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Jeff Edwards
Gillian Lieberman, MD
Hydrocephalus in Children:Hydrocephalus in Children:
Diagnostic Imaging andDiagnostic Imaging andRadiological CharacteristicsRadiological Characteristics
January 2002
Jeff Edwards, Harvard Medical School, Year III
Gillian Lieberman, MD
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AgendaAgenda
Introduction to the Patient
Macrocephaly
Basics of Hydrocephalus
Diagnostic Imaging of Hydrocelphalus
Ultrasound, CT, MR
Shunts
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The PatientThe Patient
6 yo boy with macrocephaly, whichmanifested in the first year of life asexcessive head growth, accompaniedby reduced activity and poor feeding.
Other significant medical hx includes
cognitive delay, osteogenesisimperfecta type 2, restrictive lungdisease.
Birth hx: born at 34 wk premature byc-section with subsequent 25 day NICUcourse significant for apneic andbradycardic spells
No family hx of large headsUsed with permission of
patients mother
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MacrocephalyMacrocephaly in Infant or Childin Infant or Child
Defined as a head circumference more than 2 SDabove the mean for age and sex
Excessive rate of head growth over time suggests
increased intracranial pressure Most often caused by hydrocephalus, extra-axial fluid
collections, or neoplasms
Macrocephaly with normal head growth rate
suggests familial macrocephaly or true
megalencephaly
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DDxDDx ofof MacrocephalyMacrocephaly
Causes ExamplesPseudomacrocephaly,
pseudohydrocephalus, catch-up growth
Growing premature infant, recovery
from malnutrition, congenital heart
disease
Increased intracranial pressure
with dilated ventricles
with other mass
Progressive hydrocephalus, subduraleffusion, hydrancephaly
Arachnoid cyst, porencephalic cyst,brain tumor
Benign familial macrocephaly
(idiopathic external hydrocephalus)
Benign enlargement of subarachnoidspaces, congenital communicatinghydrocephalus, benign subduralcollections of infancy
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DDxDDx ofof MacrocephalyMacrocephaly (cont(contd)d)
Megalencephaly
with neurocutaneous disorder
with gigantism
with dwarfism
metabolic
lysosomal
other leukodystrophy
Benign familial (see above)
Neurofibromatosis, tuberous sclerosis
Soto syndrome
Achondroplasia
Mucopolysaccharidoses, Krabbesdisease, Ganglioside storage disease
Metachromatic leukodystrophy
Canavan spongy degeneration
Thickened skull Fibrous dysplasia (bone), hemolyticanemia (marrow), sicklemia,thalasemia
Modified from Hay, WW, et al. Current Pediatric Diagnosis & Treatment.
15th ed. New York: Lange Medical Books/McGraw Hill, 2001, p. 669.
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Workup ofWorkup of MacrocephalyMacrocephaly
History including family medical hx
Physical exam Neurological exam
Plotting measurement of head circumference for age and sex
Palpation of anterior fontanelle (if not closed) and of head forasymmetries or ridges
Listen for bruits in neck and head
In infants, transillumination of skull in a darkened room may reveal
subdural effusions, hydrocephalus, hydranencephaly, or cystic defect
Imaging studies
Depending on hx, possible labs include toxoplasmosis serum
antibody levels, lumbar puncture, subdural tap
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NarrowedNarrowed DDxDDx for our Patientfor our Patient
Hydrocephalus
Space-occupying lesion (e.g., tumor or cyst)
Extra-axial fluid collection (e.g., subduraleffusion)
Growing premature infant
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Pathophysiology of HydrocephalusPathophysiology of Hydrocephalus
Imbalance of CSF formation andabsorption, resulting in an excess of CSFwith subsequent increase in intracranial
pressure
CSF basics
Normal CSF production 02.-035 mL/min with amajority produced by the choroid plexus
Total volume of CSF in an adult ~ 120 mL
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CSF Circulation & Ventricular SystemCSF Circulation & Ventricular System
From Nolte, J. The Human Brain: An Introduction to ItsFunctional Anatomy. 4th ed. St. Louis: Mosby, 1999.
