cysts.

Kyle L. Cabbell, Donald A. Ross / 251-256H e m i s p h e rectomy. Benjamin S. Carson, Aaron L. Zuckerberg / 257-264

Volume VII

Posterior Lumbar Interbody Fusion Augmented With the Ray Threaded Fusion Cage.Peter Klara, Berkley Rish, Charles D. Ray / 1-10

Total Sacre c t o m y . Ziya L. Gokaslan, Marvin M. Romsdahl, Stephen S. Kroll, T h e resa A. Gillis, David W. Wildrick, Milam E. Leavens / 11-20

Treatment of Fractures at the Thoracolumbar Junction with Kaneda Anterior SpinalInstrumentation System. Seth M. Zeidman, Randy F. Davis / 21-28

Cannulated Screws for Odontoid and Atlantoaxial Transarticular Screw Fixation.Curtis A. Dickman, R. John Hurlbert / 29-42

Anterior Microforaminotomy for Cervical Radiculopathy: Disc Preservation Te c h n i q u e .Hae-Dong Jho / 43-52

Pedical Subtraction and Lumbar Extension Osteotomy for Iatrogenic “Flatback.”Gary L. Lowery, Atul L. Bhat, A. Eugene Pennisi / 53-58

The Surgical Treatment of Dolichoectactic and Fusiform Aneurysms. Michael T. Lawton, John A. Anson, Robert F. Spetzler / 59-68

P e t rosal Approach for Resection of Petroclival Meningiomas. William T. Couldwell / 69-82S u rgical Resection of Esthesioneuro b l a s t o m a . Scott L. Henson, John A. Jane, Sr. / 83-92

S t e reotactic Radiosurgery of the Trigeminal Nerve Root for Treatment of Trigeminal Neuralgia. Ronald F. Young / 93-98

Techniques of Peripheral Neurectomy for Control of Trigeminal Neuralgia. Raj Murali / 99-106


P e rcutaneous Balloon Compression for the Treatment of Trigeminal Neuralgia.

J e ff rey A. Brown, Jan J. Gouda / 107-116M i c rovascular Decompression for Hemifacial Spasm. Thomas J. Lovely / 117-124

Thalamic Deep Brain Stimulation for the Control of Tre m o r. A n d res Lozano / 125-134Magnetic Resonance Image-Guided Stereotactic Cingulotomy for Intractable Psychiatric

D i s e a s e . Osama S. Abdelaziz, G. Rees Cosgrove / 135-140Magnetic Resonance Image-Guided Pallidotomy. Antonio A.F. De Salles, Marwan Hariz / 141-148

Endoscopic Carpal Tunnel Release via a Biportal Appro a c h . David F. Jimenez / 149-156Thoracic Sympathectomy. J. Patrick Johnson, Samuel S. Ahn / 157-162

Blood Flow-Monitored Transthoracic Endoscopic Sympathectomy.R i c a rdo Segal, Peter M. Ferson, Edwin Nemoto, Sidney K. Wolfson Jr. / 163-172S u rgical Management of Craniopharyngiomas. H a rold J. Hoffman / 173-182

S u rgical Resection of Craniopharyngiomas. Ali F. Krisht, Ugur Türe / 183-190Optic Nerve Sheath Fenestration in the Management of Pseudotumor Cere b r i .

Eric L. Berman, Jonathan D. Wirschafter / 191-200S u rgical Correction of Unilateral and Bilateral Coronal Synostosis.

Ann Marie Flannery, Jack C. Yu / 201-210Te t h e red Cord Syndrome: Management of Myelomeningocele, Diastematomyelia, and

H y p e r t rophied Filum Te rm i n a l e . Robert F. Keating, James Tait Goodrich / 211-218Te t h e red Cord Syndrome: Management of Lipomyelomeningoceles.

James Tait Goodrich / 219-226Excision of Colloid Cyst via the Transcallosal Appro a c h . Deepak Awasthi, John J. Kruse /

2 2 7 - 2 3 4L a p a roscopy Assisted Lumboperitoneal Shunt Placement in the Management of

P s e u d o t u m o r C e re b r i . F l o rence C. Barnett, Dennis E. McConnell / 235-240The Transparaspinal Approach to Dumbbell-Shaped Spinal Tumors.

Stephen T. Onesti, Ely Ashkenazi, W. Jost Michelsen / 241-248Posterior Occipito-axial Fusion for Atlantoaxial Dislocation Associated with

Occipitalized Atlas. Vijendra K. Jain, Sanjay Behari / 249-256Evaluation and Management of Severe Facial Nerve Injury Resulting From

Temporal Bone Tr a u m a . Aijaz Alvi / 257-260

Volume VIII

S u rgical Management of Paraclinoid Carotid Aneurysms.Murali Guthikonda, Fernando G. Diaz / 1-12

S u rgical Management of Middle Cerebral Artery Aneurysms.Philip E. Stieg, Robert M. Friedlander / 13-22

S u rgical Removal of Tentorial and Posterior Fossa Dural Arteriovenous Malform a t i o n s .Adam I. Lewis, John M. Tew Jr. / 23-34

S u rgical Resection of the Arteriovenous Malformations of the Posterior Fossa.Thomas Kopitnik, Duke Samson, Michael Horowitz / 35-46

S u rgical Treatment of Arteriovenous Malformations of the Ventricular Tr i g o n e .Daniel L. Barrow, Roger H. Frankel / 47-56

Dural Arteriovenous Malformations of the Transverse and Sigmoid Sinuses. Todd A. Kuether, Gary M. Nesbit, Stanley L. Barnwell / 57-68


Operative Management of Anterior Fossa, Superior Sagittal Sinus, and Convexity DuralArteriovenous Malform a t i o n s . Aman B. Patel, Wesley A. King, Neil A. Martin / 69-78

Use of the Operating Arm System in Skull Base Surg e r y .J e ff rey J. Larson, Ronald E. Warwick, John M. Tew Jr. / 79-86

The Orbitocranial Zygomatic Approach to Aneurysms of the Upper Basilar Trunk. T. C. Origitano / 87-94

Extradural Approaches for Resection of Trigeminal Neurinomas. J. Diaz Day / 95-106S u rgical Management of Trigeminal Schwannomas.

Madjid Samii, Ramesh Pitti Babu, Marcos Tatagiba / 107-120S u rgical Management of Cholesterol Granulomas of the Petrous Apex.

Mark B. Eisenberg, Ossama Al-Mefty / 121-126S u rgical Management of Angiographically Occult Vascular

M a l f o rmations of the Brainstem, Thalamus, and Basal Ganglia.Gary K. Steinberg, Steven D. Chang / 127-134

Management of Jugular Foramen Tu m o r s . J e ff rey Bruce, Ian Storper / 135-142S u rgical Management of Esthesioblastomas. Ramesh Pitti Babu, Mark S. Persky / 143-152

S u rgical Treatment of Brainstem Gliomas. Mark R. Lee, Michael Cowan / 153-160Brainstem Gliomas. Harold J. Hoffman / 161-170

The Contralateral Transcallosal Approach to Lesions In or Adjacent to the Lateral Ve n t r i c l e .Michael T. Lawton, Robert F. Spetzler / 171-178

Posterior Fossa Decompression Without Dural Opening for the Treatment of Chiari I Malform a t i o n . Jonathan Sherman, Jeff rey J. Larson, Kerry R. Crone / 179-184Computed Tomography-Assisted Pre f o rmed Prosthesis for Repair of Cranial Defects.

Manuel Dujovny, Celso Agner, Fady T. Charbel, Lewis L. Sadler, Raymond Evenhouse, D i e rd re McConathy / 185-194

C h ronic Subthalamic Nucleus Stimulation for Parkinson’s Disease. Ali R. Rezai, William Hutchison, Andres M. Lozano / 195-208

A r t h roscopic Microlumbar Discectomy.Kenneth F. Casey, Parviz Kambin, Marc Chang / 209-216

Excision of Herniated Thoracic Disc Via the Transthoracic Appro a c h .Mary Louise Hlavin, Russell W. Hardy / 217-224

S u rgical Management of Advanced Degenerative Disease of the Lumbar Spine withM u l t i p l a n a r D e f o rm i t y . Michael F. O’Brien, Gary L. Lowery, A. Eugene Pennisi / 225-234

The Retropleural Approach to the Thoracic and Thoracolumbar Spine.T h e o d o re H. Schwartz, Paul C. McCormick / 235-242

S u rgical Treatment of Lateral Lumbar Herniated Discs.Giuseppe Lanzino, Christopher I. Shaff rey, John A. Jane, Sr. / 243-252

“ Trap Door” Exposure of the Cervicothoracic Junction.Ziya L. Gokaslan, Garrett L. Walsh / 253-260

Peripheral Nerve Suture Te c h n i q u e s .Rajiv Midha, Margot Mackay / 261-269

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AAblative epilepsy surgery, 6:131-146Acoustic neuromas, 4:159-164Acrylic cranioplasty, 5:214-215Acute subdural hematoma, 5:57-63Allogeneic bone matrix, 5:233-239Aneurysms

basilar bifurcation, 5:33-42broad-based siphon, 8:3-4; 8:10-11carotid cave, 8:3-4carotid ophthalmic, 8:2-3; 8:10-11carotid-superior hypophyseal, 8:3-4dolichoectatic, 7:59-67fusiform, 7:59-67middle cerebral artery, 8:13-22paraclinoid carotid artery, 8:1-12superior hypophyseal, 8:1-2; 8:10-11upper basilar trunk, 8:87-94ventral paraclinoid, 8:3-4; 8:10-11

Angiographically occult vascular malformations, 8:127-133

Angioma, cavernous, 4:13-18Anterior cervical spine

discectomy, 5:233-239implant systems, 5:101-108stabilization, 6:157-166

Anterior foramen magnum meningioma,5:23-32

Anterior fossa dural AVMs, 8:69-78Anterior microforaminotomy, 7:43-52Apert syndrome, 7:201Arteriovenous fistulas (AVFs)

cranial dural, 6:75-84dural, 4:3-7; 6:51-56intradural, 4:11-16perimedullary, 4:11-13

Arteriovenous malformations (AVMs)anterior fossa, 8:69-78basal ganglia, 4:43-58cerebellar hemisphere, 8:36; 8:40-42cerebellar tonsil, 8:36; 8:43-44cerebellar vermis, 8:35-36, 8:38-40deep parenchymal, 8:36dural, 8:23-34; 8:69-79glomus, 4:9-10juvenile, 4:8-10posterior fossa, 8:23-46spinal cord, 4:7-10

superior sagittal sinus dural, 8:69-78tentorial dural, 8:23-34thalamic, 4:43-58upper basilar trunk, 8:87ventral paraclinoid, 8:3-4; 8:10-11ventricular trigone, 8:47-56

Astrocytomasbrainstem, 8:162; 8:164; 8:165-169craniocervical, 8:169-170

Atlantoaxial dislocation with occipitalizedatlas, 7:249-256

Atlantoaxial instability, C1-2 screw fixation,4:19-28

Atlantoaxial transarticular screw fixation,7:29-41

BBanked fibula, 5:233-239Basal ganglia AVMs, 4:43-58Basilar bifurcation aneurysms, 5:33-42Bilateral coronal synostosis, 7:201-210Birth defects, 5:219-225Bone graft harvesting

fractures, 7:24-25atlantoaxial dislocation, 7:251-254calvarial defects, 5:199-217; 6:201-211posterior lumbar interbody fusion,

7:6-10Bone-wiring procedures, 5:91-100Brainstem

AVMs, 8:36; 8:43; 8:45-46craniocervical astrocytomas, 8:169-170dorsally exophytic gliomas, 8:161-163diffuse intrinsic astrocytomas, 8:162;

8:164focal intrinsic astrocytomas, 8:165-169gliomas, 8:153-159

Bridge bypass coaptation, 6: 43-50Broad-based siphon aneurysms, 8:3-4;

8:10-11Burst fractures, 5:110; 6:173-182

CCallostomy, 7:227-233Calvarial defects, 5:199-217Calvarial reconstruction, 6:201-211Cannulated screws, 7:29-41

Carotid cave aneurysms, 8:3-4Carotid endarterectomy, 6:57-64Carotid-cavernous sinus fistulas, 6:1-4Carotid ophthalmic aneurysms, 8:2-3;

8:10-11Carotid-superior hypophyseal aneurysms,

8:3-4Carpal tunnel syndrome, 6:99-108;

7:149-156Cavernous angiomas, 4:13-18Cavernous sinus tumors, 4:199-207Cerebellar hemisphere AVMs, 8:36; 8:40-42Cerebellar tonsil AVMs, 8:36; 8:43-44Cerebellar vermis AVMs, 8:35-36; 8:38-40Cerebral palsy, 4:183-190Cervical fusion, 5:233-239; 6:167-171Cervical nerve root avulsion, 6:43-50Cervical neurinoma, 6:35-41Cervical radiculopathy, 7:43-52Cervical spine

C1-2 screw fixation, 4:19-28degenerative disc disease, 7:43-52discectomy, 5:233-239extradural tumors, 5:135-141implant systems, 5:101-108stabilization, 6:157-166stabilization (articular mass), 5:91-100stabilization (Orion system), 5:101-108

Chiari I malformation, 8:179-183Children

cerebral palsy, 4:183-190moyamoya syndrome, 4:139-146

Cholesterol granulomas of petrous apex,8:121-125

Chondrosarcoma, 5:129Cingulotomy for psychiatric disease,

7:135-140Clivus, 5:129-133Codman locking plate system, 6:157-166Colloid cyst, 6:109-114; 6:251-256;

7:227-233Complex spinal schwannomas, 7:241-242 Convexity dural AVMs, 8:69-78Coronal synostosis, 4:67-73; 6:201-211;

7:201-210Corpus callosum sectioning, 4:38-39;

4:107-116Cranial defects, 8:185-194Cranial dural arteriovenous fistulas,

6:75-84Craniocervical brainstem astrocytomas,

8:169-170Craniopagus twins, 6:5-11Craniopharyngiomas, 7:173-181; 7:183-190Craniovertebral junction lesions,

5:177-184Crouzonís syndrome, 7:201Cubital tunnel syndrome, 4:235-249Cushingís disease, 4:165-172Cyst

colloid, 6:109-114; 6:251-256; 7:227-233fenestration, 6:85-98

DDecompressive corpectomy, 5:101Deep brain stimulation

control of tremor, 7:125-134subthalamic nucleus, 8:169-197;

8:200-201; 8:205-206Deep parenchymal AVMs, 8:36Degenerative disc disease, 7:43-52;

8:225-233Denervation for spasmodic torticollis,

4:59-65Diastematomyelia, 7:219-226Direct end-to-end repair of peripheral

nerves, 8:263-269Disc herniation

far lateral, 5:85-89far lateral lumbar, 5:185-197lateral, 8:243-251thoracic, 8:217-224

Disc preservation, 7:43-52Discectomy, cervical, 5:233-239Dolichoectatic aneurysms, 7:59-67Dorsal column stimulation, 6:221-235Dorsal lipomyelomeningocele, 7:221-225Dorsal rhizotomy, 4:183-190Drug infusion pumps, 6:237-250Dumbbell-shaped cervical neurinoma,

6:35-41Dumbbell-shaped spinal tumor, 7:241-248Dural AVFs, 4:3-7; 6:51-56; 6:75-84Dural AVMs

anterior fossa, 8:69-78convexity, 8:69-78inferior petrosal sinus, 8:29-32

petrous apex, 8:24-27posterior fossa, 8:23-46superior sagittal sinus, 8:69-78tentorial, 8:23-34

EElbow, ulnar nerve transposition,

4:225-233Electrode implantation, 6:131-146Endarterectomy, carotid, 6:57-64Endoscopy

approaches to the ventricular system,6:65-74

carpal tunnel release, 6:99-107;7:149-156

colloid cysts, 6:109-114fenestration of the third ventriculosto-

my, 5:241-246intraventricular, 6:85-98pituitary surgery, 5:1-12thoracoscopic sympathectomy,

7:157-162; 7:163-171Ependymoma, fourth ventricular, 4:95-106Epilepsy

ablative surgery, 6:131-146corpus callosum sectioning, 4:107-116medial temporal onset, 5:75-83

Esthesioblastomas, 7:83-91; 8:143-151Exophytic gliomas, 8:161-163Extradural non-neoplastic lesions,

5:177-184Extradural cervical spine tumors,

5:135-141

FFacial nerve injury, 7:257-260Facial pain, 5:227-232Far lateral disc herniation, 5:85-89;

5:185-197Fascicular peripheral nerves repair, 8:267Fields of Forel, 8:200Fistulas

carotid-cavernous sinus, 6:1-4dural arteriovenous, 4:3-7; 6:51-56; 6:75-

84intradural, 4:11-16

Flat-back syndrome, 7:53-58

Focal intrinsic brainstem astrocytomas,8:165-169

Foramen magnum, 5:23-32Fourth ventricular ependymoma, 4:95-106Frameless stereotaxy, intracranial lesions,

5:121-128Full facetectomy, 5:190-191Full thickness calvarial bone graft,

5:215-217Functional hemispherectomy, 5:155-164Fusiform aneurysms, 7:59-67Fusion tension band wiring, 6:167-171

GGalen, vein of, 8:32-34Gamma Knife radiosurgery, intracranial

lesions, 4:215-224Gliomas, brainstem, 8:153-159Glomus AVM, 4:9-10Glomus tumors, intracranial, 4:117-130Grafts, 5:233-239; 8:267-269

bone, 5:199-217; 7:6-10; 7:24-25;7:251-254

Granulomas, petrous apex cholesterol,8:121-125

HHematoma, acute subdural, 5:57-63Hemicorticectomy, 5:155Hemifacial spasm, 7:117-124Hemispherectomy, 5:155-164; 6:257-264Herniation

far lateral disc, 5:85-89far lateral lumbar disc, 5:185-197thoracic disc, 8:217-224

Horner’s syndromeand anterior microforaminotomy, 7:51complication of thoracoscopic

sympthectomy, 7:162Hydrocephalus, 5:241-246; 6:65; 6:76; 6:98;

6:261-264Hyperhidrosis, 7:158Hypertrophied filum terminale, 7:219-226

IIdiopathic intracranial hypertension,

7:191-200Implantation of drug infusion pumps,

6:237-250Infection of ventriculoperitoneal shunt,

6:193-200Inferior dental neurectomy, 7:103-104Inferior petrosal sinus dural AVMs, 8:29-32Infraorbital neurectomy, 7:101-103Interbody fusion, 4:147-157Intercostal neuralgia, 7:162Interhemispheric corridor and third-

ventricle exposure, 4:37-42Internal stabilization, 5:109-119; 5:233-239Intervertebral disc damage, 7:51-52Intracranial glomus tumors, 4:117-130Intracranial hypertension, 7:191-200Intracranial lesions, 4:75-83; 4:85-93;

4:215-224; 5:121-128Intracranial pressure monitoring, 5:65-74Intradural arteriovenous fistulas, 4:11-16Intraventricular endoscopy, 6:85-98Intraventricular shunt, 6:85-98Isthmic spondylolysis/spondylolisthesis,

4:147-157

JJugular foramen tumors, 8:135-142Juvenile AVMs, 4:8-10

KKambin instrumentation for microlumbar

discectomy, 8:211Kaneda anterior spinal instrumentation

system, 7:21-27

LLabbé, vein of, 8:58-60Lambdoidal synostosis, 4:44-45; 4:209-214Lateral disc herniation, 8:243-251Lateral mass plate and screws, 5:91-100Lateral orbitotomy, 4:81-83Lateral ventricles, 5:67-69Lipomyelomeningoceles, 7:219-226Lobectomy, temporal, 4:131-137; 5:75-83Locking anterior cervical plate, 5:233-239

Locking plate system, 6:157-166Low back pain, 5:227-232Lower clivus-anterior foramen magnum

meningioma, 5:23-32Lumbar decompression, 5:227-232Lumbar disc herniation, far-lateral, 5:185-

197Lumbar extension osteotomy for flat-back

syndrome, 7:53-58Lumbar spine

arthroscopic microlumbar, 8:209-216degenerative disease, 8:225-233far lateral disc herniation, 5:85-89far lateral lumbar disc herniation,

5:185-197foraminal stenosis, 8:227thoracolumbar fractures, 5:109-119

Lumboperitoneal shunt placement forpseudotumor cerebri, 7:235-240

MMeningioma

anterior foramen magnum, 5:23-32lower clivus, 5:23-32petroclival, 7:69-81torcular/peritorcular, 5:13-21

Meningoceles, 6:213-219Mental neurectomy, 7:103-106Mesiotemporal lesions, 6:147-156Microelectrode-guided pallidotomy,

6:27-33Microforaminotomy, anterior, 7:43-52Microsurgery

carotid endarterectomy, 6:57-64craniotomy for colloid cysts, 6:251-256lumbar decompression, 5:227-232root entry zone decompression,

5:165-170Microvascular decompression for

hemifacial spasm, 7:117-124Middle cerebral artery aneurysms, 8:13-22Moyamoya syndrome, 4:139-146MRI-guided pallidotomy, 7:141-148MRI-guided stereotactic cingulotomy,

7:135-140Multiple subpial transection, 6:125-129Myelomeningocele, 7:219-226

NNerve root avulsion, 6: 43-50Nerve root injury, 7:51Neurectomy for trigeminal neuralgia,

7:99-106Neurinoma, 6:35-41; 8:95-105Neuroblastomas, olfactory, 7:83-91; 8:

143-151Neuroma, acoustic, 4:159-164Non-neoplastic lesions of the cranioverte-

bral junction, 5:177-184

OObstructive hydrocephalus, 5:241-246Occipitalized atlas, 7:249-254Occipitoaxial fusion, 7:249-254Odontoid transarticular screw fixation,

7:29-41Olfactory neuroblastomas, 7:83-91;

8:143-151Operating Arm System, 8:79-85; 8:133Optic nerve injury, 8:12Optic nerve sheath fenestration, 7:191-200Orbit

anatomy, 4:75-81craniotomy, 4:85-93lateral orbitotomy, 4:81-83

Orbitotomy, 4:81-83Orion anterior cervical plate system,

5:101-108

PPain

facial, 5:227-232low back, 5:227-232relief, 6:221-235trigeminal neuralgia, 5:165-170

Pallidotomymicroelectrode-guided, 6:27-33MRI-guided, 7:141-148posteroventral, 5:143-153; 6:13-26subthalamic nucleus, 8:196-197;

8:200-201; 8:205-206Paraclinoid carotid artery aneurysms,

8:1-12

Parkinsonís diseasedeep brain stimulation for control of

tremor, 7:125-134MRI-guided pallidotomy, 7:141-148posteroventral pallidotomy, 5:143-153;

6:13-26subthalamic nucleus, 8:196-197;

8:200-201; 8:205-206Pedical screw, 5:112-113; 5:116-117Pedicle subtraction for flat-back syndrome,

7:53-58Percutaneous balloon compression for

trigeminal neuralgia, 7:107-116Perimedullary AVFs, 4:11-13Peripheral nerve suture techniques,

8:261-269Peripheral neurectomy for trigeminal

neuralgia, 7:99-106Peritorcular meningiomas, 5:13-21Petroclival meningiomas, 7:69-81Petrous apex

cholesterol granulomas, 8:121-125dural AVMs, 8:24-27

Pfeifferís syndrome, 7:201Pial synangiosis, 4: 139-146Pineal region masses, 4:29-36Pituitary

Cushing’s disease, 4:165-172surgery, 5:1-12

Plagiocephaly, posterior, 5: 43-55Pneumothorax, postoperative, 7:162Posterior C1-2 screw fixation, 4:19-28Posterior cervical fusion with tension band

wiring, 6:167-171Posterior fossa dural AVMs, 8:23-46Posterior lumbar interbody fusion, 7:1-10Posterior occipitoaxial fusion for

atlantoaxial dislocation, 7:249-254Posterior plagiocephaly, 5: 43-55Posterior stabilization, 5:91-100Posterolateral tentorium dural AVMs,

8:25-29Posteroventral pallidotomy, 5:143-153;

6:13-26Pseudotumor cerebri

lumboperitoneal shunt placement,7:235-240

optic nerve sheath fenestration,7:191-200

Psychiatric disease, surgery for, 7:135Pulse generator for subthalamic nucleus

stimulation, 8:205-206

RRadiosurgery of intracranial lesions,

4:215-224Radiosurgical dose planning, 7:94-96Radiosurgical localization, 7:94-96Ray Threaded Fusion Cage, 7:1-10Raynaud’s syndrome, 7:158Revascularization and

dolichoectatic/fusiform aneurysms,7:61-65

Rhizotomydorsal, 4:183-190spasmodic torticollis, 4:59-65

Rod placement and thoracolumbar junction fractures, 7:24-27

Root entry zone decompression,5:165-170

SSacrectomy, 7:11-20Sacrum tumors, 7:11-20Sagittal synostosis, 5:219-225Sathre-Chotzen syndrome, 7:201Scalp reconstruction, 5:199-217Schwannomas

complex spinal, 7:241-242trigeminal, 8:107-120

Screw fixationatlantoaxial instability, 4:19-28atlantoaxial transarticular, 7:29-41odontoid transarticular, 7:29-41

