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NS36 Neurosurgery Toronto Notes 2023

Investigations

• spinal injury precautions(cervical collar) are continued until C-spine is cleared

• C,T,L-spine and headCT scan

AH, lateral,odontoid views for C-spine (must see from Cl toTl;swimmer’

s view if necessary)

look for fractures, loss of mastoid orsinus airspaces, blood in cisterns, pneumocephalus

-50% of injuries happen at the junction of the cervical and thoracic spines,T1 should be well

visualized in the image to detect this occurrence

rarely done: oblique viewslooking for pars interarticularisfracture (“Scottie dog" sign)

if CT is unavailable,can do C-spine x-ray with Tl well visualized,but not recommended since

injuries at C and Tspine junction are seldom adequately visible with x-ray

• cross and type, arterial blood gas (ABG),CBC, drug screen (especially alcohol)

• chest and pelvic x-ray as indicated

• Never do IP in head injury unless

increased ICP has been ruled out

• All patients with head injury have

C-spine injury until proven otherwise

• Suspect hematoma in alcoholicrelated injuries

• Low BP after head injury means

injury elsewhere

• Must dear spine both radiologicalty

AND clinically

TREATMENT

Couparatire Effectnreaessd UiiajCcopited

Tcnsgrapby Mow toEicMt CervicalSpin

la j inesia Ob‘jaJed or btobated Petieals:M eta

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Treatment for Minor Head Injury (GCS 13-15)

• observation over 24-48 h

• wake every hour

• judicious use ofsedatives or pain killers during monitoring period

• outpatient: advise patients to undergo stepwise approach to return to play and return to school (for

latest recommendations,refer to 2019 Parachute Canada Concussion Guidelines)

Treatment for Moderate (GCS 9-12) and Severe Head Injury (GCS <8)

• clear airway and ensure breathing; intubate if necessary

• secure C-spine

• maintain adequate BP

• monitor for clinical deterioration

• monitor and manage increased ICP if present (see Herniation Syndromes, NS7)

Admission required if:

• skull fracture (indirect signs of basal skull fracture,see Head Injury)

• confusion,impaired consciousness, concussion with >5 min amnesia

• focal neurologicalsigns, extreme H/A, vomiting,seizures

• unstable spine

• use of alcohol

• poorsocialsupport

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Head Injury

Epidemiology

• M:F=2-3:1

Pathogenesis

• acceleration/deceleration:contusions,SDH, axon and vessel shearing/mesencephalic hematoma

• impact:skull fracture,concussion, epidural hematoma

• penetrating:worse with high velocity and/or high missile mass

low velocity:highest damage to structures on entry/exit path

high velocity: highest damage away from missile tract

Scalp Injury

• rich blood supply

• considerable blood loss (vessels contract poorly when ruptured)

• minimal risk of infection due to rich vascularity

Skull Fractures

• depressed fractures:double density on skull x-ray (outer table of depressed segment below inner table

ofskull),CT with bone window is gold standard

• simple fractures(closed injury): no need for antibiotics, nosurgery

• compound fractures (open injury):increased risk of infection,surgical debridement within 24 h is

necessary

internal fractures into sinus may lead to meningitis, pneumocephalus

risk of operative bleed may limit treatment to antibiotics

• basal skull fractures: not readily seen on x-ray, rely on clinical signs

retroauricular ecchymosis (Battle'

ssign)

periorbital ecchymosis (raccoon eyes)

hemotympanum

CSF rhinorrhea, otorrhea (suspect CSF if halo or target sign present);suspect with Lefort 11/111

midface fracture

rWJ '

—r-Retroauricular R

/ /

ecchymosis >5

/ / (Battle’

s sign) £

Periorbital

:chymosis

racoon

>

= ,

= s

I

\

+

Figure 28.Signs of basal skull

fractures

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XS37 Neurosurgery Toronto Notes 2023

Cranial Nerve Injury

• most traumatic causes of cranial nerve injury do not warrant surgical intervention

• surgical intervention

C.