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EpidemiologyEpidemiology
Incidence of congenital hydrocephalus is 2-3 per 1,000 live births
Incidence of acquired hydrocephalus is not
known
About 100,000 shunts are implanted each
year in the developed countries
Incidence is equal in males and females
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Symptoms of Hydrocephalus inSymptoms of Hydrocephalus inInfantsInfants
Poor feeding
Irritability
Reduced activity
Vomiting
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Signs in InfantsSigns in Infants
Macrocephaly with excessive rate of head growth
Dysjunction of sutures
Dilated scalp veins
Tense/bulging fontanelle
Setting-sun sign: Eyes are deviated downward, theupper lids are retracted, and superior sclerae may
be visible.
Lower limb spasticity and hypertonia
Papilledema often not present in infants
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Symptoms in ChildrenSymptoms in Children
Altered behavior
Slowing of mental capacity or decreased level ofconsciousness
Headaches (initially in AM)
Neck pain (2 to tonsilalar herniation)
Vomiting (worse in AM)
Blurred vision (2 to papilledema)
Double vision (2 to Abducens nerve palsy)
Stunted growth and sexual maturation from third ventricledilatation obesity, precocious or delayed onset ofpuberty
Difficulty in walking 2 to spasticity
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Signs in ChildrenSigns in Children
Papilledema optic atrophy and vision loss (if increasedintracranial pressure (ICP) goes untreated)
Failure of upward gaze (2 to pressure on tectal plate through thesuprapineal recess)
Macewen sign: A "cracked pot" sound is noted onpercussion of the head.
Unsteady gait (2 to spasticity in lower extremities)
Macrocephaly (sutures are closed, but chronic ICP will lead toprogressive abnormal head growth)
Uni- or bilateral sixth nerve palsy
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Classifications of HydrocephalusClassifications of Hydrocephalus
Congenital v. Acquired
Communicating v. Noncommunicating
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Congenital HydrocephalusCongenital Hydrocephalus
Most common category in children
Usually present during infancy
Hydrocephalus presenting after age 6 months is
less likely to be congenital, and neoplasm mustbe excluded
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Congenital CausesCongenital Causes
Aqueduct (of Sylvius) stenosis
due to malformation (10% of all cases in newborns)
Arnold-Chiari I &II, Vein of Galen, Klippel-Feil
Postinfectious: toxoplasmosis, cytomegalic inclusiondisease, rubella, syphilis
Obstruction of foramina of Luschka and Magendie
Dandy-Walker malformation (2-4% of newborns)
Agenesis of foramen of Monro
Bickers-Adams syndrome
Achondroplasia
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Acquired CausesAcquired Causes
Mass lesions
account for 20% of all cases in children
usually tumors (eg, medulloblastoma, astrocytoma), but cysts, abscesses,or hematoma also cause
Intraventricular hemorrhage
2 to prematurity, head injury, or rupture of a vascular malformation.
Infections Meningitis, especially bacterial, Mumps, cysticercosis
Increased venous sinus pressure
2 to achondroplasia, craniostenoses, or venous thrombosis.
Iatrogenic Hypervitaminosis A.
Idiopathic
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Communicating HydrocephalusCommunicating Hydrocephalus
Overproduction of CSF (rare)
Choroid plexus papillomas (more common of the two)
Diffuse villous hyperplasia of choroid plexus
Extraventricular (not between ventricles andsubarachnoid space) obstruction by tumor,hemorrhage, infection, vascular abnormality, orstructural abnormality
Possible sites: cerebellar subarachnoid space, basalcisterns, tentorial hiatus (Chiari malformation,achondroplasia) cerebral subarachnoid space
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NoncommunicatingNoncommunicating HydrocephalusHydrocephalus
An intraventricular obstruction by tumor, hemorrhage,
infection, vascular abnormality, or structural abnormality
Most common cause is aqueductal stenosis, often in
association with Chiari II
Common sites of obstruction
Lateral ventricle
Foramina of Monro Third ventricle
Aqueduct
Fourth Ventricle
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Fetal Diagnosis ofFetal Diagnosis of VentriculomegalyVentriculomegaly
Primarily by obstetric ultrasound
Defined as an atrium of a lateral ventricle largerthan 11 mm
However, ultrasound cannot confirm whether
ventriculomegaly is result of hyrdocephalus or loss ofperiventricular brain tissue in which the vacant space is
passively filled with CSF
May be detected as early as latter part of 1sttrimester. Around 20-24 weeks, abnormal dilation
of ventricles is more clearly detectable.
