NS Neurosurgery

Brian G. Ballioe, Habert Lee and Alireza Mansouri, chapter editors

Alaina Garbens and Modape Oyewwni, associate editors
Adam Gladwish, EBM editor
Dr. Todd Mainpriu and Dr. Taufik Valiante, staff editors

Basic Anatomy Review ................... 2 Lumbar Disc Syndrome

Cauda Equina Syndrome
Differential Diagnoses of Common Lumbar Spinal Stenosis
Neurosurgical Presentations .............. 4 Neurogenic Claudication

INTRACRANIAL PATHOLOGY Intradural Intramedullary Lesions . . . . . . . . . 28

Intracranial Pressure (ICP) Dynamics ....... 4 Syringomyelia
ICPNolume Relationship
Cerebral Blood Flow (CBF) Spinal Cord Syndromes ................. 28
ICP Measurement Spinal Cord Injuries
Elevated ICP
Peripheral Nerves . . . . . . . . . . . . . . . . . . . . . . 29
Herniation Syndromes ................... 6
Treatment of Elevated ICP SPECIALTY TOPICS
Neurotrauma •••••••••••••• , •••••• , •••• 29
Hydrocephalus ••• , •••••• , ••••••••••• , •• 7 Trauma Assessment
Head Injury
Benign Intracranial Hypertension Brain Injury
(Pseudotumour Cerebri) . . . . . . . . . . . . . . . . . . 9 Late Complications of Head/Brain Injury
Spinal Cord Injury (SCI)
Tumour ................................ 9 Fractures of the Spine
Metastatic Tumours Neurologically Determined Death
Astrocytoma Altered Level of Consciousness
Meningioma Coma
Vestibular Schwannoma (Acoustic Neuroma) Persistent Vegetative State
Pituitary Adenoma
Pediatric Neurosurgery . . . . . . . . . . . . . . . . . 36
Pus .................................. 14 Spinal Dysraphism
Cerebral Abscess Intraventricular Hemorrhage (IVH)
Hydrocephalus in Pediatrics
Blood ................................ 15 Dandy-Walker Malformation
Extradural (uEpiduraln) Hematoma Chiari Malformations
Subdural Hematoma Craniosynostosis
Pediatric Brain Tumours
Cerebrovascular Disease ................ 17
Subarachnoid Hemorrhage (SAH) Functional Neurosurgery ................ 40
Intracerebral Hemorrhage (ICH) Movement Disorders
Intracranial Aneurysms Neuropsychiatric Disorders
Carotid Stenosis Chronic Pain

vascular Malformations ................. 22 Surgical Management of Epilepsy ......... 41

Arteriovenous Malformations (AVMs) Neurosurgical Treatment of Epilepsy

Cavernous Malformations................ 23 Surgical Management for Trigeminal

Neuralgia ............................. 42
EXTRACRANIAL PATHOLOGY Medical Therapy for Trigeminal Neuralgia
Dermatomes/Myotomes •• , ••••••••••• , • 24 Surgical Therapy for Trigeminal Neuralgia

Approach to Limb/Back Pain ••••••••••• , • 24 Common Medications .................. 43

Extradural Lesions . . . . . . . . . . . . . . . . . . . . . 24 References . . . . . . . . . . . . . . . . . . . . . . . . . . . . 44

Root Compression
Cervical Disc Syndrome
Cervical Stenosis (Cervical Spondylosis)

Toronto Notes 2011 Neurosurgery NSI

NS2 Neuroaursery 1'oroDio 2011

n IBB Func:liaDBI
NBui'CIBndamy Sllftwln Basic Anatomy Review
MRI Brain

frDnllllloba
Corpus calloeiJn
Th•lamu. Caudltll nuclau.
llypothallmu.
Occipital lobe Lderll vantricl•

Midblain
Pons
Four1h V8111rida
Cerabllllum
ThiiiiiiUI

Madl41a

DansofCZ
Spinal cord Occipillllobe

BadrafC3
A. lagil:lllllal:tion B.AxiiiSacli•

F"111•ra 1. MRI
Flllns.rtP H-. IJJ1rt.21Q.

Cl l.2
C2
r:::J C3
l.l LA

cj, C4 LA
r.;:;J C5
... C6

i
G8 C7
CB
Tl I I
:1!1
:0::
0

F"111•ra Z. RllhrtioiiSiip af Nerve RDots ta Vertebral Llml in tlla Cenilll81 and Lumbar Spina
Nota: AP views depict left-sided C4-5 and L4-5 disc herniation, and correlating nerve root impingement
'IbroDlo Nota 2011 Buic Anatomy Review Neumaurgery NS3

A B

..2.. '6 1. Am.iDr carebralartay

7 2. Midcll centnl ll'lllry
...11 3.
4.
Postarior cammlricating artary
Postarior Clf8bralartay
a:
I! 5. Besilanrtary
6. AICA
7. PICA
0
c 8. Var1abrllartary
9. cerabllll•artary
Arblry IBgn: 1D. AniBriar ID!ruidal arl8ry
At. - Antariar carebral 11. Am.ior spinalllllry
AcDIII - Antariar CGIIIIIUliCIIilg , 2. l'ol18rior spin!. arl8ry
n: -
MC - Ft.tddla canllllll
PCGIII - Po&telior CGIIIIIUliCI!iV
PC - Po&telior cerebnll
SC -
B
P -Pontine
AIC - Anblriar inl8rior
V - Vlltabrll
PIC - Po&telior inl8rior cerabell•
AS - Anblriar i!Jinal

Figure 3. s..ply af ... Bnia. PIBIIH T'lfBr to laglfld for artBTY namas
Figure 3A. Circle of Wlllll. MOlt Cemmmon Vllrlant
Figure 31. Vaculer Tanitorias oftha Brllin end Breinstem, Sagitbll Viaw, Seen Llltllnllly
Figun 3C. . ..r Tarritaria af ... lnin and Bninstam. Saailbll V'I8W, Sean Medially

1. eGITIIIUnieating artery, 301

2. Middlll cerebnl artary, 20%
3. lnmn.l Clnltilfpcnllariar
conwnunicllling artary, 30'1.
4. Buiar tip, 71.
5. Superior canbelar arlely, 3%
B. Vertlilnllui• jlrlction. :5
7. P08Uiriar ileriar canbelar artary, 3%

Figure 4. Anallryama af tfla Cin:la of Wllia

NS4 Neurosurgery Toronto Notes 2011

Differential Diagnoses of Common

Neurosurgical Presentations
Intracranial Mass Lesions
• tumour
• metastatic tumours
• astrocytoma
• meningioma
• vestibular schwannoma (acoustic neuroma)
• pituitary adenoma
• primary CNS lymphoma
• pus/inflammation
• cerebral abscess, extradural abscess, subdural empyema
• encephalitis (see Infectious Diseases, ID7)
• tumefactive multiple sclerosis (MS)
• blood
• extradural (epidural) hematoma
• subdural hematoma
• ischemic stroke
• hemorrhage: subarachnoid hemorrhage (SAH), intracerebral hemorrhage (ICH),
intraventricular hemorrhage (IVH)
• C}'5t

Disorders of the Spine

• extradural
• degenerative: disc herniation, canal stenosis, spondylolisthesis/spondylolysis
• infection/inflammation: osteomyelitis, discitis
• ligamentous: ossification of posterior longitudinal ligament (OPLL)
• trauma: mechanical compression/instability, hematoma
• tumours (55% of all spinal tumours): lymphoma, metastases (lymphoma, lung, breast,
prostate), neurofibroma
• intradural extramedullary
• vascular: dural arterio-venous fistula, subdural hematoma (especially if on anticoagulants)
• tumours (40% of all spinal tumours): meningioma, schwannoma, neurofibroma
• intradural intramedullary
• tumours (5% of all spinal tumours): astrocytomas and ependymomas most common; also
hemangioblastomas and dermoid
• syringomyelia (common causes: trauma, congenital, idiopathic)
• infectious/inflammatory: TB, sarcoid, transverse myelitis
• vascular: AVM, ischemia

Peripheral NeiVe Lesions

,, ,
• neuropathies
• traumatic
• entrapments
Ma•o-KIIIill Hyplllll•i• • iatrogenic
Vm. + Vlil>od + VcsF + Vlooion = •inflammatory
v- = conslllnt • tumours

INTRACRANIAL PATHOLOGY

100Ll
ICPmmHg

60
80
'-.
r·-.. . .2040. --,••-. ,-
...-I
i
I
Intracranial Pressure (ICP) Dynamics
ICPNoluma Relationship
I 1
II 0 I
I
1 Vollda : • adult skull is rigid with a constant intracranial volume
Wh.n a mass IIICjlllllds Evantualy finl&
I
• contents (CSF, blood, brain) are incompressible
withilthe slut small inCielllents • increase in one constituent/space-occupying lesion = increase in ICP
compensatury in voklme produce • however, ICP docs not rise initially due to compensatory mechanisms (autoregulation):
mechanisms initially larger and 1.-ger
maintain a nonnaiiCP increments in ICP • immediate: displacement of CSF to lumbar theca, blood
• delayed: displacement of extracellular fluid (ECF) or intracellular fluid (ICF); displacement
Figure 5. ICP-Volume Curve of brain tissue into compartments under less pressure (herniation)
Adlpled lrom Unduy llW, lbl9 t NtwtrJ1Jw IIIII
Ne!mst6puy 1lu.mrrled. Copyright 2004 with parmilliln
• once compensation is exhausted, ICP rises exponentially
lromB18Viar.
Toronto Notes 2011 Intracranial Pressure (ICP) Dynamics Neurosurgery NSS

Cerebral Blood Flow (CBF)

• CBF depends on cerebral perfusion pressure (CPP) and cerebral vascular resistance (CVR)
• normal CPP >50 mmHg in adults
• cerebral autoregulation maintains constant CBF by compensating for changes in CPP, unless:
• high ICP such that CPP <60 mmHg
AulcngtJation: CBF maidllilad daspitl
• MAP >150 mmHg or MAP <50 mmHg ch111gein CPP
• brain injury: e.g. subarachnoid hemorrhage (SAH), severe trauma

ICP Measurement
Acute Monitoring
• lumbar puncture (LP) (see sidebar) LDw BP or High ICP
• intraventricular catheter/ventriculostomy/external ventricular drain ("gold standard", permits Clllllbllll parfusioo prBI$Irll
therapeutic drainage of CSF to decrease ICP)
Figura 6. Carabral Autoregulation
Chronic Monitoring Curve
• fibreoptic monitor (intraventricular, intraparenchymal, subdural), subarachnoid bolt Ad1pted fnlm liiiiiiY et II. Neii!Jiogf and NeiiDstlr,ay
Alsl1rltd. Copyright 2004 with pennitlion from Elsevier.
(Richmond screw), and epidural monitor
• normal ICP <15 mmHg (8-18 em H 20) for adult, 3-7 mmHg (4-9.5 em H 20) for child; varies
with patient position
..... ,,

• moderate elevation: increase in mean pressure >20 mmHg
Consider Monilllring of ICP in 1lle
• severe elevation: increase in mean pressure >40 mmHg following Sitllltians
• waveform: comprised of respiratory and blood pressure pulsations (Traube-Hering 1. Patianll will1an abnoiiTIIII halld CT
waves); the amplitude increases with ICP IJid Glngow Coma Scale {GCSI
• beta-waves: coarse, variably increased amplitude, frequency Yz-2/min, often related to scors of 3 111 8 llfl8r cardiopulmonary
resuscitation.
respiration Or
• plateau waves: elevation ofiCP over 50 mmHg lasting 5-20 min, precursor of further 2. Patianll will11 noiiTIIII hald CT and
deterioration GCS liCOr& af 3111 8 AND the pra&enCe
of two or more of the following:
• Age over 4C yen
• Unilabral or billbnll motDr posturing
Elevated ICP • Systulic blood pniSIUI'IIIess than
90mmHg
Etiology 3. Postoperative monitoring
4. Investigation of normal prenura
• intracranial space-occupying lesion:
hydrocsphalus {NPHI
• tumour
• pus
• blood [trauma-+ hematoma (most common), subarachnoid hemorrhage]
• depressed skull fracture
..... ,,

• foreign body
Lumbar punctura is contnlindic8tad with
• increased intracranial blood volume known/suspected intracranial mus.
• vasodilatation (increased pC02 /decreased p02/decreased extracellular pH,
e.g. hypoventilation)
• venous outflow obstruction (venous sinus thrombosis, superior vena cava syndrome, space
occupying lesion)
• cranial dependency
• cerebral edema
• vasogenic (vessel damage, e.g. hypertensive encephalopathy, tumour)

•
• cytotoxic (tissue/cell death, e.g. hypoxia, brain injury)
• osmotic (acute hyponatremia, hepatic encephalopathy)
impaired autroregulation (hypotension, hypertension, brain injury)
..... ,,

• hydrocephalus (obstructive, non-obstructive)
• tension pneumocephalus (gas within the cranial cavity) Cushing's Triad af AcllllllaiiM ICP
• pseudo tumour cerebri !full triad- in ,13 of - 1
1. Hypartansion
• status epilepticus (chronic seizure resulting in brain edema) 2. Bradyclll'dia {late finding)
3. AbnoiiTIIIIrespil'lllllry pllttllm
Clinical Features
1. Acute Blevated ICP
• headache (HIA) - worse in the morning, aggravated by stooping and bending
• nausea and vomiting (NN)
• decreased level of consciousness (LOC) ifiCP =diastolic BP, or midbrain compressed
• drop in Glasgow Coma Scale (GCS) =best index to monitor progress and predict outcome of
acute intracranial process (see Neurotrauma, NS29)
• papilledema± retinal hemorrhages (may take 24-48 hours to develop)
• abnormal extra-ocular movements (EOM):
• CN VI palsy: often falsely localizing (causative mass may be remote from nerve}
• upward gaze palsy (especially in children with obstructive hydrocephalus)
• herniation syndromes (see Herniation Syndromes, NS6}
• focal signs/symptoms due to lesion
NS6 Neuroaursery lntrac:ranlal Preuure (ICP) Dyaamia/Herniation Syndromes 1'oroDio 2011

2. Chronic Elmated ICP

• H/A
• postural: worsened by coughing, straining, bending over
• morning/evening HIA-+ VIUIOdfiatation due to increased COz with recumbency
• visual changes
• due to papilledema
• enlarged blind spot. ifadvanced-+ eplsodJ.c constrictl.ons ofvisual. fields ('"grey-outs")
• optic atrophy/blindness
• differentiate from papillitis (usually unilateral with decreased visual acuity)
• decreased level ofc:onsd.ousness

Investigations
• patients with suspected elevated ICP require an urgent Cf/MRI
• ICP monitoring where appropriate

Herniation Syndromes
Table1. Hemllllon Syll*ome•
Cl1lcal FN1u111
o Letalll aurnta*Jriallaaill'l • Usualy
• Wlms af impnling 1nntan1Drial haniatian

I. Sublalcila
2. Cllllni DispB;anent ci • lesion • Small pupila, dilltad. fixed (I'Oitnll
3. UIICII clencephalon 11raugh o Diffuse C818b111l tD caudal dataliaration), sapntill flllue of
tentDrii!l nab:h o Lata uncal hamimon diancephahn 1111ckla
S.TDRSillr • Daaaased l.DC (nidbrain EOt.V