'

N II: local eye/orbit injury

• CN III, IV, VI: if herniation secondary to mass

• CN VIII: repair of ossicles

• CN injuries that improve

CN 1: recovery may occur in a few months; most do not improve

CN III, IV, VI: majority recover

CN VII: recovery with delayed lesions

CN VIII: vestibular symptoms improve over weeks, deafness usually permanent (except when

resulting from hemotympanum)

AAN Concussion Classification

Grade 1: altered mental status <15 min

Grade 2: altered mental status >15 min

Grade 3: any loss of consciousness

Concussion Grades

UK Management Options

Grade

IS mm for amnesia ardother symptoms

Return to normal activity if symptoms

dear within IS min

Rtmow from activity for 1d , then

re-eiamine

Cl or MRI if H® or othersymptoms

worsen or last »1v«k

Return to normal activity after

1 wk withoutsymptoms

Emergent neurological eiam and

imaging:if initial eram is normal,may go

home with dosefollow-op

Admit if any signs of pathology or

persistent abnormal mentalstatus

Cl or Mil if H A or othersymptoms

If brief loss of consciousness(

'

1min),

return to normal activity after1wk

without symptoms

If prolonged lossof consciousness(>1

arlii).return to normal activity only aflnr

iwhwithoulsymptoms

1 Arterial Injury

• e.g. carotid-cavernous (C-C) fistula, carotid/vertebral artery dissection

2

Intracranial Bleeding

• see Blood, NS20 and Cerebrovascular Disease, NS2I

Brain Injury

3

Primary Impact Injury

• mechanism of injury determines pathology: penetrating injuries, direct impact

low velocity:local damage

high velocity:distant damage possible (due to wave of compression), concussion

• concussion: a trauma-induced alteration in mental status

refer to American Academy of Neurology (AAN ) guidelines for classification and management

no parenchymal abnormalities on CT

• coup (damage at site of blow) and contrecoup (damage at opposite site of blow)

acute decompression causes cavitation followed by a wave of acute compression

• contusion (hemorrhagic)

• high density areas on CT ± mass effect

• commonly occurs with brain impact on bony prominences (inferior frontal lobe, pole of temporal

lobe)

• diffuse axonal injury/shearing

• wide variety of damage results

• may tear blood vessels (hemorrhagic foci)

• often the cause of decreased loss of consciousness if no space-occupying lesion on CT

Coup

ContreSecondary Pathologic Processes coup

• same subsequent biochemical pathways for each traumatic etiology

• delayed and progressive injury to the brain due to

high glutamate release > NMDA receptor activation > cytotoxic cascade

• cerebral edema

intracranial hemorrhages

ischemia/infarction

raised ICP, intracranial HTN

• hydrocephalus

Figure 29. CT showing coupcontrecoup injury

A Trial of Intracranial-Pressure Monitoring in

IranmaticSrain Injury

NEJU 2012:367:2471-2481

Background:ICP monitoring isfrequently used

to monitorsevere TBI. but controversy exists over

whether it isbeneficial.

Methods:Studysanple (n»

324 patients, >13 yr|

consisted of those who had severe TBI and were being

treated n ICU in Bolivia or Ecuador. Patentswere

randomly assigned to one management group:

1.ICP-monitoring based management.

2.Management based on imaging and clinical

tiaamabon.

Primary outcome was a composite of survival time,

impaired consciousness,functionalstatus (al 3, $

mo),and neuropsychologicalstatus(at 6 mo).

Results: ho significant difference belween

management groups based on primary outcome. G mo

morlah!y.median length ol ICU stay, or occuiieoce of

sereus adveise events. However, duration ol brainspecie beaineets(e.g. use of hyperosmolar flu ids or

hypervtnWafenl was higher m the imaging-clinical

eianinalon group (4.8 d vs.3.4 d,P*

0.002).

Conclusion. Maintaining monitored ICPalJOmiiiHg

or lessis notsuperer to caie based on Imaging and

cbniul anamination.