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Postnatal DiagnosisPostnatal Diagnosis
Diagnosis of hydrocephalus is made whenthe ventricles are enlarged in the absence ofcerebral atrophy or dysgenesis
Radiological Modalities Plain film
Ultrasound
CT
MR
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Structural characteristics ofStructural characteristics of
hydrocephalushydrocephalus
Dilation of temporal and frontal horns of thelateral ventricles (often first sign)
Enlargement of anterior or posterior
recesses of third ventricle
Narrowing of mamillopontine distance
Narrowing of ventricular angle
Effacement of cortical sulci
= will return to point again
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Hydrocephalus v. Cerebral AtrophyHydrocephalus v. Cerebral Atrophy
Enlargement of temporal horns commensurately
with the bodies of the lateral ventricles is probablymost sensitive and reliable sign in thedifferentiation of hydrocephalus from atrophy
In atrophy, there is less dilatation of the temporal hornsthan the lateral ventricles bodies
If sylvian fissures are enlarged, dilated temporal hornsare not reliable sign
Large or rapidly enlarging head suggestshydrocephalus
Small or diminishing head circumference suggestsatrophy
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Hydrocephalus v. Cerebral AtrophyHydrocephalus v. Cerebral Atrophy
Ventricular Angle (left) tends to be smaller in hydrocephalus
(shown above) than in atrophy. Frontal horn radius (right) tends
to be larger in hydrocephalus than in atrophy.
Courtesy of Dr. Nedda Hobbs and Childrens Hospital Boston Film Library
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Plain Films and HydrocephalusPlain Films and Hydrocephalus
Prior to newer modalities, diagnosis was made byskull films showing:
split sutures
disproportionate craniofacial ratio bulging of the anterior fontanel
erosion of the dorsum sellae
hammered silver appearance of calvarium
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Ultrasound and HydrocephalusUltrasound and Hydrocephalus
If anterior fontanlle is open, intracranial structures including
ventricles, parenchyma, and vessels are readily visualized in thecoronal and sagittal planes.
From Kirks, DR. Practical Pediatric Imaging: Diagnostic
Radiology of Infants and Children. 3rd
ed. Philadelphia:Lippincott-Raven Publishers: 1998, p. 66.
Used to evaluate for
ventricular size,parenchymal and
intraventricular
hemorrhage,
extracerebral fluid
collections, cystic
lesions, and solid
parenchymal masses.
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Normal UltrasoundNormal Ultrasound
Anterior to posterior coronal images of the patient at age 10 days (study
done to look for intraparaenchymal or intraventricular hemorrhage)Courtesy of Dr. Nedda Hobbs and Childrens Hospital, Boston Film Library
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Normal UltrasoundNormal Ultrasound
Anterior coronal image of patient at
10 days
Superior aspect
of orbits
Frontal lobe
Courtesy of Dr. Nedda Hobbs and Childrens Hospital, Boston Film Library
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Normal UltrasoundNormal Ultrasound
More posterior coronal image of
patient at 10 days
Interhemispheric
fissure
Corpuscallosum Frontal horn of
lateral ventricle
Sylvian
fissure
Courtesy of Dr. Nedda Hobbs and Childrens Hospital, Boston Film Library
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Normal UltrasoundNormal Ultrasound
Body of lateralventricle
Corpus
callosum
Sylvianfissure Area of
thalamus and
third ventricle
Courtesy of Dr. Nedda Hobbs and Childrens Hospital, Boston Film Library
More posterior coronal image of
patient at 10 days
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Normal UltrasoundNormal Ultrasound
Patient at 10 days
Sagittal Right Parasagittal
Courtesy of Dr. Nedda Hobbs and Childrens Hospital Boston Film Library
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Normal UltrasoundNormal Ultrasound
Patient at 10 days
Sagittal
Courtesy of Dr. Nedda Hobbs and Childrens Hospital, Boston Film Library
Corpus callosum
Third
ventricle
Fourth
ventricle
Thalamus
Pons
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Normal UltrasoundNormal Ultrasound
Patient at 10 days
Right Parasagittal
Courtesy of Dr. Nedda Hobbs and Childrens Hospital, Boston Film Library
Body of lateralventricle
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Abnormal UltrasoundAbnormal Ultrasound
Anterior to posterior coronal images of