-
gaze iqlaiment eyes"):
CaqliiBIIill'l of )l8leCtwn end supelill' c*uli
: I! • Bninstem IIII!ICIIhaga secondaly
i0 11:1 sh111ring af be&ilar lrtary perfa!Biing VBSS81s)
• llillblti!S illlipidus (tractiiJI on pillitary d and
end-s!IQI s9'1
F"111•ra 1. H1miltian Types- Sua
Tabla 1 for dascription Uncus af l8f11)llnll o Llbnl sl4)l'llenblrilllaaion • lpslallnii1101H111Ctiva dilll8d pupil(estialt,
laba hami1181 down (oflllll'l)ily opanding mast ralllble sign) + ip&i&tlnl EOM pRy$i&.
'llmlgh IIODrial nab:h trauiT'IIIIic lllll'llllamll) plosis (CN II
• Daaaased l.DC (nidbrain
1 Contralaleral hemiplegia :!: extensor (upgoRg)
plril' response :!: ipsilateral hemiplegia
("Karnallln's natd( -1 fll&a lacelizilg aign
re&Uiting from pr8&1lll8 from the adga of 1111
tentorium an 1M cadnllallllll cerrl:nl pedurda)
CerBJellar Willis 1 large posterior fossa l1lii5S o CII8Jellar infarct (sl.pl'ior cerebelar artery
hamiates llnugh (cmman afta' VP lhi.IIIRg) ISCA) COI11Niian)
tentDrii!l inciBIA • Hydf11C8Phakll !Cinbnllaquecllct
Cerabell•tonsis o llinltadorilllaaiiJI • Neck stiffness head tilt ftcnsllar. .,
hemiatell"f'DIQI o FltawiJ.I central tanllrili • Daaaased l.DC (nidbrain
funmen011gnum heniation 1 Flaccid pnysis
o Fltawng LP in praaance al • Raapiii1DIV irra(paritiaa.flll)iratrry IIT8IIt
intrlcranial mass IB&ian (CIIII)I'IS&ian of macklllaly raspil'llclly centres)
• Blood pr111111 illllllility (camii'BIIIian af
m&GJIII'f cardDY8SCIB cantras)

Treatment of Elevated ICP

• Cf or MRI to identify etiology, assesa for midline shlft/hemiation
• treat primary cau.se (ie. remow mass lesioru, ensure adequate ventilation)
• if elevated ICP persists following treatment ofprimary cause, consider therapy when
'hdnllllof E..,_.ICP: ICP>20mm.Hg
ICPHEAD • goals: keep ICP <20 mmHg. CPP >65 mmHg, MAP >90 mmHg
lnllmiB
calm (sldiiiJ,II:cma General Measures (,CP HEAlY see sidebar)
Place .nivParlllylil • elevate head of bed at 30-45•, maintain neck in neutral position increases intracranial venous
ltypemntiltll outflow
Bewle head • prevent hypotension with fluid and vasopressor&, dopamine, norepinephrine pm
AdaqudaBP • ventilate to nonnocarbia (pCOz 35-40 mmHg) -+ prevents vasodilatation
Dinlllic (malllilol)
• prn to maintain J'02 >60 mmHg -+ prevents hypoxic brain injury
'IbroDlo Nota 2011 Herniation Syndromet/Hydrocephalus Neumaurgery NS7

Spec:Hic Me•sures
• osmolar diuresis (mannitol20% IV solution 1-1.5 glkg. then 0.25 glkg q6h to serum osmolarity
of315-320)
• can give rapidly, acts in 30 minutes, must maintain sBP >90 mmHg
• sedation \light" e.g. barbiturates/codeine ... "heavy" e.g. fentanyVMgSO.J
• paralysis with vecuronium -t reduces sympathetic tone, reduces HTN induced by muscle
contraction
• hyperventilate to pCOz 30-35 mmHg
• use for brief period& only- also resulta in decreased cerebral blood .flow (CBF)
• drain 3-5 m1 CSF via ventricles. assess each situation independently
• insert external ventricular drain (lf acute) or shunt
• corticosteroids ... decrease edema over subsequent days around brain tumour, abscess, blood
• no prawn value in head injury or stroke
• hypothennia - cool body tn 34"C
• no proven value in head injury
• barbiturate coma induced with pentobarbital to reduce cerebral blood flow and metabolism
(10 mglkg aver. 30 min, then 1 mglkg q1b continuous infusion)
• decreases mortality, but no improvement in neurological outcome
• decompressive craniectruny is a last resort

Hydrocephalus
Definition
• increased CSF volume

Etiology
• ob&truction to CSF 8ow
• decreased CSF absorption
• increased CSF production (rarely) - e.g. choroid plaus papilloma (0.4-1% of intracranial
tumours)

Epidemiology
• estimated prevalence 1-1.5%; incidence ofcongenital hydrocephalus -1-2/1000 live births
• hydrocephalus in children, see Pediatric Neurosurgery, NS37
1. Clloroid plsxu.
Classification 2. l..lltalll wntricllll
3. Third venlricle
4. Cerebral aqueduct (Df
Tllllllle 2. Cl&lllllcatlon of Hydrocephalus 5. Four1h vanlrida iii
6. Fo111men l.ulchklland MIQIIIIdie
7. Aracmoid gnmliltions
1
of
Obllrur:linl Ciculllliln blacUd willin Acqund • Vantriclilr pruxinlll 8. Subal'lll;l'noid •par;• j
(tm.Cimlllllil:llill) Vldricular sy1l8m pmximal • AIJJeduclal stenosis (lllh!sians to lilck 9. Segilllll sinus o
to the 8111CI'IIDid IJlftllatiJnS !GU- o Periwnbiclilr hypodensily Figure I. 'Ilia Flow of CSF
Racticxl, hllllllllhaga) lllln8ependymal ri{plian li CSF
• lnlrllv8nlrii:U• lnians {lllnaurs
e.g. 3nl wnbicle aJIIaid cyst.
hemibms)
mat illo spacal
• Sulcal aflacemllll .... ',

• Mall tnariallaniltian, CSF prodlad by choroid pillllul. ftOWI
Vllllric:l& CD11118Uian ID: vanbiclaa -o of l..uiCI'b
• Otlllrs: .. abscaa/ (lllll'lll)and MIQardll (medial) ...
tpllllamas, aracmaid cysts •lblrachnoid spac;e -o ablsofbld by
Bl'llchnoid vlflgranuldiona illo ve1111111
lii'IDM.
• AcrJ&ductal S1811asis. CSF production - CSF l'fllbsorptian -
malbmalim -sao mVday i'l nonnalld.llll
(188 PrMiifllric NflutDJutgety, NS36) Normal ml (501
spinal, 5D'Io intracl'llnill -o 25 ml
N...OIIIInl:liR CSF absarplian blac:bd at • Post-infactiaus (#1 C8US1) • All wnbicles dilaled idn.VIIItriculllr. 50 mlaubncl'noid)
(er.r...lil:ltilg) l!ldnlvmlriculll' site = meniVfis, cysticercosis
nchnaid IJllniJI!ian& • Post-hemonhegic (#2 cause)
SAil. MI. tnunatic
• Dlamid 1)11111111 papilams (rm,
c:ausas ilcraased CSF pmcllctian)
• nannal pi8SSU8
hydracephils NPH I'NaNAiol
AID
Parlisl:8lt vantric:Uar o ldiapllhic (50%) o Enlarged vllllriclaa withaut
AlaxiVApiiXia of gait
dlllalian il the CDI'IIald: of • Othe111: lllilereclrlaid lananhllga. incraased pnlfliniiiC8 of cnbrel lncantinanca
IIDIIII1II CSF pniSSin malingitis, 1nlu1111, radiaticD- U:i D1111entia
iJcU;ed
0 Normal aging 0 E'nllllved venbides and mci
• Alzllairnar'a, Crautzlaldt-Jacob • Carelnllllqlhy
Diiea&a
NS8 Neurosurgery Hydrocephalus Toronto Notes 2011

Clinical Features (see also Pediatric Neurosurgery, NS36)

• acute hydrocephalus
• signs and symptoms of acute raised ICP (see Elevated ICP, NSS)
• impaired upward gaze ("sunset eyes") and/or CN VI palsy
• chronic/gradual onset hydrocephalus [i.e. normal pressure hydrocephalus (NPH)]
• gradual onset of classic triad developing over weeks or months
• pressure ofventricle on LE motor fibres -+ gait disturbance (ataxia and apraxia usually
initial symptoms)
• pressure on cortical bowc:l/bladder centre -+ urinary incontinence
• pressure on frontal lobes -+ dementia
• CSF pressure within clinically "normal" range, but symptoms abate with CSF shunting

Investigations
• CT/MRI
• periventricular lucency suggests raised CSF pressure
• ultrasound (through anterior fontanelle in infants)
• ICP monitoring (e.g. LP) may be used to investigate NPH, test response to shunting (lumbar
tap test)
• radionuclide cisternography can test CSF flow and absorption rate (unreliable)

Treatment
• ventricular drainage
• surgical removal of obstruction (if possible) or c::xcision of choroid plexus papilloma
• shunts
• ventriculoperitoneal (VP) - most common
• ventriculopleural
• ventriculo-atrial (VA) - not first choice because of increased infections, shunt emboli
• lumboperitoneal- for communicating hydrocephalus and pseudotum.our cerebri
• third ventriculostomy (for obstructive hydrocephalus) via ventriculoscopy
• LPs [for transient hydrocephalus (e.g. subarachnoid hemorrhage), IVH in premature infants, etc.]

Shunt Compli«:ations

Table 3. Shunt Complications

Complication Etiolour Clinical Features lnvestiplians
Obstnlction • Obstruction by choroid plexus • Acute hy!Rcephakls • "Silmt series" (plain X-fiVS of
(most common) • Buildup of proteinaceous • h:l8iiS8d ICP entire shunt that only rule·out
accretions, blood, cells discomection. break. tip
(illlaiTII'IIItory or tumour) mi!JIIIion)
• Infection ·CT
• Di&connaction or dal!lilge • Radionuclide "shunto!Jlllf"
lnf8c:tion (3-6%) • s. epidermidis • Fever, NN, anorexia, initabiity • CBC
• S.lMR'fiiRl • Meningitis • Blood culture
• P.ICII8S • Peritonitis • Tap shunt for C&S (LP usualy NOT
• Gram-negative bacilli • Signs and symptoms of shunt recommended)
obstruction
• Shunt naplritis NA shunt)
Ovarsllunting • Slit ventricle synctoma • CIYonic or reculring • CTIMRI
(HI% over • Collapse of ventricles leading headaches often raliavad
6.5yea11) to occlusion of shunt ports by when lying down
ependymal lining • ventricles on imaging
• Seconday crMiosyno510Sis
(childran)

• Subdural hamillumll • A&ymptornatic ·CT

• Collapsing brain tears bridging • Headaches, wmiting.
veins {especially common in somnolence
NPH patients)

• Apposition and overlapping of • Abnormal head shape • Clinical

tha cranial sutures in an infllll oCT
following decorqnssion of
hy!Rcephakls
Saizun11 • EEG
(5.5% risk in 151 year,
1.1% attar 3rd year)
...auinal Hamil • Increased inlrllperitonaal • hguinal swelling. discomfort • U/S
(1 7% incidence with VP results in hernia
shunt inserted in inflrlcy) becoming apparent
± skin breakdown over
hardware
'IbroDlo Nota 2011 Neumaurgery NS9

Benign Intracranial Hypertension

(Pseudotumour Cerebri)
Definition
• rai&ed int:racranial. pressure and papilledema wiJ:hout evidence of any mass lesion,
hydrocephalus, infection or hypertensive encephalopathy (diagnosis ofexclusion)

Etiology
• unknown (majority), but aS&Ociated with:
• lateral venous sinus thrombosis
• habitus/diet: obesity, hyper/hypovitaminosis A
• endocrine: reprodw:tive age, menstrual irregularities, Addison'&/Cushing's disease, thyroid
irregularities
• hematological: iron deficiency anemia, polycythemia vera
• drugs: steroid administration or withdrawal, tetracycline, nalidixic acid, etc.
• risk factors overlap with those ofvenous sinus thrombosis; similar to those for gallstones ('"fat,
female, fertile, forties")

Epidemiology
• incidence -0.5/100,000 per year
• usually In 3rd and 4th decade (F>M)
Clinical Features
• symptoms and signs ofra1secl ICP (HIA in >9096, pulsatile intracranla1 noJse), but NO decreased
LOC or diplopia ....
• decreased visual acuity. papilledema, visual field defect. optic atrophy (key morbidity)
• usually self-limited. recurrence is common, chronic In some patientB
,.----------------,
111,.rlanl f'llltura to nubian CT a..t
• risk ofblindnes.s is not reliably correlated to symptoms or cl1nica1 course
IIRI(:t cantrMt
• t.e.ia"' (:t ld11111B. nKro.i,,
Investigations hsmarrhlgs)
• CT:nonnal • Midline shifts 1nd h1111ialians
• CSF studies: normal • Elfat:oment of ventric:lee and aulei
• MRI: must look fur venous sinus thrombosis (olbln ipllilatn), batal
• Single or mLitijlle implies
mebllbllil)
Treatment
• rule out conditions that cause intracranial hypertension
• discontinue offending medicatioDS, encourage weight loss, fluid/salt R:5triction ....
• pharmacotherapy: acetazolamide CSF production), thiazide diuretic or furosemide
• ifabove fail: serial LPs, shunt Primary CNS l',mphar.-. npcn11d il
• optic nerve sheath decompression (if progressive impairment ofvisual acuity) 6-201 of HIV inf\lcl8d patienta.
• 2-yea.r follow-up with imaging to nde out occult tumour, ophthalmology follow-up

Tumour
Vllllric...r: CGUDid, chomid prDC81S
pep•ma. apandymoma.
germiloma. tntoma. DDx far Rmg (nlllnci.. Laeia1 01 CT
wllht:antrAt
hpnllmut..
irrlnr--:
...,.._..
IUOICALDR

Ablcass*
lltrDI:Y!Dmt.
1gliobllllluma, •blastnma(high .,Ualllracytama)•
aligadlillllllllioma. lnfllrct
QMglioma. Contuaion
lymphoma, AIDS (lmulplasmosis)

LY!l1111ollll
DliiiJY'Iinalion
IIBIIDiving homlllllma
piUtaJy (" 3 mo.t conrnon Dx's)
adnma.
craniopharyngioma.
apt£ narva glioma. cyst
....