Seizuresablative epilepsy surgery, 6:131-146corpus callosum sectioning, 4:38-39;

4:107-116temporal lobectomy, 4:131-137

Shuntintraventricular, 6:85-98ventriculoperitoneal, 6:193-200

Sinus fistulas, carotid-cavernous, 6:1-4Sinus skeletonization technique, 6:51-56

Sinus, sagittal, 8:74-77Sinus, transverse-sigmoid, 8:57-68Spasmodic torticollis, 4:59-65Spasticity, 4:183-190Spina bifida, 7:219-226Spinal cord AVMs, 4:7-10Spinal exposure, upper thoracic, 4:173-182Spinal instrumentation, 7:21-27Spinal plate/screw placement, 7:23-25Spinal stabilization

cervical spine, 6:157-166cervical spine with articular plates and

screws, 5:91-100cervical spine with the Orion system,

5:101-108posterior, 5:91-100thoracolumbar fractures, 5:109-119

Spinal tumor, dumbell-shaped, 7:241-248Spinal vascular malformations, 4:1-18Spondylolisthesis, 4:147-157; 6:183-191Spondylolysis, 4:147-157Stabilization

cervical, 6:157-166lateral, 4:147-157posterior, 5:91-100thoracolumbar fractures, 5:109-119

Stereolithography for cranial repair, 8:188Stereotactic cingulotomy for psychiatric

disease, 7:135-140Stereotactic depth electrode implantation,

6:131-146 Stereotactic imaging and deep brain

stimulation for control of tremor,7:127-128; 7:141

Stereotactic microsurgical craniotomy,6: 251-256

Stereotactic radiosurgery of trigeminalnerve root, 7:93-97

Stereotaxy, frameless, 5:121-128Subclavian steal syndrome, 4:191-198Subdural hematoma, 5:57-63Substantia nigra pars reticulata/pars

compacta, 8:201Subthalamic nucleus, 8:196-197; 8:200-201;

8:205-206Superior hypophyseal aneurysm, 8:1-2;

8:10-11Superior sagittal sinus dural AVMs, 8:69-78Supraorbital, supratrochlear neurectomy,

7:99-101Sympathectomy, 7:157-162Synostosis

coronal, 4:67-73; 6:201-211; 7:201-210lambdoidal, 4:44-45; 4:209-214sagittal, 4:219-225

TTemporal bone trauma, 7:257-260Temporal lobe, 4:131-137; 5:75-83;

6:115-124Tension band wiring, 6:167-171Tentorial apex, 6:51-56Tentorial dural AVMs, 8:23-34Tethered cord syndrome, 7:219-226Texas Scottish Rite Hospital

forceps, 6:183-191system, 5:109-119

Thalamic AVMs, 4:43-58Thalamic mapping for control of tremor,

7:125-134Third ventricular colloid cysts, 6:251-256Third ventriculostomy for obstructive

hydrocephalus, 5:241-246Third-ventricle exposure, 4:37-42Thoracic disc herniation, 8:217-224Thoracic spine exposure, 4:173-182Thoracolumbar spine

burst fractures, 6:173-182fractures, 5:109-119junction fractures, 7:21-27

Thoracoscopic sympathectomy, 7:157-162Thrombectomy, 7:61-62Torcular/peritorcular meningiomas,

5:13-21Transthoracic endoscopic sympathectomy,

7:163-171Transverse-sigmoid sinus, 8:57-68Tremor, 7:125-134Trigeminal neuralgia

percutaneous balloon compression,7:107-116

peripheral neurectomy, 7:99-106microvascular decompression of root

entry zone, 5:165-170stereotactic radiosurgery of the trigemi-

nal nerve root, 7:93-97Trigeminal schwannomas, 8:107-120

Tumorscavernous sinus, 4:199-207dumbell-shaped spinal, 7:241-248ependymomas, 4:95-106extradural cervical spine, 5:135-141intracranial glomus, 4:117-130jugular foramen, 8:135-142orbital region, 4:87-90pineal region, 4:36sacrum, 7:11-20

Twins, craniopagus, 6:5-11

UUlnar nerve

entrapment, 4:235-249submuscular transposition, 4:225-233

Unilateral coronal synostosis, 4:67-73;7:201-210

Upper basilar trunkaneurysms, 8:87-94AVMS, 8:87

Upper clivus dural AVMs, 8:24-27

VVascular malformations

angiographically occult, 8:127-133spinal, 4:1-18

Vein of Galen, 8:32-34Vein of Labbé, 8:58-60Ventral intermediate thalamotomy, 7:125;

7:134Ventral paraclinoid

aneurysms, 8:3-4, 8:10-11AVMs, 8:3-4; 8:10-11

Ventricular AVMs, 8:52-58Ventricular system, 6:65-74Ventricular trigone AVMs, 8:47-56Ventriculoperitoneal shunt, 6:193-200Vertebral artery, 5:135-141

WWrist, ulnar nerve entrapment, 4:235-249

ZZona incerta, 8:200

1

SURGICAL REPAIROF TRIGONOCEPHALY

KEN R. WINSTON, M.D.MICHAEL J. BURKE, D.V.M., M.D.

INTRODUCTIONThe metopic suture is functional for approximately thefirst two years of life. Premature fusion of this suture istypically associated with a specific cranial dysmorphia,termed trigonocephaly. While associated brain deformi-ties have been reported (i.e., holoprosencephaly andarhinencephaly), trigonocephaly is most commonly an iso-lated type of cranial dysmorphia in a neurologically nor-mal child.

DESCRIPTION OF THE DEFECTThe dysmorphia is apparent at birth. When the head isviewed from the vertex, the frontal area has a wedge ortriangular shape. A keel of bone extends vertically acrossthe forehead and may appear to continue below thefrontonasal suture. The keel does not necessarily extendposteriorly to the bregma. Very characteristic of trigono-cephaly is the severely retropositioned lateral parts of thesupraorbital ridges. The bifrontal cranial dimension is ab-normally narrow, with a widening of the biparietal diam-eter which accommodates normal brain volume but ac-centuates the cosmetic defect.

Although the eyes often appear hyperteloric, mea-surement of the orbits may show hypotelorism. The lat-eral canthal angles and therefore the lateral eyebrows mayappear elevated, but extraocular muscle functions are nor-mal. The term “startled coon” has been applied to the fa-cies of these children.

The diagnosis is made by inspection of the head. If thecharacteristic abnormality cannot be identified, then eitherthere is no trigonocephaly or it is clinically insignificant.Skull films will show the suture to be absent anteriorly(lower portion). Computed tomography scanning shouldbe done on patients with other congenital malformations(i.e., palatal defects). These patients with trigonocephalyare at higher risk for forebrain abnormalities.

INDICATIONS FOR SURGERYSurgery for trigonocephaly is cosmetic. Most parents ofchildren with trigonocephaly find the dysmorphia to bevery noticeable and extremely undesirable. The defect doesnot improve with time; there is no reason to delay thecorrective procedure. We strongly prefer surgical repairby four to six weeks of age but there is no upper age limit.

RISKSRisks associated with this procedure include blood lossand the need for transfusion. Dural lacerations, if not rec-ognized and repaired, can lead to enlarging skull defectswith cerebral herniation and brain injury. The osteoto-mies may fuse too early or, conversely, reossification maybe incomplete. Additional surgical procedures may be re-quired to achieve a desired satisfactory cosmetic result.Injury to an eye or to periocular structures is possible,with resulting damage to the visual system. Although rare,it is possible for the brain to be injured.

Parents should also be informed that, while most chil-dren have an excellent cosmetic result, a perfectly shapedskull is not likely to be achieved. A good result is one inwhich the child’s resulting craniofacial morphology willnot adversely affect normal psychosocial development.After surgery, the region of the forehead and orbits is usu-ally normal in appearance to all but the most detailed ex-amination.

PREPARATION FOR SURGERYPreoperative laboratory evaluation generally consists ofroutine complete blood counts, electrolyte determinations,and urinalysis. A prothrombin time, partial thromboplas-tin time, and platelet count are also usually obtained. Ashampoo with a chlorhexidine solution is done 8-24 hoursbefore surgery. Prophylactic antibiotics are started in theoperating room and continued for 24 hours.

SELECTION OF SURGICAL REPAIRChildren under six months of age, and perhaps up to© 1992 The American Association of Neurological Surgeons

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NEUROSURGICAL OPERATIVE ATLAS, VOL. 2

age nine months, are repaired by the “floating forehead”procedure. This method corrects the almond shape of theorbits and midline ridge and takes advantage of the pro-gressively expanding brain to correct any remaining ab-normality. Children who are one year of age or older andsome children under this age are best repaired by the“tongue-in-groove” procedure. In older children, the brainis expanding more slowly and it is necessary to make amore rigidly structured repair. Also, it is not safe to leavelarge bony defects because they occasionally do notreossify satisfactorily.

DESCRIPTION OF FLOATINGFOREHEAD OPERATION

Position, Preparation of Scalp, and DrapingThe patient is placed in the supine position with the shoul-ders elevated by a transverse roll and the neck slightlyextended. An arterial line (usually a radial artery), a singleperipheral venous line, and a Foley catheter are placed.

We do not shave or clip the hair, although this is com-monly done by most neurosurgeons. Using a sterile combor hemostat, the hair is parted along the proposed inci-sion line. The scalp, including the ears and cheeks, arescrubbed with a chlorhexidine solution and the head isdraped for a transcoronal incision.

Chemical HemostasisThe skin is infiltrated with 0.5% lidocaine with epineph-rine (1/400,000) along the planned incision line.

Initial Soft Tissue DissectionA coronal incision is made, beginning about 5 mm abovethe insertion of each pinna and crossing the midline nearthe anterior fontanelle (Fig. 1). Skin edges are retractedand clips (preferably children’s or Cone clips) are appliedto the scalp edge for hemostasis. Periosteal elevators areused to free the pericranium anteriorly to the level of thesupraorbital rims. The periorbita are then dissected fromthe superior half of each orbit. Medially this dissection iscontinued well below the frontonasal suture and laterallybelow the frontozygomatic sutures. The supraorbitalnerves can be preserved by using a thin osteotome to openthe supraorbital foramen and reflecting the nerve anteri-orly with the skin.

OsteotomiesThe frontal convexity and supraorbital rims are removedseparately. A high-speed craniotome (e.g., Midas Rex) isused for all osteotomies in the frontal convexity. No burrholes are made. Blunt dissection in the anterior fonta-nelle is used to separate the dura from the frontal bone

and is the starting point for the osteotomies. If the ante-rior fontanelle is closed, a small oval hole just anterior tothe coronal suture can be made with the craniotome.

The frontal convexity bone is removed first. An os-teotomy is made just anterior to each coronal suture. Theosteotomy is continued anteriorly across the foreheadapproximately 1.5 cm superior to the supraorbital rims(Fig. 1). The resulting triangular piece of bone is sepa-rated from the underlying dura. and removed from thefield. The only firm dural attachment to the frontal boneis at the midline along the area of the superior sagittalsinus. A wide periosteal elevator will usually disrupt thisattachment with safety. Bleeding from the dura. is con-trolled with bipolar coagulation and microfibrillar col-lagen (Avitene). Bleeding from bone is controlled withmicrofibrillar collagen. Bone wax is used only if the abovemeasures fail to control a point of active bleeding.

Both supraorbital ridges are removed with a frontalbar en bloc, using osteotomes (Fig. 2). The frontal dura isretracted superiorly and posteriorly. This necessitates sepa-ration of the dura. from the midline of the frontal fossaanterior to the crista galli. An osteotomy is made across thefloor of the frontal fossa (i.e., across each orbital roof) andextended laterally across the sphenoid wings (Fig. 2). Thisosteotomy is approximately 1-1.5 cm posterior to the su-praorbital rims. The zygomaticofrontal suture is dividedvertically with an osteotome. A vertical osteotomy is madein the sphenoid bones down to the level of thefrontozygomatic suture. When necessary, a horizontal os-teotomy is made to connect the above two osteotomies.

An inverted “V”-shaped osteotomy is made throughthe region of the frontonasal suture to free the supraor-bital rim. If an abnormal nasal ridge exists, it is removedwith a high-speed burr.

Remodeling of the Supraorbital Rims, Frontal Bar, andForeheadThe supraorbital bar is straightened. This almost alwaysrequires division in the midline. Posterior reinforcementwith a strip of bone taken from the frontal convexity maybe required. Straightening of the bar causes the lateralorbital margins to swing medially. A large Leksell rongeuris used to resect this protrusion and also to remodel thesuperior orbit (Fig. 3).

Remodeling of the forehead first involves divisionof the frontal bone in its midline (Fig. 1). Switching rightfor left and rotating the two fragments 90° often achievesan acceptable appearance but sometimes other incisionsin the frontal fragments are performed as needed to moldthem into an acceptable cosmetic appearance.

Prior to replacing the above remodeled bones, thenarrow anterior biparietal diameter is addressed.

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WINSTON AND BURKE : SURGICAL REPAIR OF TRIGONOCEPHALY

Figure 1. Removal and remodeling of the forehead bone. A, a coronalincision is made. The dura is bluntly separated from bone at the anteriorfontanelle and is the starting point for osteotomies. Osteotomies are madejust anterior to the coronal sutures and 1.5 cm superior to the supraorbital

rim (inset). B, the forehead bone is removed and divided in its midline. Cand D, switching right for left and rotating the fragments 90° will oftengive a satisfactory shape. E, other osteotomies and smoothing of the fron-tal bone are performed as needed to improve the shape of the forehead.

© 1992 The American Association of Neurological Surgeons

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Figure 2. Removal of the supraorbital bar. The supraorbital ridges and a1.5-cm frontal bar are removed en bloc. This necessitates separation of thedura from the frontal fossa anterior to the crista galli. Osteotomies acrossthe frontal fossa (orbital roofs) are indicated. The zygomaticofrontal suture

is divided. An inverted V-shaped osteotomy through the frontonasal sutureis made. If the tongue-in-groove technique is required, osteotomies are madeposteriorly to form a 2-4 × 1.5-cm “tongue” of bone which is continuouswith the frontal bar.


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Figure 3. Remodeling of the supraorbital bar. A and B, the supraorbitalbar is straightened by division in the midline. B, straightening of the barcauses the lateral orbital margins to protrude antermedially and may in-crease the distance between the orbits. C, on each side, the lateral orbitalprotrusion is resected and the interorbital distance is narrowed by vertical

osteotomies from glabella to nasion; using a large Leksell rongeur, thesuperior orbital margin is rounded. D and E, osteotomies are made in thebone of the frontal fossa, facilitating a more natural curve to each su-praorbital margin. F, the supraorbital bar is reinforced posteriorly with astrip of bone (generally obtained from the remodeled forehead bone).


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Using the high-speed craniotome, the anterior 1-2 cmof the parietal bone is morcellated and the resultingtwo to four fragments are left attached to the dura (Figs.5 and 6).

Replacement of Remodeled ForeheadThe frontal bones are sutured together at the midline

with 2-0 Vicryl (Figs. 1 and 4). The forehead is thenattached to the supraorbital bar with 2-0 Vicryl sutures(Fig. 4). Only rarely do we use a few wires and thenonly in children over one year of age. The entire rigidcomplex is then replaced and anchored with a single 3-0 Vicryl suture in the frontonasal region (Fig. 4). Theresult is a “floating forehead” (Fig. 5).

Figure 4. Replacement of remodeled bone. The forehead bone isattached to the supraorbital bar using 2-0 absorbable sutures. Theentire rigid complex is replaced and anchored with a 3-0 absorb-

able suture in the frontonasal region. Wire is occasionally used toattach the forehead to the supraorbital bar in children over one yearof age.


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Closure and DressingIf the upper face has been prepared and draped appropri-ately, the scalp should be returned to its normal position,temporarily at first, so that the appearance of the upperface and orbits can be assessed. It may be necessary tomake some corrective adjustments in the forehead andorbits at that time. After the surgeon is satisfied with theappearance, the galea and underlying pericranium aresutured (single layer) with 3-0 Vicryl sutures (interruptedor continuous technique). Skin edges are approximatedwith staples. Drains are occasionally required. Postop-eratively the head is wrapped snugly but never tightly.

DESCRIPTION OF TONGUE-IN-GROOVEOPERATIONThis procedure is identical to that described above for thefirst three steps. The removal of the convexity of the frontalbone and the osteotomy in the orbital roofs (floor of fron-tal fossa) are the same as in Step 4 above. The lateralosteotomies are, however, totally different. The high-torque craniotome is used to outline a posteriorly directed“tongue” of bone which remains in continuity with the

frontal bar (Fig. 6). This tongue should be at least 1.5 cmwide and about 2-4 cm in length. This tongue always ex-tends posteriorly into the squamous portion of the tem-poral bone beyond the coronal suture. The osteotomiesalong the lateral orbits are the same as described above.

The remodeling of the supraorbital rim and frontalbar should include all the steps described above. As a re-sult, the tongue of bone will rotate outward on each sidewhen the midline angle in the frontal bar is corrected.Therefore, the sphenoid ridges will need to be notched ontheir inner (medial) surfaces and the lateral bony frag-ments bent (green stick fracture) inward. It is very impor-tant that the fragment to which the tongue is attached re-main firmly continuous with the whole frontal bar.

The remodeled forehead is returned to the operativefield and sewed in the middle with one or two 3-0 Vicrylsutures. The posteriorly directed tongues of bone are re-turned to their respective grooves and secured 11.5 cmanterior to their original location to give the desired cor-rection. The tongues are sewed in place with wire and/or2-0 Vicryl (Fig. 6). The closure and application of thedressing are accomplished as described above.

Figure 5. The floating forehead operation. This technique is used in chil-dren under nine months of age. The remodeled forehead is replaced andanchored with an absorbable suture at the frontonasal region. The entire

complex then floats over the growing brain. Morcellation of the anteriorparietal bones, leaving the fragments attached to the dura, corrects the nar-row anterior biparietal diameter.


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Figure 6. The tongue-in-groove operation. This technique is used in olderchildren where a more rigid reconstruction is required. A posteriorly di-rected tongue of bone which is continuous with the frontal bar is createdwhile the lateral osteotomies are performed. The tongue is 1.5 cm wide and2-4 cm long. Upon straightening the supraorbital bar the tongue protrudeslaterally. Notching of the sphenoid wing facilitates moving the tongue of

bone medially. The tongue must remain attached to the supraorbital bar.The forehead bone is replaced and secured in the frontonasal region. Thetongues of bone are secured 1-1.5 cm anterior to their previous location,thereby rigidly fixing the supraorbital bone in an advanced position. Bipa-rietal morcellation is performed to correct the narrow anterior biparietaldiameter.

POSTOPERATIVE MANAGEMENTThe head of the patient’s bed is elevated. A hematocrit ischecked in the immediate postoperative period and twicedaily for the first 48 hours. We transfuse packed red cellswhen the hematocrit drops to 22 or below. The dressing shouldbe monitored at approximately 4-hour intervals for the first24 hours to ensure that it is not too tight. Facial swellingreaches its maximum at around 48 hours. The worst of theperiorbital and facial edema resolves over the next 24 hoursand the child is generally discharged at about the time botheyes are clearly open (usually the third to fifth postoperativeday). A helmet is not used unless the child is a toddler.

FOLLOW-UP AND EXPECTED OUTCOMEThe child is usually seen five to seven days postopera-tively for staple removal. Examinations are at aboutthe six-week, six-month, and one-year anniversaries.Follow-up radiographs are not necessary unless the cos-metic result is questionable or clearly unsatisfactory.An enlarging skull defect should alert the surgeon tothe presence of a dural tear and is an indication forimmediate surgical attention. No clinically significantdefects in bone should be palpable at a one-year post-operative follow-up.


9

DORSAL ROOT ENTRY ZONE(DREZ) LESIONING

BLAINE S. NASHOLD, JR., M.D.AMR O. EL-NAGGAR, M.D.

INTRODUCTIONThe dorsal root entry zone (DREZ) operation was origi-nally reported in 1976 as a focal destruction of the sub-stantia gelatinosa of Rolando. It was done on a patientwith intractable arm pain following a brachial plexus avul-sion injury. Since then it has been performed at the DukeUniversity Medical Center in over 500 patients with in-tractable pain of various etiologies. Pain due to deaffer-entation responds best to the DREZ operation, which in-volves the creation of lesions in the dorsal root entry zoneareas, destroying Rexed layers I through V using aradiofrequency current delivered through a specially de-signed thermocouple electrode. These lesions are mainlytargeted toward the cells of origin of the second-orderneurons in Rexed layers II and V which give rise to thespinothalamic and spinoreticular tracts. The dorsal rootentry zone extends from the upper cervical cord to theconus medullaris deep to the intermediolateral sulcus. Itintermingles cephalad with the trigeminal nucleus caudaliswhich is the caudal portion of the trigeminal nucleus. Thenucleus caudalis receives the major pain afferents fromthe trigeminal system. Radiofrequency (RF) lesions in thenucleus caudalis have the same functional effect as thedorsal root entry zone lesions, and are performed to treatintractable pain of head and facial origin, especially paincaused by deafferentation.

PATIENT SELECTIONCareful patient selection is the key to the success of anyoperative procedure. Patients with deafferentation painsyndromes, especially brachial and sacral plexus avulsionpains, benefit the most from this operation. The DREZoperation is also very successful in paraplegic patientswith intractable pain, including central pain and radicu-lar pain, in postamputation phantom pain, and inpostherpetic neuralgia. Trigeminal nucleus caudalis le-

sions are successful in the treatment of intractable facialpain secondary to postherpetic neuralgia or anesthesiadolorosa, as well as in patients with trigeminal dysesthe-sia for whom all other surgical treatments have failed.Combined nucleus caudalis-nucleus solitarius lesions inthe floor of the fourth ventricle are performed for the treat-ment of intractable visceral pain of pharyngeal origin. Thenucleus solitarius contains the second-order neurons en-coding pain from cranial nerves IX and X from the tongue,pharynx, larynx, and esophagus.

PREOPERATIVE EVALUATIONA thorough evaluation of the patient’s pain is thus essen-tial, especially for patients who have undergone previousmultiple surgical procedures. Plain roentgenograms areobtained routinely to study the details of the bone anatomy,which is especially helpful in patients who have had pre-vious operative interventions. Other preoperative radio-logical studies are essential in most cases to confirm thediagnosis (as in cases of brachial plexus or sacral plexusavulsion injuries where myelography and magnetic reso-nance imaging (MRI) usually show evidence ofpseudomeningoceles along the avulsed roots (Fig. 1)) aswell as to visualize the spinal cord at the proposed opera-tive site for evidence of scar tissue or traumatic syringo-myelia (Fig. 2). All patients are given 10 mg of dexa-methasone by mouth the evening prior to surgery. We donot use perioperative antibiotics.

OPERATIVE PROCEDUREAll DREZ operations are performed under general an-esthesia with appropriate physiologic monitoring as de-termined by the patient’s general condition; however, aFoley catheter and an arterial line are essential. Thepatient is then placed in the prone position. Patientsundergoing nucleus caudalis lesions as well as patientsundergoing cervical DREZ lesions or lesions involv-ing the upper four thoracic segments require immobi-lization of their head in a Mayf ield head holder© 1992 The American Association of Neurological Surgeons

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Figure 1. A, a cervical myelogram showing traumatic pseudo-meningoceles along several cervical nerve roots in a case of brachialplexus avulsion injury. B, a lumbar myelogram showing traumatic

pseudomeningoceles along the L5 and S1 nerve roots in a case of sacralplexus avulsion injury.

to ensure anatomical alignment. Full flexion and elevationof the head is also essential in nucleus caudalis cases aswell as in cases involving the uppermost cervical levels. Areverse Trendelenburg position is then used to position theoperative site horizontally (Fig. 3). Patients undergoing le-sions below T4 are placed in the prone position with thehead turned to one side. Adequate cushioning by placingsoft rolls under the chest, hips, arms, and legs will preventpressure injuries (Fig. 4). Particular care should be takento avoid injury to the ulnar and peroneal nerves. Intraop-erative steroids are given in the form of intravenous 1-2mg/kg/hr Solu-Medrol throughout the procedure along with50 mg of ranitidine intravenously every eight hours. Musclerelaxants are used in cases where intraoperative evokedpotential monitoring is used.

The level and extent of the surgical exposure re-lates directly to the level and number of dermatomesaffected. Patients undergoing cervical DREZ lesionsrequire laminectomies extending one level rostral tothe highest dermatome affected, whereas those under-going thoracic DREZ lesions require laminectomiestwo levels higher. The number of laminectomies per-Figure 2. A cervical MRI showing a traumatic syrinx in a patient with

cervical spinal cord injury.