patient at age 14 months
Courtesy of Dr. Nedda Hobbs and Childrens Hospital Boston Film Library
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Abnormal UltrasoundAbnormal Ultrasound
Anterior coronal image of patient at 14
months
Superior
aspect of orbitDilated
frontal horns
of lateralventricles
Courtesy of Dr. Nedda Hobbs and Childrens Hospital, Boston Film Library
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Abnormal UltrasoundAbnormal Ultrasound
More posterior coronal image of
patient at 14 months
Dilated
frontal horns
of lateral
ventricles
Dilated
temporal
horn of
lateralventricle
Dilated
temporal
horn of
lateralventricle
Courtesy of Dr. Nedda Hobbs and Childrens Hospital, Boston Film Library
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Abnormal UltrasoundAbnormal Ultrasound
Dilated
bodies of
lateralventricles Dilated
temporal
horns of
lateralventricles
Dilated
third
ventricle
Courtesy of Dr. Nedda Hobbs and Childrens Hospital, Boston Film Library
More posterior coronal image of
patient at 14 months
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Abnormal UltrasoundAbnormal Ultrasound
Patient at 14 months
Sagittal Right Parasagittal Left Parasagittal
Courtesy of Dr. Nedda Hobbs and Childrens Hospital, Boston Film Library
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,
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Abnormal UltrasoundAbnormal Ultrasound
Patient at 14 months
Sagittal
Courtesy of Dr. Nedda Hobbs and Childrens Hospital, Boston Film Library
Dilated
thirdventricle
Dilated body of
lateral ventricle
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,
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Abnormal UltrasoundAbnormal Ultrasound
Patient at 14 months
Right Parasagittal
Courtesy of Dr. Nedda Hobbs and Childrens Hospital, Boston Film Library
Dilated
body of
lateral
ventricle
Dilated frontal
horn of lateral
ventricle
Dilatedtemporal
horn of
lateral
ventricle
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Comparison of Ultrasound SectionsComparison of Ultrasound Sections
Coronal images of patient at 10 days
Coronal images of patient at 14 months
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Comparison of Ultrasound SectionsComparison of Ultrasound Sections
Patient at 14 monthsSagittal Right Parasagittal
Patient at 10 days
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CT/MRI Findings inCT/MRI Findings inAcuteAcute
HydrocephalusHydrocephalus
Temporal horns are preferentially dilated antero-
posterially
Size > 2 mm
Normally, temporal horns are slit-like and barely visible
Ballooning of frontal horns of lateral ventricles and
third ventricle (ie, "Mickey mouse" ventricles)
Periventricular interstitial edema
Sylvian and interhemispheric fissures are not visible
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CT/MRI Findings inCT/MRI Findings inAcuteAcute
Hydrocephalus (contHydrocephalus (contd)d)
Fourth ventricle is usually normal in size
Ratio between largest width of the frontal horns
and the internal diameter from inner-table to
inner-table at this level should be greater than 0.5
Ratio of largest width of frontal horns to maximal
biparietal diameter > 30%
Upward bowing of corpus callosum on sagittal
MRI
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CT/MRI Findings inCT/MRI Findings in ChronicChronic
HydrocephalusHydrocephalus
Temporal horns may be less prominent than inacute hydrocephalus
Third ventricle may herniate into sella turcica,which may be eroded
Corpus callosum may be atrophied (best appreciatedon sagittal MRI)
With long-standing untreated hydrocephalus,white matter will undergo irreversibledemyelination
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PeriventricularPeriventricular Interstitial EdemaInterstitial Edema
Transependymal CSF resorption from ventricularlumen to the parenchyma
On CT, appears as hypodensity in periventricularregion with indistinct ventricular margins
On MR, appears as rim of prolonged T1 or T2relaxation times surrounding lateral venticles
proton density image or a fluid attenuated inversionrecovery (FLAIR) image is much more sensitive
Seen particularly at the superlateral angles of thefrontal horns
Not seen in neonates or young infants (immaturebrain has normally high water content)
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PeriventricularPeriventricular Interstitial EdemaInterstitial Edema
Courtesy of Dr. R. Michael Scott and Childrens Hospital, Boston Film Library