MMrySGu- rl
TIIIIIIIIS
lu1g 44lli
8r'llql 10%
(RCC) 7'!1i
Gl 0.
Figura 9. Tu•aurs M•noma 3%
NSIO Neurosurgery Tumour Toronto Notes 2011

Classification
..............
.........................:A

Cwr()lc;d'11X11; 14(41:131-43
Patiantt idan1lJid a hiving !ida lnin ma111ta1is
oodelgo llliltmlln11hlt inlilde wide liRin
lldillian tllapy (WIIRij, 111111ical,..ctian and
sfnlllctic llldidon..,-, (SRSI. Given 1hlt
conllc:ting Mlanctlu beln !Wplflld witli 1l5pacl
1D lhe best IPProacli 1D lilgle brlin rne11st1ses. 1he
..._cologylli.- SiQ Grlql r-r
Clf'l Onlllio Progrmn I:Onlb:tld 1 sysllmltic
lll'iuw rJ 1hel¥idlnculnd prldi:u uuidllil8.
c.:lllin: Surgicalmilion sllould be
consider8d fw IJitiartl wMh pd perfonnlnce
IIIU. or no lll'idiiiCI rJ ablcmill
cli-.lnd 1 Sllllicdy ICCeslible qe bnlin
maiiSIIsis amanllila 1D
Becue 1rea1ment il lingle hrail
ma1lllalis i1 canlidllllld plliiiiMI, iMIMIIDcll
1lllllnlnlllllllt be indiloiludlld. To rda 1111
1llnllll' l'llCU'ItiiC8 fw pl1iants who 11M
oodalgont miCii:ln rJ a•lnilll'lllltiiU.
poslupef1live W8I!T should be canlider8d. As an
llllmiiM ID up fii8Ction. WBI!Tfollawld lrt
SRS boost slwld be CCIIIIidenid lor pa1ien1s wi1h
liJ9a llllill mallltlliL Tile Mane& is ildciant
1D lllCDIIIrnendSAS lliorle IS I
llilrlpy.
• primaryvs. metastatic, intra-axial (parenchymal) vs. extra-axial, supratentorial vs. infratentorial,
adult vs. pediatric
• benign: non-invasive, but can be devastating due to expansion of mass in fixed volume of skull
• malignant: implies rapid growth, invasiveness, but rarely extracranial metastasis
• types of intracranial tumours (• = most common)
• neuroepithelial
• glial•: astrocytomas, oligodendrogliomas
• neuronal: ganglion cell tumours, cerebral neurocytomas/neuroblastomas
• poorly differentiated: glioblastomas, medulloblastomas
• other: pineal tumours, ependymomas, choroid plexus papillomas
• meningeal: meningiomas•
• nerve sheath: schwannoma, neurofibroma
• blood vessels: hemangioblastomas
• germ cells: genninomas, teratomas
• pituitary adenomas*
• craniopharyngiomas
• cysts: epidermoid/dermoid cysts, colloid cysts
• local extension: chordomas, glomus jugulare tumours
• other: primary CNS lymphomas, metastatic tumours
Clinical Features
• progressive neurological deficit (7096) - usually motor weakness, ± CN deficits, sensory,
cognitive, personality, endocrine deficits (these may localize lesion)
• H/A (5096) ±raised ICP (acute or chronic depending on growth rate), H/A classically worse
in am but non-specific (likely hypoventilation during sleep causing vasodilatation -+ increased
ICP), may worsen with bending forwardlvalsalva
• N/V (4096)
• seizures (25%)
• papilledema, vision changes
• symptoms suggestive ofTIA (ictal, post-ictal, or ischemic 2° to "steal phenomenonD)
• rarely presents with hemorrhage
• familial syndromes associated with CNS tumours
• von Hippel-Lindau (hemangioma)
• tuberous sclerosis (astrocytoma)
• neurofibromatosis type 1 and 2 (astrocytoma, acoustic neuroma respectively)
• Li-Fraumeni (astrocytoma)
• Turcot syndrome (glioblastoma multiforme)
• multiple endocrine neoplasia type 1 (MEN-1) (pituitary adenoma)

Investigations
• CT, MRI, stereotactic biopsy (tissue diagnosis), metastatic work-up

Treatment
• conservative: serial Hx, Px, imaging for slow growing/benign lesions
• medical: corticosteroids to reduce cytotoxic cerebral edema, pharmacological
(see Pituitary Adenoma, NS13)
• swgical: total or partial excision (decompressive, palliative), shunt if hydrocephalus
• radiotherapy: conventional fractionated radiotherapy (XRT), stereotactic radiosurgery
(Gamma Knife•)
• chemotherapy: e.g. alkylating agents (temozolomide)

Table 4. Tumour Types: Age, Location

<15 ye1n Astrocytoma (all grades) (511%) Medulloblaslllma (15·211%)

• Incidence: 2-&'100,000/y&llr
• 60% infratentorial
>15 High IJ!Ide astrocytoma (12-15%. e.g. GBM)
• 80% supratentorial
Craniophlryn.jiorna (2-5%) Ceraballar asbocytoma (15%)
Others: pineal region tumours, choroid Ependymoma{!!%)
plexus twnours, ganglioglioma, DNET Brainstem asbocytoma
Metastasis
Metastasis (15-311%, includes infratentorial) Acoustic neuroma (schwannoma) (5·1II%)
Meningioma (15-211%) Hamangiablaslllma {2%)
Low IJ!Ide astrocytoma (8%)
Pituillry adentma (5-8%)
Oligodendroglioma (5%)
Othar: CQIIoid cyst. CNS
darmoidfepidarmoid cyslll
'IbroDlo Nota 2011 Tam.our Neurosursery NSll

Metastatic Tumours
• most common brain tumour seen clinically
• 15-3QlJ6 of cancer patients present with cerebral metastatic twnoUI'!I
• most common sites = lungs, breast
• other sites = kidney, thyroid, stomach. prostate, testis, melanoma
• hematogenous spread most common

Location
• 80% a.re hemispheric, often at grey-white matter junction or junction of temporal-parietal-
occipitallobes (likely emboli spreading to terminal MCA branches)

Investigations
• identify prlmary tumour
• metastatic work-up (CXR, CT chest/abdo, abdominal U/S, bone scan, mammogram)
• cr with contrut -+ round, well-drcumscrtbed, often ring enhancing, ++ edema, often Figura 1D. M11tiple Bniin
multiple Mlll:astaas (see 111111WS)
• MRI more sensitive, especially fur posterior fossa
• oonsider biopsy in unusual cases. or if no primary identified
1- metubrtic work-up negative -+ brain biopsy
2. metubrtic work-up p011itive biopsy of affi:cted lritc:s other than brain

Treatment
• medlcal
• phenymin for seizure prophylaxis ifpatient presents with seizure z
• dexamethasone to reduce edema given with ranitidine
• chemotherapy (e.g. small cell lung cancer)
• radiation
• stereotactic radiosurgery: for discrete. deep-seatc:dJinoperable tumours 3
• multiple lesions: use whole brain radiation therapy (WBRT); consider stereotactl.c 1. HIIIBruganoos conlnlllarll.,callllnt
radiosurgery If<3lesions Z. 1-deliled bardn(infltraiM)
• post-op WBRT 1.1 commonly used 3. l'lritumaur adarra
4. CantriiiiiCIIISis
• surgical 5. CamprvAion of vedricla, m•e shit
• single/solitary lesions: use surgery+ radiation
Fia•re 11. Hig. Grelle
Prognosis AstrDcyiDma 01 CT
• median survival without treatment once symptom.at.k is -1 month, with optimal treatment
6-9 months but varies depending on prlmary tumour type

Astrocytoma
• most common primary intra-uial. brain tumour '' ,
ICamof*Y lllnlfll c.-
Tillie 5. Astnlcytuma Grading S.,.... PIIffGin- 1t1tue Sclll
lldlg Qtlerhl
T,.al CT.tiiRI FWd1p ('II.I
1- Pilocytic amocytama ± IIIIISS affect. ± anhanc£11111nt >10 yan. CWBI ps 111111 rasactian 100 No compeints; no evidanca of
di-
II- Low (plldr/dilfusa Mia allact. no anllllranat Syaars Abla 111 1:11ny on narmlll activity;
minor signs or symptoms of
Ill- Anapaslic Cllqllex eManc:ann 1.5-2 yellS di-
IV - GliOOiastoma rrUiimme (GBM) Necrosis (rilg emal'll:ef11ID) 12 manlbs, 10% at2 yess 80 NIJIIIIIilldivity with dart; ..,.
- . , . Dr symptoms af di-s
70 c.. fw •elf: unable 111 carry
Clinical Features on normal activity ur to do
• epidemiology: most common in 4th_(ilh decades lctiva Wllrk
• sites: cerebral hemispheres » cerebellum. brainstc:m, spinal cord 80 Requil88 occuionalllllil1lnce.
but ilable 111 Cln for 111011: of
• symptoms: recent onset of new/worsening HIA, Ntv; seizure, ± focal deficits or symptoms of hit needs
increased ICP 50 Requiras considlllble
881i111nce 4lld fnlquant medical
ClQ
Investigations
40 Disabled; l'llfJJiras . . care
• CT with contrast: va.rl.able appearance depending on grade (see Table 5) and -illance
• tissue biopsy: WHO grade and histology correlates with prognosis, but 25% chance of sampling 30 S8VIlnlly -.blld;
error due to tumour heterogeneity missicn is indicltad .U.ough
dflllh not i11111L'11nt
20 V.ry lick; hospital million
ldivB .upportiva
1llltlnBIIt II8C8SWY
10 Mcriluld; fiiii110C88118
prugllllling lllpidly
0 Delli
NS12 Nearomrgery 10ronto Nota 2011

Tralltment
• low grade diffuse astrocytoma
• close follow-up, radl.ation, chemotherapy, surgery all valid options
• not curative, trend towards better outcomes
• radiotherapy alone or post-op pmlongs survival (retrospective evidence)
• chemotherapy: usually reaerved for tumour progression
• high grade astrocytomas (anaplastic astrocytoma and GBM)
• surgvy
• gross total resection: IDIWmal safe resection + fractionated radiation with 2 em margin +
concomitant and adjuvant temozolomide
- a.cept: enensive dominant lobe GBM. slgnlfica.nt bllatenl involvement, end ofllfe
near, extensive brainstem involvement
• stereotactic biopsy ifresection not possible, followed by fractioned radiation with 2 em
margin
• expectant (based on functional impairment - Kamofsk:y score <70; petient'slfamily's wishes)
• aim to pmlong '"quality" survival
• chemotherapy: -2096 response rate. temozolomide (agent of choice); better response to
temozolomide predicted by MGMT gene hypermethylation
• multiple gliomas: WBRT ± chemotherapy

Meningioma
• mostly benign (1-2% anaplastic), slow-growing. extra-axial, drcumsc.ribed (non-iDfiltrative),
arise from arachnoid membrane
• often calcified, cause hyperostosis ofadjacent bone
• classically see Psammoma bodies on histology

Common Locations
• parasagittal convexity or falx (70%), sphenoid wing, tuberculum sellae, foramen magnum,
olfactory groove

Clinical Features
• middle aged, slight female preponderance (male:female = 2:3), high progesb:rone receptor&
(increase in size with pregnancy), symptoms of increased ICP, focal deficits, usually solitmy
1. Homogenous contmt emancement (10% multiple, likely with lollS ofNF2 gene/22q12 deletion)
2. Dui'IIIIIIIBctmmt
3. Dillinc:t margill lnvestiglltions
Figure 1Z. Meningiam1 on CT • cr with contrast: homogeneouB, densely enhancing. along dural border ("dural tall"), well
drcumsc.ribed (Figure 12}
o contrast enhanced MRI provides better detail
• angiography
• most are supplied by extmtal. carotid feeders (meningeal vessel&)
• also assesses venous sinus Involvement, "tumour blush"' commonly seen (prolonged contrast
.... ,'

Treatment
image)

WHO Clluification of Mlnq;.IM • conservative .management for non-progressive, asymptomatic le8lons

111r •iltoltm • surgeryis treatment ofchoice ifsymptomatic or progression on sequential imaging (curative if
Grade 1: low n.k IJf
Grada 2: intamedialll risk of NC.-ce complete resection)
Grade 3: high rilk of recul'l'lnce • stereotactic zadiosurgery (SRS) may be an option for lesions <3 em
• endovascular embolization to facilitate surgery
• SRS or XRT for recurrent atypical/malignant meningiomas

Prognosis
• >90% 5-year survival. recurrence rate variable (often -10-2096}
• depends on enent of resection (Simpson's classification)

.... ,,
Proglllllive ll'lillltlll'lll or
sansorineul'lll '-ing loss - acoustic
nauroma ll'1li pmvan lltharwi•.
Vestibular Schwannoma (Acoustic Neuroma)
o slow-growing (average of 1 mm/yr), benign posterior foll&a tumour
• arises from w:stibular component of CN vm in internal auditory canal, expanding into bony
canal and cerebella-pontine angle (CPA)
• ifbflateral, dl.agnosth: of neurofibromatosis type II
• epidemiology: all age groups affected, peaks at 4th-(ilh decades
'IbroDlo Nota 2011 Tam.our Neurosursery NS13

Futures

• compression of structures in CPA, often CN VIII (hearing loss 98%, tinnitus, d}'!ICquilibriwn),
then V. then VII
• ataxia and raised ICP are late features

Investigations
• MRI with gadolinium or T2 FIESTA sequence (>9896 sensitive/specific), CT with contrast 2nd
choice
• audiogram. bminstem auditory evoked potentials, caloric testll

Treatment
• conservative: serlal imaging
• radiation: stereotactic radiosurgery is the trea1ment of choice Figure 13.. Vestibular SchwaMJOIII
o surgery if: I. lesion >3 em; 2. bn.in8tem compression; 3. edema; 4. hydrocephalus (tumour in ceraballo-pantina angle)
• curable ifcomplete resection (almost always possible)
• operative complications: CN VII, VIII dysfunction (only sigDificant dissbility ifbilateral),
CSF leak

Pituitary Adenoma
• primarily from anterior pituitary, 3rd-4th decades, M=F
• incidence in autopsy studies approximately 20%
• classification
• miaoadenoma <1 em; maaoadenoma 0!:1 em
• endocrine active (functlonal/seaetory) vs. inactlve (non-functional)

Clinical Features
• mass effects
• HJA
• bitemporal hemianopsia (compression of optic chiasm) (see NeuroloBf. N21 for details of GD LDak Far ...... AIIIMIH ..._ -
visual field deficlt) OH. ut, FSH. TSII. AC1H. Prollc&l
A co..-ive adenoma in the pilllibrf
• CN m, IY. V 1, V a. VI palsy (compression of cavernous sinus) wil impair honnone produdion in !hit
o endocrine effects ardar (i.a. GH-•I:nllinv calbl •ra mDSI
• hyperprolactinemla (prolactinoma): lnfe:rtlllty, amenorrhea. galactorrhea, deaeased Ubido S8IISitivrl tD co,..-.ssiDII}.
• ACTI:I production: Cushing's disease, hyperpigmentatln
• GH production: acromegaly/gigantism
• panhypopituitarism (hypothyroidism, hypoadrenalism, hypogonadism)
• associated MEN-I syndrome
• diabetes insipidus
• pituitary apoplexy
• apoplexy (sudden expansion of mass due to hemorrhage or neaosis)
• abrupt onset HIA, visual disturbances, ophthalmopl.egl.a, reduced mental status, and
panhypopltuitarism
• CSF rhinorrhea and seizures (rare)
• signs and symptoms ofsubarachnoid hemorrhage (rare)