Extracranial Conditions

• hypoxemia

due to trauma to the chest, upper airway,brainstem

extremely damaging to vulnerable brain cells

leads to ischemia, raised ICP

• hypercarbia

leads to raised ICP (secondary to vasodilation)

systemic hypotension

caused by blood loss (e.g. ruptured spleen)

loss of cerebral autoregulation leads to decreased CPP, ischemia

• hyperpyrexia

leads to increased brain metabolic demands > ischemia

caused by severe infections (e.g. meningitis,sepsis)

• fluid and electrolyte imbalance

• iatrogenic (most common)

• SIADH caused by head injury

• Dl

• may lead to cerebral edema and raised ICP

• coagulopathy

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NS38 Neurosurgery Toronto Notes 2023

Intracranial Conditions

• raised ICP due to traumatic cerebral edema OR traumatic intracranial hemorrhage

SLADH -» hyponatremia

Brain Injury Outcomes DI-»hypernatremia

• mildly traumatic (GCS 13-15):post-concussive symptoms: H/A,fatigue, dizziness, nausea, blurred

vision, diplopia, memory impairment,tinnitus,irritability, low concentration; 50% at 6 wk, 14% at 1

yr

• moderately traumatic (GCS 9-12):outcome proportional to age (>40) and CTfindings; 60% good

recovery,26% moderately disabled, 7% severely disabled,7% vegetative/dead

• severe (GCS <8):difficult to predict, correlates with post-resuscitation GCS (especially motor) and age

Late Complications of Head/Brain Injury

• seizures:5% of head injury patients develop seizures

incidence related to severity and location ofinjury (increased with local brain damage or

intracranial hemorrhage)

post-traumatic seizure may be immediate, early, or late

• presence of early (within first wk) post-traumatic seizure raises incidence of late seizures

• meningitis:associated with CSF leak from nose or ear

• hydrocephalus:acute hydrocephalus or delayed N PH

• Post-Concussion Syndrome: H/A,dizziness, cognitive changes, psychological symptoms, and

behavioural symptoms

Spinal Cord Injury

Alignment

columns

anterior vertebral tine (II

posterior vertebral line (21

spinolaminar line (31

posterior spinousline (4)

• see Orthopaedic Surgery,OR25 and Emergency Medicine. EK9

Neurogenic and Spinal Shock

1. neurogenic shock: hypotension that follows SCI (sBP usually <80 mmHg) caused by

interruption ofsympathetics(unopposed parasympathetics) below the level of injury, usually

with injuries above T6 level

loss of muscle tone due to skeletal muscle paralysis below level of injury -» venous pooling

(relative hypovolemia)

neurogenic shock isto be distinguished from hemodynamic shock due to blood loss from

associated wounds (true hypovolemia)

neurogenic shock -> hypotension, bradycardia, warm and well-perfused extremities

hemodynamic shock -> suspect in multisystem trauma and ifthere is peripheral vascular

shut-down

2. spinal shock: transient loss of all neurologic function below the level ofthe SCI, associated with loss of

bulbocavernosus reflex,flaccid paralysis and areflexia for variable periods

Whiplash-Associated Disorders

• definition: traumatic injury to the soft tissue structures in the region of the cervical spine due to

hyperflexion, hvperextension,or rotational injury to the neck

Initial Management of Spinal Cord Injury

• major causes of death in SCI are aspiration and shock

« the following patientsshould be treated as having a SCI until proven otherwise:

all victims of significant trauma

minor trauma patients with decreased LOC or complaints of neck or back pain, weakness,

abdominal breathing, numbness/tingling, or priapism

Stabilization and Initial Evaluation in the Hospital

1 . ABCs, immobilization (backboard/head strap), oxygenation, l-

'

oley catheter to urometer,

temperature regulation

2. hypotension: maintain sBP >90 mmHg with pressors (dopamine), hydration, and atropine

deep vein thrombosis(DVT) prophylaxis

3. monitor CBC/electrolytes

4. perform a mental status and cranial nerve function assessment as many patients with SCI have cooccurring traumatic brain injury

5. focused history and exam asthe patient is being immobilized (see Trauma Assessment, NS35)

6. spine palpation:point tenderness or deformity

7. motor lev el assessment (including rectal exam for voluntary anal sphincter contraction)

8. sensory'level assessment:pinprick,light touch, and proprioception

9. evaluation of reflexes

10.signs ofautonomic dysfunction: altered level of perspiration, bowel or bladder incontinence,

priapism

11. radiographic evaluation

3 views C-spine x-rays(AP,lateral, and odontoid) to adequately visualize Cl to C7-T1 junction

flexion-extension views todisclose occult instability

CTscan (bony injuries) typically most trauma centres use CT as the modality of choice for

looking at fractures, very sensitive with the high-resolution scanners

MR1 mandatory if neurological deficits (soft tissue injuries)

