Compressive Myelopathy
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Transcript of Compressive Myelopathy
CME on Spinal cord Diseases Compressive Myelopathy
ByProf .TITO`s Unit
Compressive Myelopathy
Intra medullary
Intradural
Extradural
Extramedullary
Extramedullary Intramedullary
Motor
a)UMN signs Common Late
b)LMN signs
1or2segments at the site of root compression
wide (Ant horn cell)
Sensory
a)Pain Root pain Funicular pain
b)Dissociated sensory loss Absent present
c)Sacral sensation Lost Preserved
d)Joint sensation Lost Late involvement
e)Lhermitte`s sign present absent
Autonamic involvement – Bowel and Bladder
Late Early
Intradural Extradural
Mode of onset Asymmetrical , acute,rapidmalignant
Symmetrical,slow, progressivebenign
Vertebral No Pain and gibbus Pain and Gibbus
Extradural Intradural Intramedullary
SpondylosisDisc prolapseTraumaTumor-Metastasis,multiple myelomaCVJ anomaliesFluorosisTB spineEpidural abscessEpidural haematoma
Tumor-NF,meningioma, lipoma,sarcoma metastasisArachonoiditisSarcoidosisCervical menigitisAVMLeukemic infiltrationArachonoid cyst
SyrinxTumor – ependymoma astrocytoma HaemagioblastomaHaematomyelia
COMPRESSIVE MYELOPATHY – CAUSES (mode compression based)
Spondylosis
• spondylosis is a general term encompassing a number of degenerative conditions– Degenerative disc disease (DDD)– Spinal stenosis–With or without degenerative facet joints–With or without the formation of osteophytes–With or without a herniated disc
• One single component as a diagnosis is rare
Disc degeneration
Annulus Fibrosis
Dehydration of disc
Loss shock absorbing capacity
Articular Facet Hypertrophy
Load ti Posterior elements of vertebra
Prolapse of annulus
Rupture of annulus
Herniation of Nucleous pulposus
Intraforaminal hermiations Posterolateral herniations Central disk herniations
narrow canaldecreased disk heightposterior osteophytesdisk protrusionsbuckled posterior longitudinal ligamentand ligamentum flavumposterior subluxation
Clinical Aspects of Spondylosis:Cervical Spondylosis:
common cause of progressive myelopathycommonly affects at cervical level;C5-C6 disc commonly involved>40yrs;M>FNeck pain,Root pain and LMN signs corresponding to compressionUMN signs and Post colmn involvement below the compression level
Axial compression test Spurling’s test Shoulder abduction relief sign
Lhermitte's Sign(Barber Chair phenomenon) Finger Escape sign
Cervical Spine - AP, lateral, and oblique disk space height Facet statusOsteophyte formation Spinal alignment
MRI SPINElow signal intensity – degenerated discfocal extension of disc material – herniationHerniated disc may extend above and belowLigaments calcification and changing contourOcclude the canalCompress the spinal cord
Conservative:Nonsteroidal anti-inflammatory Tricyclic antidepressants for chronic caseshort courses of collarstretching (traction),dynamic, isometric, strengthening exercises, aerobic exerciseLifestyle modification- low high pillows
SURGERY Indications: Moderate to severe myelopathy
progressive motor/gait impairment Static deficits with significant pain
Anterior Cervical Diskectomy With FusionMultiple – Level Laminectomy
MANAGEMENT:
LUMBAR DISC PROLAPSEAge 20-40 yrs; L4-L5 common siteAcute or chronic Back acheSciatic pain – S1compPostero lateral calf and heel
L5comanterolateral aspect of leg and ankleFemoral pain-L2-L3 to front of thigh
SLR test
Bragaard test
lasegue test
Most of the time it needs Surgery – Fenestration,Laminotomy,Hemilaminectomy,Laminectomy
Manage ment similar to Cer spondylosis
LUMBAR CANAL STENOSIS
Congenital narrowing of lumbar canalL4-L5 commonly affectedCauda equina lesionM>F;40-50 yrsNeurogenic claudicationStoop test positive
Usually surgery needed- laminectomy
CRANIOVERTEBRAL JUNCTION ANOMALIES
1. CONGENITAL MALFORMATIONS
Malformations of occipital boneBasilar invagination, Remnants around foramen magnum,Clivus segmentations)
Malformations of atlasFailure of atlas segmentation from occiput, Atlantoaxial fusion
Malformations of axisAtlantoaxial segmentation failureSegmentation failure of C2-C3Dens dysplasias – os odontoideum, odontoid hypoplasia/apla
ossiculum terminale persistens
2. DEVELOPMENTAL AND ACQUIRED ABNORMALITIES
Foramen magnum abnormalities
ATLANTOAXIAL INSTABILITY
SKELETAL ANOMALIES
NEURAXIAL ANOMALIES
-Foraminal stenosis (eg.achondroplasia ,MPS )
-Secondary basilar
invagination eg.