Investigations
o formal visual :fi.elda, CN testing
o endocrine tests (PRL level. TSH. 8 a.m. cortisol. fasting glucose. FSH/LH, IGF-1), electrolytes,
urine electrolytes and osmolar.lly
• imaging (MRI with and without contrast)

Differential
• parasellar tumours (e.g. craniopharyngioma. tuberculum sellae meningioma), carotid aneurysm

Treatment
• medical
• for apoplexy: rapid corticosteroid administration ± surgical decomptession
• for prolactinoma: dopamine agonists (e.g. bromocriptlne)
• for Cushing's: serotonin antagonist (cyproheptadine), inhibition ofcortisol production
(ketoconazole)
• for acromegaly: somatortati.n analogue (octreotide) ± bromocriptine
• endoaine replacement therapy
• surgical
• trans-sphenoidal, trans-ethmoidal, trans-cranW. approaches
NS14 Neuroaurgery
Brain Allscass on CT
. , . . _ iii4Zpllillll: ll&tn
.......... Tlillb.ty .... »lllrtfy
modllyin • immunocompmmised: fungi and protozoa: Toxoplasma. Noamlia. Candids a1&iams, Listeria
patinDM!IInil--.
.... . , I I ( 'II! patiaJDiamlhl
Nalilnll TIMan Lllivnty fiDsPtal wara rl'liiMid
irWIId f(a) aloc-.t
lnil pmlCirjmlllllill wilt rq .t.amrt
br conlrllt rMntilantrII'MRIIIIII lbl
-_.,wilt at IIIII I !l)llliliull*Kid
1:11hnt, ,_1M 1:11luw Ill irCnlclnDIIIIIIBBI
rrhilab.rJIIIIhlirDII:rinllilianiUJIIIIIIi!g
lninabtcMI42(tlllllle. 1111111111!'41!
• Immunosuppression (e,g, AIDS)
IIUII:Gn'lrM ....tm:odrGtDihiGII!gCM
o...:an. ko1e IOOSI- M IDrUwtnnDI
Wth!VIIIIiiDicslurlllllllt4Mib.
llldmilioa- primlld 11111iens >tS IIIII in
- -dimBIIL!I
,._..:A1ullli
llllr:Grnl: 13 !44,411 hid ful _ . , - 42
I2SAI hid rril dRill, 3'l Plliml hid Ill
lll:ll:llnl, Hlild il hGIPII!anl13
hldliiiiBD»-dllblly, !AJIMrill
loil1ic Nllll"iln llhllwld in'fiiNII M:omll
..:illal Mil bqii'IIIIIIIUR Ul, P=O:Im),
tmJJ• GCS >IZ lOR &.20. P=O.OII),
lOR • CSF obstruction
781 A8. P<D:0011rr l'lllmiiiiMI-'POii!M eocci
1J1M11ian llblcla 1:11lln 111142.3.
atlawriiiNspr!Mid ID ba
c.a.- !knjcll mnamat ICIII'itanTi
lhill8':11nG11diLIIPillirlnG18IIiliGn)
iii8CIIIII'BIIId il .. pllildl Mill19*1D
• imaging of choice
il11111111<2.i 111111 dlllitf-'"1 11'1111. . . il
nnn. 1hlin,nr.wl progllllliiiiDIICilllll wilt
(white)
cocci, lbt{IIIUis il ,.rrran hlwi'cl culln
llldlll'liliriJ...,.IDflill._u
llllirmliii11W11Q1111111.
1'oroDio 2011
Sources of Pus/Infection
• four mutes of microbial access to CNS
1. hematogenous spread (most common): arterial and retrograde venous
• adults: chest is #l source Oung abscess, bronchiectasis, empyema)
• children: congenital cyanotic heart disease with R to L shunt
• immunosuppression (AIDS - tomplasmo!ds)
2. dire<:t implantation: dural disruption due to
•trauma
• iatrogenic (e,g, following LP, post-op)
• congenital defect (e.g. dermal sinus)
3. contiguous spread (adjacent infection): from air sinus, nasa/oropharynx, surgical site
(e.g. otitis media, mastoiditis, sinusitis, osteomyelitis, dental abscess)
4. spread from PNS (e.g. viruses: rabies, herpes zoster)
• common examples
• epidural abscess: In cran1.al. and spinal epidural space, associated with osteomyelitis
• treatment: immediate drainage llJld antibiotics, smgical emergency if cord compression
• subdural empyema: bacteriallfungallnfection, due to contiguous spread from bone or air
sinus. progresses rapidly
• treatment: smg!cal drainage and antibiotics, 20% mortality
• me:nlngitlB, encephalit:l8 (see lnfectlous Diseases. ID6)
• cerebral abscess (see Cerelml Abscess, below)
Carabral Abscess
Definition
• pus in brain substance, surrounded by tissue .reaction (capsule formation)
Etiology
• modes ofspread (see above): 10-60% of patients have no cause identified
• pathogens
• Streptococcus (most common), often anaerobic or microaerophilic
• Staphylococcus (penetrating injury)
• Gram-negatives, anaerobes (.Btu:teroides, Fusobacterium)
• in neonates: Proteus and Citrobat:ter (exclusively)
monocytogmes, Mycobacterium and Aspergillus
Riskflleton;
• lung abnormalities [infection, AV fistulas; especially Osler-Weber-Rendu syndrome (aka
hereditary hemorrhagic telengiectaaia)]
• congenital coronary heart disease: R-to-L shunt bypasses pulmonary :filtration of
micro-organisms
• bacterial endocarditis
• penetrating head trauma
• dental abcess
Clinical Features
• focal neurological signs and symptoms
• HJA.. deaeased LOC; hemiparesis and se:lzures in 5096
• mass effect:. increased ICP and sequelae (cnnial enlargement in chlldre:n)
• hemipareslB llJld seizures in 50%
• ± sJg:ns and symptoms ofsystemic Infection (low-grade fever, l.eukocytosls)
Complications
• with abscess rupture: ventriculitis, meningitis. venous sinus thrombo!ds
• transtentorial herniation
Investigations
• cr scan often lst test in emergency department
• MRI
• apparent diifusion coefficient (ADC) used to differeot:iate abscess (black) from tumour
• WBC/ESR may be normal. blood cultures rarely helpful and LP contraindicated iflarge mass
• CSF: nonspecific (high ICP, high WBC, high protein. normal carbohydratt:), rarely helpful,
usually negative culture
'IbroDlo Nota 2011 PwiBlood Neurosursery NSlS

Treatment
• aspiration ± excision and send for Gram stain, acid fast bacillus (AFB), C&S, fu.ngul culture
• exdsl.on preferable lflocation suitable
• antibiotics
• empirically: vancomycin + ceftriaxone + metroniduole or chloramphenl.rol or rifiunpin
(6-8 weeks therapy)
• revise antibiotics when C&S known
• anti-convulsants (1-2 years)
• follow up cr is critical (do weekly initially, more frequent if condition deteriorates)

Prognosis
• mortality with appropriate therapy -10%, permanent defidts in -50%

Blood
Tllllla &. Cum)lllrisun uf Epi..........,. •• EtiDIDIIf Ill lntnn:rasial BIDIIds
Tna of EtiDIDar EpidamiCIIDgy Clnical FtlbJIII CT Fllllnl
11..11111111
11.......
fpanllallluma SkYI fraelln c:ausing M. > F111111la (4:1) lucid inllMI bafonl LOC Lanticlilr DIISS Good with prorr¢
nicHe me.qeal lllllliiiJI!Illenl
bleed !Nota: nspmay ernst e1r1
DCal' from unc:al hamiml)

AartalkDiml Ruptured AQB >50. No lucid inllML Crascen1ic OilS$ Cnriatamy if bleed Paar
11....... uan11amid IISSOCiated with henipsesis, >1cm
vessels tmuma Pupilary chqes
Cl111ic SUWanl Ruptured AQa >50.BOH Often lllylqiiDIIllltiC HypadaiiiB Burr bola to IRil; Good
11....... sdlnclnlid abusn, Minar WA. confusion, CIIRiCBID: lll8iS Cllllliotumy Hreoccurs
bridgill! vassels antk:ollguilred signs of ilcreased ICP
Traum11, spmaneous Aae 55-SO Sudden onset Hit#J density IDxl CIIISIIVlllive: Paar: 511% mortality
llllllllllhlge (111811¥811'11. m C8888 under thundan:lap headllcha, (snitivity dacrealas NPO, rl NS, ECG, Foley, 3D% of IUrvMn haw
Dopethic, AVMI ega 45 signs of inctaad ICP ova"tima) modnta to IIMr8 cisabiity
prophylaxis (nlnod'*-);
opan vs. llldovascular
surgery to repair if rebleed
HTN, wsc.-r Aaa >55, • 11A-ll8 ..,......, Hit#J dnity IDxl Medical: dacnssa BP. Paar: 44'hlortality dua to
abnormality, ci'ug use (CIICIIile, sip of ilcfelsad ICP cam!ICP c:aralnl hamildion
11lnDW's, Raclions. BOH, -B1llnila) Slillil:al: Cnlliotomy

Extradural (•Epidural'") Hematoma

Etiology
• temporal-parietal sJwll fracture: 85% are due to ruptured middle meningeal artery. Remainder
ofcaaes are due to bleeding from middle meningeal vein. dural sinus, or bone/diploic veins

Epidemiology
• young adult, male > female= 4:1; rare before age of2 or after age 60

Clinical Features
• in 6096, there is lucid interval of several houn between conCI158ion and coma
• then, obtundation. hemlpareals, .ip6Jlateral pupillary dilatation
• signs and symptnms depend on severity but can Include H/A. NJV; amnesia. altered WC, HTN 1. Comp1'81Sion of van1ridas
and respiratory distress (miclile llhilll
• deterioration can talce hours to days 2. Bload
Figura 15. Eatndural Hama1Dm1
lnvestigtdions DICT
• CT without contrast: high density biconvex mass against skull, usually with
unlfonn density and sharp margins. usually lim:iJ:ed by suture Unes

Treatment
• admit, observe, bead elevation
• mannitol pre-op If elevated ICP!brain herniation
• craniotDmy to evacuate clot, follow up CT
NS16 Neurosurgery Blood Toronto Notes 2011

Calcilm antaganisiJ for aneurysmal

Prognosis
subaracllloid haemonhage (Review) • good with prompt management, as the brain is often not damaged
Cochrane Review 2008; Issue 3. • worse prognosis if bilateral Babinski or decerebration pre-op
Introduction: This sbJdy looked to review the • death is usually due to respiratory arrest from uncal herniation (injury to the midbrain)
evidence in regards as to whether calcium
antagonists improve the outcome in patients with
aneUJysmal subarachnoid haemonhage.
Mathods/Papulation: The review included 3361 Subdural Hematoma
patients presenting aneurysmal subarachnoid
haemorrhage from 16randomised controlled trials
comparing treatment with calcium antagonists vs.
ACUTE SUBDURAL HEMATOMA
control from 1980 ID March 2006.
Results: The results were based mainly on one Etiology
large trial of oral nimodipine, which showed aRR • rupture of vessels that bridge the subarachnoid space (e.g. cortical artery, large vein, venous
of 0.67(95% Cl 0.551D 0.811 and the evidence sinus) or cerebral laceration
for other calcium agonists was not statistically
significant
Con'*sion: The authors endorse the use of Risk Factors
oral nimodipine in patients aneurysmal • trauma, anticoagulants, alcohol, cerebral atrophy, infant head trauma (see Pediatrics)
subarachnoid haemonhage.
Clinical Features
• no lucid period, signs and symptoms can include altered LOC, pupillary irregularity,
hemiparesis
CT Density and MRI Appearance of
Blood Investigations
Time CT MRI MRI • CT: high density concave mass, "crescentic" usually less uniform, less dense and more diffuse
·T1 -T2 than extradural hematoma
Acute Hyper. Grey Black
(<72hl Treatment
Subacute Iso. White White
• craniotomy for clinically symptomatic subdural hemorrhage, or subdurals greater than 1 em;
1<4wl optimal if surgery <4 hrs from onset
Chronic Hypo. Black Black
1>4wl Prognosis
• poor overall since the brain is often injured (mortality range is over 50%)
MRI-Tl: "George Washington Bridge"
MRI-12: "Oreo" cookie -
Black/White/Black
CHRONIC SUBDURAL HEMATOMA

Etiology
• many start out as acute subdurals
• blood within the subdural space evokes an inflammatory response:
• fibroblasts invasion of clot and formation of neomembranes within days -+ neocapillaries
growth -+ fibrinolysis and liquefaction of blood clot
• course is determined by the balance of rebleeding from neomembranes and resorption of fluid

Risk Factors
• older, alcoholics, patients with CSF shunts, anticoagulants, coagulopathies

Clinical Features
• often due to minor injuries or no history of injury
• may present with minor H/A, confusion, language difficulties, TIA-like symptoms, symptoms of
raised ICP ± seizures, progressive dementia, gait problem
• obtundation disproportionate to focal deficit; "the great imitator" of dementia, tumours

Investigations
• CT: hypodense (liquefied clot), crescentic mass

Treatment
• seizure prophylaxis only if posttraumatic seizure
• reverse coagulopathies
• burr hole drainage as clot liquefies; craniotomy if recurs more than twice

Prognosis
Figure 16. Subdural Hematoma • good overall as brain usually undamaged, but may require repeat drainage
on CT
Toronto Notes 2011 Cerebrovascular Disease Neurosurgery NS17

Cerebrovascular Disease
Ischemic Cerebral Infarction (80%)
• embolic (heart, carotid artery, aorta) or thrombosis of intracerebral arteries
(see Carotid Stenosis, NS21 and Neurology. N45)

Intracranial Hemorrhage {20%)

• subarachnoid hemorrhage (SAH), spontaneous intracerebral hemorrhage (ICH),
intraventricular hemorrhage (IVH)

Subarachnoid Hemorrhage (SAH)

---------------------
Definition
• bleeding into subarachnoid space (intracranial vessel between arachnoid and pia)

Etiology
', ,

• trauma (most common)

• spontaneous Grad1 Finding
• aneurysms (75-80%) Normal scan
• idiopathic (14-22%)
2 <1 mm thick blood
• AVMs(S%)
• coagulopathies (iatrogenic or primary), vasculitides, tumours (<5%) 3 >1 mm thick blood
4 IVH or ICH ± SAH
Epidemiology
• -10-28/100,000 population/year
• peak age 55-60, 20% of cases occur under age 45

Risk Factors
• hypertension
', ,

• pregnancy/parturition in patients with pre-existing AVMs, eclampsia Huntlmlllus Grade