T2-weighted image of 5 yo boy who presented with 3 weeks
of bifrontal headache, morning vomiting, and blurred vision
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Computed Tomography andComputed Tomography and
HydrocephalusHydrocephalus
Pros: widely available, rapid, compatiblewith life support devices, often requires no
patient sedation
Should be performed with and without
contrast
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CTCT
Patient at 14 months
Courtesy of Dr. Nedda Hobbs and Childrens Hospital, Boston Film Library
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CTCT
Patient at 14 months
Courtesy of Dr. Nedda Hobbs and Childrens Hospital, Boston Film Library
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CTCT
Patient at 14 months
Courtesy of Dr. Nedda Hobbs and Childrens Hospital, Boston Film Library
Expansion ofextra-axial
CSF spaces
Brachycephaly
Enlarged frontal
horns + third
ventricle =
Mickey Mouse
ventriclesGray-whitematter junction
is intact
Note: no evidenceof periventricular
interstitial edema
Widened sulci
with overalleffacement of
sulci
Enlarged
temporal horns
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Comparison ofComparison of CTsCTs at Similar Levelsat Similar Levels
of Sectionof Section
PatientNormal adult
Normal from Mori, K. MRI of the Central Nervous System: A Pathology
Atlas. Tokyo: Springer-Verlag, 1991, p. 15.
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CTCT
Patient at 23 months s/p Ventriculoperitoneal
(VP) shunt placement
Courtesy of Dr. Nedda Hobbs and Childrens Hospital, Boston Film Library
Flattening of posterior occiput
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Patient 2: MRI andPatient 2: MRI and HyrdocephalusHyrdocephalus
11 yo girl who presented with three days of headache and
nausea/vomiting
Courtesy of Dr. R. Michael Scott and Childrens Hospital, Boston Film Library
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MRIMRI
11 yo girl who presented with three days of headache and
nausea/vomiting
Courtesy of Dr. R. Michael Scott and Childrens Hospital Boston, Film Library
Decompressed left
lateral ventricle
Slight periventricular
edema
Shift of midline
structures to left
Dilated right
lateral ventricle
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MRIMRI
Same 11 yo girl with non-enhancing hyperintense mass
most consistent with colloid cyst
Courtesy of Dr. R. Michael Scott and Childrens Hospital, Boston Film Library
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Comparison of MRIs at SimilarComparison of MRIs at Similar
Levels of SectionLevels of Section
Our 11 yo girlNormal 11 yo girl
Normal from Bisese, JH, Wang, AM. Pediatric Cranial MRI: An Atlas of
Normal Development. New York: Springer-Verlag, 1994, p.94
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MRIMRI
Same 11 yo girl s/p colloid cyst removal one
day prior
Courtesy of Dr. R. Michael Scott and Childrens Hospital, Boston Film Library
Postoperative
edema in left
thalamus
Right
pneumocephalu
and small
subdural
hematoma
causing mass
effect on right
frontal lobe
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Comparison of MRIsComparison of MRIs
11 yo girl with colloid cyst
Before surgery After surgery
Ventricles
are mildly
dilated butimproved
from the
prior study
Courtesy of Dr. R. Michael Scott and Childrens Hospital, Boston Film Library
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Patient 3: MRIPatient 3: MRI
5 yo boy who presented with 3 weeks of bifrontal
headache, morning vomiting, and blurred vision
Stenotic aqueduct
Courtesy of Dr. R. Michael Scott and Childrens Hospital, Boston Film Library
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Comparisons of MRIsComparisons of MRIs
5 yo boywith stenotic
aqueduct
Stenotic aqueduct
Normal adult
Normal from Truwit, CL, Lempert, TE. High Resolution Atlas of Cranial Neuroanatomy.
Baltimore: Williams & Wilkins. 1994, p2
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ShuntsShunts
Principle of shunting is to establish a communicationbetween the CSF (ventricular or lumbar) and a
drainage cavity (peritoneum, right atrium, pleura)
In principle, a shunt is a plastic tube less than 1/8of an inch thick that allows one-directional flow of
CSF by responding to pressure differencesbetween the ventricle and the cavity to which theshunt terminates.
There is a valve system that regulates the flow aswell as a reservoir, which can be felt through theskin. This reservoir allows for sampling of CSF by
needle aspiration.