Paget’disease, osteomalacia, hyperparathyroidism
-Traumatic atlantoaxial / occipitoatlantal dislocation-Degenerative (ligamentous disruption at CV junction)-Inflammatory (RA, ankylosing spondylitis)-Tumours ( chordoma, syringomyelia, NF )-Down’s syndrome
-Platybasia-Basilar invagination ( 10 / 20)
-Klippel-feil anomaly-Occipitalisation of atlas-Atlanto-axial dislocation
-Arnold Chiari malformation-Dandy Walker syndrome-Occipito cervical myelo meningiocoele-Posterior fossa cysts
CV junction malformation Vs Neurological symptoms
Mechanisms:– Bone and soft tissues compress directly on medulla or
upper cervical cord– Associated CNS developmental anomalies – Raised ICT due to impaired CSF flow
Around 20-25 yrs; both sexes Painful or restricted cervical movements Pyramidal signs with varying motor disabilities in
one or mostly all limbs. Muscle wasting in UL;progressive over 5yrs
Cerebellar signs usually;sensory symptoms(lat and Pos)
Neuro vascular symptoms rare. transient reversible weakness may present
CHAMBERLAIN’S LINE -joins posterior tip of hard palate to posterior rim of foramen magnum dense 3.6mm below it-Basillar invagination
McRae’s LINEJoins anterior and posterior edges of foramen magnum: sagittal diameter of foramen magnum. (Avg – 35mm);dense below the line
foramen stenosis
MCGREGOR’S LINE (Basal line)-Joins hard palate to lowest point of occipital boneTip of dens should not exceed 5 mm above this line
FISHGOLD’S DIGASTRIC LINE – paramedian abnormality
HEIGHT INDEX OF KLAUS – dense to tuberculam line < 30basillar invagination
Spinolamellar line – atlas not intersected in ant fusion of atlasatlanto axial dislocation
CLIVUS CANAL LINE – basillar invagination
KLIPPEL FEIL SYNDROME• Congenital fusion of cervical vertebrae• Failure of normal segmentation of the cervical vertebrae/somite
between 3rd and 8th weeks of fetal development (rather than a secondary fusion)
• Incidence – 1 in 42,000 births ;more in females• Autosomal dominant inheritance – C2-C3 fusion. Autosomal recessive –
C5- C6 fusion
FEIL’S TRIAD :1. Low posterior hair line(<L4)2. Short neck3. Limitation of head and neck movements / decreased range of motion in cervical spine
upper cervical spine earlier ageRotational loss and lateral bending is usually more pronounced than loss of flexion and extensionScoliosis, Sprengel deformity/ high scapulapterygium colli - Webbing of soft tissues on each side of the neck ; Assocd torticollis Facial asymmetryCardiovascular- VSD, PDAUrinary tract abnormalities – agenesis of kidney, horseshoe kidney, hydronephrosis,Deafness (absence of auditory canal and microtia)Neurologic deficit- facial nerve Palsy, rectus muscle palsy, ptosis of eye, cleft palate, etc
Cervical spine routine x-ray followed by flexion/extension lateral X-rays. - flattening and widening of vertebrae, hemivertebrae or block vertebrae, instability. MRI with head flexed and extended - subluxation and cord compression
cord anomalies.