• oral contraceptive pill ar•...._ -1• for SAKI
• substance abuse (cigarette smoking, cocaine, alcohol) Grad1 O.Crlptlan
• conditions associated with high incidence of aneurysms (see Intracranial Aneurysms, NS20)
No Sx or mild IVA and/or mild
meningismus
Clinical Features of Spontaneous SAH
• sudden onset (seconds} of severe "thunderclap" headache usually following exertion and 2 Features of 1 + CN palsy
described as the "worst headache ofmy life" (up to 97% sensitive, 12-25% specific) 3 Confusiorv1ethlrgy, mild
• nausea/vomiting, photophobia hemiparnil or aphqia
• meningismus (neck pain/stiffness, positive Kernig's and Brodzinski's sign) 4 GCS <15 but >&,moderate-
• decreased WC (due to either raised ICP, ischemia, seizure) s.-a hemiparnis, mild
• focal deficits: cranial nerve palsies (CN III, IV), hemiparesis rigidity
• ocular hemorrhage in 20-40% (due to sudden raised ICP compressing central retinal vein) 5 Coma (GCS <91.
• reactive hypertension moribund appearanc1
• sentinel bleeds Morblity of Grade 1-2 20%,
• SAH-like symptoms lasting <1 day ("thunderclap H/ A,) iiiCI'IIIIslld wilh grads
• may have blood on CT or LP
• -50% of patients with full blown SAH give history suggestive of sentinel bleed within past
3weeks
• differential diagnosis: sentinel bleed, dissection/thrombosis of aneurysm, venous sinus
thrombosis, benign exertional HIA
', ,

World Fedlndion Ill N-ological

Investigations Surpans Grlllling of SAH
• non-contrast CT (Figure 17) WFNS GCS Aphuia,
• 98% sensitive within 12h, 93% within 24h; 100% specificity Grad• Scare llllmiparlllia, ar
• may be negative if small bleed or presentation delayed several days llllmiphagil
• acute hydrocephalus, IVH, ICH, infarct or large aneurysm may be visible o•
• CTA/MRA/ cerebral angiography for localization and treatment planning
15
• positive history for SAH with negative CT - MUST do LP to look for blood or xanthochromia
(may be negative <12h) 2 13·14 -
• lumbar puncture (LP) findings (highly sensitive): 3 13·14 +
• elevated opening pressure (> 18 em HzO)
4 7-12 +or-
• bloody initially, xanthochromic supernatant with centrifugation ("yellow") by -12h, lasts
2 weeks 5 3-6 +or-
• RBC count usually> 100,000/mm3 without significant drop from 1st to last tube (in contrast •1nt11ct anltr{sm
to traumatic tap)
• elevated protein due to blood breakdown products
NS18 Neuroaurgery CerebroYascular DJnase 1'oroDio 2011

• four vessel cerebral angiography ("gold standard" for aneurysms)

• demonstrates source of SAH in 80-8596 ofcases
• "angiogram negative SAH": repeat angiogram in 7-14 days, ifnegative -+ •perimesencepbalic
SAH"
• magnetic resonELilce angiography (MRA) and cr angiography
• sensitivity may be up to 95% for aneurysms

F"IJara 1'1. DiaiJDalia af SAH

HiiiDry af..W.n • -... da... BP

• l.OC
.-ent ----+ linb mMm!lnll
I Stiff neck
• Fundi
CTicen
I
+ +

. •
NBQI1ive fllr blood I'DiiiMI fur bllllld ancVor
pllliant chlwsy, uncanacious,
locelizina nuv!Dgicel findinae
puncture
I
.....-------'----,.
----+ Flafa'1D NIIUtiU'Qiry
no mic7ie
CSF: clw, cololll'lass,
blood
CSF: bllllld ±
XWIIhochramil

DIC heme
f"IJIFI 18. Appraacii1D SAH

Treatment
• admit to ICU or NICU
• oxygenlventilation pm
• NPO, bed rest, elevute head ofbed 30D, minimal external stimulation, neurological vitals qlh
• aim to maintain sBP =120-150 (balance of vasospasm prophylaxis, risk of re-bleed, risk of
hypotension since CBF autoregulation impaired by SAH)
• cardiac rhythm monitor
• Foley pm, strict monitoring of ins and outs
• IV NS with 20 mmol KClJL at 125-150 cclb.
• phenytoin ifseizure or temporal lobe clot
• mild sedation pm
• nimodipine fur vasospum neuroprotection for 21 day5; may discontinue earlier ifpatient is
clinkally well
Toronto Notes 2011 Cerebrovascular Disease Neurosurgery NSHI

Complications
• vasospasm - vessel constriction in response to extravascular blood irritation
• clinical features: confusion, decreasedwe. focal deficit (speech or motor)
• onset 4-14 days post-SAH (deterioration within first 3 days is NOT caused by vasospasm)
• risk factors: large amount of blood on CT (high Fisher grade), smoking, increased age, HTN
• "symptomatic· vasospasm in 20-3096 ofSAH patients
• "radiographic" vasospasm in 30-70% of arteriograms performed 7 days following SAH (peak
incidence)
• diagnosed clinically, and/or with transcranial Doppler (increased velocity of blood flow)
• risk of cerebral infarct and death
• treatment
• "triple W therapy using fluids and pressors (examples: norepinenphrine, phenylephrine)
• angioplasty for refractory cases
• hydrocephalus (15-20%} - due to blood obstructing CSF drainage
• can be acute or chronic, requires extraventricular drain (EVD) or shunt, respectively
• neurogenic pulmonary edema
• hyponatremia - SIADH, cerebral salt wasting
• diabetes insipidus lri!N H" '"'-•PY fvr V.aapum
Hyparllnsion
• cardiac- arrhythmia (>50% have ECG changes), MI, CHF Hypervolemia
H1111odilution
Prognosis
• 10-15% mortality before reaching hospital, overall 50% mortality (majority within first 2-3 weeks)
• 30% of survivors have moderate to severe disability
• a major cause of mortality is rebleeding, for aneurysms:
• risk of rebleed: 4% on first day, 15-20% within 2 weeks, 5096 by 6 months
• if no rebleed by 6 months, risk decreases to same incidence as unruptured aneurysm (296)
• only prevention is early clipping or coiling of"cold" aneurysm
• rebleed risk for "perimesencephalic SAH" is approximately same as for general population

Intracerebral Hemorrhage (ICH)

----------------------------
Definition
• hemorrhage within brain parenchyma, accounts for -10% of strokes
• can dissect into ventricular system (IVH) or through cortical surface (SAH)

Etiology
• hypertension (usually causes bleeds at putamen, thalamus, pons and cerebellum)
• hemorrhagic transformation (reperfusion post stroke, surgery, strenuous exercise, etc.)
• vascular anomalies
• aneurysm, AVMs and other vascular malformations (see Vascular Malformations, NS22)
• venous sinus thrombosis
• arteriopathies (cerebral amyloid angiopathy, lipohyalinosis, vasculitis)
• tumours (1%}- often malignant (e.g. GBM,lymphoma, metastases)
• drugs (amphetamines, cocaine, alcohol, anticoagulants, etc.)
• coagulopathy (iatrogenic, leukemia, TTP, aplastic anemia)
• CNS infections (fungal, granulomas, herpes simplex encephalitis)
• post trauma (immediate or delayed, frontal and temporal lobes most commonly injured via
coup/contre-coup mechanism)
• eclampsia
• post-operative (post-carotid endarterectomy cerebral reperfusion, craniotomy)
• idiopathic

Epidemiology
• 12-15 cases/100,000 population/year

Risk Factors
• increasing age (mainly >55 years)
• male gender
• hypertension
• Black/Asian > Caucasian
• previous CVA of any type (23x risk)
• both acute and chronic heavy alcohol use; cocaine, amphetamines
• liver disease
• anticoagulants
NS20 Neurosurgery Cerebrovascular Disease Toronto Notes 2011

Clinical Features
• TIA-like symptoms often precede ICH, can localize to site of impending hemorrhage
• location: basal ganglia/internal capsule (50%), thalamus (15%), cerebral white matter (15%),
cerebellumlbrainstem- usually pons {15%}
• gradual onset of symptoms over minutes-hours, usually during activity
• HJA, NN and decreased WC are common
• specific symptoms/deficits depend on location ofiCH

Investigations
• hyperdense blood on noncontrast cr

Treatment
• medical
• decrease BP to pre-morbid level or by -20%; check PTT/INR, and correct coagulopathy
(stop anticoagulation for 1-2 weeks)
• control raised ICP (see Intracranial Pressure Dynamics section, NS4)
• phenytoin for seizure prophylaxis
• follow electrolytes (SIADH common)
• angiogram to r/o vascular lesion unless >45 yrs, known HTN, and putamen/thalamid
posterior fossa ICH (yield - 0%)
• surgical
• craniotomy with evacuation of clot. treatment of source of ICH {i.e. AVM, tumour,
cavernoma), ventriculostomy to treat hydrocephalus
• indications
• symptoms of raised ICP or mass effect
• rapid deterioration (especially if signs ofbrainstem compression)
• favourable location, e.g. cerebellar, non-dominant hemisphere
• young patient (<50 yrs)
• if tumour, AVM, aneurysm, or cavernoma suspected (resection or clip to decrease risk of
rebleed)
• contraindication&
• small bleed: minimal symptoms, GCS >10
• poor prognosis: massive hemorrhage (especially dominant lobe), low GCS/coma, lost
brainstem function
• medical reasons [e.g. very elderly, severe coagulopathy, difficult location (e.g. basal
ganglia, thalamus)]

Prognosis
• 30-day mortality rate 44%, mostly due to cerebral herniation
• rebleed rate 2-6%, higher if liTN poorly controlled

Intracranial Aneurysms
Epidemiology
• prevalence 1-4% (20% have multiple)
• female > male; age 35-65 years

Risk Factors
• autosomal dominant polycystic kidney disease ( 15%)
• fibromuscular dysplasia (7-21 %)
• AVMB
• connective tissue diseases (Ehlers-Danlos, Marfan's)
• family history
• bacterial endocarditis
• Osler-Weber-Rendu syndrome (hereditary hemorrhagic telangiectasia)
• atherosclerosis and HTN
• trauma

Types (Figure 4, NS3)

• saccular (berry)
• most common type
• located at branch points of major cerebral arteries (Circle of Willis)
• 85-95% in carotid system, 5-15% in vertebrobasilar circulation
• fusiform
• atherosclerotic
• more common in vertebrobasilar system, rarely rupture
• mycotic
• secondary to any infection of vessel walL 20% multiple
• 60% Streptococcus and Staphylococcus
• 3-15% of patients with SBE
Toronto Notes 2011 Cerebrovascular Disease Neurosurgery NS21

Table 7. 5-year Cumulative Rupture Risk in Unruptured Aneurysms Based on Size and Location
Cmlmo111 Cuolid ACJMCIIC V.llllbmbuillrJPC./PCIIIIIII
<7 mm 0% 0% 2.5%
7-12mm 0% 2.6% 14.5%
13-24mm 3% 14.5% 18.4%
<!:24 rnn 6.4% 40% 50%
It,- rilrior C8111bniV11118rior n.y; MC- middle c8lllbnll nry; K:- inllrnll ci!Oiid llllllry; PC- pnrior cnbmlllllllry; Ff.omm - po6Q
corrmuriclting 1r1Bry
1111 t.at2003;362:10J.IO

Clinical Presentation
• rupture (90%), most often SAH, but 30% ICH, 20% IVH, 3% subdural bleed
• sentinel hemorrhage ("thunderclap HIN) -+ requires urgent clipping/coiling to prevent
catastrophic bleed
• mass effect (giant aneurysms)
• internal carotid or anterior communicating aneurysm may compress:
• the pituitary stalk or hypothalamus causing hypopituitarism
• the optic nerve or chiasm producing a visual field defect
• basilar artery aneurysm may compress midbrain, pons (limb weakness), or CN III
• posterior communicating artery aneurysm may produce CN III palsy
• intracavemous aneurysms (CN III, IY, V1, V2, VI)
• distal embolization (e.g. amaurosis fugax)
• seizures
• headache (without hemorrhage)
• incidental CT or angiography finding (asymptomatic)

Investigations
• CT angiogram (CTA), magnetic resonance angiography (MRA), angiogram

Treatment
• ruptured aneurysms ,._,.. Tlill

• overall trend towards better outcome with early surgery or coiling (48-96 hours after SAH) CGiq il ZIU l'lliln with
• treatment options: surgical placement of clip across aneurysm neck, trapping (clipping .....,_lnlacrllill"-¥-: A....-..d
of proximal and distal vessels), thrombosing using Gugliemi detachable coils (coiling), ea..n-nrllh:ll• Slniwa, Dlf-llnllll
wrapping (last resort) - - 111111............. 11111Ani1J11111
• choice of surgery vs. coiling not yet well defined, consider location, size, shape, and Occbiln
1Mce!2005;36&:D17
tortuosity ofthe aneurysm, patient comorbidities, age, and neurological condition. In Thill randomilld trilllinld
general: endcMac:ullr dellc:l1lbll coiled 1rellment IQiinst
• coiling: posterior> anterior circulation, deep/eloquent location, basilar artery nialamy •nd rfppinvfor inlrlcllnilll
bifurcation/apex, older age, presence of comorbidities, presence of vasospasm IIIIIUfVIIIII il Pllients who were conside!ld elglile
fur eilhel rnoddly ct1herlpr.
• clipping: superficial > deep, broad aneurysmal base, branching arteries at the aneurysm Canlbin: In pllilnls v.itll rupblfld illrlc!will
base, tortuosity/atherosclerosis of afferent vessels, dissection, hematoma, acute brainstem IIIIIUfVIIIII Utili! fur bcJtb treldJnlrQ,
compression lllikMscull' coing ilmorelklly fD in
• unruptured aneurysms independent suM¥1111 1year 'dl111 nUIIUfgiCII
cipping; 11i11.1Niw11 bllllfit continUII far Ill lint
• average 1% annual risk of rupture: risk dependent on size and location of aneurysm 7years. The risk af lllllllbB!q il klw. but is
• no clear evidence on when to operate: need to weigh life expectancy
• risk of morbidity/mortality of SAH (20%/50%) vs. surgical risk (2%/5%) 1'IUOIIIViCII clppilg.
• generally treat unruptured aneurysms > 10 mm
• consider treating when aneurysm 7-9 mm in middle-aged, younger patients or patients with
a family history of aneurysms
• follow smaller aneurysms with serial angiography

Carotid Stenosis
Definition
• narrowing of the internal carotid artery lumen due to atherosclerotic plaque formation, usually
near common carotid bifurcation into internal and external carotids

Risk Factors
• for atherosclerosis: HTN, smoking, DM, CVD or CAD, dyslipidemia

Clinical Features
• may be asymptomatic
• symptomatic stenosis may present as TIA, reversible ischemic neurologic deficit (RIND), or
stroke
• retinal insufficiency or infarct permanently or temporarily (amaurosis fugax), (see Neuroloi}'> N47
and OP37)
• middle cerebral artery (MCA) occlusive symptoms
NS22 Neurosurgery Cerebrovaac:ular Disease/Vascular Malformations Toronto Notes 2011

,..__of!IIQqllldFIIII._IIJ Investigations
Sui:CIIIful Clnlid &IIIIIIIII:IDIIJ ill'dlnll • CBC, PTT/INR (hypercoagulable states)
MhlltRICIIIINUIIagi:ll • fundoscopy: cholesterol emboli in retinal vessels (Hollenhorst plaques)
lluilonUid C.allll Trill • auscultation over carotid bifurcation for bruits
Llnc:et2004; 363:1491-1502 • carotid duplex Doppler ultrasound: determines size oflumen and blood flow velocity, safest but
Slllly: AlympiDnwlic Carotid Sllgary Trill {ACST),
least accurate, unable to scan above mandible
a lilldomized, controlled 1rial will
5)WTI. • angiogram: "gold but invasive and 1/200 risk of stroke (not for screening)
l'llilnll: 3120 asymplomllic pl1ients NUl • MRA: safer than angiogram, may overestimate stenosis