Bone

vertebral bodies

facets

spinous processes

Cartilage

Disc

disc space

interspinousspace

Soft tissues 1

J

Pre-vertebral soft tissues(A)

g

Figure 30.Assessment of spine

CT/X-Ray (parasagittal view)

Images used withpermission from

Dr. Ferco Berger and Dr.Michael

O'

Keeffe

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XS39 Neurosurgery Toronto Notes 2023

Medical Management Specific to Spinal Cord Injury

• option:methylprednisolone (given within 8 h of injury) is controversial; must confer with

Neurosurgery service

± decompression in acute, non-penetrating SCI

Resolution of spinal shock is indicated

by the return of reflexes (most commonly

the bulbocavernosus reflex)

Fractures of the Spine

FRACTURES AND FRACTURE-DISLOCATIONS OF THE THORACIC AND LUMBAR

SPINE

• assessligamentous injury/instability using MR1 ± llexion /extension x-ray views

• thoracolumbar spine unstable if 4/6 segments disrupted (3columns divided into left and right)

• anterior column: anterior half of vertebral body, disc, and anterior longitudinal ligament

• middle column:posterior half of vertebral body, disc,and posterior longitudinal ligament

posterior column:posterior arch, facet joints, pedicle,lamina and supraspinous, interspinous,

and ligamentum ligaments

See lanfcfiiNeurosurgery trials tablelot more

efsraatosKBe SIASC1S tnal for effectiveness ol

*

j

- yis.l£e decompressive surgery lor traumatic

cerocalspMlcordwjsy.

Type 1

Types of Injury

Table 25. AO Spine Classification System for Subaxial Cervical Spine Injury and Thoracolumbar

Spine Injury

Type Description

Compression fractures

Involves anlerior elements (vertebral body andor disc)

No injury/process fracture

Wedge compression (fracture of single endplate wo involvement of posterior vertebral body

wall)

Split/pincer type (fracture of both endplates w o involvement of posterior verlebral body wall)

Incomplete burst (involvement of posterior vertebral body wall and only a single endplate)

Complete burst (involvement of posterior vertebral body wall and both endplates)

A

0

t

2

3

4

B Tension band injuries

Posterior transoesseous disruption

Posterior ligamentousdisruption

Anlerior ligamentous disrupbon

1

2

3

C Translationinjuries (displacement dislocation)

F (only for subaxial cervical spine injury) Facetinjuries

Non-displaced lacetfracture (fragment <1cm,<40% lateral mass)

Facet fracture with potential lor instability (fragment >1cm,>40%lateral mass or displaced)

Floating lateral mass (disconnection of superior and inferior articular processes)

Pathologic subluxalion or dislocated facel

1

2

Figure 31.Odontoid fracture

classification

3

4

Management of Thoracolumbar Injury

• severity and management based on thoracolumbar injury classification and severity (TLICS)

classification

FRACTURES OF THE CERVICAL SPINE

Types of Injury

Table 26. AO Spine Upper Cervical Spine Injury Classification System

Type Description

Occipital condyle and occipital cervical jointcomplex injuries

Cl ting and C1-2 joint complex injuries

C2 and C2-3 joint complex injuries

1

2

3

A.B. and C sub-categorcations apply to each type ol Injury

A-booyinjures only (stable|

B *tensionband injuries(potentially unstable)

C -tuniimonil Injuries(unslablcl

r1

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NS-10 Neurosurgery Toronto Notes 2023

Table 27. Fracture Patterns of the Cervical Spine

Fracture Type Description

C1Vertebral Fracture Veitical compression forces the occipital condyles ol the skull down on the C1 vertebra ( atlas), pushing the lateral

(Jefferson fracture! masses of the atlas outward and disrupting the ling of the atlas

Also can cause an occipital condylai fracture

Causes C1 and odontoid of C2 to move independently of C 2 body

this occurs because

NormallyCl vertebra and odontoid of C2 aie a single functional unit

Alar and transveisc ligaments on posteiior aspect ol odontoid usually remain intact after injury