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NASHOLD AND EL-NAGGAR : DORSAL ROOT ENTRY ZONE LESIONING

Figure 3. Positioning of a patient undergoing nucleus caudalis DREZ lesions or cervical DREZ lesions.

Figure 4. Positioning of a patient undergoing thoracic or conus medullaris DREZ lesions.



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formed is based directly, in a one-to-one ratio, upon thenumber of painful dermatomes. For patients undergoinga conus medullaris DREZ lesioning for intractable lowerextremity pain, as in patients with phantom pain, T10through L1 laminectomies are performed. For trigeminalnucleus caudalis lesions a small suboccipital craniectomyand C1-C2 laminectomies are performed (Fig. 11, upperleft). Determination of the level is based on palpation ofthe spinous processes and is confirmed by obtaining anintraoperative radiograph as necessary.

The anatomy of the spinal roots varies according tothe level of their origin from the spinal cord. Thecervicodorsal roots are made up of five to eight individualrootlets that form the main sensory branch and exit viathe intervertebral foramen at the level of origin from thespinal cord. In contrast, the thoracic dorsal roots are madeup of two to four rootlets which are much smaller in di-ameter that form the main dorsal root and they exit atleast two to three vertebral levels below their origin fromthe spinal cord. Whereas the cervical sensory rootletsoriginate close together, the thoracic roots often are sepa-rated by several millimeters with a distance of 5 mm be-tween successive thoracic dorsal roots. This so-calledblank space between the thoracic roots should also be in-cluded in the DREZ lesioning.

At the level of the conus medullaris, the lower lum-bar and sacral roots are close to each other and may over-lap the conus and hide the lower sacral sensory roots. The

avulsed area on the spinal cord at the level of the conus isoften hidden by these superficial sensory rootlets fromhigher levels and the surgeon must carefully retract theseroots to expose the avulsed area. Anatomical identifica-tion of the sacral sensory roots is often difficult. The S1dorsal root is the largest, and the best way to identify itvisually is for the surgeon to find the last sacral root, whichis extremely small, and count up from that point to thelargest dorsal root which should be the level of S1. Themost accurate method of dorsal root localization is theuse of somatosensory evoked potentials. Electrical stimu-lation over the femoral triangle, stimulating the femoralnerve, will give a good L1 localization. With the record-ing electrodes placed on the spinal cord while stimulat-ing over the popliteal fossa (posterior tibial or sciaticnerve) and recording on the conus will give good S1 lo-calization. Where there is an area of unilateral avulsionon the conus or loss of a leg from trauma, the intact legcan be used for somatosensory localization (Fig. 5).

The thoracic dorsal roots are the most difficult toidentify precisely at their origin on the spinal cord. Weuse the “rule of two”: the origin of the dorsal root fromthe spinal cord is approximately two vertebral levelsabove its exit at the intervertebral foramen. In patientswith postherpetic pain involving the thoracic or abdomi-nal areas, the surgeon may note after opening the durathat certain of the dorsal roots appear abnormal. Thisis a good indication that the proper roots for

Figure 5. Localization by somatosensory evoked potentialmonitoring. The site for DREZ lesioning is determined by the

most positive wave recorded when stimulating the affected der-matome.


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the DREZ lesion have been localized. These involvedherpetic dorsal roots usually appear thin, dull, and gray-ish-red in color. A biopsy of the dorsal root reveals lossof the large myelinated fibers.

The advantage of the DREZ lesion is that the clinicaleffect can be localized to specific dermatomes or der-matomal levels. As we have indicated above, precise ana-tomical localization is important to restrict the lesion justto the painful areas of the body.

Following a thorough skin preparation and draping,a midline incision is made down to the subcutaneous tis-sue, and using electrocautery the midline cervical orlumbodorsal fascia is incised. In most instances a stan-dard multilevel bilateral laminectomy is done following asubperiosteal dissection of the paraspinous muscles fromthe spinous processes and laminae. After adequate con-firmation of the desired levels, bilateral laminectomiesare performed in almost all patients. Hemilaminectomiesare performed in patients with thoracic postherpetic neu-ralgia and in patients with unilateral intractable radicularpain secondary to spinal cord injury. Postoperative recov-ery is faster and incisional pain is less in patients under-going hemilaminectomy.

We prefer to use the Midas Rex drill to perform thelaminectomies to save operative time and for its safety whenused by an experienced surgeon. We use the S-1 drill bitsfor lumbar and thoracic laminectomies and hemilaminec-tomies, and the B-1 drill bits for the cervical region. Wefirst use the AM-8 drill bit to drill the lower portion of themost caudal lamina to expose the ligamentum flavum bi-laterally. The S-1 or B-1 bit is then used to cut through thelaminae one after the other, rostrally (Fig. 6A). This is per-formed on both sides. The supraspinous and interspinousligaments above and below are cut with Mayo scissors andthe laminae and spinous processes are removed en toto.The AM-8 bit is then used to widen the laminectomy asnecessary. The use of the Midas Rex drill is not essentialand the laminectomies can be performed the conventionalway using rongeurs. A hemilaminectomy is used to exposethe dorsal roots in the thoracic region in patients withpostherpetic pain. The dorsal roots are well visualized us-ing the microscope. Lesser postoperative pain and earlymobility are advantages in this group of patients who areoften elderly. We do not use the Midas Rex drill in caseswhere epidural scarring is suspected from previous sur-gery, trauma, or infection. Bone bleeding is controlled byapplying bone wax to the edges of the laminae. Epiduralvenous bleeding is controlled with bipolar cautery and smallpieces of Surgicel. Cottonoid strips are placed over the sidesof the wound and the dura is then opened.

In patients undergoing nucleus caudalis lesions, thesuboccipital craniectomy is performed using a perforator

and rongeurs or using the Midas Rex M-3 bit as a perfo-rator followed by a suboccipital craniotomy and removalof the bone in one piece. Care should be taken duringdissection of the paraspinal muscles at the C1-2 area dueto the presence of large veins in that location. Carefuldissection of the periosteum above and underneath theposterior arch of C1 should be performed prior to the useof rongeurs or the drill. The craniectomy needs to extendabout one-third to one-half the distance from the fora-men magnum to the inion and extend bilaterally just shortof the mastoid processes. The rim of the foramen mag-num is carefully dissected and preferably removed piece-meal. The atlanto-occipital membrane is then dissectedand cut using Dandy scissors. Bone wax and Surgicel areused to control bleeding as mentioned above and the durais then opened.

The dural opening is accomplished with or withoutthe aid of the operative microscope. Either way a 2-mmopening in the midline is made with a small-blade scal-pel, sparing the arachnoid. The dura is then openedsharply in the midline along the entire extent of the bonyexposure (Fig. 6B). Using 4-0 silk sutures placed ap-proximately 1 cm apart, the dural edges are retractedlaterally, thus maximizing the exposure. In patients withtrauma or prior operative procedures, the dura and arach-noid may be adherent and scarred down to the spinalcord. Gentle and blunt dissection using the microscopeis required to separate them. In nucleus caudalis DREZoperations, care should be taken when opening the duraacross the area of the foramen magnum due to the fre-quent presence of a circular sinus. Control of bleeding,from the sinus is achieved using hemostatic clips untilthe dura is opened followed by replacing the clips witha running 4-0 silk suture. Once the dura is opened be-yond this point the incision is then curved laterally to-ward the side of the pain.

If the microscope was not used for the dural openingit is then brought into the field to open the arachnoid. Thearachnoid is opened directly over the dorsal root entryzone in patients undergoing unilateral DREZ lesions. Thearachnoid is first opened in the middle of the exposure bythe use of a sharp hook and scissors and then its edges aresecured to the dural edges using small hemostatic clips(Fig. 6C). It is then opened caudally and rostrally using amicrobayonet forceps and sharp microscissors. It is im-portant to keep the arachnoid edge secured to the duraledge with hemostatic clips so that when the dura is closedthe subarachnoid space is maintained and adhesion of thedura to the spinal cord is prevented. In patients undergo-ing nucleus caudalis lesions, the posterior inferior cer-ebellar artery is almost always encountered and careshould be taken to avoid injury to this impor-

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Figure 6. A, a laminectomy performed using the Midas Rex AM-8 and S-1 drills. B, opening of the dura. C, opening of the arachnoid.


15


tant vessel. This is especially important in patients whohave undergone a previous retromastoid craniectomy formicrovascular decompression of the fifth cranial nervefor tic douloureux, in whom scarring and thickening ofthe arachnoid can obscure the vessel.

Once the arachnoid is satisfactorily opened, any ad-herent structures over the dorsal root entry zone shouldbe dissected and retracted. Commonly, multiple serpen-tine vessels located along the intermediolateral sulcusmust be mobilized to allow for the introduction of theDREZ electrode. If bleeding is encountered, a small pieceof Surgicel placed on the vessel is almost always suffi-cient for hemostasis; if the bleeding is significant, bipo-lar coagulation at a low setting is used. The descriptionof the DREZ electrodes as well as the specifics of theoperation for various indications are mentioned later. Ingeneral, the DREZ electrode is placed first into the mostcaudal aspect of the region to be lesioned, and is thenmoved stepwise in cephalad direction. This allows theneurosurgeon to visualize the upper dorsal rootlets as aguide. The electrode is placed into the entry zone at thesame angle as the dorsal root, i.e., approximately 45°.The electrode is placed into the spinal cord to a depth of2 mm, at which point the insulating collar prevents fur-ther ingress. Lesions are made at 75°C for 15 secondsusing the radiofrequency generator. The lesions are madeat 1-mm intervals along the entire affected dorsal rootentry zone. The spinal region to be lesioned can be mea-sured, and if the distance is 10 mm then 10 lesions shouldbe made. A comparison of the improvement in pain af-ter DREZ procedures between the earlier patients oper-ated on in the late 1970s and the more recent cases re-veal improved results with a greater number of DREZlesions. Blood vessels which are encountered are gentlyretracted and the electrode slipped into the entry zoneavoiding the coagulation of all except the smallest ves-sels adherent to the DREZ area. The laser has been usedby some neurosurgeons to create DREZ lesions, and theearly clinical reports regarding relief of pain and com-plications appear to be satisfactory. We believe the laserlesion may be more difficult to control because of thelack of detailed laboratory studies, but this may be cor-rected in the future.

After all lesions are made, total hemostasis is ob-tained within the thecal sac and all residual blood isgently irrigated away. The dura and arachnoid arereapproximated in a single layer of continuous 4-0 Vicrylsuture, removing the silver clips gradually as the sutureapproaches the site of the clip to avoid any gaps in thearachnoid closure. Dural tack-up sutures are placed toavoid compression in the event of the development of apostoperative epidural hematoma. A tack-up suture is

placed at each end of the dural exposure between the su-ture line and the adjoining supraspinous or interspinousligament. Central tack-up stitches are also used: two infour-level laminectomies and three in five-level laminec-tomies. These are placed between the dural suture lineand the connective tissue overlying the adjoining jointcapsule in the lumbar and thoracic regions, or to the cer-vical fascia and nuchal ligament in the cervical region.We prefer to place tack-up stitches in all cases, whetherbilateral laminectomies or hemilaminectomies are per-formed. Copious amounts of bacitracin irrigation are usedafter each layer of the wound is closed. The paraspinalmuscles are sutured with 2-0 Vicryl sutures, followed byclosure of the subcutaneous tissue in two or three layersof 2-0 Vicryl sutures depending on its thickness. The skinis then sutured using 4-0 continuous nylon sutures. Weordinarily do not use epidural drains. If drains are usedthey are preferably removed on the first postoperative dayto avoid infection and the development of a cerebrospinalfluid (CSF) fistula.

ELECTRODES AND LESION PARAMETERSThe three types of DREZ electrodes in use at Duke aremanufactured by Radionics who also make the RF lesiongenerator used in the DREZ operation (Fig. 7). The stan-dard DREZ electrode has a lesion tip of 2 mm and is 0.25mm in diameter (Fig. 7A). The caudalis nucleus electrodehas a tip length of 3 mm, a diameter of 0. 25 mm, a 1-mmproximal insulation, and a 2-mm lesion tip (Fig. 7B). Theproximal 1-mm insulation at the base is designed to pre-vent lesioning the ascending spinocerebellar tract whichlies superficial to the trigeminal nucleus caudalis. A newtype of caudalis electrode is made with a 90° angle at thetip to facilitate its use at the higher levels of thecervicomedullary junction (Fig. 7C). The electrodes aremade of a hollow stainless steel tube tapered and pointedat the end with an internal thermister at the tip to measurethe temperature of the lesion. The RF lesions are made at75°C for 15 seconds and this results in a lesion (2 × 4-5mm) which will destroy the upper 5 or 6 Rexed layers inthe dorsal horn. Two postmortem studies have confirmedthe focal nature of the lesions of the Rexed layers. The heatproduced at the tip of the electrode is produced by theradiofrequency current generator. Spinal cordotomy-typeelectrodes are not satisfactory to make DREZ lesions.

BRACHIAL PLEXUS AVULSION INJURYA laminectomy usually extending from C5 to T1 is per-formed, although it is imperative that at least a portionof the healthy roots above and below the avulsion bevisualized to avoid any residual postoperative pain.The intermediolateral sulcus marking the entry

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Figure 7. The various DREZ electrodes: A, standard DREZ electrode. B, nucleus caudalis DREZ electrode. C, El-Naggar-Nashold right-angled nucleus caudalis DREZ electrode.

zone of the avulsed rootlets is readily identified in most casesand is easily seen along an imaginary line connecting theentry zone of the first attached root above and the first at-tached root below the avulsed area. Also, identification ofthe DREZ area on the normal contralateral side helps in iden-tifying the overall anatomy of the area. DREZ lesions arethen placed 1 mm apart extending between the healthy root-lets above and below as described above (Fig. 8).

CONUS MEDULLARIS ROOT AVULSIONSAvulsion injuries of the conus medullaris differ from thosein the cervical region in that usually only one or two lum-bosacral roots are avulsed (L5 or S1). When the conus isexposed at operation, the lumbosacral dorsal roots on ei-ther side can be seen along with the avulsed area on theconus. The dorsal roots on the side of the avulsion mustbe carefully retracted laterally until the avulsed root levelis visualized (Fig. 9).

PARAPLEGIA WITH INTRACTABLE PAINMeticulous dissection of the arachnoidal scarring andadhesions commonly found in these cases is necessary toidentify the DREZ area. Intraoperative ultrasound is alsoused whenever there is a suspicion of the presence of atraumatic syrinx either on clinical, radiological, or surgi-cal grounds. If present, the syrinx should be drained byplacement of a syringo-subarachnoid or syringo-perito-neal shunt in addition to the DREZ lesions (Fig. 10).

POSTHERPETIC NEURALGIAEvoked potentials are very helpful in localizing the re-

sponsible dorsal rootlets as shown below; we find this tobe crucial to avoid incomplete pain relief. Both soma-tosensory evoked potential (SEP) and motor evoked po-tential (MEP) studies are carried out intraoperatively.Anatomic localization is most difficult with the thora-columbar dorsal roots and those dorsal roots originatingfrom the conus medullaris. Careful SEP studies from thepainful areas of the body give a precise dorsal root local-ization, allowing the neurosurgeon to confine the DREZlesions to the involved painful area of the body.

We now routinely monitor somatosensory evokedpotentials intraoperatively. The potential recorded is pro-duced by simultaneous firing of dorsal horn neurons, themaximal discharge being in the spinal cord segment(s) ofentry of the nerve stimulated (Fig. 5). This allows for pre-cise localization of the level for lesion production. Stimu-lating electrodes are placed bilaterally near affected nervesas determined from the preoperative sensory exam, andalso on the contralateral side near the comparable intactnerves. This allows for a comparison of normal with ab-normal signals.

For stimulating the body or the extremities, we usesubcutaneous bipolar needle electrodes; bipolar gold discsare used when stimulating the face. The evoked poten-tials are recorded from the surface of the spinal cord orthe cervicomedullary junction using platinum-irridiummulticontact disc electrodes and also from the depth us-ing the lesion-generating electrode.

The largest amplitude negativity is determined af-ter stimulation of the intact side. The negativity is usu-ally comparatively much reduced or otherwise ab-


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Figure 8. DREZ lesions in brachial plexus avulsion injuries.


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Figure 9. DREZ lesions in conus medullaris sacral avulsion injuries.


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first and wired or plated into position (labeled C inFig. 6). The nasal bone and cribriform plate are usu-ally the most solid structures to work with. The medialcanthal ligament also has to be reattached, which canbe done easily through a small drill hole. Next, a pieceof bone is fashioned to form the orbital roof. This is animportant structure which must be solidly placed (Fig.


Figure 10. DREZ lesions and drainage of a traumatic spinal cyst in cases with intractable pain due to spinal cord injury.


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normal on the affected side. We have found that in manyinstances after DREZ lesions are produced, the negativewave is replaced by a positive one. This positive potentialgenerally signals the volume-conducted approach towardthe electrode of neural activity, but without neuronal dis-charge at the electrode site. This positivity, then, providesfor an immediate feedback on the technical success ofthe operation.

NUCLEUS CAUDALIS DREZ LESIONINGThe DREZ lesions are made using the special caudaliselectrodes described above. The special design of theseelectrodes takes into account that the caudalis nucleus liesbeneath the surface of the cervicomedullary junction.Therefore, the electrode tip is 3 mm in length and 0.25mm in diameter, with a proximal 1 mm insulated area anda distal 2-mm lesion tip. The RF lesions are made alongthe same line as the cervical dorsal root entry zones overa distance of 15-20 mm from the level of the C2 dorsalrootlets to the tuberculum cinereum of the medulla at alevel slightly above the obex. Due to the larger cross-sec-tional diameter of the nucleus caudalis, two rows of RFlesions are made 1 mm apart using the same parametersof 75°C for 15 seconds. The first row of lesions begins atthe level of the dorsal rootlets of C2 and is extended ceph-alad to 5 mm above the obex. The second row begins atC2 but just dorsal to the exit of the rootlets of the spinalaccessory nerve (Fig. 11, middle and lower left).

Currently, we perform a unilateral limited exposureof the nucleus caudalis. This is associated with less post-operative pain and earlier ambulation. It involves a para-median skin incision (Fig. 12A). The incision is carrieddown to the subcutaneous tissue, cervical fascia, andtrapezium muscle using electrocautery. The semispina-lis capitis muscle is then split at the point of emergenceof the greater occipital nerve (Fig. 12B). The rectus capi-tis posterior minor muscles are divided at their insertionon the posterior tubercle of C1 and reflected upward.The rectus capitis posterior major is retracted downwardand laterally using a Leyla retractor (Fig. 12C). A uni-lateral suboccipital craniectomy with removal of the ip-silateral half of the arch and whole tubercle of C1 isthen performed. The ligamentum flavum between C1 andC2 is also removed (Fig. 12D). The C2 lamina and themuscles attached to C2 are left intact. The dura and arach-noid are then opened as discussed previously. The le-sions are made using the right-angled nucleus caudalisDREZ electrode (Fig. 13A), which provides a better angleto target the lesion on the nucleus caudalis (Fig. 13B).The lesions are made starting above the C2 rootlets inline with the DREZ area of the spinal cord in the inter-mediolateral sulcus proceeding upward until the C1 root-lets are encountered. The lesions are then made into the

trigeminal tubercle between the border of the cuneatetubercle and the emerging cranial roots of the accessorynerve (Fig. 13C). Only one row of lesions is made. Fa-miliarity with the bilateral exposure of the nucleuscaudalis is advised prior to performing the unilateralexposure.

COMBINED NUCLEUS CAUDALIS-NUCLEUSSOLITARIUS DREZ LESIONINGThe exposure is the same as for nucleus caudalis DREZlesioning. After arachnoid dissection, standard nucleuscaudalis DREZ lesions are made; then two lesions aremade to destroy the nucleus solitarius in the floor of thefourth ventricle 1 mm above the obex and 1 mm lateral tothe midline on the side of the pain (Fig. 11, middle). TheRF lesions are made using the straight nucleus caudaliselectrode, thereby avoiding injury to the overlying cra-nial nerve nuclei. Transient bradycardia and a slight dropof the blood pressure may occur during lesioning. Theuse of 0.5-1 mg of atropine intravenously will prevent thevascular changes which are due to the proximity of theafferent input from the carotid body into the ventral por-tion of the nucleus solitarius. The combined nucleuscaudalis and solitarius lesions give good pain relief inpatients with head and neck cancer, especially those withposterior pharyngeal and esophageal pain.

POSTOPERATIVE CAREPostoperative care is the same as for laminectomy patients.We prefer, however, progressive ambulation of the patientsdepending upon the clinical condition. Patients who un-dergo conus medullaris DREZ lesioning or lower thoracicprocedures are nursed in the flat position for three to fourdays followed by progressive ambulation. Patients withupper thoracic, cervical, and caudalis DREZ surgery arekept with the head of the bed up 30° for three days fol-lowed by progressive ambulation. Steroids are continuedin the postoperative period for three days followed by rapidtapering over three to four days to avoid the deleteriouseffect of steroids on wound healing. Analgesics are lim-ited to those necessary to control postoperative pain.Parenteral narcotics for 24-48 hours are used followed byoral codeine or oxycodone for a few days. We prefer notto give narcotics in high doses for extended periods oftime to be able to assess the results of surgery.

COMPLICATIONSPostoperative complications are in the order of 3-5%,including CSF leakage and postoperative epidural he-matoma formation, in addition to ipsilateral lower ex-tremity weakness or incoordination, especially follow-ing DREZ lesions in the thoracic cord. Nucleuscaudalis DREZ lesioning can be especially compli-

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Figure 11. Nucleus caudalis DREZ lesions using a bilateral exposure. Nucleus solitarius lesions are also shown.


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Figure 12. Unilateral exposure of the nucleus caudalis.


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Figure 13. Precise location of lesions of the nucleus caudalis.


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cated by upper and/or lower extremity ataxia, usuallyresolving in a few days. Cerebrospinal fluid leakage canbe prevented by having a tight dural closure and nursingthe patient in the appropriate position postoperatively.In nucleus caudalis DREZ operations we almost invari-ably place a dural graft at the time of closure to avoidundue tension on the dura, which in turn allows for abetter, tighter closure. Epidural hematomas can be pre-vented by having a dry field prior to closure in additionto the use of tackup stitches as mentioned above. Rou-

tine antibiotics are not used; however, if signs of infec-tion develop, we obtain blood cultures as well as woundcultures followed by the administration of broad spec-trum antibiotics until the final results of the cultures areobtained. Neurologic deficits in the form of ipsilateralor bilateral upper and lower extremity weakness can beavoided by careful monitoring of evoked potentials aswell as downstream electromyographic recording in ad-dition to thorough adherence to the above mentionedprinciples of lesion making.

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OPHTHALMIC SEGMENT ANEURYSMSARTHUR L. DAY, M.D.

PERTINENT ANATOMYThe ophthalmic segment (OphSeg) is the longest sub-arachnoid portion of the internal carotid artery (ICA). Itbegins below the level of the anterior clinoid process atthe point where the ICA penetrates the dura to enter thesubarachnoid space and ends at the origin of the posteriorcommunicating artery (PComArt) (Fig. 1). Removal ofthe anterior clinoid process (AC) to expose the proximalportion of the OphSeg reveals an ICA segment that liesbeneath the subarachnoid space and outside the cavern-ous sinus. This portion, known as the clinoidal segment(ClinSeg), is limited superiorly by the dural reflectionsfrom the medial roof of the anterior clinoid process to-ward the optic nerve and canal that mark ICA entry intothe subarachnoid space, a point known as the dural ring(DR). Inferiorly, the clinoid segment is bordered by a thinlayer of periosteum, bridging from the ICA to the oculo-motor nerve (carotid-oculomotor membrane (COM) ormembranous ring), that separates this segment from thevenous wall of the cavernous sinus.

Two named branches arise from the OphSeg, both ofwhich typically originate just above the dural ring. Theophthalmic artery (OphArt) usually arises from the dor-sal or dorsomedial ICA surface. Several perforating ves-sels also arise from this segment, the largest of which hasbeen named the superior hypophyseal artery (SupHypArt).These perforators typically arise from the medial or ven-tromedial ICA surface. Their ventromedial origin, togetherwith the gentle downward slope of the dural ring posteri-orly, often places the SupHypArt origins on a horizontalplane below the level of both the anterior clinoid processand OphArt.

Ophthalmic segment aneurysms are divided hereininto two large categories, depending on association of theaneurysm neck with the named arterial branches withinthe segment. Aneurysms arising in clear relation to theophthalmic artery are termed OphArt aneurysms (Fig. 2).These lesions arise from the ICA just distal to the originof the ophthalmic artery, and initially project dorsally ordorsomedially from the carotid surface toward the lateralhalf of the optic nerve.