111lllllr blllwlan immllilll carotid andulnclmny Treatment
(CEA) UJ1 indafuitB dafumll ri CEA IIIII \'MII • control ofHTN,lipids, diabetes
followad for up 1D 5years {maan 3.4 yBIIII. • antiplatelet agents (ASA ± dipyridamole, clopidogrel) -25% relative risk reduction
Mlil Oldaml: flirt stroke (incliding flllll or
dillblingl- • carotid endarterectomy (generally if symptomatic and >70% stenosis, see Tables 8 and 9)
c.:llli•: In pi!ien1swilh • endovascular angioplasty ± stenting
•CIIII CI!Qiid QlyQno5ia. immdlbl CfA
Nduced the nets..,.
stroke riskflom lllout Prognosis
1D llbaullft.. lid rltlis5-yalr bnlit iMMd
dillbling or fllal Slnla Table 8. Symptomltic Carotid Stenosis: North American Symptomatic Carotid Endarterectomy Trial
(NASCET)
%Stun• on Angiogr111
Medal Rx Medal + Sllf1liCII Rx
70-99% 26% over 2 years !1% over 2years
50-6!1% 22% over 5years 16% over 5 years
<50% Surgery has no benefit with 5% complicatiCillllte

Table 9. Asymptomltic Carotid Stenosis: Asymptomltic Carotic Atllerosclerosis Study (ACAS) and
Asymptomatic Carotid Surgery Trial (Acsn
%S1anosis on Angiogr111 Risk af Major Strub or Dllllh
MadicaiRx
60-9!1% 11% over 5 yea'S 5.1% over 5 years {ACASI
70-9!1% 11.8% over 5 years 6.4% over 5years {ACSTI

Vascular Malformations
Types
• arteriovenous malformations (AVMs)
• cavernous malformations (cavernoma, cavernous hemangioma/angioma)
• venous angioma
• capillary telangiectasias
• arterio-venous fistula (AVF) (carotid-cavernous fistula, dural AVF, vein of Galen aneurysm)
• "angiographically occult vascular malfonnations" (any type:, 10% of malformations)
• clinical significance:
• AVMs and cavernous malformations produce intracranial hemorrhages and scizu.rcs

Arteriovenous Malformations (AVMs)

,
..._.
..----------------.
Spetzler-M1rtin AVM Grading Scale
Definition
• tangle of abnormal vessels/arteriovenous shunts, with no intervening capillary beds or brain
parenchyma
• congenital
Itam Sc:ere
Size Epidemiology
0-3cm 1 • prevalence -0.14%, male:female = 2:1, average age at diagnosis= 33 years
3.1-6.0 em 2
• 15-20% of patients with hereditary hemorrhagic telengiectasia (Osler·Weber· Rendu syndrome)
>6cm 3
will have cerebral AVMs
Location
Noneloquent 0
Eloquent 1
Clinical Features
• hemorrhage (40-60%) - small AVMs are more likely to bleed due to direct high pressure AV
Deep vwn- dl'lin111 connections
Not prllllent 0
Present 1 • seizures (50%) - more common with larger AVMs
• mass effect
A'iM gl'llla8 Clbilbld tr;" addirQ tlla 3 inllvidull
Spallllr-MI11in Scala -.s 11om Ilia abova table. • focal neurological signs secondary to ischemia (high :O.ow -+ "steal
E.g. A2em 1llnDur in nonaloq.lllnt bcaliDn wilhout • localized headache:, increased ICP
daap wnoiJI chinaga Gradel. • bruit (especially with dural AVMs)
• may be asymptomatic ("silenn
'IbroDlo Nota 2011 Vucular MalfonnaHona/Cnemoua Malformations Neurosursery NS23

Investigations
• MRI (Bow void), MRA
• angiography (7% will also have one or more associated aneurysms)

Tnatment
• decreases risk offuture hemorrhage and seizure
• surgical excision is treatment of choice
• stereotactic radiosurgery (SRS) is preferred for small {<3 em) or very deep lesions
• endavascular emboliza.tion (glue. balloon) am facilitate surgery or SRS for larger lesions
• conservative (e.g. palliative embolization, seizure control ifnecessary)

Prognosis
• 10% mortality, 3D-50% morbidity (serious neurological defidt) per bleed
• risk of major bleed In untreated AV'Mk. 2-4% per year

Cavernous Malformations
Definition
• benign Vl!llcular hamartoma consisting of irregular sinUIIoidal vucular channels located within
the brain without intervening neural tissue or associated large arteries/veins

Epidemiology
• 0.1-0.2%, both sporadic and hereditary forms described
• several genes now described: CCMI, CCM2, CCM3

Clinical Features
• seizures (60%), progressive neurological deficit (5096), hemorrhage {20%), HIA
• often an incidental finding
• hemorrhage risk less than AVM, usually minor bleeds

Investigations
• T2WI MRI (non-enhancing); gradient echo sequencing {best for diagnosis)
• usually not seen with angiography or cr

Treatment
• surgical acision
• only appropriate for symptomatic lesions that are surgically accessible (supratentorial lesions
are less likely to bleed than lnfratentorialleaions)

Prognosis
• good with surgicallnterventlon

Figure 19. MRI uf CIV8IIIous

Mlllfennallon
A. T2 weighted imaging MRI
B. Gradient Echo aaquancing MRI
NS24 Neuro1urgery 1'oroDio 2011

,, ,
EXTRACRANIAL PATHOLOGY
..,...._
IIIIIOIWII Dlrlllll1181 IIIII

C2 - Anti• of jBw
C4 - Colar Df shirt Dermatomas/Myotomas
"C3A.5 lileP11hl diaplnam alive"
T4 - Nippla line
T6-Xiphoid
TIO-lnbiliCIII
l12-S..,apubil:
'1.3 abava lha knaa"
"S2,3,4 - Klllpl YIU' s1Dol olf1111 flw"

..... ,

Mvnnl•
C5 - Sho!Mir abductioNellow fllllion
Cl - Wrist IXIInsors
C7 - Bbow IDdlnlion
ca - Squ- hand
T1 - Abduct fiiG'ers
12-8 -lntlrcolllal (Abdominal n&.l
Tt-1 0 - Upperlbclomillll•
Tll-12 -I.Jiwar abdominall
l2-Fiax.hip
L3 - Hip addulrtion
L4- Knaa IDIIIInlliDIIand BJtla
L5 dorsiflaxian and big tDa
IIXtlnlion
Sl - Planlarflelt f11111 i
J
...i
(t

IIIIIIIDa F'11•r• 20. DanniiiDmas

1, 2 tia my shoe -> S1-2 Anlda jerk
3. 4 kidt lhe door-> LJ-4 ICMe
5, I pick up sticks -o C5-l Bicaps/
Brac:lioradilli•
7, Slay!hem *-ight -> C7-8 Triclpl
Approach to Limb/Back Pain
• see Orthqpaedics. OR22

RED FLMI fw IHII: 1'1111 Extradural Lesions

Cudlr.rlnl
Urilary rvtention or ineontinenc., f8eal
incontinanca or loss of anal spiW!ctar Root Compression
.......,
tone. IIddie an.U.ia. unLibilllel'll.lea
WAkneWpain.
Differential Diagnosis
Aga >50, prwiDUI hx of cancer; pain • herniated disk
lllr'lliaved by bad rast,. constitutional • neoplasm (neurofibroma, schWllllllOinll)
fYI'I1P1DmL • synovial c:}'!t. abscess
lnr.:tian.
lnCI'IIUtld ESR.. IV drug use. • hypertrophic bone/spur
fwlr.

c.....-.nfrlcb,. Cervical Disc Syndrome

Aga >SO.Irlllna. prolonged $hroid u.a.

Etiology
• nucleus pulposus herniates through annulus fibrosis and impinges upon nerve root
J

RED FLAGS fw lladl ..... Epidemiology

BACK PAIN • most common levels C6-C7 (C7 root) > C5-C6 (C6 root)
Bowel/lllddar ll'llllltion or
incontinence) Clinical Features
AnNihllillllldlte)
Constitutionel symptoms • pain down arm in nerve root distribution, worse with neck extension, ipsilateral rotation and
IChronic disease lateral flexion (all compress the ipsilateral neural foramen)
l'lrulhNil • LMN signs and symptoms
AQ1>5Dar<2D
• central cervical disc protrusion causes myelopathy as well as nerve root deficits
IYG'ug uu
NIUIIIIIotDr dlficihl
Investigations
• Ifred flags: C-splne x-ray, CT, MRI (imaging of choice)
• consider EMG, nerve conduction studies Ifdiagnosis uncertain
'IbroDlo Nota 2011 JW:radural Leal.ODI Neurosursery NS25

Treatment
• conservative
• no bedrest: unless severe radicular symptoms
"',.--------------.
, .
Disc hamidions lnpinga tha 111M root
• activity modiftcation, patient education (reduce sitting, lifting) It thaiMI below the illtnpaca (i.e.
• phys1otherapy. exerd8e programs C5-ti dise C& 1111rve 1\!111).

• analgesl.cs, collar, tractl.on may help

• surgical indications
• in:tnu:table pain despite adequate conservative treatment for >3 months
• progreMM: neurological deficit
• llll12rior cervical discectomy is usual ru.rgical choice

Prognosis
• 95% improve spontaneously in 4-8 weeks

Tillie 1D. Latenl Cervical Disc Syndrom11

Cl-7 C7-T1
lloGt hdvtMI C5 C& C8
•••rrFibras
2\ 10% FascicuUI gl'lcilirlcunllllul: joint
po.ition. fine txlueh, villnltion
SIIJuldar Rilg fing• 5th finger Spiullhlllamil: lnll:l: Pain 11'11
Delblid, biceps, Digillll flexors, nmsics
tampemn
tuplllpinlltul
CGrticaiPilll tract BkiBd movements
No clwlga llicapl. Bnlclial'lldillis Triceps Fingar jllk (Haffmam's iign)

Cervical Stenosis (Cervical Spondylosis)

Definition
• cervical spondylosis is chronic disc degeneration and usodated facet arthropathy
• resultant syndromes include mechanical neck pain. radiculopathy (root compreasion),
myelopathy (spinal cord compression) and combinations

Epidemiology
• typically begins at age 40-50, men >women, most commonly at the C5-C6 > C6-C7levels

Pathogenesis
• with neck atenslon. the c:ervical. cord is pinched. With neck flalon. the canal dimensions
increase slightly to relieve pressure on the cervical cord

Fetdures
• insidiOUII onset of mechanical neck pain exa.cerbated by excess vertebral motion (particularly Figu111 Z1 A. AliiaI uctian Df
rotation and lateral bending with a vertical compressive force - Spurling's test). Pain is worse Cervical Spine with Vasc•r Wid
with neck extension. relieved with flenon Functional Terltlclrlll
• ocdpltal headache is common
• radiculopathy may Involve 1 or more roots, and symptoms include neck. shoul&W" and arm pain,
paresthesias and numbness
• cervical myelopathy may be characterized by weakness (upper > lower extremity), decreased
derterity and sensory changa. UMN findings such as hyperreflexia, clonw and Babinslri reflex
may be present 1he most worrisome cmnplaint is lawex extremity weakneM (corticospinal tracts)
• myelopathy may be associated with funicular paiD. characterized by burning and stingiDg ±
Lhermitte's sign (lightning-like sensation down the back with neck flexion)

lnvutlgatlona
• x-ray of cervical spine ± flmOD!emnslon or oblique views (studied for changes in LU8chka and
fe.cet: joints, osteophytes and disc space narrowing), MRI, cr, EMG

Treatment
• NSAIDS, moist heat. strengthening and range of motion exercises, analgesics. cervical collar,
cervical traction
• surgical indications: myelopathy with motor impairment, progressive neurologl.c impairment. FlgUI'II 21 B. Axial secllon of
intractable pa.ln Tbonlcic Spine wilfl Vaacul• end
fiiiCiional TarritDria
NS26 Neuroaurgery 1'oroDio 2011

Lumbar Disc Syndrome

Etiology
• laterally herniated lumbar disc compre&lleS nerve root, central hernilllion caUIIes cauda
equina or lumbar stenosis (neurogenic claudication)

Epidemiology
• common (>95% of herniated lumbar disks) - L5 and Sl roots

Figure 21 C. Axial slldion of
Lu..bar Spinu with Vascul• and
Functloaal Terrllerlea
Clinical Fntures
• leg pain > back pain
• limited back movement (especially forward flexion) due to pain
• motor weakness. dermatomalsensory changes, reflex changes
• exacerbation with coughing. sneezing or straining. Relief with flexing the knee or thigh
• nerve root tension signs
• straight leg raise (SLR: Lasegue's test) or aossed SLR (pain should occur at less than 60
degrees) suggests LS, Sl root ilivolvement
• femoral stretch test suggests L2, L3 or L4 root involvement

Investigations
• x-ray spine (only to rule out other lesions), Cf, MRI
• myelogram and post-myelogram cr (only ifMRI ls contraindicated)

Treatment
• conserwtive (same as cervical disc disease)
• surgical indications
• same as cervical disc + cauda equina syndrome

Prognosis
• 9596 improve spontaneously within 4 to 8 weeks

Tablu11. Lllt:Dral Llnbar Disc Syu*a..us

Figure 21 D. AKial semion of S111:111l
Spine wltll Ya&cular aad Root ....... L4 L5 S1
Functloaal Terrllerlea
llcidaiC8 <10% 451. 45%

.....,.
Ptin flllllllllpattam
Madill leg
Sciatic patllm
Darsal foot to hab.
l..nnlleg
Sciatic palbln
l..a1inll !oat

MaiDr Tibillislllllerior Exlnar hal!cia Gntrocnemius, ealu

(dorlillsxion) \ballux lllnkln) (pllmr fl&Xian)
Raila. Klwejerk AM!ejerk

Tablu12. Diffl11111iating Ca1us Mldullaris Syu*a..u from Cauda Eq1ina Syndi'DIJII

Onset Suct:!an. blataral IDllal unilateral

SpaiDneaus Pain Rare. H11111111 usually symmallic Savan, radii:Uar type: in periniJJ11. 1hiP,
in pllileum ar thip legs,IB:k. or bladder
Sensory Deficit Saddle; bilill2nllllld symmelric; seRIIliV Sadcle; no sensiiY dissociation; may be
dilaociltion unilllarll end asymmetric
22.. 11-waightad MRI of
SVmmalric; pn&i& lass nBkad; AsyrrmaiJE; pnsi& IWJI9 mar1cld; lllqlby
l.umbllr Disc Humilltion fasciculatians may be IIISR may be llf8Sid; fascil:ulatians nn
Rellees Dnly lrile jett Bbslft (presEM!d blee jerk) Knee end 111kle jllk lllll'f be absent
Autonomic (bladder !mary retEntion end lltlmic -1 Sphincter dyWJdian presents IE;
dysfunction, elc.) II'Dftilant 811fv; iq)otanca impatBnca lass fnlcpn
Toronto Notes 2011 Extradural Lesions Neurosurgery NS27