Occipitalization of Atlas Atlando Axial Dislocation
Diagnosis- Atlas-Dens interval of more than 5 mm in children and more than 3 mm in adults is diagnostic
Platybasia >135
Arnold-Chiari Malformation
1) Extension of a tongue of cerebellar tissue, posterior to the medulla and spinal cord, into the cervical canal 2) displacement of the medulla into the cervical canal, along with the inferior part of thefourth ventricle
Type I – Cerbellar tonsilar herniation – adult onset,syrinxType II-Part of Vermis, Medulla & 4th Ventricle herniating upto mid cervical region – early ages;ass with mengiomyeloceleRxto do nothingPregessive symptomaticupper cervical laminectomy andenlargement of the foramen magnum
1) Increased ICTheadache,2) progressive cerebellar ataxia, 3) progressive spastic quadriparesis,4) downbeating nystagmus5) cervical syringomyelia6)lower cranial nerves palsieshydrocephalus,
Syringomyelia (syrinx, “pipe” or “tube”)
A chronic progressive degenerative or developmental disorder ofthe spinal cord, characterized by cavitation of the central part of Cervical Canal
Associated with Vertebral and Base of Skull Anomalies90% syrinx ass with Type-I chairy malformation20-40yrs initial ;M=FInsidious onset ,irregular progressive over 5-10yrsPt cant say when disease beganDisease depends on1.cross sectional extent 2.longitu extent.
Classic elements: a) segmental weakness and atrophy of the hands and arms b) loss of some or all tendon reflexes in the arms
c)segmental anesthesia of a dissociated type (loss of pain and thermal preservation of touch)over the neck,shoulders,and arms(cape sensation)
Pyramidal tract: UL : Reflexes preserved or brisk amyotrophy of shoulders and hands spastic
LL: Spastic typePost column,spinothalamic tract involvement laterHorner syndrome can occurUsually have tropic ulcers; vague pain may be presenting feature
BARNETT`s Classification
Syringobulbia : affect the brainstem(medulla ,pons)1. Vestibular nuclei Vertigo & nystagmus2. Nucleus ambiguus dysphagia & hoarseness of voice3. Spinal trigeminal nucleus Analgesia & thermal anesthesia on ipsilateral face (Onion skin pattern )4. hypoglossal nucleus Weakness of lingual muscles & dysarthria
Patho: Gardners hydrodyanamic theory
Inves: MRI with contrast – slow filling cavity ; look other skeleatl manifestationsCT Myelogram; X ray of cervical spine and skull
DD for Dissociated sensory loss:Pseudosyringomyelia-small fib polyneu; DM,amyloia,heriditary sensory,fabrys ant Spinal arte thrombosisPICA
RxType I-surgical decompression of foramen
magnum and upper cervical canal(relieve headache, pain,mildy improve motor sym;ataxia&nystagmus persist
Syringostomy or Shunting by T tube by syringotomyin Type I and some II
Other types – surgery not useful
INFECTIVE EPIDURAL ABSCESS :
Triad – Fever;Midline dorsal pain over spine;progressive limb weakness
2/3 – hematogenous spread 1/3 – extension of a local infection
Lesion mainly – compress venous plexus direct compression
Staph. Aureus is commonStrepto,gram neg bacilli
Inc ESR/CRPMRI; CSF analysisBacterial culture pods <25%
Rx: Decompressive laminectomy /drainage + long term parentral(6-8wk) antibioticweakness several days – not improve with surgery
Cauda equina – antibiotics is enough mostlyEmpiric Abx:Nafcillin plus metronidazole plus either cefotaxime or ceftazidimeVancomycin (1 g every 12 hours) can be substituted for nafcillin
Syndrome of painful root and spinal cord symptoms;patchy motor symptoms
adhesions between the arachnoid and dura
Causes;TB,syphilis,viral & bacterial meningitis,anesthesia,LP
acute or delayed for weeks, months, or even yearsLumbo-Sacral(cauda equina) commonly involvedRoot pain one side next sidereflex changes
motor weaknessspastic ataxia&sphincter disturbance
CSF: moderate lymphocytosis,elev protein – acute stagesometimes normal due to complte block
MRI:loss of normal ring of CSF,loculationsCT myelogram: candle gutter appearance
ManagementSteroids can be triedSurgery if cyst formedPain relieving medications and surgeries
ARACHNOIDITIS
POTT`S DISEASE
skeletal TB spinal is commonCommon in paediatric and adolscence groupDorsal 42% >Lumbar>Dorsolumbar , Cervical
Lesion could beFlorid - invasive and destructive lesion Non destructive - lesion suspected clinically but identifiable by investigations Carries sicca Hypertrophied Periosteal lesion.