Other aneurysms originating within this segment in-variably incorporate the perforating branches to the hy-pophysis and are herein called SupHypArt aneurysms(Fig. 3). Small SupHypArt aneurysms usually arise fromthe inferior or inferomedial surface of the ICA just oppo-site and slightly distal to the origin of the OphArt. Theselesions may remain lateral to the sella, burrowing beneathand medial to the ICA under the anterior clinoid process.Because the space beneath the carotid is limited, how-ever, most larger lesions will eventually expand mediallyor superomedially above the diaphragma sellae into thesuprasellar space.

PATIENT SELECTIONThe typical patient harboring an OphSeg aneurysm is afemale in her mid-fifties who presents with a subarach-noid hemorrhage (SAH) or visual changes, or whose an-eurysm is discovered incidentally. If bleeding has oc-curred, surgery is performed on the earliest day possiblefollowing the hemorrhage, as long as the patient is not apoor medical risk or has not sustained significant and ir-reversible brain injury.

Approximately one-half of symptomatic OphSeganeurysms are giant lesions presenting with visual loss.The high frequency of OphSeg lesions reaching large orgiant proportions without bleeding is probably explainedby their reinforcement by adjacent structures, such as theoptic nerve or dura of the lateral sellar wall and cavern-ous sinus. Lesions presenting with mass-related symp-toms are often much larger on computed tomography thanthe angiographically apparent lumen size would suggest,indicating a significant incidence of partial luminal throm-bosis.

Because 40-50% of patients with one OphSeg lesionalso have at least one other intracranial aneurysm, thesurgeon often must decide which lesion bled. SmallSupHypArt lesions that remain purely paraclinoid have avery low rate of hemorrhage compared with those at otherlocations, and asymptomatic lesions are often best treatedconservatively unless intervention is planned for otherreasons. Larger aneurysms, or those with medial supra-sellar extension, appear to bleed with higher frequency.

If intervention is planned, the ideal treatment of© 1992 The American Association of Neurological Surgeons

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DAY : OPHTHALMIC SEGMENT ANEURYSMS

Figure 1. Paraclinoid anatomy. A, lateral view (schematic) with theclinoid intact. The three paraclnoid segments of the ICA can be iden-tified, including the intracavernous segment (CavSeg), the clinoidalsegment (ClinSeg), covered by the anterior clinoid process (AC), andthe ophthalmic segment (OphSeg). The OphSeg begins just proximalto the OphArt origin and ends at PComArt. Note the posterior bend ofthe ICA just beyond the ophthalmic artery (OphArt) origin, which isusually obscured by the AC. ON = optic nerve; SupHypArt = superiorhypophyseal artery; PComArt = posterior communicating artery;AChorArt = anterior choroidal artery; CavSin = cavernous sinus. B,lateral view (schematic) with the clinoid removed. The dura overlying

and reflecting from the medial surface of the AC delineates theparaclinoid segments. DR = dural ring; COM = carotid-oculomotormembrane (also called membranous ring); OSt = optic strut. In mostinstances, the OphArt and SupHypArt arise from the OphSeg, abovethe dural ring. C, dorsal view (schematic) with the anterior clinoidintact. Note the medial-to-lateral curve of the ICA that actually beginsjust beyond the anterior bend of the CavSeg. The SupHypArt perfora-tors usually arise from the inferomedial surface of the OphSeg as theICA curves laterally. The right ON has been retracted superiorly toexpose the OphArt origin. Occasionally, both or either branch mayarise from the ClinSeg, beneath the dural ring. Pit = pituitary gland.

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Figure 2. Typical anatomy of ophthalmic artery aneurysms. A, a largeophthalmic artery aneurysm (schematic, lateral view, clinoid intact). Notethe position of the optic nerve (ON) and the sharp angulation of its supe-rior surface (arrow) against the edge of the falciform ligament. Note alsothat the anterior clinoid process (AC) limits the view of the proximal an-eurysm neck and the origin of the ophthalmic artery (OphArt). DR = du-ral ring; OphSeg = ophthalmic segment; AN = aneurysm. B, a large OphArtaneurysm (schematic, dorsal view, clinoid intact). Note the medial dis-

placement of the lateral aspect of the optic nerve. The ON often creates agroove in the superomedial surface of the aneurysm, and its position re-stricts medial extension of the AN across the midline until late in theclinical course. FalcLig = falciform ligament. C, a lateral arteriogram ofa typical large OphArt aneurysm. Note that the lesion originates just be-yond the OphArt takeoff and projects largely dorsally, above the bend ofthe carotid artery. As the lesion expands, the superior restriction imposedby the overlying optic nerve tends to close the carotid siphon.

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Figure 3. Typical anatomy of superior hypophyseal artery aneurysms. A,a small superior hypophyseal artery aneurysm. 1, lateral view (schematic).The aneurysm (AN) arises ventromedially above the dural ring (DR), op-posite the ophthalmic artery (OphArt) origin, and appears to project intothe cavernous sinus. The AN lies partly below the level of the anteriorclinoid process (AC) but is still within the subarachnoid space. ON = op-tic nerve. 2, anteroposterior (AP) view (schematic). The AN projects ven-tromedially above the DR toward the lateral sellar wall. SupHypArt =superior hypophyseal artery; Pit = pituitary gland. B, a larger superiorhypophyseal artery aneurysm. The lesion size now exceeds its ventralconfines and expands into the suprasellar space below the optic nervesand chiasm. 1, lateral view (schematic). Note that the AN projects bothdorsal and ventral to the OphSeg of the ICA, and its lumen is widelysplayed. The SupHypArt drape over the aneurysm’s superior surface, whilethe posterior communicating artery (PComArt) is displaced posteriorlyand laterally. The AC limits the view of the ventral and medial aspects of

the aneurysm neck. Note also that the AN does not sharply angulate theoptic nerve at the falciform ligament. 2, AP view (schematic). Note thetwo bulges at the aneurysm, one ventrally at the site of aneurysm origin.and the second into the suprasellar space. To totally obliterate this lesion,the ventral bulge (arrow) lateral to the sella must be incorporated in theclip down to the dural ring. C, a giant superior hypophyseal aneurysm,dorsal view (schematic). Note the suprasellar extension beneath the chi-asm, with the pituitary stalk (PitSt) displaced and allowing extension acrossthe midline. D, a lateral arteriogram of a typical large SupHypArt aneu-rysm. In this projection, the AN balloons both above and below the pro-jected course of the ICA, which appears to run through the aneurysmlumen. The part of the aneurysm below the ICA represents the initialventral origin, whereas the suprasellar extension lies superior. The ca-rotid siphon appears to open as the lesion enlarges, due to the bulge be-neath and medial to the ICA. Note that the region of the typical OphArtorigin is independent of the aneurysm.


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OphSeg aneurysms is clipping, with preservation of theinternal carotid artery and its branches. Major risks ofsurgery include blindness, stroke, or inability to com-pletely secure the aneurysm neck. With proper exposureand a firm understanding of parasellar and vascularanatomy, however, most of these lesions are clippable, withlow risks to the brain or visual apparatus. Carotid ligationshould be considered a secondary alternative, as the risksof stroke are higher from parent vessel sacrifice, the vi-sual system is not as effectively decompressed, and com-plete thrombosis of the aneurysm is not ensured.

PREOPERATIVE PREPARATIONBleeding from OphSeg aneurysms is managed in the samefashion as SAE from aneurysms in other locations, usingsuch measures as bedrest, calcium channel blockers, hy-dration, ventricular drainage (when indicated), steroids,and anticonvulsants. Prophylactic antibiotics are given toall patients when they enter the operating suite and arecontinued for 24 hours.

Preoperative bedside testing of visual fields is oftenoverlooked in the SAH patient, but should be dutifullyperformed in those harboring large or giant OphSeg an-eurysms. The early visual sign of an OphArt aneurysm(an inferior nasal field cut) is often not noted by the pa-tient. Establishment of this visual field loss pattern notonly documents the deterioration preoperatively, but also

provides key knowledge to the surgeon about the anatomylikely to be encountered in the operating room.

SURGICAL TECHNIQUE

Anesthesia and MonitoringThe ispilateral cervical carotid region should be unen-cumbered by any anesthetic equipment. If temporary clip-ping of the ICA is anticipated, intravenous barbituratesare administered until burst suppression is achieved onelectroencephalography (EEG) and are continued untilpatency in the carotid system is restored. Blood pressure,monitored with an indwelling radial artery catheter, isgenerally maintained at normal levels. Continuous evokedpotential and EEG monitoring is also utilized, and theblood pressure is elevated during ICA clipping if focalchanges are noted. Spinal drainage is not utilized rou-tinely.

Operative Positioning and DrapingThe patient is placed in the supine position, with the headelevated above the heart to promote good venous drain-age (Fig. 4). The patient’s head is turned 45° toward theopposite side, with the vertex lowered, to allow gravita-tional distraction of the frontal and temporal lobes fromthe skull base. A shoulder roll is used to minimize distor-tion of the cervical carotid bifurcation.

Figure 4. Operative position and craniotomy exposure (schematic). Thearrow points to the “keyhole,” marking the external surface of the sphe-

noid ridge. The carotid incision is draped into the operative field but isnot opened in most instances.


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The head is draped to permit visualization of the fron-tal and temporal regions from the midline to below thezygoma. For giant lesions, especially those with calcifi-cations or luminal thrombosis, the cervical region is alsodraped to allow sterile access to the carotid bifurcationfor proximal control or bypass source as desired.

Operative ProcedureThe skin incision for craniotomy extends from the mid-line to the zygoma, one finger’s breadth behind the hair-line (Fig. 4). An incision is also marked over the cervicalcarotid bifurcation, paralleling the anterior margin of thesternocleidomastoid muscle, but is not opened in mostinstances.

The temporalis fascia is sectioned 1 cm below its skullattachment superiorly, and just posterior to the fat padcontaining the frontal branch of the facial nerve. Thetemporalis muscle with its remaining fascial covering isreflected inferiorly and posteriorly to expose the pterion.A frontotemporal free bone flap is elevated, opening lowenough anteriorly so that 2-3 cm of the posterior frontalfossa floor is exposed. The sphenoid ridge is removedextensively, and a temporal craniectomy is enlarged toallow an unobstructed view of the anterior aspect of themiddle cranial fossa.

Proximal visualization of the carotid and ophthalmicarteries is mandatory for both aneurysm types (OphArtand SupHypArt), and, at this point, a decision is madewhether to remove the anterior clinoid processextradurally. While not always necessary for smaller le-sions, clinoidal removal is frequently required for safeand accurate clipping of large or giant lesions. Withunruptured aneurysms, extradural clinoid removal canusually be done quite safely, without exposing the sub-arachnoid space to bone debris. Generally, and especiallyfollowing SAH, the clinoidal tip is removed intradurallywhile the surgeon simultaneously visualizes the aneurysm,thereby avoiding inadvertent rupture during extraduralmanipulation.

If done extradurally, the posterior roof of the orbitand the lesser wing of the sphenoid bone covering thesuperior and medial surface of the superior orbital fis-sure are removed with a rongeur (Fig. 5). As the base ofthe clinoid process and optic nerve are approached, a high-speed diamond drill is utilized to thin the bone, which isthen fractured away with microcurettes. After the durahas been stripped away from the remaining clinoid tip,the process is grasped with a hemostat, gently rocked freeof any remaining attachments, and removed. Bleeding isquite easily controlled with bone wax, Gelfoam, andSurgicel. This extensive bone removal exposes the extra-dural optic nerve and the clinoidal space, a pocket of vari-

able size (usually <5 mm) that houses an ICA segment(clinoidal segment) below the dural ring but outside themain venous channels of the cavernous sinus. Althoughcovered by thin reflections of periosteum and small venouschannels, the ClinSeg can be freed up from its loose at-tachments, thus providing proximal exposure for tempo-rary clipping if required.

The dura is then opened and reflected to expose theproximal portions of the sylvian fissure. The fissure issplit widely to allow an unobstructed view of the opticnerve, ICA, and aneurysm with minimal retraction.

If indicated and not already performed, the clinoidprocess is now removed intradurally (Fig. 6). After cau-terization, a cruciate incision is made into the dura cover-ing the anterior clinoid process and the optic canal roof.The clinoid process is then carefully thinned and removedwith small rongeurs and a highspeed drill. The removalshould extend laterally to include the medial roof of thesuperior orbital fissure, inferomedially to trim the opticstrut, and superomedially to unroof the optic canal.

Optic nerve displacement, if not already done by theaneurysm, is often necessary to visualize the proximalneck. The falciform ligament should be sectioned beforeany aneurysm dissection is undertaken. This structureforms a knife-like edge against the superior aspect of theoptic nerve, and mobilization of the nerve against it mayfurther increase visual morbidity.

The neck of the aneurysm is now ready to be de-fined. Before beginning the dissection, the ClinSeg shouldbe prepared to receive a temporary clip if the need is an-ticipated. Extradural clinoidal removal requires that theclinoidal dura now be opened from within, thereby delin-eating clearly the dural ring and the clinoidal ICA seg-ment. The dural ring is thicker laterally but thins on itsmedial surface. Its circumferential section allows mobili-zation of the ICA and accurate identification of the OphArtand aneurysm neck. Cervical carotid exposure is a rea-sonable alternative to proximal control within the clinoidalspace, but neither is a substitute for extensive clinoidaland optic strut removal.

The proximal neck of OphArt aneurysms originatesjust distal to the OphArt and can be separated with gentleretraction of the aneurysm base and spreading dissectionwith micro-bayonetted forceps (Fig. 7). The distal neck isusually unencumbered by major branch attachments, butany perforators to the optic nerves, chiasm, or hypophy-sis should be dissected free. Straight or side-angled clips,closed down parallel to the course of the ICA and sparingthe OphArt, satisfactorily secure most OphArt lesions.Clips placed perpendicular to the ICA are often ineffec-tive in collapsing larger lesions and risk avulsion of theproximal aneurysm neck.

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Figure 5. Extradural clinoid removal (schematic). A, the extent of theosseous removal is outlined in the crosshatched area. OC = optic canal;AC = anterior clinoid process; SOF = superior orbital fissure; OSt = opticstrut. B, the operative view. 1, the right frontal and temporal lobes areretracted extradurally to expose and permit removal of the posterior por-tions of the orbital roof back to the sphenoid ridge. The SOF is unroofed,advancing toward the AC and the extradural portion of the optic nerve(ON). 2, the AC is removed with a high-speed irrigating drill until only a

thin shell remains, which is then fractured off the optic strut and detachedfrom the dura. The superior, lateral, and inferior walls of the extraduralportion of the ON are removed carefully. 3, the completed exposure re-veals the clinoidal segment (ClinSeg) of the carotid artery, and the opticstrut (OSt). The cavernous sinus lies posterior, inferior, and lateral to theClinSeg and is covered by the inferior projection of dura from the ACknown as the carotid-oculomotor membrane (COM). DR = dural ring, thepoint where the ICA penetrates the dura to enter the subarachnoid space.


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Figure 6. Intradural clinoid removal, operative view (schematic). A, thedural incision (right pterional frontotemporal craniotomy). The sylvian fis-sure has been opened widely, and the frontal and temporal lobes retracted.The dotted lines mark a cruciate dural incision overlying the anterior cli-noid process (AC), with an additional limb sectioning the falciform liga-ment (FalcLig) to untether the optic nerve (ON). OphArt = ophthalmic ar-tery; SupHypArt = superior hypophyseal artery; ICA = internal carotid artery;ACA = anterior cerebral artery; PComArt = posterior communicating ar-tery. B, the AC, roof, and lateral wall of the optic canal, and adjacent orbital

roof have been removed. The clinoidal segment (ClinSeg) has been ex-posed, covered by the thin dura medial to the AC. The dural ring (DR)surrounds the ICA and marks its entrance into the subarachnoid space. Thecarotid-oculornotor membrane (COM) covers the cavernous sinus (CavSin).The oculomotor nerve (III ) can be seen through the COM, in the wall of theCavSin. Bleeding is usually due to small venous tributaries that traverse thearea and is easily controlled with pledgets of Gelfoam and gentle suction.Extensive removal of the optic strut (OSt) provides enough exposure ofthe ClinSeg to permit temporary ICA clipping if necessary.


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SupHypArt aneurysms project medially and inferi-orly, just distal to the dural ring (Fig. 8). Small SupHypArtaneurysms may be initially hidden from the surgeon bythe overlying ICA and anterior clinoid process. In largeand giant varieties, the ICA is displaced slightly laterallyand superiorly toward the surgeon, and the neck of thelesion often appears so wide and long that the entire ca-rotid wall appears incorporated into the aneurysm. AsSupHypArt aneurysms enlarge, their walls become ad-herent to the dura of the sella, diaphragma, and lateralcavernous sinus wall. Although the arteriogram may sug-gest otherwise, these lesions rarely if ever project into thecavernous sinus, and the walls of the two structures canbe separated. By carefully adhering to the dural ring sur-face, the part of the aneurysm wall that bulges beneaththe clinoid process is separated from the clinoidal dura,thus freeing up the proximal neck.

The hypophyseal stalk may be adherent to the poste-rior and medial surface of larger SupHypArt lesions. Theposterior communicating artery or its thallamoperforatingbranches are often draped over the distal end of the aneu-rysm, and these vessels must be carefully identified, sepa-rated, and preserved.

SupHypArt lesions are usually best obliterated witha fenestrated clip whose blades pass over and then runparallel to the ICA, spanning the distance between thePComArt and the dural ring. Although the OphSeg per-forators (superior hypophyseal arteries) do not generallysupply brain parenchyma, some reach the optic chiasm,and every attempt should be made to spare them from thesurgical clip. Visual loss, either unimproved or somewhatworsened following surgery, can perhaps be caused byinterruption of these vessels. The pituitary stalk receivesblood supply from both sides, however, and endocrinedeficits secondary to unilateral interruption of thesebranches are rarely noted.

When large, both types of lesions (OphArt andSupHypArt) tend to be associated with arteriosclerosis inthe carotid artery and/or adjacent aneurysm neck. Broadnecks are commonplace and are best secured by placingthe clip parallel to the parent (ICA) vessel. The bulk ofthese aneurysms and the thickness of their necks oftencause the initial clip to slip downward and partially ob-struct the parent artery lumen. A second clip, applied more

distally on the neck and in the same direction as the first,is often helpful in keeping the neck and aneurysm col-lapsed. If placement of the first two clips results in a com-promised ICA lumen, a third clip is applied distal to thesecond, and the original clip is removed. This process isrepeated until wide carotid patency is ensured. The aneu-rysm is then opened and its contents evacuated withoutbleeding. The entire aneurysm wall does not need to beremoved, but the visual apparatus must be thoroughlydecompressed.

Some OphSeg lesions may be judged “unclippable”because of marked calcification within their walls. Usingbarbiturate anesthesia and temporary ICA clipping, thelaminated calcific walls are removed through an incisioninto the aneurysm interior. The resultant neck is much morepliable and accepting of the clip, with less risk of parentvessel compromise by fractured or displaced calcificationor atheroma. A hemostat may occasionally be used to fa-cilitate creation of a surgical neck, but this instrument mustbe applied distal enough so as not to injure the parent ves-sel. Debris should be irrigated thoroughly from the parentvessel before final clip placement.

Because of their superior or medial projection, smallOphSeg aneurysms can often be clipped from a contralat-eral approach between or behind the optic nerves. OphArtaneurysms are much easier to clip from a contralateralapproach than are SupHypArt lesions. This capability maybe quite important when deciding which side to treat firstin a patient harboring bilateral lesions, one of which is anOphSeg type. In general, the craniotomy should be doneon the side of the symptomatic aneurysm. The surgeonmay then choose to explore the opposite carotid artery,with plans to obliterate the contralateral lesion if feasible.Attempted clipping of large or giant OphSeg lesions froma contralateral approach should be avoided except in emer-gent situations.

Once the aneurysm is clipped and aspirated, thedura is closed, including the opening over the anteriorclinoid process. The clinoid often incorporates an ex-tension of the sphenoid sinus, and the residual boneedges must be inspected and carefully sealed withmuscle, bone wax, or acrylic to prevent cerebrospinalfluid leakage. A drain is left in the epidural space, andbrought out posterior to the skin incision through a

Figure 7. Ophthalmic artery aneurysm clipping (right side, sche-matic). A, exposure (see also Fig. 6B). The falciform ligament(FalcLig) is sectioned before any aneurysm manipulation is under-taken. AN = aneurysm; ON = optic nerve; OphArt = ophthalmic ar-tery; SupHypArt = superior hypophyseal artery; PComArt = poste-rior communicating artery; ClinSeg = clinoidal segment; OphSeg =

ophthalmic segment; DR = dural ring; OSt = optic strut. B, definingthe proximal neck with microforceps dissection and suction-retrac-tion. C, defining the distal neck. D, clip application. A side-angledclip has been placed parallel to the long axis of the ICA. The AN isthen aspirated and carotid artery patency inspected.

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Figure 8. Superior hypophyseal artery aneurysm clipping (right side,schematic). A, exposure (see also Fig. 6B). AN = aneurysm; ON =optic nerve; OphArt = ophthalmic artery; SupHypArt = superior hypo-physeal artery; PComArt = posterior communicating artery; ClinSeg= clinoidal segment; OphSeg = ophthalmic segment; DR = dural ring;OSt = optic strut. B, defining the proximal neck with microforcepsand suction-retraction. Separation of the ventral AN bulge from thedura adjacent to the DR is often aided by circumferential section of

the dura alongside the ring. C, defining the distal neck. D, clip appli-cation. A right-angled fenestrated clip is passed over the broadenedcarotid wall and carefully placed parallel to the ICA, with the fenes-tration reconstructing the parent vessel lumen. The butt of the clipmust spare the PComArt, while the tips are advanced to the ventralborder (arrow) of the DR. The AN is then aspirated, and carotid pa-tency confirmed. If possible, the SupHypArt should also be spared, asthey may provide critical blood supply to the ON or chiasm.

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Figure 9. Clinoidal segment aneurysm (schematic). A, AP view. Theaneurysm (AN) arises below the dural ring (DR) and erodes throughthis membrane to enter the subarachnoid space medial and usuallyanterior to the ICA. AC = anterior clinoid process; ON = optic nerve;COM = carotid-oculomotor membrane. B, operative view, right side.Removal of the optic strut (OSt) is essential to gain access to theaneurysm neck, which usually originates just above the COManteromedially. Note that the clinoidal segment (ClinSeg) is not avail-

able for proximal arterial control, and cervical exposure may be veryuseful. Circumferential section of the DR is required to allow pas-sage of a fenestrated clip around the ICA. The clip tips are then ad-vanced as far proximally as to obliterate the neck, using great care toavoid injury to the cranial nerves within the cavernous sinus. Bleed-ing can be easily controlled with gentle Gelfoam or Surgicel pack-ing and suction. III = oculomotor nerve within cavernous sinus wall;OSt = optic strut.


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separate stab wound. When the frontal sinus is violatedby the craniotomy, the mucosa should be removed, andthe space packed with Gelfoam soaked with an antibi-otic. The sinus is then obliterated with acrylic and in ques-tionable cases is oversewn with periosteum. The bone flapis then anchored in position, and the temporalis muscleand skin are closed in traditional fashion.

POSTOPERATIVE CAREPatients are thereafter managed according to their pre-senting symptoms. Patients with an unruptured aneurysmare mobilized the following day, with rapid normaliza-tion of medications and fluid intake. SAH patients withhigh vasospasm potential are hydrated aggressively forthe duration of their risks.

COMPLICATIONS AND THEIRMANAGEMENTTransient or fixed postoperative hemibody deficits maybe an indication of carotid compromise and occur withhigher frequency in patients with a calcified or partiallythrombosed aneurysm with atherosclerosis within the ICAwall. Digital subtraction arteriography can be useful inthe operating room or immediately postoperatively whenparent vessel patency or embolization is questioned.

Visual deterioration after surgery may occur if theoptic nerve, already distorted medially and superiorly bythe underlying aneurysm, is further manipulated againstthe falciform ligament. Perforator sacrifice may harm the

blood supply of the optic nerve and chiasm.Postoperative diplopia may be due to either an ab-

ducens or oculomotor nerve paresis. When the dural ringis opened, these nerves lie in a relatively superficial posi-tion within the wall of the clinoidal space. They may bedisturbed within the cavernous sinus either by clinoid re-moval or by the clip blades as they are advanced proxi-mally beyond the aneurysm neck.