Patients often report a feeling of instability and picsent holding llicli head with their hands

lype It fracture the most common

C2 Vertebral Fracture Bilateral fracture thiough the pars intcraiticulaiis ol C2 with subluxation ol C2 on C3 (spondylolisthesis of axis)

(hangman fracture) Usually ncurologically intact

Clay Shovelcr Fracture Avulsion of spinous pioccss. usually C6 01 C7

Odontoid Fracture

'The AOSpine dasslllcatlon is prelcuud to charocletirc liadores ol the cervical spine, but the teimlnolugy described above may still be

encountered on the wards

Imaging

• AP spine x-ray (open-mouth and lateral view),CT

Treatment

• immobilization in cervical collar or halo vest until healing occurs (usually 2-3 mo)

• type 11 and 111 odontoid fractures:consider surgical fixation for comminution, displacement,or

inability to maintain alignment with external immobilization

type 11 odontoid fractures more likely to require surgery than type 111 due to higher risk of nonunion (fracture line in watershed zone)

• confirm stability after recovery with flexion-extension x-rays

Thoracolumbar Injury Classification

and Severity Scoring

Parametei Points

Morphology

Compression fracture

Burst fracture

Trarslaboaaltotational fracture

Distraction

Neurologic Status

Intact

Nerve loot injury

Spinal CoidStatus

Incomplete

Complete

Cauda equina

Posteiini ligamentous Complex

Intact

Neurologically Determined Death 1

2

Definition

• irreversible and diffuse brain injury resulting in absence of clinical brain function

• cardiovascular activity may persist for up to 2 wk

3

4

0 Criteria of Diagnosis

• prerequisites: no CNS depressant drugs/neuromuscular blocking agents, no drug intoxication/

poisoning, temperature >32°C, no electrolyte/acid-base/endocrine disturbance

• absent brainstem reflexes: pupillary light reflex, corneal reflexes, oculocephalic response, caloric

responses (e.g. no deviation of eyes to irrigation of each ear with 50 cc of ice water allow I min after

injection, 5 min between sides), pharyngeal and tracheal reflexes, cough wilh tracheal suctioning,

absent respiratory drive at PaCO’

2:6(1 mniHg, 2:20 mmHg rise above baseline, and pH 27.28 (apnea

test)

• 2 evaluations separated by time, usually performed by two specialists (e.g. anesthetist, neurologist,

neurosurgeon)

• confirmatory testing: flat btCi, absent perfusion assessed with cerebral angiogram

2

3

2

3

0

Injury MptctedMtttunmatt 2

Injnitd 3

UlCSMciing tacdon motpliotogy ol injury. ol

pmlffio

*

tynwiTlonitonplc

*

. andn«jiolog<iililatui

Ncn-cfWfdlnt nuMgtfnrnlIITIICS 0-3. opcMlhft

nunapfiicnt 4 IUCSs S\cilhct opuat/rto» noncpcfotwilUICS 4

Coma

Definition

• an unrousable state in which patients show no meaningful response to environmental stimuli

Pathophysiology

• lesions affecting the cerebral cortex bilaterally, the reticular activating system, or their connecting

fibres

• focal supratentorial lesions do not alter consciousness except by herniation (compression on the

brainstem or on the contralateral hemisphere) or by precipitating seizures

Prenatal vs.PostnataIRcpaii of

MyelomeningocclelMMC)

NE JU 2011:364:9931004

Puipose: loconpare outcomes of in utero leaaii of

myelomeningocele with standard postnatal repair of

myelomeningocele.

Methods: PCI comparing pre-ratal surgery (be'oie 26

wk of gestation)and standard postoperative sugeiy.

12 mooutcomes included death 01 need for placement

of a CSF short.30 mo outcomesincluded mental

development and mcCoi function.

Besults: 40'

t of p-f -aial-scigeiy patients, compared

to12« of postnatal-surgery patients, regnted

CSF shunt (M.001).Prenatalsurgery resn rted i n

improvement in medal developmenl and motor

function (P-0.0071.However, prenatalsurgery was

associated nrrth an increased risk of gynaecological

compilations

Conclusion: Prenatalsurgery lot MMC redjeed the

need forshunting and improved motor outcomes but

was associated with maternal and fetal lisksrelated

to preterm delivery.