Anatomically the lesion could be :Paradiscal - destruction of adjacent end plates Appendeceal (Posterior) - involvement of pedicles, laminae, spinous process Central - Cystic or lytic, concertina collapse Anterior –longitudinal lig Synovitis in post facet
Pathophysiology:xtraspinal source of infection osteomyelitis and arthritis
(anterior aspect of the vertebral body adjacent to the subchondral plate)
spread to adjacent intervertebral disksChild may de direct invasion
bone destruction
vertebral collapse and kyphosis(throcic>lumbar>cervical)
abscesses, granulation tissue, or direct dural invasion
spinal cord compression and neurologic deficits
Kyphotic deformity
Healing by fibrous tissue
bony ankylosis vertebrae.
Paravertebral abscess anterior longitudinal lig
Groin abscess Thoracic abscess
Clinical Features:Back pain is the earliest and most common symptom Duration of symptoms at the time of diagnosis is 3-4 months fever and weight lossPain can be spinal or radicular Neurologic abnormalities - 50%
spinal cord compression with paraplegiaparesis, impaired sensation, nerve root pain, cauda equina syndrome
InvestigationsMantoux;IFN release assays; sputum AFBCXR;Xray Thracolumbar spine;CT spineMRI
X Ray appearancesLytic destruction of anterior portion of vertebral bodyanterior wedging Collapse of vertebral body Reactive sclerosis Intervertebral disks shrunk or destroyed Vertebral bodies may show destruction Enlarged psoas shadow with or without calcification Fusiform paravertebral shadows
MRI
Tb spine with PARAPLEGIA
INCIDENCE 10-30% Dorsal spine (MC) Motor functions affected before /greater than sensory Sense of position & vibration last to disappear
Patho of Tuberculoses Paraplegia
1. Inflammatory Edema –vascular stasis,toxin 2. Extradural Mass – Tuberculous ostetis,abscess 3. Bony Disorder – Sequestra, Internal Gibbus 4. Meningeal changes – ‘dura as rule not involved’ Extradural granulation
–contractcicatrizationperidural fibrosis paraplegia 5. Infarction of spinal cord - Ant spinal artery Endarteritis, Periarteritis,
Thrombosis6. Changes in Spinal cord- Myelomalacic,Syringomyelic change
Seddon’s Classification: GROUP A_-Early onset - in active stage of the disease within first 2 years(active disease - Caseous material, debris, sequestrated disc or bone, internal gibbus, stenosis and deformity can cause compression) GROUP B -Late onset- Usually after 2 years of onset of the disease(Healed disease - Usually internal gibbus and acute kyphotic deformity)
Kumar’s classification(paraplegia) 1 Negligible :Unaware of neural deficit, Plantar extensor/ Ankle clonus 2 Mild :Walk with support 3 Moderate :Nonambulatory, Paralysis in extention,sensory loss <50% 4 Severe :3+ paralysis in flexion/sensory loss>50%/ Sphinters involved
MANAGEMENT:ATT – prolonged pack and surgery
Surgical indications:1. No sign of Neurological recovery after trial of 3-4 weeks therapy 2. Neurological complication during treatment 3. Neuro deficit becoming worse 4. Recurrence of neuro complication 5. Prevertebral cervical abscesses,neurological signs 6. Advanced cases- Sphincter involvement, flaccid paralysis, Severe flexor spasms7.severe neuro deficcit