Aneurysms may arise from the clinoidal segmentand may be quite difficult to differentiate from OphSeglesions (Fig. 9). These aneurysms probably account forsome lesions formerly termed ophthalmic aneurysmswhich at surgery were “unclippable” or ruptured cata-strophically. ClinSeg aneurysms probably represent casesin which the OphArt or SupHypArt arises from theclinoidal rather than the ophthalmic segment of the ca-rotid artery. As the space beneath the dural ring is lim-ited, these lesions may eventually erupt through the durainto the subarachnoid space, where they appear along-side the ICA and resemble OphSeg aneurysms. Proxi-mal exposure is much more difficult to obtain in theselesions, as the dural ring does not define its proximalextent. Clinoidal segment aneurysms are often adherentto the undersurface of the anterior clinoid process andoptic strut, and extradural clinoidal removal may causepremature aneurysm rupture before proximal or distalvascular control has been established. If this type of an-eurysm is anticipated, proximal ICA exposure in thecervical region is essential.

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CHRONIC SUBDURAL HEMATOMAJAMES E. WILBERGER, JR., M.D.

INTRODUCTIONSince first described by Virchow in 1875 as pachymenin-gitis haemorrhagica interna, the pathophysiology andtreatment of chronic subdural hematoma (SDH) has beena controversial neurosurgical topic. Through the years,concepts on the pathophysiology of chronic SDH havebeen reviewed and revised. Similarly, a variety of treat-ments have been advocated—observation for spontane-ous resolution, steroid and osmotic therapy, manipulationof intracranial pressure, radical calvariectomy to collapsethe subdural space, shunting procedures, and exterioriza-tion of the subdural space. Currently, the favored surgicaltreatments for chronic SDH are twist drill or burr holecraniostomy with or without closed system external drain-age of the subdural space. More extensive procedures arenow usually reserved for the 10-25% of patients who donot respond clinically to these treatments. This chapterwill focus on the techniques of twist drill and burr holecraniostomy for chronic SDH.

DIAGNOSISThe incidence of chronic SDH has been estimated to be1-2 per 100,000 population per year with an increasingoccurrence as age advances. Over 50% of patients mayhave no history of trauma and, even in those that do, theinciting incident is often mild and poorly remembered.Predisposing factors have been shown to include advancedage, chronic alcoholism, epilepsy, coagulopathy, and in-tracranial shunting procedures.

Chronic SDH may present in a variety of ways, mak-ing the clinical diagnosis difficult. A frequent misdiag-nosis is “dementia” because the patient is often elderly, ahistory of trauma is missing, and symptoms such asmemory loss and personality change may be prominentand slowly progressive. Chronic SDH can present withacute or slowly progressing focal neurologic signs, mim-icking a stroke or tumor. Other infrequent but well de-scribed presentations include meningismus, seizures, andataxia. Chronic SDH is not commonly associated with

impaired consciousness, but headache may be a veryprominent complaint.

In the era before computed tomography (CT), thediagnosis of chronic SDH was not made until postmor-tem examination in over one-third of patients. Presently,CT is rarely incorrect in confirming or establishing thediagnosis. The typical finding is a focal hypodense len-tiform lesion over the surface of the hemisphere. Occa-sionally, the CT may be unreliable if the SDH is isodensewith the brain. In such situations, use of intravenouscontrast may result in visualization of the vascularizedsubdural membranes, giving indirect evidence of thehematoma’s existence. Magnetic resonance imaging(MRI) can also assist in diagnosis when the CT is “nor-mal” or equivocal. An acute subdural hematoma isslightly hypointense on T1 weighted images and mark-edly hypointense on T2 images. The hypointense signalis due to the presence of deoxyhemoglobin, a strongparamagnetic substance. As the deoxyhemoglobin isconverted to methemoglobin, the T2 image becomes veryintense. When the subdural hematoma becomes chronic,and the conversion to methemoglobin is complete, thehematoma will appear intense on both T1 and T2 im-ages (Fig. 1).

When considering radiographic imaging for chronicSDH, it should be borne in mind that there is no clearcorrelation between hematoma size and clinical symp-toms and signs. Thus, selection of patients for surgicaltreatment should rely more on clinical than on radio-graphic criteria. In addition, a significant finding in manychronic SDH treatment series has been that remission ofthe clinical syndrome may significantly precede radio-graphic resolution of the SDH—an important consider-ation in evaluating treatment results and the need for fur-ther intervention.

PATHOPHYSIOLOGYThe initial stages in the formation of a chronic SDH in-volve a proliferative response to blood in the subdural space.Fibroblasts from the dura invade the area to form both anouter and an inner membrane to “encapsulate” the SDHwithin approximately three weeks of its initial presence.© 1992 The American Association of Neurological Surgeons

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WILBERGER : CHRONIC SUBDURAL HEMATOMA

Theories about the subsequent enlargement of thehematoma have been numerous. For years, it was heldthat an osmotic gradient developed across the membranesand that fluid was drawn into the subdural hematoma.Others have held that fragile neocapillaries within themembranes rupture repeatedly and fill the subdural cav-ity with recurrent hemorrhage.

Recent research has focused on disordered hemostaticmechanisms with increased fibrinolytic activity within themembranes. Following the initial hemorrhage, abundanttissue thromboplastin is released into the subdural space,activating local clotting mechanisms. Thrombin is gener-ated and crossed-linked fibrin is formed from fibrinogen.Clotting activation leads to mobilization of the intrinsicfibrinolytic system. Fibrin is split into fibrin degradationproducts which affect further clot formation. Defective clotformation causes recurrent hemorrhage. As this process isrepeated, the dura reacts to fibrin nonspecifically to gradu-ally form the vascularized outer membrane. As this mem-brane proliferates, the extrinsic fibrinolytic system is acti-vated and a self-perpetuating vicious cycle is repeated. Ithas been postulated that the primary effect of surgical drain-age procedures is to remove such self-perpetuating factorsfrom the subdural space and to allow restoration of normalhemostatic mechanisms.

SURGICAL TREATMENTThe surgical treatment for chronic SDH has evolved fromcraniotomy for radical membranectomy to burr hole andtwist drill drainage of the fluid collection. Given the factthat chronic SDH may resolve spontaneously with com-plete and lasting recovery, it is not unreasonable to treatalert patients who have few signs of cerebral dysfunctionwith repeated clinical and CT follow-up. In those patientswhose clinical symptoms and signs from the subdural fluidcollection warrant intervention, burr hole or twist drillcraniostomy with or without closed system external drain-age has become the preferred initial treatment option.

Twist Drill Craniostomy with External Closed SystemDrainageThis treatment approach should be considered when CTand/or MRI demonstrates subdural fluid of homogenousliquid character without septations and with sufficientthickness (>1 cm) to ensure safety of blind dural perfora-tion. This procedure maybe performed at the bedside un-der aseptic conditions using local anesthesia supplementedby intravenous sedation if necessary (Fig. 2).

The site for drainage is selected based on CT find-ings—placement of the twist drill hole is over the maxi-mal thickness of the SDH. The scalp in this area is shavedto cover an area 3-4 cm in diameter from the selectedtwist drill hole site. After skin preparation with Betadineor other antiseptic solutions, sterile drapes are placed aboutthe site. Xylocaine (0.5% with 1:100,000 epinephrine)infiltration of the surrounding skin is accomplished, a No.15 scalpel blade is used to nick the skin, a 5/8-inch twistdrill bit attached to a hand-powered drill is placed per-pendicular to the skull’s outer table, and drilling is begun(Fig. 2A). Drilling may be continued in a perpendiculardirection or may then be slanted obliquely. Perforation ofthe outer table is appreciated by a lessening of tension onthe drill bit; engagement of the inner table results in abinding of the drill bit and should lead to caution as onlyone to two more turns on the drill are usually needed tobreak through into the epidural space. The dura and outerSDH membrane are then blindly perforated with a sharptrocar or a 14- or 16-gauge needle to enter the subduralspace. Only rarely does a significant amount of subduralfluid escape spontaneously at this point.

A standard ventriculostomy catheter may be usedas the subdural drain. This catheter is modified by cut-ting off the blunt end and adding several side holesalong the shaft to facilitate fluid and particulate drain-age. The stylet is left in the catheter as it is passedthrough the twist drill hole and is removed as soon asthe catheter is in the subdural space to prevent intra-cerebral penetration. The catheter is then directed

Figure 1. MRI appearance of a chronic subdural hematoma.


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Figure 2. Twist drill craniostomy with external closed system drain-age. A, placement of the twist drill hole after the injection of a localanesthetic and the creation of a small stab wound in the scalp. B,

introduction of the subdural drainage catheter. C, tunneling of thedrainage catheter. D, connection of the catheter to an external drain-age system.


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anteriorly or posteriorly for approximately 10 cm depend-ing on the location of the hole in relation to the SDH cav-ity (Fig. 2B). The catheter is then checked for patency byallowing spontaneous gravity drainage of fluid or by as-pirating 15-20 ml of the hematoma. Subcutaneous tun-nelling of the catheter is accomplished after first anes-thetizing the skin for 2-3 cm lateral to the twist drill site(Fig. 2C). A trocar is used to guide the catheter to an exitsite 2-3 cm away from the twist drill site. The catheter isrechecked for patency before connecting to a sterile closeddrainage system (Fig. 2D). All wounds are sutured closedwith 3-0 nylon sutures.

Postoperatively, prophylactic antibiotics—nafcillinand cefotaxime—are given during the time the subduraldrain is left in place. Anticonvulsants are not given rou-tinely unless there is a seizure history. The collection bagof the drainage system is positioned 10-15 cm below headlevel to promote gravity drainage of the subdural fluid.The patient is kept in bed with the head elevated no morethan 30°. Hydration, intravenous and oral, is encouragedto promote brain reexpansion.

Within 24 hours, a follow-up CT scan is obtained(Fig. 3). If the patient’s initial symptoms and signs haveresolved, the CT scan shows substantial reduction (>50%)in the size of the fluid collection, and/or output from thesubdural catheter is minimal or clear, the catheter is re-moved. If these criteria are not met, the catheter may beleft in place for several more days, and CT scans obtaineddaily. Subdural fluid samples are sent daily and on re-moval of the catheter for Gram stains, cultures, and sen-sitivity determinations. If the clinical symptoms and signsare not satisfactorily resolved after two to three days andthe CT scan shows persistence of a significant SDH, al-ternative treatment approaches should be considered.

Burr Hole CraniostomyBurr hole craniostomy holds several advantages over thetwist drill technique: burr holes permit wider visualiza-tion of the subdural space and of the outer and inner sub-dural membranes; hemostatic control of the vascularizedouter membrane can be accomplished; the larger openingpermits freer drainage of thicker blood collections andparticulate matter; the subdural space may be cross-irri-gated between burr holes for more complete emptying ofthe hematoma; brain reexpansion may be directly visual-ized; and, if necessary, the burr holes can be converted toa full craniotomy for further treatment as indicated.

Burr hole craniostomy can be accomplished with lo-cal anesthesia supplemented by intravenous sedation. Sit-ing of the burr holes should be done with two factors inmind: they should relate to the location of the maximalsubdural fluid collection, but skin incisions and hole place-

ments should be able to be converted to a full craniotomywithout compromise of the vascular supply of the scalp(Fig. 4A).

Once the site is selected, the scalp is shaved for 3-4 cm around the area; antiseptic skin preparation is ac-complished and local anesthesia is induced withXylocaine (0.5% with 1:100,000 epinephrine). A2.53.0-cm skin incision is made to accommodate anairpowered cranial perforator and the periosteum isstripped away from the area. A small mastoid retractorcan be used to retract the skin edges. After the burrhole is made, the inner table is removed with a smallcurette or a Penfield No. 1 dissector. Bipolar coagula-tion of the dura is accomplished and a No. 11 scalpelblade is used to incise the dura in a cruciate fashion.The outer subdural membrane is also coagulated andopened sharply. The subdural fluid often runs out orgushes out spontaneously at this point. A small red rub-ber catheter (7 or 9 French) can then be directed intothe subdural space. Warm saline irrigation is carefullyflushed through the subdural space until the effluent isclear and the inner membrane brain surface is visual-ized (Fig. 4B). A subdural catheter and closed externaldrainage system can then be left in place as describedpreviously. Careful hemostatic closure of the skin in-cision with galeal and subcutaneous sutures should beperformed to avoid any bleeding that may gain accessto the subdural space and cause an acute reaccumulationof the hematoma. If the subdural fluid is too thick toevacuate through the burr hole, or septations are en-countered which prevent effective drainage of the sub-dural space, conversion to a full craniotomy is possiblefor stripping of the inner and outer membranes andcomplete evacuation of the hematoma (Fig. 4C).

The postoperative management of patients with burrhole craniostomy is not significantly different from thatdescribed for twist drill craniostomy.

COMPLICATIONS AND TREATMENTRESULTSThe outcome of surgical treatment of patients with chronicSDH is quite variable. A compilation of treatment resultsover the past 30 years yields a cure rate ranging from 39to 100%, a recurrence rate of 1-37%, a rate of neurologicsequelae of 7-32%, and a mortality rate of 0-28%. Suchvariation could not be explained adequately by a differ-ence in surgical techniques alone, but more likely it re-flects varying trends in patient selection and the meansand mechanisms of follow-up.

Comparison of burr hole versus twist drill tech-niques yields somewhat more consistent results, yet 10-25% of patients usually require some form of addi-

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Figure 3. A, CT scans of a chronic SDH immediately after twistdrill drainage. B, 24 hours later with the subdural drain still in place.

C, 4 weeks later showing substantial resolution of the SDH.


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Figure 4. Burr hole craniostomy. A, siting of the burr holes. B, cross-irrigation of the subdural spacebetween holes. C, conversion of burr holes to a full craniotomy.


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tional treatment. When evaluating results of treatment inany given patient, however, as noted previously, it mustbe borne in mind that remission of the clinical syndromeof chronic SDH does not necessarily require radiographicresolution of the fluid collection. Camel et al. found intheir series of twist drill craniostomy treatment that 41 of45 patients (91%) having residual SDH on follow-up CTscan had complete or nearly complete resolution of symp-toms. Similarly, CT scans did not normalize followingburr hole treatment until after three weeks in 92% of casesreported by Richter and after 40 days in 84% of casesdescribed by Markwalder. Thus “recurrence” of the SDHafter twist drill or burr hole treatment must be consideredin light of such findings.

Excluding the need for reoperation, the compli-

cation rate from burr hole or twist drill drainage isquite low. Infection rates range from 1.5% to 4.2%;subdural empyema has been reported in approximately2% of treated patients. Richter reported two epiduralhematomas in a series of 120 patients after burr holeSDH evacuation. Several authors have reported ten-sion pneumocephalus after drainage of the subduralspace.

Burr hole or twist drill craniostomy thus appears tobe a safe and reliable method of dealing with a clinicallysymptomatic chronic SDH. Other more invasive and ex-tensive procedures, however, may be necessary in the fewpatients who are not appropriate candidates for these pro-cedures or who have recurrent or residual clinical prob-lems in spite of this mode of treatment.

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TAILORED TEMPORAL LOBECTOMYUSING SUBDURAL ELECTRODE GRIDS

ISSAM A. AWAD, M.D., M.S.JOSEPH F. HAHN, M.D.

PATIENT SELECTIONPatients with intractable epilepsy where noninvasive tech-niques do not clearly define the zone of epileptogenicityto the mesial temporal lobe structures need further delin-eation of the epileptic zone prior to resective surgery. Inthese cases, noninvasive electroencephalographic (EEG)recording or the presence of a structural lesion may sug-gest basal frontal or lateral temporal epileptogenicity.Especially on the dominant side, these regions cannot beresected safely without tailored mapping.

In the following illustrated text, we describe the tech-nique of insertion of subdural electrodes in the circum-stance where surface recording alone suggests left fron-totemporal epileptogenicity (interictal epileptiformactivity and seizure-onset EEG data) but does not defineit further to the mesial temporal structures. The strategyfor electrode implantation is designed to allow coverageof basal frontal areas, lateral frontotemporal structures,and basal temporal structures. The electrodes are subse-quently used to map interictal and ictal-onset epileptiformactivity. Subsequent extraoperative stimulation using theseelectrodes defines areas of cortex involved in speech func-tion (zones of Broca and Wernicke). A tailored temporalresection is then designed to accomplish maximal resec-tion of epileptogenic tissue, while sparing eloquent re-gions of brain involved in speech function.

The general techniques of subdural electrode inser-tion and brain mapping may also be used in extratemporalregions of the brain, or in cases where a structural lesion(i.e., neoplasm, vascular malformation, etc.) is locatedadjacent to eloquent brain.

PREOPERATIVE PREPARATIONAnticonvulsant therapy is titrated to levels near the toxicrange prior to the insertion of subdural electrodes. In-travenous antibiotics aimed to cover the skin flora (i.e.,

oxacillin, vancomycin, etc.) are administered at the timeof skin incision for electrode implantation and are con-tinued prophylactically until electrode removal and re-section of the epileptogenic tissue. The patient wouldhave donated autologous blood two to three weeks priorto surgery and/or would have been typed and screenedfor possible blood transfusion. Partial thromboplastintime, prothrombin time, and bleeding time are checkedpreoperatively to rule out coagulopathy which may berelated to chronic anticonvulsant use.

SURGICAL TECHNIQUE

Operative PositioningThe patient is placed in the supine position on the operat-ing table; the head is extended 45° and rotated 60° awayfrom the operative side (Fig. 1). It is helpful to place thehead at the “foot” of the operating table to provide moreknee room for the sitting surgeon and to allow the anes-thetist or nurse to raise or lower the operating table at therequest of the operating team. The head is fixed in thedesired position using a Mayfield head clamp or otherskull fixation device. The whole head is shaved becausemeticulous scalp hygiene will be required in view of theexiting electrode cables. The presence of hair near theelectrode exit sites will invariably interfere with propercare and hygiene at these sites.

Draping and Skin IncisionA skin incision is marked to allow wide exposure of po-tential areas of brain resection. Because the precise ex-tent of the zone of resection is not known at this time, alarge frontotemporal incision is generally performed.Draping should allow exposure of not only the skin inci-sion but also sites of potential cable exit. Because of this,the scalp is prepared in a wide area beyond the proposedincision. Otherwise, draping is performed as for a routinecraniotomy.© 1992 The American Association of Neurological Surgeons

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Figure 1. Patient positioning for frontotemporal insertion of subdural electrodes.

Implantation of Subdural ElectrodesThe skin is incised through the galea aponeurotica, andRaney clips are applied to both edges of the scalp. Thescalp is reflected in the subgaleal plane, preserving at-tachment of the underlying temporalis muscle to the cra-nial bone for subsequent osteoplastic craniotomy. Osteo-plastic bone removal (with a muscle nutrient pedicleattached) is thought to minimize the risk of flap infectionin the setting of chronically implanted subdural electrodes.If a free bone flap is elevated, consideration must be givento maintaining this bone in a sterile fashion in a freezeruntil removal of the subdural electrodes and final replace-ment of the bone.

The scalp is reflected in the subgaleal plane and isheld anteriorly and inferiorly using fishhooks (Fig. 2).The temporalis muscle is then incised in the line of theproposed osteoplastic flap, making sure to preserve a vi-able vascularized muscle pedicle inferiorly. Three burrholes are placed, one at the pterion, one in the posteriortemporal area, and one in the posterior frontal area. Theseare connected using a power craniotome, except inferi-orly where the bone is rongeured under the preservedmuscle pedicle (Fig. 2). This facilitates elevation of theosteoplastic flap and its reflection inferiorly along thetemporalis muscle pedicle.

The dura mater is tacked to the edges of the surround-ing craniotomy using 4-0 Nurolon sutures. The dura materis opened in a C-shaped fashion and flapped anteriorly(Fig. 3). Prior to dural opening, if the brain appears tense,

intravenous mannitol is administered in the dose of 1 g/kg, in addition to ensuring hyperventilation to a pCO

2 of

25-30 mm Hg. The dural opening should allow exposureof the inferior frontal regions and the lateral temporal lobe.

The selection of subdural grids, including size andnumber of electrodes, is dictated by the areas of the brainto be covered. Subdural electrode grids consist of stain-less steel (or platinum for magnetic resonance imagingcompatibility) discs embedded in a sheet of Silastic, typi-cally 1 cm apart. These are available through several com-mercial manufacturers. In the particular instance beingdescribed, a 4 × 4 grid is used to cover the basal frontalregion (orbitofrontal cortex). A large 8 × 8 grid is usedto cover the lateral frontotemporal neocortex, and thisis folded inferiorly to cover the inferior temporal andfusiform gyri. Another two 1 × 4 strips of electrodes areinserted transversely under the temporal lobe to coverthe anterior and posterior basal temporal areas (Fig. 3).

Wound ClosureAdditional mannitol may be infused intravenously toensure continued brain relaxation prior to dural clo-sure. The dura mater is closed in a watertight fashionaround the electrode cables using 4-0 Nurolon sutures(Fig. 4). The suture is passed in purse-string fashionaround the electrode cables for maximal watertight ef-fect. A piece of Gelfoam is placed around the site ofcable exit from the dura mater. The osteoplastic flap isreplaced and kept free-floating or fixed loosely using


51

AWAD AND HAHN : TAILORED TEMPORAL LOBECTOMY USING SUBDURAL ELECTRODE GRIDS

Figure 2. Elevation of an osteoplastic bone flap.


52


Figure 3. Insertion of subdural electrodes. The choice of size and num-ber of electrode grids depends on the areas of the brain to be covered. Inthis particular instance, a 4 × 4 electrode grid is used to cover the basal

frontal regions (orbital frontal cortex), an 8 × 8 grid is used over thelateral frontotemporal convexity, and two 1 × 4 strips are placed trans-versely to cover the basal temporal area.

Figure 4. Wound closure including watertight dural closure around the cable exit sites. The cables are tunneled subcutaneously andare brought out via a separate scalp incision.



53


temporalis muscle sutures. The cables are brought out viathe posterior burr hole and are tunneled subcutaneouslyto a separate stab scalp incision from which they exit. Atthe site of skin cable exit, 3-0 Nurolon sutures are usedonce again in a purse-string fashion to ensure a water-tight closure. The scalp is then closed in two layers usinginverted interrupted 2-0 Vicryl sutures for the galea apo-neurotica and interrupted 3-0 Nurolon sutures for the skin(Fig. 4).

BRAIN MAPPINGFollowing electrode implantation, the patient is nursed ina critical care unit for 24-48 hours. Throughout this pe-riod, close attention is paid to the serum electrolyte val-ues, ensuring a sodium level greater than 140 mEq/dl.Frequent infusions of mannitol or other diuretics and strictfluid restriction are adopted. Inappropriate antidiuretichormone secretion and other factors may induce signifi-cant brain edema during this critical period, necessitatingremoval of the subdural electrodes. We have not encoun-tered the need to remove electrodes because of brainedema in any patient maintained on strict fluid restrictionand where the serum sodium concentrations were main-tained in an elevated range. Intravenous dexamethasoneis also administered at a dose of 4 mg every six hours.Two to three days following electrode implantation, fluidrestriction may be eased as tolerated, and the steroids aretapered. The patient is transferred to a special epilepsymonitoring unit where the anticonvulsant medications aregradually tapered for the first phase of brain mapping.

This first phase of brain mapping will consist ofinterictal and ictal-onset monitoring of epileptiform ac-tivity. The special monitoring unit is equipped with video-EEG capabilities for real-time correlation of seizure symp-tomatology with EEG phenomena. Monitoring ofepileptiform activities is continued until suff icientinterictal abnormalities are recorded and mapped and untilseveral of the patient’s typical seizures have been recorded.This phase of the monitoring typically lasts 5-10 days.

Following this, the serum anticonvulsant levels aregradually titrated once again to near-toxic ranges, in prepa-ration for cortical stimulation. The second phase of brainmapping will consist of stimulation of each of the subdu-ral electrodes in a systematic fashion, to map eloquentbrain regions. This is performed in the epilepsy monitor-ing unit in an unhurried fashion, with retesting performedas needed to ensure accurate localization of frontal andtemporal speech areas. The location of the electrodes iscorrelated closely with surface landmarks as noted intra-operatively and as documented by intraoperative draw-ings and photographs. Each electrode is stimulated dur-ing wakefulness starting initially with a current intensityof 1 mA. As long as there are no clinical symptoms orEEG afterdischarge, subsequent trials are used with gradu-

ally increasing amperage. If there are no symptoms orsigns with stimulation at a maximum of 15 mA or at am-perage just below the afterdischarge threshold, then test-ing is repeated for reading or speech interference.

Information gathered from recording and electricalstimulation will consist of delineation of zones of maxi-mal interictal epileptiform activity, seizure-onset epilep-tiform activity, and eloquent cortical regions (Fig. 5). Aplan of resection is then designed to excise a maximalextent of epileptogenic brain, while staying at least 1 cmaway from eloquent brain regions.