Cauda Equina Syndrome

---------------------------------------
Etiology
• compression or irritation oflumbosacral nerve roots below conus medullaris (below L2level)
• decreased space in the vertebral canal below 1.2
• common causes: herniated disk ± spinal stenosis, vertebral fracture and tumour

Clinical Features
• usually acute (develops in less than 24 hours); rarely subacute or chronic
• motor (LMN signs)
• weakness/paraparesis in multiple root distribution
• reduced deep tendon reflexes (knee or ankle)
• autonomic
• urinary retention (or overflow incontinence) and/or fecal incontinence due to loss of anal
sphincter tone
• sensory
• low back pain radiating to legs (sciatica) aggravated by Valsalva maneuver and by sitting;
relieved by lying down
• bilateral sensory loss or pain: depends on the level affected
• saddle area (S2-S5) anesthesia
• sexual dysfunction (late finding)

Treatment
• urgent investigation and decompression (<48 hrs) to preserve bowel, bladder and sexual
function and/or to prevent progression to paraplegia

Prognosis
• markedly improves with surgical decompression
• recovery correlates with function at initial presentation: if patient is ambulatory, likely to
continue to be ambulatory; if unable to walk, unlikely to walk after surgery

Lumbar Spinal Stenosis

Etiology
• congenital narrowing of spinal canal combined with degenerative changes (herniated disk,
hypertrophied facet joints and ligamentum flavum)

Clinical Features
• gradually progressive back and leg pain with standing and walking that is relieved by sitting or
lying down {neurogenic claudication - 60% sensitive)
• neurologic exam may be normal, including straight leg raise test

Investigations
• spine x-ray, cr, MRI, myelogram

Treatment
• conservative - NSAIDs, analgesia
• surgical-laminectomy with root decompression

Neurogenic Claudication ----------------------------------

Etiology
• ischemia oflumbosacral nerve roots secondary to vascular compromise and increased demand
from exertion, often associated with lumbar stenosis

Clinical Features
.... ,,

• dermatomal pain/paresthesia/weakness of buttock, hip, thigh, or leg initiated by standing or
walking IC8y fAtu8l uf Neurogenic w.
v-1u CIMit:don
• slow relief with postural changes (sitting >30 min), NOT simply exertion cessation
• induced by variable degrees of exercise or standing Claudlclltian: denmrtolllll
distribution with positional relief
• may be elicited with lumbar extension, but may not have any other neurological findings, no accurrilg over minutes.
signs of vascular compromise (e.g. ulcers, poor capillary refill, etc.)
Vacular CIMit:don: sclarotomll
distribution with relief accurrilg with
Investigations rest owr s1condl.
• bicycle test may help distinguish neurogenic claudication (NC) from vascular claudication (the
waist-flexed individuals on the bicycle with NC can last longer)

Treatment
• same as for lumbar spinal stenosis
NS28 Neuro1urgery Intradural Intramedullary Lai.ODI/Spinal Cord 1'oroDio 2011

Intradural Intramedullary Lesions

Syringomyelia
Definition
• cystic cavitation of the spin81 cord
• presentation is highly variable, usually progresses over months to years
• initially pain and weakness; later atrophy and loss ofpain and temperature sensation
Etiology
• 7096 are associated with Chiari I malfoi'IIl8tion
• post-traumatic
• tumour
Clinical Features
• nonspecific features for any intramedullary spin81 oord pathology:
• sensory loss similar to central cord syndrome
• pain and temperature loss with preserved touch and joint position sense in a cape-like
distribution at level ofcervical syrinx
• dysesthetic pain often occurs in the distrlbution of the &eDllory l.o&a
• LMN arm/hand weakness or wasting
• painless arthropathles (Charcot's joints), especially in the shoulder and neck due to loss of
pain and temperature sensation (seen in less than 5%)

Flg1re Z3. T1 WelgMid IIIRI of Investigations

SyringDmyalil • MRI is best method, myelogram with dela}'M CT
Treatment
• treat underlying cause (e.g. posterior fossa decompression for Chiarl I. surgical removal of
tumour ifcausing a syrinx)

Spinal Cord Syndromes

Spinal Cord Injuries
• N4. for spinal cord anatomy
....... , Complete Spinal Cord Lesion
• bilateral loss of motor/sensory and autonomic function at :M segments below lesion/injury, with
Compartmentalize spillll cord UMNsigns
lllllomil:lllv by loaation. • about 396 of patients with complete in:jurie& will develop some recovery within 24 hours, beyond
24 hours, no dlstaJ. function will recover
Incomplete Spinal Cord Lesion
• any residual function at :2:4 segments below lesion
• signs include sensory/motor function in lower li.mbs and "sacral sparing" (perianal sensation,
voluntary rectal sphincter contraction)

II
'1i!
.B T•ble13. CDmJMriiOn b8tween IIICGIIIplete Spinal Card l..eiiDn Syndrom11

Hemiseetion of card lpsilatinl Lt.lll weakness Ipsilateral loss of vibration and pra!Jiacaptian
at tha l11im Cormlataralloss of pail111d ta'npnure
lpsilatanll UMN waakness PmiMIII lii#Jtlauch
bllaw lha l11ian
A111H Canl Anterior spinal .my BilatemllMN weakness Presi!M!d vlnlion and proprioceplion
1:011_.eaion r. at the lesioo Bilteralloss d pain and lefl1llnlure
occlusim Bilateml UMN 'ltoelkness Presi!M!d lii#Jt tuul:h
belaw the lesion
Urillry 1'818nti111
Celml Card Sytivlmytlia_ tlmaur&, BiiUDI mlltlr Wlllkna&s: Vllilbla blldsi'IIIIU&pal1dad slll&aly loa
(most commm) spinal Uppa' 1mb W8lkna&s (l.llfi lesion) Loss d pain and tsiJ'C)III'Era 1han lass
iniiiY (J8Itsr 1Im of vibl'llian and
LDwer liiD waalcness (UMN lasianl
Urillry llllantian
P'allllriar Cord IU!arir. spinal allay PmiMIII Blalaralloss of vibration. ptapriocaptian. light
infarction. 'lnUIII twch at and balcrN lha !asian
Presi!M!d pail MJd

Figure 24. Spi•ll CaniLBsian

Spdi'DIIIIIS
Toronto Notes 2011 Peripheral Nerves/Neurotrauma Neurosurgery NS29

Peripheral Nerves
• see Neurology; N30

Classification and Clinical Course

• neurapraxia: axon intact but fails to function, recovery within hours to months
• nerve entrapment: nerve compressed by nearby anatomic structures, often secondary to
localized, repetitive mechanical trauma with additional vascular injury to nerve -+ sensory loss
in nerve distribution (often discriminative touch lost first)
• axonotmesis: axon disrupted but nerve sheath intact -+ Wallerian degeneration of axon segment
distal to injury-+ axonal recovery of I em/month, max at 1-2 years
• neurotmesis: nerve completely severed, need surgical repair for recovery

Investigations
• neurological exam (power, sensation, reflexes), localization via Tinel's sign (paresthesia& elicited
by tapping along the course of a nerve}
• electrophysiological studies (EMG, nerve conduction study) may be helpful in assessing nerve
integrity and monitoring recovery; not helpful unti12-3 weeks post-injury
• labs: bloodwork, CSF
• imaging: C-spine, chest/bone x-rays, myelogram, CT, MRI "neurography" to rule out cerebral/
spinal cord lesions, identify etiology
• angiogram if vascular damage is suspected

Treatment
• early neurosurgical consultation if injury is suspected
• entrapment
• conservative: prevent repeated stress/injury, physiotherapy, NSAIDs, local anaesthesia!
steroid injection
• surgical: nerve decompression ± transposition for progressive deficits, muscle weakness/
atrophy, failure of medical management
• stretch/ contusion
• follow-up clinically for recovery; exploration if no recovery in 3 months
• axonotmesis
• if no evidence of recovery, resect damaged segment
• prompt physical therapy and rehabilitation to increase muscle function, maintain joint range
of motion, and maximize return of useful function
• recovery usually incomplete
• neurotmesis
• surgical repair of nerve sheath unless known to be intact [suture nerve sheaths directly if
ends approximate or nerve graft (usually sural nerve)]
• clean laceration: early exploration and repair
• contamination or associated injuries: tag initially with nonabsorbable suture, reapproach
within 10 days

Complications
• neuropathic pain: with neuroma formation
• complex regional pain syndrome: with sympathetic nervous system involvement

SPECIALTY TOPICS

Neurotrauma
Trauma Management (see also Medicine, ER7}

Indications for Intubation in Trauma

1. depressed WC (patient cannot protect airway): usually GCS
2. need for hyperventilation
3. severe maxillofacial trauma: patency of airway is doubtful
4. need for pharmacologic paralysis for evaluation or management
• ifbasal skull fracture suspected, use orotracheal instead of nasotracheal intubation
• note: intubation prevents patient's ability to verbalize for determining GCS
NS30 Neurosurgery Neurotrauma Toronto Notes 2011

Trauma Assessment
..... ,

INITIAL MANAGEMENT

Glaqaw Corllll Scale

ABC's of Trauma Management
• see Emeri!=DQ" Medicine. ER8
4......... 5orinlld NEUROLOGICAL ASSESSMENT
lOIDI!II 400lhslil
••
Z-1!1111 3lllllnldii!MIIII 4lllllnllflllnlllll
Mini-History
• period of LOC, post traumatic amnesia, loss of sensation/function, type of injury/accident
Plil

-.
1noeyeopllilg 3lelionl0poil
.... . .. pa!UiiQ
Neurological Exam
• Glasgow Coma Scale (GCS)
, .. ,...... 2lllllm0110poil head and neck (lacerations, bruises, basal skull fracture signs, facial fractures, foreign bodies)
,........ •
• spine (palpable deformity, midline pain/tenderness)
ln1- • eyes (pupillary size and reactivity)
• brainstem (breathing pattern, CN palsies)
• cranial nerve exam
• motor exam, sensory exam (only if GCS is 15), reflexes
• sphincter tone
It'
• record and repeat neurological exam at regular intervals
Assessment of Spl• CT/X-ray
IPII'IIAtlittll vilwl Investigations
ABCDS
• spinal injury precautions (cervical collar) are continued until c-spine is cleared
Al9mlent (Columns: lllllerior • C,T,L-spine x-rays
v.n.bnlllin1, portarior vtlrtablllllinl, • AP,lateral, odontoid views for C-spine (must see from Cl to T1 (swimmer's view if
spinolaminar line, posterior spinou5 tine) necessary) or CT
IIane (vartebral bodies, facets, spinous
proce5Ses)
• rarely done: oblique views looking for pars interarticularis fracture ("Scottie dog" sign)
Cartilqa • CT head and upper C-spine (whole C-spine if patient unconscious) look for fractures, loss of
Disc (disc space and inbnpinous mastoid or sinus air spaces, blood in cisterns, pneumocephalus
spiC8) • cross and type, ABG, CBC, drug screen (especially alcohol)
Softtissun
• chest and pelvic x-ray as indicated

TREATMENT

Treatment for Minor Head lniury

• see Canadian CT Head Rule sidebar, Emer.senc:y Medicine. ER8
• observation over 24-48 hours
• wake every hour
• judicious use of sedatives or pain killers during monitoring period

Treatment for Severe Head lniury (GCS s8)

• clear airway and ensure breathing (if GCS sa, intubate)
• secure C-spine
• maintain adequate BP
• monitor to detect complications (GCS, CT, ICP)
• monitor and manage increased ICP if present (see Herniation Syndromes, NS6)

Which patients should be admitted to hospital?

• skull fracture
Wblch !'dents Need CT Hull or
Tl'llllf1lr to 1 Nlm'DIUf1llcll C.ntrl1 • indirect signs of basal skull fracture
• Remains aftar • confusion, impaired consciousness
resuscitation • focal neurological signs
• Faclll neurological signs • extreme headache, vomiting
• Deterianrtilg
• seizures
• concussion with >5 minutes amnesia
• unstable spine
• use of alcohol
• poor social support (i.e. no friend/relative to monitor for next 24 hours)
• if there is any doubt, especially with children

KEY POINTS
• never do lumbar puncture in head injury unless increased ICP has been ruled out
• all patients with head injury have C-spine injury until proven otherwise
• alcohol may not be the cause of coma - there may also be a hematoma
• low BP after head injury means injury elsewhere
• must clear spine both radiologically AND clinically (will require re-assessment if/when patient
improves clinically)
Toronto Notes 2011 Neurotrauma Neurosurgery NS31

Head Injury
-------------------------------------------------
Epidemiology
• male to female: 2-3:1

Pathogenesis
• acceleration/deceleration: contusions, subdural hematoma. 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 Etioloaill
• high velocity: highest damage away from missile tract • WNA (30-55')(,1
• Falls (1 >35%1
• Gun Shot Wound (S.20'1'ol
Scalp Injury
• rich blood supply
• considerable blood loss (vessels contract poorly when ruptured) .... ,,

• minimal risk of infection due to rich vascularity
U,.rsllf Sclllp
Skull Fractures SCALP
• depressed fractures: double density on skull x-ray (outer table of depressed segment below inner Skin
table of skull), CT with bone windows is gold standard Comective tissue (dense)
Aponeurosis {galea)
• simple fractures (closed injury): no need for antibiotics, no surgery Loou connectiw tissu1
• compound fractures (open injury}: increased risk of infection, surgical debridement within Periostllum
24 hours 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 ecchymoses (Battle's sign)
• periorbital ecchymoses (raccoon eyes)
• hemotympanum
• CSF rhinorrhea. otorrhea (suspect CSF ifhalo or target sign present); suspect with Lefort II/
III midface fracture

Cranial Nerve Injury

• most traumatic causes of cranial nerve injury do not warrant surgical intervention
• surgical intervention
• CN II -local eye/orbit injury
• CN III, IY, VI- if herniation secondary to mass
• CN VIII - repair of ossicles
• CN injuries that improve
• CN I - recovery may occur in a few months; most do not improve
• CN III, IY, VI - majority recover
• CN VII - recovery with delayed lesions
• CN VIII - vestibular symptoms improve over weeks, deafness usually permanent (except
when resulting from hemotympanum)

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

Intracranial Bleeding
(see Blood, NS15 and Cerebrovascular Disease, NS17)