Classification

• structural lesions (tumour, pus, blood,infarction,CSF):1/3 of comas

supratentorial masslesion:leads to herniation

infratentorial lesion: compression of or direct damage to the reticular activating system (RAS) or

its projections

• metabolic disorders/diffuse hemispheric damage: 2/3 of comas

deficiency of essential substrates(e.g.oxygen,glucose, vitamin B12)

exogenous toxins (e.g.drugs, heavy metals,solvents)

endogenous toxins/svstemic metabolic diseases (e.g. uremia, hepatic encephalopathy, electrolyte

imbalances, thyroid storm)

infections (meningitis, encephalitis)

trauma (concussion, diffuse shear axonal damage)

r 1

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NSll Neurosurgery Toronto Notes 2023

Investigations and Management

. ABCs

• labs: electrolytes, extended electrolytes, TSH, LET'

S, Cr. BUN, toxin screen, glucose

• CT/MRI, LF (after ruling out space-occupying lesion/increased ICE), EEG

Persistent Vegetative State

Definition

• a condition of complete unawareness of the self and the environment accompanied by sleep-wake

cycles with either complete or partial preservation of hypothalamic and brainstem autonomic

function

• “awake but not aware"

• follows comatose state

Subarachnoid

space

Etiology/Prognosis

• most commonly caused by cardiac arrest or head injury

• due to irreversible loss of cerebral cortical function but intact brainstem function

• average life expectancy is 2-5 yr

Arachnoid

Dura s

S

Spinal S

cord t

—i

Paediatric Neurosurgery Vertebrae f

Spinal Dysraphism Meninges

« spinal dysraphism refers to a spectrum of congenital anomalies resulting in a defective neural arch

through which CNS elements are herniated

• the spectrum is divided largely into aperta (visible lesion; no skin covering) and occulta (no visible

lesion;skin covering)

2_-

£

—Si

Table 28. Summary of Spinal Dysraphic Anomalies &

Spina Bifida Occulta Meningocele (SpinalBifida Myelomeningocele (Spina

Bifida Aperta)

Subarachnoid Aperta)

space

Congenital absence of a spinous Herniation of meningeal tissue

process and a variable amount

of lamina

No visible exposure olmeninges herniation olneural tissue

or neural tissue

15-20% of the general population;

most common at IS or S1

failure of fusion of vertebral

bodies resulting fiom abnormal

fusion of posterior vertebral

aichcs

No obvious clinical signs

Presence ollumbosacral

cutaneous abnormalities (dimple, incidence of associated

sinus,port

- wine stain,or hair anomalies, and hydrocephalus

lull) should increase suspicion of

an underlying anomaly (lipoma,

dermoid,diastematomyclia)

Definition Herniation of meningeal and

CNS tissue through a defect in

the spine

and C&F through a defect in

the spine,without associated

Epidemiology 0.1-0.2% of live births

Etiology Failure of fusion of posterior

neural arch

Primary failure of neural lube

closure

ClinicalFeatures Most common in lumbosacral area Sensory and motor changes distal

Usually no disability,low to anatomic level producing

varying degrees of weakness

Urinary and fecal incontinence

Hydrocephalus (65- 85% of

patients)

Most have Type IIChiari

malformation

|sce ChioriMalloimaliom. W43)

Meninges

Spinal

1 cord

Plain film:Absence of the spinous Plain films.CT, MRI. U/S.echo,CU

process and minor amounts ol the investigations

neutal arch

U S. MRI to exclude spinal

anomalies

Requires no treatment

Plain films.Cl. MRI. U/S.echo.GU

investigations

Investigations

Subarachnoid Spinal cord

space

Surgical excision and tissue repair Surgical closure to preserve

neurologic status and prevent CNS

infections

Closure rnofero shown to

decrease hydrocephalus and

improve postnatal motor scores

Operative mortality close to 0%,

95% 2-yr survival

80% have 10 >80 (but most are 80-

95).40-85% ambulatory,3-10%

have normalurinary continence

Early mortality:usually due to

Chiari malformation complicabons

(respiratory arrest,aspiration),

late mortality:due to shunt

malfunction

Treatment

Prognosis Generally good prognosis Good prognosis with surgical

treatment

r T

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