In the particular case illustrated here, epileptiformregions are noted in lateral and basal temporal areas. Thesecan be resected just close to but not including the tempo-ral speech area (Wernicke’s area). Electrical stimulationmay induce speech interference near the temporal tip andin the fusiform gyrus (basal temporal speech area). Re-section of these areas (non-Broca, non-Wernicke) has notbeen associated with any untoward sequelae.

In addition to cortical stimulation, evoked potentialstudies of the lateral cortical plate may be performed todefine the rolandic fissure (as per standard neuro-physiologic techniques). Other specialized studies of

Figure 5. Results of cortical mapping in a hypothetical case. Frontaland temporal speech areas have been delineated by cortical stimulation.Prolonged monitoring has revealed a zone of interictal epileptiform ac-tivity, and another zone of seizure-onset epileptiform activity. Theplanned resection (dashed line) will include maximal excision of theseepileptogenic areas while sparing mapped eloquent brain regions.


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Figure 6. Tailored temporal lobectomy. At the second operation, thewound is reopened and the subdural plate is used to guide the planned

resection line. This will extend posteriorly to (but not include) the mappedtemporal lobe speech area (Wernicke’s area).

Figure 7. Temporal lobectomy is performed along the planned resec-tion line using bipolar electrocautery and suction. The Cavitron ultra-sonic aspirator used at low settings is very helpful for such brain inci-

sions. The diagram illustrates the extent of temporal lobectomy as guidedby extraoperative brain mapping.



55


speech and memory and of movement-induced potentialscan be performed as per institutional protocols. The wholeperiod of brain mapping (recording of epileptiform activ-ity and electrode stimulation) usually does not exceed threeweeks (mean, 10 days). Throughout this time, prophylac-tic antibiotic coverage is continued and meticulous scalphygiene is maintained. Leakage at the cable exit sites isnot infrequent during this time. If it becomes excessive,additional purse-string sutures at the cable exit sites maybe placed at the bedside.

REMOVAL OF SUBDURAL ELECTRODES ANDTAILORED TEMPORAL LOBECTOMYThe patient is returned to the operating room followingthe period of brain mapping and is placed once again un-der endotracheal anesthesia. The head is fixed in the sameposition and the areas of previous scalp incision and cableexit sites are prepared and draped according to routineneurosurgical procedures (Fig. 6). The wound is reopenedwith cultures taken from every layer prior to copious an-tibiotic irrigation. At this time, the cable is cut and re-moved (by pulling out) prior to dural opening. The duramater is opened and the cortical surface is once againexamined through the subdural grids, and correlations aremade with previous photographs and diagrams. The pro-posed line of resection is then marked on the cortical sur-face prior to removal of the subdural electrodes (Fig. 6).Basal electrodes are left in place until completion of thebasal resection, for they can be quite helpful in delineat-ing the extent of such resection.

Cortical resection is performed along the proposed lineusing bipolar electrocautery and suction (Fig. 7). TheCavitron ultrasonic aspirator used at low setting is particu-larly helpful in this regard. Following excision of the de-sired portion of the temporal lobe, a decision must be madewhether to also excise mesial temporal structures.

Meticulous hemostasis is ensured. The wound isclosed in layers, including watertight dural closure. A pieceof the osteoplastic bone flap is sent for culture along with

the multiple cultures obtained during wound opening. Thesubdural plates themselves are sent for cultures. The cableexit site is debrided and closed in a single layer. Steriledressings are applied.

POSTOPERATIVE CAREPostoperatively, anticonvulsants are continued at or neartoxic levels, and intravenous antibiotics are maintaineduntil final intraoperative culture results. Frequently (one-third of cases), these cultures reveal bacterial coloniza-tion of at least one layer of the wound or the subduralplates. In this case, intravenous antibiotics are continuedfor 14 days following surgery and are followed by onemonth of oral antibiotics, all aimed against the culturedorganism. This is done even in the absence of any clinicalevidence of wound infection. In the circumstance of apositive bone culture, intravenous antibiotics are contin-ued for four weeks even in the absence of clinical evi-dence of wound infection.

The above aggressive regimen of antibiotic treat-ment of bacterial colonization of the wound has elimi-nated frank wound infections (purulence or meningitis)in the last 80 consecutive cases of subdural electrodeinsertion. Prior to this, wound purulence in the settingof implantation of subdural electrodes was not infrequentat our institution.

OUTCOME AND COMPLICATIONSUsing the above precautions, infection should not be morefrequent with this procedure than with any other neuro-surgical operation. Other complications are related to thearea of cortical resection. As long as the zone of resectionis at least 1 cm away from mapped eloquent areas, wehave not encountered any instances of permanent neuro-logic deficit related to focal cortical function.

Favorable seizure outcome is accomplished in nearlytwo-thirds of patients undergoing this operation. This ishighly dependent on patient selection and other factorsrelated to the etiology and severity of the epilepsy.

56

GUNSHOT WOUNDS OF THE BRAINSUZIE C. TINDALL, M.D.

ALI KRISHT, M.D.

PATIENT SELECTIONMost patients with gunshot wounds to the head requiresurgery. Any depressed fracture due to a penetrating mis-sile is an open fracture and requires exploration, debride-ment, and elevation in order to prevent complications suchas infection or cerebrospinal fluid (CSF) leakage. As pa-tients reach the more serious end of the injury spectrum,decisions regarding surgical intervention become moredifficult, as surgery may have little to offer. We list somecriteria for and against surgical intervention, realizing thateach situation will need individual assessment.

Criteria in favor of surgical intervention:Glasgow coma scale (GCS) 8 or above;GCS 5-8 with good response to cerebral resuscitation;Limited nondominant hemisphere injury;Tangential wounds;Young age.

Criteria against surgical intervention:GCS 3-5;GCS 5-8 with no response to cerebral resuscitation;Extensive dominant hemisphere injury;Brain stem injury;Injuries crossing the midline;Old age;Associated major multisystem injuries.

PREOPERATIVE PREPARATIONPatients with cerebral gunshot wounds are evaluated uponarrival into the emergency facility. In addition to routinetrauma evaluation and care, coma grade and neurologicalfunction are assessed, and measures for cerebral resuscita-tion (intubation, hyperventilation, and mannitol) are insti-tuted if indicated. Entrance and exit wounds are evaluatedand temporary dressings applied. All patients receive teta-nus prophylaxis and broad spectrum antibiotics.Anticonvulsants are administered if there has been obvi-ous cortical damage. Plain anteroposterior and lateral skullradiography followed by noncontrasted CT scanning of the

head completes the preoperative radiological evaluation.

SURGICAL PROCEDUREThe goals of surgery in patients with gunshot wounds tothe head are to remove all devitalized tissue, debris, andhematoma, to control hemorrhage, and to provide duralclosure and scalp coverage.

General endotracheal anesthesia is induced and thepCO

2 is maintained between 28 and 32 torr. Mannitol and

furosemide are used if increased intracranial pressure isbelieved to be a potential problem. The head is widelyshaved. Hair and debris are removed from the irregularedges of the scalp defect. The head is positioned to facili-tate extension of the scalp incision if necessary. For un-complicated superficial wounds, the head may rest softlyon a foam headrest, but for more complicated deep woundsin which brain retractors will be needed a three-point headfixation device is used. The scalp is prepared with a gentlescrub of Betadine soap followed by painting with Betadinesolution. Sterile towels are secured circumferentially witha surgical stapler and cranial drapes are positioned.

Three major objectives are kept in mind when plan-ning the scalp incision:

1. To preserve blood supply to the scalp edges;2. To incorporate the entry and/or exit wounds into the inci-

sion;3. To establish adequate exposure of the limits of fractured

bone and any adjacent structures that might need repair.

We find the simple linear or modified linear inci-sions (Fig. 1A) to be adequate in most injuries involvingthe hair-bearing scalp. For injuries of the forehead, abicoronal scalp incision is used (Fig. 1B). The anteriorbranch of the superficial temporal artery should be pre-served. Such a scalp incision facilitates adequate expo-sure of the frontal cranial base and avoids cosmeticallyunacceptable scars about the face. Raney clips are usedon healthy scalp edges, but clips are avoided on scalp edgesmacerated or injured at the entrance or exit sites.

After completing the scalp incision, the bony defect© 1992 The American Association of Neurological Surgeons

57

TINDALL AND KRISHT : GUNSHOT WOUNDS OF THE BRAIN

Figure 1. A, for wounds within the hair-bearing scalp, the best scalpincision is usually a linear or curvilinear incision centered over the en-try or exit wound. B, for injuries of the face or forehead in which wideexposure of the frontal or anterior temporal fossa may be required, a

bicoronal scalp incision is used. The incision is located behind the hair-line and positioned so as to preserve the anterior branch of the superfi-cial temporal artery if there is potential disruption of the supraorbitalblood supply from the injury.

is widened to expose all edges of the torn dura (Fig. 2A).This can be achieved by craniectomy or craniotomy. Largepieces of bone are kept and soaked in Betadine solution.The dura is opened back to healthy brain all around.

Control of active bleeding is accomplished using bi-polar cautery or clips for very large vessels. Torn venoussinuses are oversewn or patched with pericranium andGelfoam.

The missile track is then explored and debrided. Onehelpful technique is illustrated in Figure 2B. The tip of anAsepto syringe is introduced into the depth of the track,and the wound is irrigated with saline under moderatepressure while the syringe is gently withdrawn. This ma-neuver will deliver debris and small indriven pieces ofbone.

Pieces of bone or bullet fragments still embedded inthe wound may be localized using intraoperative ultra-sound (Fig. 2C). In removing these fragments, the gelati-nous pedicle should be coagulated, cut, and allowed toslip back in the wound as it frequently contains a smallblood vessel that has been previously tamponaded by thebone fragment (Fig. 2D).

If the track is very deep, it is a good idea to set up aself-retaining retractor system to aid in maintaining ex-posure. This helps to keep the track well defined and aidsin obtaining hemostasis deep in the wound.

Bacterial contamination of metallic bullet fragmentsis much lower than that of bone fragments. For this rea-

son and because bullet fragments usually travel to muchgreater depth, we often leave bullet fragments behind.

Necrotic brain, readily identified by its purple colorand soft fragile texture is removed with suction. Hemo-stasis is achieved with bipolar coagulation and gentle tam-ponade with Gelfoam. We try not to leave foreign hemo-static agents in the wound, as we think that they mightserve to increase the incidence of cerebritis and brainabscess. Once all bleeding has been controlled, hemosta-sis is checked by asking the anesthesiologist to increasethe patient’s intrathoracic pressure as in Valsalva’s ma-neuver.

At this stage, the wound is ready to be closed. A peri-cranial patch is used to close the dura (Fig. 2E). Water-tight dural closure helps to prevent CSF leakage or fun-gus cerebri. Sometimes taking a pericranial graft mayprove difficult because of a lack of exposure; in certaincircumstances, attempts at harvesting a graft may furtherthreaten an already tenuous blood supply to the injuredscalp edges. Under such circumstances, graft material maybe taken from fascia lata or other body fascia through aseparate incision.

Whether or not to replace the bone remains a con-troversial issue. If the wound is extremely dirty andcontaminated, the bone is left out and the patientbrought back for cranioplasty in six months; if thewound is relatively clean, large (cleansed) fragmentsof bone or a craniotomy bone flap is replaced and an-


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Figure 2. A, adequate exposure of the injured area is essential. Boneremoval by craniectomy or craniotomy back to normal dural edges isdesirable. B, an excellent technique for removing indriven bone frag-ments and other debris is with gentle warm saline irrigation with anAsepto syringe. C, intraoperative ultrasound is occasionally useful for

localizing residual bone or bullet fragments. D, the gelatinous strandadherent to an extracted bone fragment is best coagulated before it isdivided as it often contains a small vascular pedicle. E, watertight duralclosure helps to prevent CSF leakage and fungus cerebri.


59

TINDALL AND KRISHT : GUNSHOT WOUNDS OF THE BRAIN

chored with nonabsorbable, monofilament, synthetic su-tures.

Scalp closure or scalp coverage is critical in prevent-ing later complications. Routinely, the scalp is closed in asingle layer with interrupted vertical mattress sutures us-ing 3-0 nylon. This prevents placing foreign suture mate-rial in the galeal layer and brings galea and epidermisinto anatomical alignment. The closure should not beunder excessive tension. If simple closure of this type isnot possible, arrangements should be made to adequatelycover the injured area by use of rotational scalp flaps or afree vascularized flap.

SPECIAL SURGICAL SITUATIONSInjuries of the major dural venous sinuses may be diffi-cult to repair. In most cases, a sinus laceration may besimply oversewn. Generous exposure of the injured sinusis mandatory for more severe sinus injuries, where sacri-fice of the sinus would prove potentially detrimental tothe patient. In such cases, the sinus can be patched withpericranium or temporalis muscle. Bleeding can be con-trolled temporarily by digital pressure or occlusion witha No. 7 Fogarty catheter.

Gunshot wounds of the frontal area frequently proveto be very challenging. The face, orbits, and frontal andtemporal fossae may be involved. A generous frontal, andsometimes bifrontal, exposure is required for adequatedebridement and repair. The involved sinuses should beexenterated. Intradural graft repair using pericranium orfascia is very important for preventing eventual CSF leak-

age. Foreign and avascular materials should be avoidedin attempts to reconstruct the bony floor.

Wounds involving the temporal bone area are asso-ciated with a high incidence of vascular injury. Hemor-rhage may be controlled with packing of the external earcanal or indirect balloon occlusion of the involved vesselor sinus.

COMPLICATIONSDisseminated intravascular coagulation may develop atthe time of operation. It is usually first recognized bynoting diffuse oozing of blood at the operative site whichis difficult to control with the usual methods. Laboratoryevaluation will document elevated coagulation times andfibrin split products in conjunction with reduced plateletcounts and fibrinogen levels. The condition is treated withinfusions of fresh blood products, including frozen plasmaand platelets.

CSF leakage may occur in the form of a cutaneousfistula, otorrhea, or rhinorrhea. Hydrocephalus must beruled out, and the leak may stop with temporary placementof a spinal or ventricular drain. If the leak persists, the woundshould be reexplored with adequate dural closure.

Meningitis, abscess, and empyema are possible in-fectious complications. All are treated with appropriateantibiotics, and surgical drainage is frequently necessarywith abscess or empyema.

Subarachnoid hemorrhage from a traumatic aneu-rysm may occur occasionally. Under these circumstances,a cerebral angiogram should demonstrate the lesion.

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INTRODUCTIONThe transvenous therapy for vascular malformations in-volving high- and low-flow shunts is nothing new. SeanMullan and others have been advocates for the incorpo-ration of this route of therapy for various lesions for manyyears. The concept that the arterial side of high-flow fis-tulas needed to be attended to first in the obliteration ofthese lesions virtually eliminated the discussion and useof the transvenous approach to these lesions for decades.The great risk of venous outlet obstruction and thereforemarked increased pressure in the thinly walled veins justdistal to the shunts could very easily result in massivehemorrhage, producing major neurologic deficit or death.This threat and potential outcome has been demonstratedgraphically to occur with transarterial endovasculartherapy for certain malformations when the embolic ma-terial, principally glue, escaped into the venous outlets,solidifying the egress and resulting in major venous out-let occlusion with hemorrhage. However, Mullan’s excel-lent results with the transvenous approach to carotid cav-ernous f istulas continued to stimulate interest in atransvenous approach to various vascular malformations,especially those lesions such as vein of Galen malforma-tions which carry high mortality and morbidity statisticswith the standard surgical and transarterial approaches.

As the burgeoning subspecialty of interventionalneuroradiology continued to grow, various technologiesincluding new thrombolytic agents and particles havemade possible the approach to lesions heretofore unreach-able. The combined interventional and neurosurgical ap-proach to vein of Galen malformations as reported byBerenstein and Epstein demonstrated the utility of thiscombined approach in improving morbidity and mortal-ity statistics. We reported in 1986 the use of the trans-torcular approach for the endovascular treatment of veinof Galen malformations.

Our enthusiasm, because of the initial successes, be-came tempered after a review of 24 patients treated in asimilar fashion revealed many of the problems with thisnew therapy. However, the overall statistics, especially inthe neonate, have prompted continued interest in this tech-nique as an adjunct of therapy for the elimination of cen-tral high-flow fistulas. Of the nine neonates we havetreated with the transtorcular approach, five are alive andthree are virtually normal except for mild spasticity inthe lower extremities. The 15 infants and older childrentreated with the transtorcular approach have fared verywell, with a 50% cure rate angiographically and one death.This death was secondary to an acute shunt malfunctionthree months after transtorcular embolization of the veinof Galen malformation.

TREATMENT CONCEPTSThe general concepts which are important to the under-standing of the utility of the transvenous treatment of veinof Galen malformations remain fairly simple. First, in allpatients the goal is to gradually occlude and thereby elimi-nate the fistula or fistulae such that acute thrombosis withacute venous outlet obstruction does not occur. Variousguidelines and experiences obtained from our series willbe discussed below as to how this goal can be attained.

Second, the goal for transvenous therapy in the neo-nate is to produce a cardiac survivor while maintain-ing neurologic integrity. This goal has often resultedin converting the neonate into a surviving infant with apersistent fistula. There seems to be a delicate balancefor the neonate: the therapist should produce a cardiacsurvivor but not eliminate the fistula completely be-cause of the major risk of venous outlet obstruction,hemorrhage, and death. Again, how this is attained willbe discussed below.

The third concept of major importance in the useof this therapy revolves around the potential for con-tinued, slow, progressive thrombosis after one or moretherapies with the transtorcular route. We have been© 1992 The American Association of Neurological Surgeons

TRANSTORCULAR OCCLUSION OFVEIN OF GALEN MALFORMATIONS

J. PARKER MICKLE, M.D.RONALD G. QUISLING, M.D.

KEITH PETERS, M.D.

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MICKLE ET AL. : TRANSTORCULAR OCCLUSION OF VEIN OF GALEN MALFORMATIONS

tempted in our 15 infants and older patients to considerother therapies to rid the patient of the fistula completely(stereotactic radiosurgery or direct surgery). In two in-stances, we have admitted patients to the hospital forprestereotactic radiosurgery angiograms and have foundin one of these the total obliteration of the fistula sincethe child’s previous angiogram three months prior to thatadmission and a substantial reduction in the flow in theother patient which allowed us to wait to see if continuedthrombosis would occur. We have therefore treated nopatients with adjunctive therapy including surgery or ste-reotactic radiosurgery and have had no patients hemor-rhage or develop other progressive symptomologies ne-cessitating further therapy. The bottom line, however, isthat, as pointed out by Hoffman and others, the prognosisof untreated or persistent vein of Galen malformationstends to be poor. Therefore, once therapy for these mal-formations is undertaken by whatever route, continuedperseverance and careful follow-up are essential for opti-mum outcome.

TECHNICAL ASPECTSThe key steps in the transtorcular approach to vein ofGalen malformations will be discussed. This simple op-eration is rapid and utilizes common materials and in-struments found in all operating rooms and radiologysuites. Various embolic materials such as coils can bedelivered to the vein of Galen malformation complex notonly through the torcular approach but through a directjugular puncture or through the femoral route if accesscan be obtained. The neurosurgeon, usually the primarycare physician in this disorder, has control over whichroute is chosen for the treatment of these malformations.Today, transarterial endovascular therapy combined withtransvenous occlusive therapy would seem to be the treat-

ment of choice for this very difficult group of malforma-tions. The transarterial approach requires the cooperationof an interventionlist trained in microcatheter manipula-tion both on the transarterial and transvenous sides. Inthe neonate, access is often difficult from the transarterialside, whereas the transvenous route, especially thetranstorcular route, is quick and easy. Of course, it is es-sential to obtain high-quality pretherapy angiograms toassess the extent of the lesion and the flow characteristicsnecessitating the therapy. Also, computed tomography(CT) scans and magnetic resonance imaging (MRI) ofthe brain and ventricular spaces are essential beforetherapy. Many of these individuals, especially in the neo-natal group, have pretherapy lesions which can be exten-sive at times and can preclude therapy. Massive encepha-lomalacia is a relative contraindication to any form oftherapy in this disease. Many of these patients have pre-treatment hydrocephalus and this often necessitates shunt-ing procedures as a major form of therapy in the vein ofGalen malformations. Once the transtorcular route fortherapy has been decided upon, the steps as outlined be-low and in the accompanying figures can be carried outrapidly and in repeated sessions to obtain optimum out-comes in the neonate, infant, and older child.

Equipment and TechniqueThe initial surgical therapy is carried out in the operatingroom, and therefore a standard craniotomy set is neces-sary. A C-arm. imaging system is necessary during theprocedure for placement of wires and also during thevenography (Fig. 1). Newer real-time subtraction unitsare available and make following the course of therapymuch easier and more accurate.

A large burr hole is placed over the area of the tor-cular herophili as identified on the angiogram. The ul-

Figure 1. An efficient arrangement of personnel and equipment dur-ing a transtorcular embolization for a vein of Galen malformation isshown. The surgeon and assistant (A and C) are seated, with the nurse(B) and equipment directly behind the patient’s head. The patient ispositioned such that the occiput is close to the edge of the table sothat manipulations with various catheters entering the torcular areunimpeded. The gantry for the C-arm fluoroscopic unit (D) can bemoved easily in and out to obtain high-quality real-time fluoroscopicimages during manipulation and deposition of coils during the proce-dure. It is very important to have the visual monitor (E) directly acrossfrom the surgeon so that all fluoroscopic manipulations can be seeneasily during the procedure. © 1992 The American Association of Neurological Surgeons

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Figure 2. These drawings depict the patient positioning (A), location ofthe incision (×), and the appearance of the torcular through the burr hole(B). The small roll under the right shoulder allows the midline occiputto be parallel with the floor. This makes the approach through the torcu-lar with the various catheters quite simple. If the torcular is not identi-fied clearly after the burr hole is completed, then the craniectomy canbe enlarged with rongeurs to better expose the structure for emboliza-

tion. The ultrasonic scanner can be used to identify the torcular, straightsinus, and aneurysm through this burr hole. Bleeding during the place-ment of the incision and burr hole is minimal, and the dura forming theouter surface of the torcular is thick and resistant to injury. It is notnecessary to place a purse-string suture through the outer layer of duraand this will result in bleeding.

trasound probe is very useful in defining the torcularherophili, straight sinus, and aneurysm (Fig. 2). Thearea of the torcular herophili is tapped with a 25-gaugeneedle to ensure free return of arterialized blood (Fig.3A). A 16-gauge Angiocath is passed through this punc-ture and the soft end of the Angiocath is left in placethrough which a short, soft guidewire is advanced un-der fluoroscopic control into the area of the aneurysm

(Fig. 3, B-D). Under fluoroscopy, an angiography cath-eter or sheath with an attached Tuohy-Borst adapteris advanced over the wire into the area of the aneu-rysm (Fig. 3F). The guidewire is removed and a veno-gram performed through the indwelling angiographycatheter to assess location and flow characteristics.Various methods of measuring pressures and flows canbe uti l ized at this point in the procedure to


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Figure 3. These drawings (A through K) represent the essential steps inthe deposition of thrombogenic wires through the torcular via the straightsinus into a vein of Galen aneurysm. The area of the torcular is tappedwith a 25-gauge needle (A), and brisk bleeding results. Contrast agentscan be injected through this 25-gauge needle if there is any questionabout the location of the penetrating needle. This needle is removed anda standard 16-gauge Angiocath (B) is placed through the same hole intothe straight sinus. The sharp inner needle of the Angiocath is removed,and then the soft outer sheath can be advanced further into the straightsinus (C). Bleeding can be vigorous at this point but is controlled nicely

with an occluding finger placed over the hub of the sheath. A standardsoft guidewire is then placed through the sheath and advanced into theaneurysm under fluoroscopic control (D). The Angiocath sheath is thenremoved while maintaining the position of the guidewire with the aid offluoroscopy. The assistant holds the guidewire in place after the sheathhas been removed (E) and then the surgeon advances a short angiographiccatheter or sheath with an attached Tuohy-Borst adapter over theindwelling guidewire into the aneurysm (F). It is extremely importantto maintain the position of the guidewire safely within the confines ofthe aneurysm during the placement of this catheter.


64


Figure 3. (Continued) The floppy guidewire is then removed and avenogram can now be performed through the indwelling angiographiccatheter (G). A 90-145-cm floppy guidewire (the mandrel was removedprior to surgery) is now advanced through the Tuohy-Borst angiographiccatheter into the aneurysm (H and I). The venogram is performed afterdeposition of this basket (I) and, if needed, Gianturco coils of various

sizes can be deposited on this basket lattice (J) to further reduce theflow and to encourage thrombosis (J and K). An occluding finger isused to control bleeding over the torcular once the angiographic cath-eter has been removed. A piece of Gelfoam is placed over this area andthe skin is closed in a standard fashion (K).