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ShuntsShunts
CSF is simply absorbed in the drainage
cavity
Ventriculoperitoneal (VP) shunt is themost common
lateral ventricle is the usual proximal
location
advantage is that the need to lengthen the
catheter with growth may be obviated by
using a long peritoneal catheter
Like all foreign bodies, shunts canmalfunction or become infected
Only about 25% of patients with
hydrocephalus are treated successfullywithout shunt placement
From
http://www.cinn.org/conditio
ns/hydrocephalus.html
Diagram of VP and VA
shunts
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Common Shunt ComplicationsCommon Shunt Complications
Ventricular end Blockage
Disconnection
Migration
Hemorrhage
Infection
Isolated or trapped fourth
ventricle Secondary craniosynostosis
Calvarial thickening
Slit ventricle syndrome
Atrial end Thrombosis
Infection
Peritoneal end Infection (peritonitis,
adhesions)
CSF pseudotumor,
encystment
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Patient 4 Shunt SeriesPatient 4 Shunt Series
Plain films used to aid in confirming proper location of shunt
3 yo boy s/p VP shunt placementCourtesy of Dr. Ron Becker and Childrens Hospital, Boston Film Library
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CSF ShuntCSF Shunt
ScintigraphyScintigraphy
In different patient
evaluated for possible
shunt malfunction, there
is normal progression of
tracer down the shunt
catheter, with free
spillage into theperitoneal cavity by 15
min. There is no reflux
into the ventricles.
From Vreeland, TH, Wallis, J. Diagnosis: Normal CSF shunt scintigraphy.
http://gamma.wustl.edu/cs001te117.html
Normal transit time ~ 10-20 min. Transit time > 30 min is abnormal.
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ReferencesReferences
Barkovich, AJ. Pediatric Neuroimaging. 3rd ed. Philadelphia: LippincottWilliams & Wilkins, 2000.
Barr, LL. Neonatal Cranial Ultrasound. Rad Clin N Am 1999; 37: 1127-46.
Bisese, JH, Wang, AM. Pediatric Cranial MRI: An Atlas of NormalDevelopment. New York: Springer-Verlag, 1994.
Chicago Institute of Neurosurgery and Neuroresearch. Hydrocephalus.http://www.cinn.org/conditions/hydrocephalus.html
Goetz. Textbook of Clinical Neurology. 1st ed. W. B. Saunders Company,1999.
Hay, WW, et al. Current Pediatric Diagnosis & Treatment. 15
th
ed. New York:Lange Medical Books/McGraw Hill, 2001.
Heilman, KM, Watson, RT, Greer, M. Handbood for Differential Diagnosis ofNeurologic Signs and Symptoms. New York: Appleton-Century-Crofts, 1977.
Hord, ED. Hydrocephalus. http://www.emedicine.com/neuro/topic161.html
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References (contReferences (cont
d)d)
The Hydrocephalus Association.http://www.hydroassoc.org/information/index.html
Kirks, DR. Practical Pediatric Imaging: Diagnostic Radiology of Infants andChildren. 3rd ed. Philadelphia: Lippincott-Raven Publishers: 1998.
Mori, K. MRI of the Central Nervous System: A Pathology Atlas. Tokyo:Springer-Verlag, 1991.
Nolte, J. The Human Brain: An Introduction to Its Functional Anatomy. 4th
ed.St. Louis: Mosby, 1999.
Rumack, CM, Johnson, ML. Perinatal and Infant Brain Imaging: Role ofUltrasound and Computed Tomography. Chicago: Year Book MedicalPublishers, 1984.
Truwit, CL, Lempert, TE. High Resolution Atlas of Cranial Neuroanatomy.Baltimore: Williams & Wilkins. 1994.
Vreeland, TH, Wallis, J. Diagnosis: Normal CSF shunt scintigraphy.
http://gamma.wustl.edu/cs001te117.html
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AcknowledgementsAcknowledgements
Gillian Lieberman, MD
Pamela Lepkowski
Lolita Lewis
Nedda Hobbs, MD
R. Michael Scott, MD
Ron Becker, MD
Daniel Saurborn, MD
Alexandru Bageac, MD
Michael Stella, MD
Larry Barbaras
Cara Lyn Damour
The Patient and his Mom