Surgical techniques: 1. Decompression -Failed response2 .Debridement+/- Failed response after 3-6 fusion months,3 .Debridement +/- Recrudescence of disease DECOMP+/- fusion 4 Debridement+/- Prevent severe Kyphosis fusion 5 .Anterior Severe Kyphosis +neural deficit- Transposition 6 .Laminectomy STS,secondary stenosis, posterior disease 7. Costotransversectomy– in tense paravertebral abscess
VASCULAR – Compressive myelopathy
Epidural Haematoma:predisposing factors:
Anticoagulation therapy,Trauma,Bleeding disorder,tumorAcute focal &/ radicular Pain Acute Spastic paraparesis or conus medularis syndromeSurgical decompression
Haematomyelia: Haemorrhage into the substances of spinal cord
Trauma,parenchymal vascular malformations,vasculitis,tumorsACUTE PAINFUL TRANSVERSE MYELOPATHY – INTRAMEDULLARYsubarachnoid hge can occur MRI; Spinal AngiographyConservative management only
surgery if AVM is the cause
AV Malformation of cord:
Reversible cause of paraparesislocated posteriorly along the surface of the cord or within the duraat or below the midthoracic level
Clinical features:middle-aged manprogressive myelopathy that worsens slowly or intermittently with
periodic remissionsincomplete sensory, motor, and bladder disturbancesmixture of upper and restricted lower motor neuron signsPain over the dorsal spine, dysesthesias, or radicular painsymptoms that change with posture, exertion such as singing, menses
Foix-Alajouanine syndrome - progressive thoracic myelopathy with paraparesis
Investigation:MRI contrast;CT myelogram;Selective spinal angiography
Management: Endovascular embolization of feeding vesselssurgical if ruptured
TUMORS AND COMPRESSIVE MYELOPATHY
METASTASIS:Metastasis is common tumor(high marrow)Epidural type of compression is commonThroacic is common; Lumbar&Sacral – Prostate and ovarianBreast>Lung>Prostate>Kidney>Lymphoma>Plasmacell dyscrasiaold age pt Vertebral pain with acute onset of neurological deficit
MRI – hypodense in T1;doesnot cross the adjacent disc spaceBone scan may be useful to detect the all other metastasis
Management:-Glucocorticoid – upto 40mg/d Dexamethasone-RT – 3000cGy in 15 daily fractions-Surgery- laminectomy or vertebral resection(neuro signs worsen even with RT)
Prognosis:Ambulatory pt – good response with RTFixed motor deficit
<12hr good response>12hr chance to improve >48hr no improvement
Intradural : Benign and slow growing ; progressive compression signsMeningioma,Neurofibroma,chordoma,lipomadermoid,sarcoma
MENINGIOMA: benignthrocic cord level or near foramen magnumfrom arachonoid cells forms Psommama bodies Radiation therapy- Gammma Knife, proton beam treatment
external beamNEUROFIBROMA: from schwwan cells
arises near posterior rootbegins with radicular symptomsasymetric progressive spinal cord syndromeneed surgical treatment
INTRAMEDULLARY: uncommoncervical commonlycentral cord syndrome or hemicord syndromeEpendymoma,Haemangioblastoma,secondaries
astrocytoma(lowgrade)Microsurgical debulking can be triedRT is not useful
Primary tumors of spinal cord common in cervical
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