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help outline the therapeutic goal (Fig. 3G). A long floppyguidewire is passed into the aneurysm very carefully inorder to create a basket onto which various sizes of throm-bolytic Gianturco coils are deposited (Fig. 3, H-K); allthis is done under fluoroscopic control. Without the in-dwelling basket the potential for embolization of the coilsinto the general venous circulation is a real threat. At thetermination of the procedure, the catheter is removed anda piece of Gelfoam is placed over the bleeding hole in thetorcular herophili and held for 5 minutes. The skin is closedin layers and the patient is returned to the intensive careunit for observation.

Individual StepsThe positioning of the patient on the operating table isshown in Figure 1. The head is placed in a position withthe sagittal suture parallel to the floor. The right shoulderis usually elevated slightly with a roll. The area of thetorcular herophili should be very close to the edge of thetable so that the table itself is not obstructing the surgeons’hands in their approach. The C-arm gantry and the visualmonitor are brought in from above and in front, respec-tively. The surgeon and assistant are operating as if anoccipital approach is being utilized in the placement of aventriculoperitoneal shunt. Angiographic localization ofthe torcular herophili on the skull is estimated and a 3-4-cm midline vertical incision is marked. Preparation anddraping are standard for a burr hole. A small adjacenttable is draped in a sterile fashion with all the necessaryequipment ready so that when embolization is begun thistable can be rolled to the juncture of the operating tablejust below the position of the child’s head. This instru-ment table is very useful in stabilizing the indwelling cath-eter during evaluation and therapy.

The incision is made down to the skull and the peri-osteum is elevated. Bleeding is minimal. A burr hole isplaced over the torcular and enlarged to 2-3 cm in diam-eter (Fig. 2). Again, bleeding is minimal. The red dilatedtorcular is easily identified from directly over the struc-ture. If ultrasound equipment is available, ultrasonic iden-tification of the torcular, straight sinus, and aneurysm isvery useful in helping the surgeon to decide on the angleof approach to the aneurysm through the torcular. If iden-tification of the torcular is not certain, then a 25-gaugeneedle can be passed easily into the area suspected of beingthe torcular. If bright red blood returns then one can beconfident that this is the area of entry. If no blood is ob-tained then a further craniectomy should be carried out inan effort to identify the torcular. It is important to realizethat a true torcular may not exist and an accessory straightsinus may have to be utilized in approaching these le-sions. In many of the patients, venous outlet obstructionis already a part of the disease process and therefore al-

ternate routes of approach may have to be chosen. Thisposes no great problem, and these routes of entry can beeasily identified on the preoperative angiogram.

Once the torcular is identified, a 16-gauge Angiocathis passed into the hole previously made by the 25-gaugeneedle (Fig. 3B). Brisk bleeding will be obtained throughthe Angiocath and the sharp needle from it can be re-moved easily with advancement of the soft outer portion.Bleeding is brisk but easily controlled with an occludingfinger over the hub of the catheter. Under fluoroscopiccontrol, a soft guidewire is advanced through the catheterinto the aneurysm (Fig. 3D). This distance ranges from 6to 9 cm from the surface of the dura to the anterior sur-face of the aneurysm. Care must be taken not to advanceeven the soft guidewire forcefully into the area of the mostanterior part of the aneurysm and malformation.

Once the wire is in place, the 16-gauge Angiocathsheath is removed. The assistant holds the wire in placeat the level of the dura and bleeding can be brisk at thispoint while the angiographic sheath or catheter is placedover the wire and advanced through the dura and intothe area of the aneurysm (Fig. 3F). The tip of the wireis carefully observed and maintained in its original po-sition during the passage of this catheter so that force-ful impingement does not occur on the anterior face ofthe malformation. Once the catheter is in the aneurysm,the guidewire is removed and the angiographic cath-eter system is flushed with heparinized saline througha side port. A Tuohy-Borst adapter is placed on the endof the catheter so that various therapeutic embolicagents can be placed through the catheter without sig-nificant bleeding.

At this point, the assistant and surgeon can rest be-cause the catheter is in place and there is no further bleed-ing. This is a good point in the procedure to perform pres-sure measurements through the side port of theangiographic catheter and to look at the venous flow pat-terns produced in the malformation with venography. Ourinitial procedure consisted of placing Gianturco coils di-rectly into the aneurysm to produce thrombosis. Thisworked in certain individuals, but in others the flow char-acteristics were so great that the coils themselvesembolized peripherally into the sigmoid sinus and, in oneinstance, into the lung. Therefore, we have modified ourprocedure by placing within the aneurysm anonthrombogenic stainless steel basket constructed froma long stainless steel guidewire with the indwelling man-drel removed (Fig. 3I). This is accomplished easily bycutting off the weld on the end and removing the stoutthin wire with a clamp. This results in the production ofa very floppy wire capable of forming a basket whenplaced within the aneurysm. Through the Tuohy-Borstadapter we advance this guidewire, which may

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range from 90 to 145 cm in length, carefully into theaneurysm. This often results in a major change in thevenous flow pattern within the aneurysm, and in sev-eral instances we stopped the procedure at this pointand elected to return later to deposit thrombogenicwires onto this basket. If a major change in the meta-bolic needs of the patient occurs with this deposition,such as a reduction or elimination of blood pressuresupport, then we suggest that the procedure be termi-nated and further therapy considered later. The philoso-phy is to do as little as is needed to get a therapeuticresponse, knowing that returning later for more therapyis always possible. If we elect to deposit thrombogenicmaterial within the aneurysm we use Gianturco coilsof various sizes and have found that these are easily

deposited within the basket both to produce a changein the flow pattern and to induce thrombosis in a gradedfashion (Fig. 3J).

At the termination of the procedure, the angiographiccatheter is removed and an occluding finger is placed overthe egress site in the torcular. A small pledget of Gelfoamis placed here and pressure applied for 5 minutes. No su-tures are required to obtain hemostasis and the skin isclosed over the Gelfoam pledget in a standard fashion(Fig. 3K). The child is returned to the intensive care unitfor careful observation.

Repeat embolizations can be performed in theneuroradiology suite transcutaneously if needed. In thissetting the procedure takes only a few minutes after anes-thesia is administered.

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DETECTION OF AN EPILEPTIC FOCUSAND CORTICAL MAPPING USING A

SUBDURAL GRIDSUMIO UEMATSU, M.D.

INTRODUCTIONThe goal of epilepsy surgery is to remove the epilepto-genic parts of the brain while sparing critical functions.To achieve this goal, two criteria are essential: preciselocalization of the epileptogenic focus and identificationof areas with critical functions.

To meet these criteria, electroencephalography (EEG)performed directly on the surgically exposed brain(electrocorticography (ECOG)) has been used intraopera-tively. However, the ECOG technique has obvious limita-tions: it must be performed in a limited time and it doesnot allow EEG recording during epileptic attacks (ictalrecording). Accumulated evidence indicates that the mostreliable information for localization of an epileptogenicfocus is obtained from the ictal recording. Epileptiformdischarges not associated with the patient’s habitual sei-zures (interictal discharges) alone are not sufficient. Tocatch and record these habitual seizures, at least severaldays of continuous EEG and video monitoring are needed.Furthermore, the physician has to determine that the re-corded attack is typical of the patient’s habitual seizures.This is best achieved by analyzing video-recorded attacksin combination with the simultaneously recorded EEG(Fig. 1).

Once the epileptogenic area has been localized, thenext task is to identify the functions of the area—mostimportantly, speech and sensorimotor function—since re-section of critical areas may result in significant func-tional impairment postoperatively. Critical functions, par-ticularly speech and language, can be tested for only onfully awake patients. Intraoperative stimulation has beenused for this purpose also, but it is restricted by the lim-ited time available and by patient discomfort, particularlyin children. To overcome the limitations of intraoperativestudies, a technique for subdural implantation of elec-trodes was developed.

The approach allows, if needed, coverage of broad

areas of the cortical convexity as well as the basal hemi-spheric regions and the interhemispheric fissure. In addi-tion to widespread coverage of the cortical surfaces, thesubdural electrodes allow direct, systematic cortical stimu-lation to be performed over a period of days.

However, as the number of electrode contacts requiredin the subdural grid increases for widespread coverage,the cable may become so bulky that skin incision andundermining of the subcutaneous tissue become neces-sary, which raises concerns about potential cerebrospinalfluid (CSF) leakage and infection of the subdural space.Therefore, a variation of the subdural grid technique thatuses a finer, multiple cable (multi-minicable) was devel-oped. The minicable has a 2-mm diameter and can bebrought out through the skin using guiding needle punc-tures. CSF leakage and grid infection have been mini-mized by sealing the burr holes with glue and placingpurse-string sutures at the site where the cable exits fromthe scalp.

Technical details include planning the craniotomy,placing the grid, closing the dura, and closing the crani-otomy wound. The techniques described here for implan-tation and use of the multi-minicable subdural grid al-low localization of epileptogenic areas and mapping ofcortical function.

PATIENT SELECTIONThe indications for grid implantation include:

1. Incapacitating epileptic attacks;2. Failure of medical management of the attacks;3. Attacks originating from one cerebral hemisphere;4. EEG abnormalities adjacent to or within function-

ally critical cortex;5. Discrepancy of location of EEG abnormality and

abnormality seen on magnetic resonance imaging.

Contraindications to implantation are:

1. Presence of active local or systemic infection;© 1992 The American Association of Neurological Surgeons

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Figure 1. Diagram of the epilepsy monitoring system: the video cameraand the computerized EEG simultaneously record the patient’s behav-

ior and brain activity. Electrical stimulation for cortical mapping is car-ried out through the implanted grid.

2. Uncorrectable bleeding tendency;3. Uncooperative or violent behavior of the patient.

Age alone is not a contraindication to grid implantation.The potential risks of the procedure are common to anycraniotomy, such as CSF leakage, infection, or hematomaformation. Every preventive precaution should be takenduring selection of candidates for implantation.

OPERATIVE METHODSTo illustrate the subdural grid technique, the operativedetails of grid implantation for a study of the language-dominant left hemisphere are described.

Preoperative Preparation

Bleeding Time and PremedicationBleeding time must be checked for all patients and shouldbe within normal limits. Prophylactic broad-spectrumantibiotics are given intravenously just prior to the skinincision and are administered daily until the removal ofthe grid. The serum level of anticonvulsant(s) should bechecked 24 hours prior to surgery and should be kept atthe therapeutic level to avoid major tonic-clonic convul-sions in the immediate postoperative period. Double dosesof the usual daily anticonvulsant may be given the nightbefore surgery to make up for anticipated loss of drugsduring intraoperative depletion of body fluid. Dexametha-sone and other antiinflammatory drugs are avoided.

Anesthesia and PositioningEndotracheal general anesthesia is used. The vertex ofthe patient’s head extends out 3 cm from the headboard ofthe operating table. The vertex is tilted down slightly tofacilitate drainage of blood out of the surgical field andto aid in opening of the base of the temporal subduralspace. The head, neck, and chest are elevated by tilting upthe upper half of the operating table about 15°, so that thevertex of the head is above heart level (Fig. 2).

Grid and Operative PlanThe patient’s entire head is shaved. The rolandic line isdrawn on the scalp (details are shown in Fig. 3A). Thesimplified midpoint to meatal (M-M) line, extending fromthe external auditory meatus to the midpoint between thenasion and inion, may also be used (Fig. 3A). After deter-mination of the amount of grid needed to encompass theentire suspected epileptogenic area, including critical sen-sorimotor cortex and language areas, the appropriate num-ber (i.e., one or more) of multi-minicable electrode grids(Ad-Tech Medical Instrument Corp., Racine, WI) are au-toclaved at 270°F (132°C) for 10 minutes just prior toimplantation.

For study over the language-dominant hemisphere,a 6 × 8 contact grid is placed over the lateral convexityof the temporal lobe and cortex superior to the sylvianfissure (Fig. 3C). The 6 × 8 contact grid is 9 cm longfrom anterior to posterior and 7 cm wide. Accordingly,the scalp incision and craniotomy opening should be


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UEMATSU : DETECTION OF EPILEPTIC FOCUS AND CORTICAL MAPPING

Figure 2. A, artist’s view of positioning of a patient for subdural gridimplantation over the left hemisphere. The vertex of the patient’s headextends out 3 cm from the headboard of the operating table. The upperpart of the operating table is elevated so that the patient’s vertex is higherthan heart level. B, the vertex of the head must extend out from the head-

board of the operating table to provide access for subcutaneous tunnel-ling using the Angiocath. C, the vertex is tilted down to allow gravita-tional pull to aid in opening the subdural space at the temporal base. Thetilted-down position of the vertex also facilitates drainage of blood fromthe surgical field.

10 × 8 cm. The extra length (1 cm) allowance around thegrid plate prevents buckling of the Silastic plate.

Surgical Procedures

Skin IncisionAfter the M-M line has been drawn on the head, four pointsare determined: the pterion; the base of the mastoid, 10cm posterior to the pterion; the parietal point, 8 cm supe-rior to the mastoid base; and, finally, the frontal point, 8cm superior to the pterion (Fig. 3B). A line connectingthe four points is drawn, beginning at the pterion and ex-tending to the frontal point, the parietal point, and towardthe base of the mastoid, and ending by curving above andin front the ear. The connecting line forms the so-calledFalconer’s question-mark incision for temporal lobectomy.During the incision, the superficial temporal artery iscarefully preserved to maintain the blood supply to theskin flap. Local anesthetic with 1/200,000 epinephrine isinfiltrated along the outer margin of the incisional out-line and around the superficial temporal artery at the neckof the skin flap.

Burr Holes and CraniotomyBurr holes are made at each of the four corner points, andtwo additional burr holes are also made; one at the mid-point between the frontal and parietal points and the otherhalfway between the parietal and mastoid points (Fig. 3B).The multiple burr holes are connected by cuts made withthe Gigli saw. The temporalis muscle should not be de-tached from the bone flap. The flap is turned outward us-ing the muscle as a hinge (Fig. 4E).

The dura is opened at the base of the craniotomyover the temporal lobe. The incision is extended an-teriorly and posteriorly and is swung superiorly to-ward the vertex; f inally, the dura is reflected towardthe midline.

The arachnoid, vessels, and cortex are inspected. Thesylvian vein and the vein of Labbé are identified. Thesylvian vein, which drains into the sphenopalatine sinusaround the tip of the temporal lobe, and the vein of Labbé,which drains into the transverse sinus at the posterior partof the lobe, are examined by gentle retraction of the lobe.The location of the vein of Labbé is measured from thetip of the temporal lobe.


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Placement of GridFirst the 2 × 8 strip-grid is inserted into the temporal base(see the inset, Fig. 3C). While the anterior quarter of thestrip is held with a bayonet forceps, the wet grid is slippedinto the subdural space as the mid-temporal base is slightlylifted with a brain spatula. The grid is advanced with gentleforce mesially and toward the tip of the temporal lobe.The first (anterior) two electrode contacts reach the tem-poral tip, and the remaining majority of electrodes coverthe fusiform and parahippocampal gyri. The tail end ofthe strip emerges from the middle fossa posterior to thetympanic prominence, crossing the fusiform and inferiortemporal gyri. The strip is anchored to the dural sleeve atthe cross-point with a single fine suture. The 6 × 8 grid isplaced over the lateral convexity of the temporal andfrontoparietal lobes. A slit 2 cm long made between thethird and fourth rows of the grid allows the upper half ofthe grid-leaf to be angled toward the inferior orbital gy-rus and the lower half toward superior temporal gyrus.The grid leaflets straddle the sylvian vein and sphenoidwing. The multi-minicables are directed toward the pos-terior margin of the craniotomy (Fig. 3C). A few looselyplaced stitches are used to anchor the grid to the dura.

Before closure, detailed drawings are made and colorphotographs are taken, with attention paid to the relationof the electrodes to the major cortical sulci and vessels.The sequential relation of the color-coded cables and elec-trode array is confirmed and recorded.

Dural ClosureDural closure begins with suturing at the posterior tem-poral base. The running suture goes around the individualcables and secures the cable with the dural closure. Theanterior and inferior or superior dural gap created by theposterior dural approximation is closed with a dehydratedhuman dural patch (Fig. 4). The closure again starts fromthe temporal base and proceeds toward the lower vertex.This facilitates drainage of subdural blood through thedural opening, which is lower with the head tilted down-ward. The subdural space is irrigated a final time with

normal saline before placement of the last sutures to com-plete dural closure.

Bone Flap and Cable PlacementAfter retaining sutures are placed to anchor the dura tothe periosteum, the bone flap is secured with sutures tiedto the skull through the drill holes. The cables emergethrough the craniotomy gap or multiple burr holes (Fig.5). An epidural Hemovac drain is placed in the anterior-most frontal burr hole, sufficiently remote from the cable.Gelfoam is packed in each burr hole. Medical adhesive isused to fill in the bone gaps created by the craniotomyand burr holes, with care taken to ensure that the adhe-sive does not contact the dura or brain or the epiduraldrain tube, since the adhesive binds with the tubing andwould make its subsequent withdrawal difficult.

In cases with a space-occupying brain lesion, wherebrain may be herniated by the mass or edema, we haveused a Raimondi peritoneal catheter or Raney scalp clipplaced around the craniotomy flap (Fig. 6A) to elevatethe bone flap off the cortical surface and avoid compres-sion of the edematous brain (Fig. 6B).

Percutaneous CablingBefore the skin flap is replaced, each cable is passed sub-cutaneously using an Angiocath 10GA (3.4 mm), 3 inches(7.6 cm). The Angiocath needle puncture is made as faraway as possible from the craniotomy margin—typically2-3 cm is sufficient (Fig. 5).

Purse-string Suture and Skin ClosuresAfter completion of the scalp closure, a purse-string su-ture is placed around the exit point of each cable (Fig. 7).

Postoperative Measures

Surgical DressingThe cable exits are painted with antibiotic ointment. Abundle of a few cables is passed through the opening ofa thick, soft pad (ABD-pad) that is used to cover the

Figure 3. A, estimation of the rolandic and sylvian lines on the scalp,based on cranial landmarks, is shown. First, the halfway point (50%)between the nasion and inion along the sagittal midline of the skull isdetermined; the point 19 mm posterior to the halfway point is the up-per rolandic point. A line is drawn from the upper rolandic point to thelower rolandic point on the sylvian fissure. The lower rolandic pointis found by constructing a line from the perpendicular point to Reed’sline (a line formed by connecting the lower ridge of the orbit to thepreauricular point (Preaur. pt.). The rolandic line is then formed byconnecting the upper and lower rolandic points. The simplified M-M

line can also be used. The line is derived by simply connecting themidpoint to meatus, as depicted in the diagram. B, a question-markincision extends from the pterion to the zygoma just in front of the ear.The superficial temporal artery is preserved to maintain the blood sup-ply to the skin flap. Extra burr holes are needed for multi-minicableexits. C, the upper three rows of the electrode contact (3 × 8) ventralto the sylvian fissure cover Broca’s speech area and the motor-sen-sory cortex; the lower three rows cover the lateral convexity of thetemporal lobe. The second grid (2 × 8) covers the fusiform andparahippocampal gyri.

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Figure 4. The dura is closed with a continuous running suture, similarto the technique used for closure of an arteriotomy (E). Note the duralpatch, which allows the subdural space to expand, thereby minimizingcompression of the arachnoid vessels and fluid space over the cortex.

Eight to ten minicables are individually passed through the dura, burrholes, and subcutaneous tunnels that traverse the midline of the vertex.An Angiocath is used for the passage of each cable through its subcuta-neous tunnel (A-D).


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Figure 5. Sealing the craniotomy opening and burr holes using Silastic medical adhesive. Note thetemporalis muscle on the bone flap.


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Figure 6. A and B, application of a Raimondi catheter or Raney scalpclips around the bone flap is shown. In patients with a space-occupy-ing lesion or edema, the grid may compress the brain. The catheter or

clip elevates the bone flap off the cortical surface and prevents com-pression of the swollen brain underneath the grid.


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Without cushioning, the bone flap collapses, put-ting presure on the cerebral cortex.

Raimondi catheter technique for cushioning the boneflap.

Scalp clip technique for cushioning the bone flap.

B© 1992 The American Association of Neurological Surgeons

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Figure 7. This diagram depicts the path of the cable from the grid overthe cortex and through the dura, skull (burr hole), galea, and scalp. The

burr hole is sealed with Gelfoam and Silastic adhesive. The Gelfoam pre-vents direct contact between the adhesive and the dura.


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surgical wound. Another pad with a slit is used to coveraround the ear, including the area in front of the ear. Asthe cable is held up out of the dressing by an assistant, anadhesive elastic bandage is applied over the skin flap andcable exit area. The tails of the cables are then coveredwith 3 × 3-inch dressing sponges.

Sitting Position and RestraintCertain precautions are unique to this procedure. As soonas the patient recovers from the general anesthesia andvital signs and neurologic condition are stabilized, thepatient is placed in a sitting position, tilted at 45°. Bothhands are restrained by the use of mittens until the patientis transferred to the epilepsy monitoring unit. Routine skullx-rays are taken in the recovery room. The epidural drainis withdrawn on the first postoperative day, and EEG re-cording begins immediately. Stimulation studies are typi-cally begun on the third postoperative day.

Postoperative MedicationsThe same anticonvulsants that the patient took prior tosurgery are administered postoperatively. No steroid oranti-inflammatory medications are given. Moderate an-algesics are given. The patient is given nothing by mouth,with fluid intake restricted for 24 hours. Prophylactic an-tibiotics are continued until the grid is removed.

COMPLICATIONS AND THEIR PREVENTIONThe success of the approach described here is heavilydependent on pre- and postoperative management as wellas intraoperative technique. The discussion is divided ac-cording to these two concerns.

Preoperative and Postoperative ManagementThe use of prophylactic antibiotics has been a subject ofcontroversy. However, we administer a prophylactic anti-biotic (Ancef) until the subdural grid is removed.

CSF leakage along a subcutaneously placed cablecould be a major cause of grid infection. Every possiblemeasure is taken to prevent this. In particular, the postop-erative sitting position discourages CSF leakage along thesubcutaneous cables. The cable should be thin and shouldtravel an extended distance in a deep subcutaneous tun-nel. Use of the finer, multicable system instead of a single,bulky cable system also reduces the chance of CSF leak-age.

Because even a millimeter-thin hematoma membranebetween the electrode and the cortex could interfere witheffective cortical stimulation and EEG recording, everyeffort is made to prevent a hematoma membrane: bleedingtime is checked preoperatively, the head is tilted down dur-ing the grid implant, and the dural opening at the lower

part of surgical field is left open until the end of the duralclosure. These measures allow blood-tinged CSF to drainout through the dural opening. Placement of an active epi-dural drain equipped with a suctioning reservoir (Hemovac)also helps to clear the fluid around the grid.

The pressure dressing using the elastic adhesive ban-dage minimizes subcutaneous bleeding. Shielding thecraniotomy opening and burr holes with Gelfoam andSilastic medical adhesive minimizes the escape ofsubgaleal blood into the cranial space. Watertight closureof the dural opening prevents the blood from running intothe subdural space and thus prevents formation of a sub-dural hematoma membrane. These wound-closure mea-sures for the scalp, skull, and dura minimize CSF leakageand prevent grid infection.

The dressing is changed and the drainage tube is re-moved 24 hours after surgery. Thereafter, the dressing mustbe changed once a week for routine wound inspectionand suture line care.

Intraoperative TechniqueThe proper positioning unique to this procedure is impor-tant. The vertex of the head must extend out from theheadboard of the operating table to provide access forsubcutaneous tunnelling using the Angiocath. I prefer notto use a head fixation device, because the metal arms andpins around the skull make the tunnelling procedure moredifficult.

Our work has shown that motor and sensory areashave considerable individual variation and cover a muchbroader area than is conventionally believed. Using therolandic line (R line) for outlining the craniotomy for gridimplantation (Fig. 3A) helps to ensure that the grid cov-ers the broadest possible cortical area for functional map-ping and localization of the epileptogenic area. We callthe modified R-line that we use the “midpoint to meatalline” (M-M line). The midpoint is the halfway point be-tween the nasion and inion, and the line is drawn from themidpoint to the external auditory meatus.

Autoclaving the grid is probably safer than gas ster-ilization because of the potential for residual chemicals(ethylene oxide) accidentally remaining after sterilizationto cause cortical irritation. Every effort should be madeto reduce surgical blood loss, because the grid procedureinvolves two stages, one for grid implantation and an-other for grid removal, within a short period of time. In-filtration of the epinephrine/local anesthetic combinationaround the skin incision is an effective hemostatic mea-sure. Use of every available hemostatic measure meansthat blood transfusion can be avoided.

The superficial temporal artery should not be ligatedor coagulated and the temporal muscle should

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not be detached from the bone flap, in order to keep thesetissues vital, which helps to minimize surgical wound in-fection. Furthermore, in the event of an infection, maxi-mum antibiotic irrigation of the wound can be achievedby the rich blood flow throughout the tissues.

Although the grid currently available is only a milli-meter thick, it can buckle, and buckling will compressthe cortical veins and the cortex. To prevent buckling, thecraniotomy opening should be 1 cm wider than the gridplate. Use of the dural patch also provides an ample sub-dural space and prevents compression.

Craniotomy using the Gigli saw instead of a high-speed craniotome is preferable. The Gigli saw allows abeveled-edge craniotomy, which prevents the bone flapfrom sinking and compressing the cerebral structures be-neath. The two extra burr holes, one halfway between thefrontal and parietal burr holes and another at the halfway

point between the parietal and mastoid, are necessary ex-its for the multi-minicable.

CONCLUSIONA nonsurgical setting, as opposed to the intraoperativeenvironment, provides comfort and support for the pa-tient and allows EEG recording during the patient’s ha-bitual attacks. Complex speech and language testing canbe carried out with maximal cooperation of the patient.

The potential for infection is a serious concern withany implanted device that has external leads. The surgi-cal technique described here is intended to minimize CSFleakage, thereby reducing the risk of infection. How-ever, it should be emphasized that careful, complete,routine pre- and postoperative antiseptic measures, notjust intraoperative technique, are needed for ultimate re-duction of the risk of infection and for surgical success.

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ANTEROMESIAL TEMPORALLOBECTOMY FOR EPILEPSY

ISAAM A. AWAD, M.D., MSPREM K. PILLAY, M.D.


PATIENT SELECTIONTemporal lobectomy is an accepted surgical treatment ofintractable complex partial seizures for patients in whomthe temporal lobe has been implicated as the site ofelectroencephalographic (EEG) seizure onset. In thesepatients, mesial temporal structures are the commonestsite of abnormal epileptiform EEG activity. Postopera-tive pathologic specimens from epileptic patients com-monly reveal histological abnormalities in the amygdalo-hippocampal region. The extent of mesiobasal resectionin temporal lobectomy has been correlated directly withseizure outcome, with higher rates of seizure controlachieved with more extensive resections of mesiobasaltemporal lobe structures. In this chapter, we describe amodified technique of temporal lobectomy with limitedlateral temporal resection and extensive microsurgicalresection of mesial temporal structures. This operationmay be performed on the left or right temporal lobe with-out mapping of speech areas, since the procedure is de-signed to spare all but the most anterior portion of lateraltemporal lobe cortex.

Candidates for this operation suffer from complexpartial seizures despite optimal medical therapy. The sei-zures are thought to be “intractable,” thereby interferingwith psychosocial function and having a significant im-pact on the patient’s life. Preoperative diagnostic studiesshould include magnetic resonance imaging (MRI) of thebrain, including coronal views, to delineate any structuralabnormalities in the temporal lobe. Other diagnostic in-formation should include prolonged EEG monitoring ofinterictal epileptiform abnormalities and seizure onset.Detailed neuropsychological studies should be performedto define baseline preoperative cognitive and memoryfunction. Any modality-specific impairment should benoted (such as impaired verbal memory in patients withsuspected left temporal epileptogenicity or impaired vi-

sual memory in patients with suspected right temporalepileptogenicity). Intracarotid injection of amobarbital(Wada test) is performed to confirm laterality of speechand memory and to demonstrate that the contralateral tem-poral lobe is able to support memory function.

Patients with unilateral or predominantly unilateralEEG epileptiform abnormalities arising from the ante-rior or anteromedial temporal lobe are selected for theoperation of anterior temporal lobectomy and microsur-gical resection of mesial structures. This operation is con-traindicated in patients with significant contralateral tem-poral pathology and in patients with epileptiform activityarising primarily from lateral temporal lobe structures.Patients with mesiotemporal epileptogenicity and an ad-jacent temporal lobe lesion should undergo this describedoperation in addition to resection of the structural lesion(i.e., neoplasm, vascular malformation, etc.).

PREOPERATIVE PREPARATIONAnticonvulsant therapy is continued through the periop-erative period at or near toxic concentrations. Preopera-tive prothrombin time, partial thromboplastin time, andbleeding time measurements are performed in all patientsin view of possible coagulopathy from prolonged anti-convulsant therapy. The patient would have donated twounits of autogenous blood two to three weeks prior to sur-gery, and/or would have been typed and screened for pos-sible blood transfusion.

SURGICAL TECHNIQUE

Operative PositioningThe patient is placed in the supine position on the op-erating table with the head toward the “foot” of a typi-cal table to provide greater room for the knees of asitting surgeon and to allow the anesthetist or nurse toraise and lower the operating table without disturbingthe operating team. The frontotemporal area is shavedand the hair is combed away from the f ield. The pa-

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tient’s head is extended 45° and turned 60° away from theside of surgery (Fig. 1), and it is fixed in that positionusing a Mayfield head clamp or other skull fixation sys-tem.

The incision is marked as a question mark startingjust in front of the tragus, extending posteriorly above thetip of the ear and anteriorly just above the superior tem-poral line. The incision is extended inferiorly and anteri-orly (along the forehead) enough to clearly expose thepterion when flapped forward (Fig. 2). In most patients,the incision will not extend anterior to the hairline morethan 2 or 3 cm. The proposed incision is marked and theoperative area is prepared and draped according to rou-tine craniotomy techniques.

Operative Procedure

Myocutaneous FlapThe scalp is incised through the galea aponeurotica, andRaney clips are applied on both sides of the incision. Thetemporalis muscle is opened along the line of the incision.The scalp and underlying temporalis muscle are turnedforward as a unit in the subperiosteal plane (Fig. 3). Themyocutaneous flap is dissected anteriorly to expose theorbital zygomatic ridge and inferiorly to expose the zygo-matic root. The myocutaneous flap is held in this positionusing multiple fine fishhooks tethered tensely with rubberbands to a Yasargil Leyla bar attached to the operating table.Such tense holding forward of the flap is essential for sub-sequent bony exposure and intradural visualization.

Bony OpeningA burr hole should be placed on the pterion and an-

other burr hole should be located at the most poste-rior aspect of the incision. These are connected via apower craniotome to elevate a frontotemporal boneflap (Fig. 4). This free bone flap should not exposemore than one or two f inger breadths of the frontallobe but should allow as much of a temporal expo-sure as possible. The key to further steps of this op-eration will consist of subsequent removal of thepterional ridge to allow a very anterior exposure ofthe middle (temporal) fossa.

Rongeurs are used to remove the remaining portionof the inferior squamous temporal bone down to the zy-gomatic root. This should allow exposure nearly flush withthe floor of the middle fossa. Mastoid air cells are fre-quently entered and should be thoroughly waxed. Anteri-orly, rongeurs are used to remove the thin temporal bonecovering the anterior temporal lobe dura. The pterionalridge is thoroughly rongeured and subsequently drilledmedially as far as the superior orbital fissure. At this point,the tip of the temporal lobe should be seen extradurally.Further intradural portions of the operation cannot becarried out without this extensive bony removal of thepterional ridge (Fig. 5).

Lateral Temporal ResectionFollowing the administration of intravenous mannitol(1 g/kg body weight) and insuring that the arterial pCO

2

tension is in the range of 25 to 30 mm Hg, the duramater is tacked to the edges of the surrounding craniotomyand is opened in a C-shaped fashion based anteriorly(Fig. 6). The dural flap is elevated anteriorly and tensedusing 4-0 silk sutures allowing a full exposure of thetemporal lobe tip and the sylvian veins. Any

Figure 1. Patient positioning. The head is extended 45° and rotated60° away from the operative side. The head is fixed in this positionusing a Mayfield head clamp or other skull fixation device.


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AWAD AND PILLAY : ANTEROMESIAL TEMPORAL LOBECTOMY FOR EPILEPSY

Figure 2. Scalp incision. The pterion is marked (two finger breadthsabove the zygoma (B) and one thumb breadth behind the lateral orbitalrim (A)). A question-mark skin incision is marked extending just ante-rior to the tragus at the level of the zygoma, swinging posteriorly above

the tip of the ear and anteriorly just above the superior temporal line.The anterior extent of the incision (on the forehead) should allow ad-equate exposure of the pterion upon anterior flapping of the scalp andmuscle.


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Figure 3. (Top) Myocutaneous flap. The scalp and temporalis muscle areflapped anteriorly and inferiorly as a single layer in the subperiosteal plane.The myocutaneous flap is extended anteriorly to expose the orbital zygo-matic ridge and inferiorly to expose the root of the zygoma.

Figure 4. (Upper middle) Free bone flap. The myocutaneous flap isheld anteriorly using multiple fishhooks which are tethered tensely withrubber bands to a Leyla bar. One burr hole is placed at the pterion and asecond one at the posterior aspect of the incision. These are connectedusing a power craniotome to elevate a frontotemporal bone flap.

Figure 5. (Lower middle) Resection of the pterional ridge. The lesserwing of the sphenoid is resected using rongeurs and then a power drillmedially to the superior orbital fissure. This is essential for subsequentintradural portions of the operation.

Figure 6. (Bottom) Dural opening. The previous pterional resectionshould allow extradural visualization of the temporal tip. The dural open-ing is performed in a C-shaped fashion and is flapped anteriorly.

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temporal lobe tip draining veins should be visualized atthis time, coagulated, and divided.

The lateral temporal lobe resection is accomplishedby connecting three separate corticectomies (Fig. 7). Thefirst or “posterior” cut extends obliquely across the lat-eral temporal surface traversing the middle temporal gy-rus 3.5 cm posterior to the temporal tip. The incision slantsslightly anteriorly across the superior temporal gyrus andposteriorly across the inferior temporal gyrus, and con-tinues transversely on the basal surface of the temporallobe to the collateral sulcus (which separates the fusiformgyrus from the parahippocampal gyrus). This posteriorcut spans across four gyri: the superior, middle, and infe-rior temporal gyri and the fusiform gyrus. The second or“superior” cut extends anteromedially below the sylvianveins just inferior and parallel to the free edge of the lesserwing of the sphenoid. It extends medially to the anteriorclinoid process which should be easily visualized (giventhe adequate bony exposure). These two cortical incisionsare then joined by a third or “inferior” cut across the basalsurface of the temporal lobe. This should totally discon-nect the temporal pole which is removed in one piece.This portion of the operation is performed with a head-light. It does not involve any violation of important sylvianstructures (superiorly) or incisural structures (medially).

Resection of Mesial StructuresThe operating microscope is brought in at this point. AGreenberg or other self-retaining retractor system is set up,and a narrow long blade is chosen. Under the operatingmicroscope, the stump of the temporal lobe is gently ex-plored to locate the tip of the temporal horn of the lateralventricle. This is opened gently using bipolar coagulation,and a long cottonoid patty is slipped into the temporal hornof the lateral ventricle. The long narrow blade of the self-retaining retractor is then inserted over the cottonoid pattywithin the temporal horn. This retractor blade is used toelevate the choroid plexus, thus opening the temporal hornlike a fish’s mouth. This allows identification of the chor-oidal fissure medially and the hippocampal formation inthe floor of the temporal horn. Upon orientation in relationto the pes hippocampus, the remaining portion of theamygdala is removed by suction, making sure not to ex-tend this resection superiorly above the plane of the sylvianfissure (into the caudate nucleus).

Mesial basal resection is completed through three sub-sequent incisions into the mesiobasal temporal structures(Fig. 8). The first or “lateral” cut extends from the lateraledge of the floor of the temporal horn (terminal sulcus) tothe collateral sulcus. The second or “medial” cut extends

in the subpial plane from the choroidal fissure to the tento-rial incisura under direct microsurgical visualization. Thiscut traverses the hippocampal sulcus which separates theparahippocampal gyrus from the dentate gyrus. The arte-rial feeders of the hippocampus (Ammon’s horn arteries)traverse the hippocampal sulcus after arising from the P

2

segment of the posterior cerebral artery; these arterial feed-ers are coagulated and divided. The leptomeninges cover-ing the perimesencephalic cisterns are not violated. Themedial and lateral cuts are extended posteriorly to the pointwhere the tentorial edge curves medially. A third or “pos-terior” cut joins the lateral and medial cuts posteriorly todisconnect the hippocampal formation and allow its removalin one piece. At this point, the tentorial edge should beseen curving medially behind the collicular plate on theposterior aspect of the mesencephalon. During this micro-surgical resection of mesiobasal structures, care should betaken not to use bipolar electrocautery at or near the tento-rial incisura (where the 4th cranial nerve may be injured)or near the petrous apex (where the intratemporal portionof the facial nerve may be injured).

Wound ClosureAfter securing meticulous hemostasis, thorough irriga-tion of the resection cavity is performed. No pieces ofSurgicel or Gelfoam are left intradurally. The operatingmicroscope is removed and intraoperative electrocorti-cography may be performed if this is a part of institu-tional epilepsy protocols. The value of intraoperativeelectrocorticography and further tailoring of the resec-tion has not been proven.

The dura mater is closed in a watertight fashion us-ing running 4-0 Nurolon sutures. The bone flap is fixedin place using 2-0 Nurolon sutures. The wound is irri-gated thoroughly and the temporalis muscle is approxi-mated using interrupted 2-0 Vicryl sutures. The galeaaponeurotica is closed using inverted interrupted 2-0Vicryl sutures. The skin is closed using interrupted 3-0Nurolon sutures behind the hairline and 4-0 nylon suturesin a plastic fashion for any portion of the incision extend-ing anterior to the hairline. Antibiotic ointment is used tocover the incision and a sterile head dressing is applied.The anesthetic is reversed. The patient is allowed to awakenand is examined in the operating room.

OUTCOME AND COMPLICATIONSPerioperative antibiotics are administered at the timeof the skin incision and are continued for 24 hourspostoperatively. These are geared at our institutionagainst the narrow spectrum of staphylococci (van-comycin or oxacillin). The patient is observed for 24hours in a critical care unit. Fluid restriction, dex-

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Figure 7. Resection of the temporal pole. This is carried out through three cortical incisions labeled 1, 2, and 3.


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Figure 8. Resection of mesial structures. A narrow self-retainingretractor blade is used to open the temporal horn of the lateral ven-tricle, allowing adequate exposure of mesial temporal structures atthe floor of the temporal horn. The roof of the temporal horn is care-

fully protected using a cottonoid patty inserted under the retractorblade (in the temporal horn itself). Mesial structures at the floor ofthe temporal horn are then resected using three incisions labeled 1,2, and 3.

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amethasone, and intermittent mannitol are used as pro-phylaxis against brain edema. Not uncommonly, follow-ing left temporal resections, the patient may awaken withnormal speech function but may develop transient dys-phasia several hours after surgery, which may last for oneor two days. Permanent dysphasia is rare following thisoperation. Visual field abnormalities are encountered inless than one-fourth of the patients, and these consist ofincomplete homonomous quadrantic field defects; theyhave been shown to be less frequent and less dense thanfollowing more extensive temporal lobectomies. Other fo-cal neurologic deficits are rare. It is extremely importantto protect structures at the roof of the temporal horn toavoid homonomous hemianopia (optic tract) or hemipare-sis (internal capsule). It is also important to avoid injuryto any structures within the perimesencephalic cistern toavoid cranial nerve or major vascular injuries.

Anticonvulsants are maintained at near toxic levels

and are monitored closely in the perioperative period.Early postoperative seizures not associated with electro-lyte abnormalities or low anticonvulsant levels are amarker for future recurrent seizures. Otherwise, completecontrol of seizures (on anticonvulsants) is expected in 70-80% of the patients. This rate may be affected by preop-erative selection protocols and other patient-related fac-tors. Patients who are seizure-free for one year followingsurgery are likely to remain seizure-free thereafter; sub-sequent seizure recurrence may be related to tapering orlack of compliance with anticonvulsant therapy, and israrely intractable.

Postoperative radiographic verification of the extentof resection (Fig. 9) is performed routinely at our institu-tion. Patients with retained temporal mesial structures aremore likely to have seizure recurrence and may be helpedby reoperation aimed at resection of these residual mesialstructures.

Figure 9. Postoperative T1-weighted MRI performed in the axial planeof the temporal lobe (axial cuts angled along the plane of the sylvian

fissure). This reveals the extent of resection of the temporal pole and ofmesial structures to the collicular level.


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ANASTOMOSIS OF THE FACIALNERVE AFTER RESECTION OF AN

ACOUSTIC NEUROMACHARLES M. LUETJE, M.D.

INTRODUCTIONThe potential for interruption of the VIIth cranial nerveduring acoustic tumor removal is present for any sizedtumor. It is incumbent upon the surgeon(s) to be pre-pared for this event and to be ready to implement animmediate plan of action should it occur. The immedi-ate plan should be that of direct VII-VIIneuroanastomosis or autogenous cable graft interposi-tion VII-VII neuroanastomosis. The plan should not beone of delay, or “inaction,” waiting for a time to per-form a substitution cranial nerve anastomosis.

OVERVIEW OF SURGICAL PROCEDUREThe author’s experience has been primarily with the op-eration of posterolateral craniectomy with translabyrin-thine exposure of the cerebellopontine angle (CPA). Thedetails of the operative procedure will be highlighted fora clearer understanding of the VII-VII neuroanastomosis.It must be clearly understood that this procedure allowsfor the removal of an acoustic tumor of any size.

The patient is supine on the operating table with thehead lying flat on a sheepskin and turned away from thesurgeon. The anesthesiologist is on the same side of theoperating table as the surgeon, with a 5-foot anesthesiatubing running along the other side of the patient, cross-ing over to the machine at the pelvis. Appropriate moni-toring equipment is used for the assessment of VIIth nervefunction and the maintenance of anesthesia.

A large postauricular incision is made just in the hair-line, the ear is rotated forward, and if bone removal is toinvolve removal of the cochlea, the external ear canal istransected and sewn shut. Bone removal is accomplishedwith the air-driven Ototome drill. The mastoid is openedand saucerized widely posteriorly behind the sigmoid si-nus to the dura. The facial recess (bounded anteriorly by

the chorda tympani nerve and posteriorly by the VIIthnerve) is opened, the incus is removed, and the eustachiantube and middle ear are filled with periosteum, fascia,and muscle to prevent postoperative cerebrospinal fluid(CSF) leakage. The sigmoid sinus is skeletonized and re-tracted posteriorly with the Silverstein retractor. The ves-tibular bony otic capsule is removed and the internal au-ditory canal skeletonized in an arc of 180°. The area ofBill’s bar separating the VIIth nerve from the superiorvestibular nerve is identified and the superior vestibularnerve is avulsed from its canal; positive identification ofthe VIIth nerve is made at this point in the operation.

Once this is accomplished, certain key anatomicpoints have been established. These include: 1) bone re-moval from the superior petrosal sinus and middle fossadural plate superiorly to the jugular bulb inferiorly; 2)posterior retraction of the sigmoid sinus; 3) opening ofthe cochlear aqueduct to allow egress of CSF and reduc-tion of intracranial pressure; 4) skeletonization of the VIIthnerve from the posterior aspect through its mastoid por-tion, lateral to the vestibule, toward the geniculate gan-glion, and at its entrance into the lateral end of the inter-nal auditory canal (IAC); and 5) complete exposure ofthe posterior fossa dura as outlined above.

If the cochlea is removed as in the case of tumorswith extension forward and into the tentorial notch, thisstep is accomplished f irst and simultaneously withskeletonization of the VIIth nerve. In essence, the ear ca-nal skin and ossicles are removed, the bony posterior earcanal wall is removed, and the cochlea is drilled away toexpose the carotid artery below the floor of the eusta-chian tube. The VIIth nerve can be skeletonized in an arcof 360° and the dural exposure extended medial to theVIIth nerve, above the jugular bulb, to the carotid artery,anteromedially, inferior to the IAC.

This exposure takes from a little less than twohours to three hours, depending upon the extent of© 1992 The American Association of Neurological Surgeons

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Figure 1. Lifting the divided VIIth nerve out of its bony canal.

Figure 2. Suture anastomosis of the VIIth nerve. Left inset, abdominalfat is used to support the suture anastomosis of the VIIth nerve. Lowerinset, an autogenous cable graft is interposed between the proximal anddistal VIIth nerve stumps.

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aeration of the temporal bone. From the induction of an-esthesia to the operation starting time is approximately30 minutes.

The dura is opened in an apron-shaped fashion andan “extradural” retraction with cottonoids only over thecerebellum is accomplished. The pCO

2 is maintained at

23 mm Hg and the patient is not paralyzed.Tumor removal is posterior first in larger tumors us-

ing the House-Urban rotary dissector to gut the interiorof the tumor, allowing for the development of arachnoidplanes and for the capsule of the tumor to be moved awayfrom cranial nerves, vessels, cerebellum, and brain stem.Once the tumor is gutted, removed partially, and reducedto smaller size, attention is turned to the lateral end of theIAC. Here, previous identification of the VIIth nerve hasbeen made. The tumor is then carefully dissected awayfrom the VIIth nerve using continuous suction and irriga-tion via the Brackmann multifenestrated suction-irriga-tor, the neurotologic scissors, and the insulated Crabtreedissector, both designed for us, the latter of which is at-tached to the Xomed Nerve Integrity Monitor.

The problem of VIIth nerve preservation occurs dur-ing the dissection of the VIIth nerve at its anterior angu-lation out of the IAC. Many tumors spread the VIIth nerveso thinly over the anterior tumor surface that the plane ofdissection can be lost in spite of lateral VIIth nerve iden-tification in the IAC and identification of its zone of exitfrom the brain stem. In fact, a histological plane betweentumor and VIIth nerve may not exist. It is at this site wherethe VIIth nerve is most commonly interrupted both ana-tomically and electrically, intentionally or unintentionally,during total tumor removal.

VII-VII NEUROANASTOMOSISUpon recognition of interruption of the VIIth nerve orthe likelihood of little if any chance of regenerationthrough thin strands of tissue that resemble arachnoid,one must be ready to perform a VII-VII neuroanastomosis.Previous skeletonization of the VIIth nerve during earlierbone removal stages of the operation now becomes anadvantage of the posterolateral craniectomy andtranslabyrinthine operation.

The proximal end of the VIIth nerve is marked witha cottonoid at its root exit zone. The CPA is sealed offwith cottonoids to prevent scattering of bone dust through-out. Bone removal is completed along the thin bone cov-ering the VIIth nerve from the stylomastoid foramen tothe geniculate ganglion using a diamond drill. The sharpangulation of the VIIth nerve from the geniculate gan-glion into the IAC does not allow for 180° of bone re-moval. However, careful diamond drilling techniques cansatisfactorily skeletonize the VIIth nerve, and bone re-

moval can be accomplished without damage to this laby-rinthine segment, allowing removal of the VIIth nerve outof its bony canal (Fig. 1). Brisk bleeding occurs from thevessels in the canal of the greater superficial petrosalnerve. The angled neurotologic scissors can be helpful inseparating the nerve from the ganglion, and Avitene canbe used for immediate hemostasis.

Once the nerve is mobilized, a 7-0 silk suture is firstpassed through the proximal stump of the VIIth nerve atthe brain stem. The suture is then passed through the dis-tal end of the nerve which is gently brought into approxi-mation with the proximal stump (Fig. 2). The first knotshould be a double (“surgeon’s”) knot so the second willhold fast. A piece of abdominal fat (taken for wound clo-sure) and Avitene are used to support the neuroanastomosis(Fig. 2, left inset). The neuroanastomosis can be some-what tenuous, and because the root exit area of the VIIthnerve may be pushed into the brain stem, this support ishelpful and is easy to place.

Rarely is it necessary to obtain an autologous cuta-neous nerve for cable grafting because the length gainedfrom the technique just described is ordinarily sufficient.If it is necessary, a segment of sural nerve from the areajust behind the lateral malleolus of the ankle is obtained.While grossly this nerve may look small, under the mi-croscope it is always much larger than the root exit seg-ment of the VIIth nerve. In this instance, the proximalneuroanastomosis is accomplished first with the techniquejust described, followed by the distal neuroanastomosis(Fig. 2, lower inset).

RESULTSOur patients have exhibited better facial animation re-sults with direct VII-VII neuroanastomosis than with adelayed XII-VII neuroanastomosis. The results producespontaneous simultaneous facial movement, do not re-quire a second operation, and shorten the time of recov-ery compared with a second substitute cranial nerveneuroanastomosis. The results with an interposition au-togenous cable graft are not as good as those with directend-to-end VII-VII neuroanastomosis but are preferablewhen compared with paralysis or XII-VII substitution.

If a patient has undergone a retrosigmoid, standardsuboccipital craniectomy, the VIIth nerve can still bemobilized and a VII-VII neuroanastomosis performed. Thelength of nerve gained from the rerouting described isnot changed because of the surgical exposure. I believethat any surgeon who performs acoustic tumor surgeryshould be prepared for the unfortunate situation of VIIthnerve interruption, intentional or unintentional, and shouldeither perform the VII-VII neuroanastomosis or call insomeone who can.

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