Brain Injury
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 ..... ,
• concu,.ion: a trauma-induced alteration in mental status
• American Academy of Neurology (AAN) Classification (see sidebar)
...----------------.
• no parenchymal abnormalities on CT AAN Clulliflc:nan
Grade I : altered lllllltll status < 15 min
• coup (damage at site ofblow) Grade 2: altered lllllltll status > 15 min
• contre-coup (damage at opposite site ofblow) Grad• 3: any loss of consciousn111
• acute decompression causes cavitation followed by a wave of acute compression
NS32 Neuro1urgery
'' ,
• Exa'ni1115 nin for .,..ill
IIIII a1N symptar.-.
• IIJblm Ia nonnaiii:IMty H
lyn¢rml willin 15 nn
2 • lllrncrw fnlm activity far
1day, 1hlln - -
• CT or MRI HIVA ar atber
lyn¢rmi1MDIII II' IIIII
>lwaek
• lllbJm 111 nannalactMly llftlr
• ischemia/infarction
3 • Em1111n1 DIIIIIIIIIKIIm +
illlllllilg;HirDIIIICMiil
1111 hOlM wi1ll
clollfaiOW up
• M'nUIIIVtip of ,-ttlllotv
« pa'Sislant abnormlll menlill
slllus
• CT or MRI HIVA or atber
IP/II1Ihllll
• fbriefooncussionl<1 ITin),
ratum 1o nannalactMly lfllr
, waek withatd:syn1fDml
• f pllllmgad OOI'ICI&Iian
I> 1nin), rWim ta nallllll
II:IMtv .nv• 2..,..
wilhaul
Direction Df Fun:a
Figure ZS. CT Showing
Ceep-Contr.Coup InJury
Neurotrauma 1'oroDio 2011
• 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 vesscll (hemorrhagic foci)
• often the cause of decreased LOC ifno space occupying lesion on cr
Secondary Pathologic Processes
• same subsequent biochemical pathways for each traumatic etiology
• delayed and progressive injury to the brain due to
• high glutamate release -+ NMDA -+ cytotoxic cascade
• cerebral edema
• intraaanial. hemorrhages
• raised ICP,lntracranial. HTN
•hydrocephalus
Extracranial Conditions
• hypoxemia
• due to trauma to the chest, upper airway, bra.instem
• extremely damaging to vulnerable brain cells
• leads to ischemia. raised ICP
• hypercubia
• 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
·hyperpyraia
• leads to increased brain metabolic demands -+ ischemia
• fluid and electrolyte imbalance
• iatrogenic (most common)
• SIADH caused by head injury
• diabetes lnslpidus (DI) from head injury
• may lead to cerebral edema and raised ICP
• coagulopathy
Intracranial Conditions
• raised ICP due to traumatic cerebral edema OR traumatic intracmnial hemorrhage
Brain InJury Outcomes
• mJl.dl.y traumatic (GCS 13-15): post-concus&l.ve symptoms: HIA. fatlgu.e, dizzine88
nausea, blurred vision, diploplia, memory impairment, tinnitus, irritability, low
concentration; 5096 at 6 weeks, 1496 at 1 ytm
• moderately traumatic (GCS 9-12): proportional to age (>40) and CT findings; 6096 good
recovery, 2696 moderately disabled. 796 severely disabled. 796 vegetative/dead
• severe (GCS S8): difficult to predict. correlates with post-reSU&dtation GCS (espedally motor)
and age
Late Complications of Head/Brain Injury
• seizurea: 596 afhead Injury patients develop seizures
-----
• inddence related to severity and location of injury (increased with local brain damage or
intracranial hemorrhage)
• post-traumatic seizure may be immediate, early, or late
• presence ofearly (within first week) post-traumatic seizure raises incidence oflate seizures
• meningitis: associated with CSF leak from nose or ear
• hydrocephalus: acute hydrocephalus or delayed normal preiSUre hydrocephalw (NPH)
Toronto Notes 2011 Neurotrauma Neurosurgery NS33

Spinal Cord Injury (SCI)

• see Orthopaedics. OR22 and EmemencyMedidne. ER9
O..RJirillw•41waa• -.._nlllal11ial
............... card iljnd pllillls?
Neurogenic and Spinal Shock ,...... ...... 1....... .....
1. neurogenic shock: hypotension that follows SCI (SBP usually S:80 mmHg) caused by

• interruption of sympathetics (unopposed parasympathetics) below the level of injury Spiii/CII'II2004;

lllrodadon: T1'il study YlliS liNd II illllrmning
• loss of muscle tone due to skeletal muscle paralysis below level of injury -+ venous pooling l'lllellierneudogi:IIIM:omewu improved will
(relative hypovolemia) early 1<24 houll) lliial WV8'Y
• blood loss from associated wounds (true hypovolemia) as C1J1111111Bd 1D lither ID 1>24 hou,.j 11111111V cr
2. spinal shock: transient loss of all neurologic function below the level of the spinal cord injury, -mMI m-uanart.

causing flaccid paralysis and areflexia for variable periods 37lllicl•. •lulll"' 1683 eligibl& plli8rQ
ltnioomic spinal iljuy), 919 lWii
Whiplash-Associated Disorders irid 764 lWii"" IIIIIIUDgicll

• definition: traumatic injury to the soft tissue structures in the region of the cervical spine due to dlficit lkill:on wu dltllriied bv' cak:ulltiig
the percenblge al pllieniJ Mil senSOIY or molD!
hyperfle.xion, hyperextension or rotational injury to the neck r..ction irnprMrnentiiCCOI'ding 1D the FninQI'1
ale.
Initial Management of SCI buill: &II;' daCIJII1IIIRion I1UIBd in imp!Md
• major causes of death in SCI are aspiration and shock wtcoma COII1llll1d 10 hotllllltand COIII8MtM
tni.......
• the following patients should be treated as having a SCI until proven otherwise: inPv IP<O.DDIIIdi
• all victims of significant trauma slides 11Milled .... pllie!O
• minor trauma patients with decreased LOC or complaints referable to neck or hack pain or illdQJing nrlv lor incomplll
SCI (weakness, abdominal breathing, numbness/tingling, priapism) inPv wu homogenous lp>O.IP.iL howeveull
iilhar .. lwtaraganaity.
Can&bln: Allilllglllllti!ti:lt{ jll1illilirQ. Mil
Stabilization and Initial Evaluation In the Hospital .... lick of pllianl bomOQIIIIIity il T8C8i1l sbilial,
1. ABC's tlil anll riCGIIIIiliidaliJn isilatMiugical
2. immobilization: maintain backboard/head-strap and use log-rolling during transfers decompression be considnl as "" optional
3. hypotension: maintain sBP mmHg with priCtica liii!JMrG 1l'lllnllic spilllll Cllld ....
• pressors ifnecessary: dopamine is agent of choice (avoid phenylephrine - causes reflex
bradycardia)
• hydration (cautiously to prevent pulmonary edema) ............ hllmnliiiCIDipi..
• atropine (for bradycardia associated with hypotension)
4. oxygenation ......,..,,...had ......
.
. . . dnugllt

7lit Spiil.lrunl/2006; 6:335-343

5. NG tube to suction: prevents NN, decompresses abdomen to facilitate breathing
lllrodlllliln: BIQng in lhlla 70's irid
6. foley catheter to urometer (to monitor ins and outs) tliraugb1DU.eerly ID's tlil Nltilll'lll Awtl Spinll
7. DVT prophylaxis CGnl ..jlly SWes INASCISI were Clllluclld in
8. temperature regulation tlir8e llrgt lliidomillld conlrolled trilll,liid lium
9. monitor CBC/electrolytes tiiCIIelriillthei'IICIIIIIIiilllllltion1Dgivepltients

10. focused history
injly. trocal Mlation "' 81Ch of these trills-
• mechanism of injury (hyperflexion, extension, axial loading, etc.) the ¥'If' led tliele din to usess1hellellm
• weakness/numbness/tingling in extremities lird.iding tlil NASCIS tri*I1D ri·MYtttlil
11. palpate spine for evidse belind
• point tenderness Malhodr,fgpulllion: Acrialllpllli5ll of the dB
the NASCIS studies alonill'lilh
• a "step-off" deformity
a
• widened interspinous space lflcl of MP on ICiill spilll injury.
12. motor level assessment - grade with American Spinal Injury Association (ASIA) Standards buill: Tlilllllhors r1il8 .-1 iau8l
• skeletal muscle exam l'tilhmh of NASCS land incliding 1111 fltt
• rectal exam for voluntary anal sphincter contraction tlllts1ldisticalanlysis wu onlv
13. sensory level assessment (grade with ASIA Standards) m ofthl NASCIS I mil blnllill
were only obserwd spinll ijlies.
• sensation to pinprick (spinothalamic tract) NASaS II was awlullad for lick of apilnllion
• sensation in face (spinal trigeminal tract can sometimes descend as low as C4) 411 oplirun MP liming Ulng Mlllaikle ID "'llO''
• sensation to light touch (anterior spinothalamic tract in anterior cord) mGtur claiiJIII post-tliellpl' on hotlllhe righl111d
• proprioception (posterior columns) 11ft lid1 oftlil body. qgasting lhll ch-.gn in

14. evaluation of reflexes
tlilliillliingkbill&!itliii'IIUI!s. Odi«llior
15. signs of autonomic dysfunction: altered levels of perspiration, bowel or bladder incontinence, sUiies lliled Ill fel)rocb:e 1lie resuls NASC1S. «
priapism IUdim is11i1 lactDrtllltlllldi•
16. radiographic evaluation Iince NASCIS lim II incUIId r.t' since it was
• 3 view C-spine x-rays (AP,lateral and odontoid) to adequately visualize C1 to C7-Tl tllrA9t 1D be LMiethiciiiD indMdulls111

junction aplacdlo111014).
CliiCbiu: 1lia Dim conclidalhat basad on
• oblique views to assess integrity of articular masses and lamina U.. mil OIW mlljarcriticilms al tlil NASCIS
• flexion-extension views to disclose occult instability II mil Ill. nny lilllrougicll depltlmaiitl liM
• cr scan (bony injuries) ± MRI (soft tissue injuries) ttopped using MP as alllnillld rwlinl iiiiCIIIIi
spinll cord inpy,liid also notetlilt its use is not
Medical Management Specific to SCI Cllllllltt IICGIIII'IIndld bythl Food mil Drug
Adirinistnltion il111e IXiW SIRs. They111ggest
• methylprednisolone (given within 8 hours of injury) liltliarinvllltigltionis"'*''llllldto-rlhil
• ±decompression in acute, nonpenetrating SCI (Fehlings and Tator, 1999) tJjeStionCOIIcUsNeiy.
NS34 Neuroaurgery Neurotrauma 1'oroDio 2011

Fractures of the Spine

Fractures and Fracture-Dislocations of the Thoracic, Thoracolumbar and Lumbar
Spine
• usessligamentous inltability wing flexion/ab:nsion x-ray views ofC-spine ± MRI
• thoracolumbar spine unstable if416 segments disrupted (3 columns divided into left and right)
• anterior column: anterior half of vertebral body, disc and anterior longitudinal ligament
• mlddle column: posterior half of vertebral body, dJsc and posterior longitudinal ligament
• posterior column: posterior arch, facet joints, pedicle, lamina and supraspinollll, interpinous
and ligamentum ligaments

Types of Injury (Dennis Classification)

• compression fracture (58%)
• produced by flexion
• posterior ligament complex (supraspinous and interspinous ligaments, ligamentum flavum
and Intervertebral Joint capsules) remain Intact
• fractures are stable but lead to kyphotk deformity
• burst fracture (1796)
• stable: a.o:rerior and middle columns parted with bone retropulsed nelll'by
• hallmark is pedicle widening on AP X-ray
• spinal cord (seen on x-ray and CO: posterior colwnn is uninjured
• unstable: same as the stable but with posterior colwnn disruption (usually llgamentous)
• fl.exl.on diatraction injury (6%)
• byperfl.exion and distra.ctl.on of posterior elements
• middle and posterior columns fail in distraction
• classic: Chance = horizontal fracture through posterior arch, pedicle&, posterior vertebral
body
• can be purely ligamentous, i.e. through PLL and disc
• fracture-dislocation (6%)
• anterior and aanial dislocation ofsuperior vertebral body -+ 3 colwnn fallure
• three types:
• flexion-rotation
• flexion-distraction
• shearthypermension (rare)

Figure 2&. Odcmtuid Fracture Fractures of the Cervical Spine

Clasalllcatlo•
'1\fpes of InJury
• Cl vertebral fracture {Jefferson fracture)
• vertl.cal compression forces the occtpltal condyles of the skull down on the Cl vertebra
(atlas), pushing the lateral massea of the atlas outward and disrupting the ring of the atlas
• also am cause an occipital condylar fracture
• odontoid process fracture
• caW!e& Cl and odontoid of C2 to move independently ofC2 body
• this occurs because
• normally Cl vertebra and odontoid ofC2 are a single functional unit
• alar and transverse Ugaments on posterior aspect ofodontoid most commonly remain
Intact following injury
• patients often report a feeling of instability and present holding their head with their hands
• C2 vertebral fracture (hangman fracture, traumatic spondylolisthesis of u:is):
• bilateral fracture through the pars interarticularis ofC2 with subluxation ofC2 on C3
• usu.ally neurologically intact
• clay shoveler's fracture
• avulsion of spinous process, usually C7

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

Trelltment
• immobilimtion in cervical collar or halo vest until healing occurs. (usually 2-3 months)
• Type II and III odontoid fractures
• consider surgical :fintion for comminution, displacement or inability to maintam alignment
with externallmmobili.zation
• onfirm stabillty after recovery with ftal.on-menslon x-rays
Toronto Notes 2011 Neurotrauma Neurosurgery NS35

Neurologically Determined Death

------------------
Definition
• irreversible and diffuse brain injury resulting in absence of clinical brain function
• cardiovascular activity may persist for up to two weeks

Criteria of Diagnosis
• prerequisites: no CNS depressant drugs/neuromuscular blocking agents, no drug intoxication/
poisoning, temperature >32<>C, no electrolyte/add-base/endocrine disturbance
• absent brainstem reflexes:
• absent pupillary light reflex
• absent corneal reflexes
• absent oculocephalic response
• absent caloric responses (e.g. no deviation of eyes to irrigation of each ear with 50 cc of ice
water- allow 1 min after injection, 5 min between sides)
• absent pharyngeal and tracheal reflexes
• absent rough with tracheal suctioning
• absent respiratory drive at PaC02 >60 mmHg or >20 mmHg above baseline (apnea test)
• 2 evaluations separated by time, usually performed by two specialists (e.g. anesthetist,
neurologist, neurosurgeon)
• confirmatory testing: flat EEG, absent perfusion assessed with cerebral angiogram

Altered Level of Consciousness

Evaluation of Patient

History
• previous/recent head injury (hematoma)
• sudden collapse (ICH, SAH)
• cardiovascular surgery, prolonged cardiac arrest (hypoxia)
• limb twitching, incontinence, tongue biting (seizure, post-ictal state)
• recent infection (meningitis)
• other medical problems (diabetes mellitus, renal failure, hepatic encephalopathy)
• psychiatric illness (drug overdose)
• telephone witnesses, read ambulance report, check for medic-alert bracelet
• neurologic symptoms (headache, visual changes, focal weakness)

Physical Examination
• Glasgow Coma Scale (see sidebar, Neurotrauma, NS30)
• pupils: reactivity and symmetry, papilledema (increased ICP)
• reflexes:
• corneal reflex: normal = bilateral blinking response
• gag reflex: normal = gag
• oculocephalic reflex (doll's eye): normal= eyes move in opposite direction of head, as if
trying to maintain fixation of a point Clleric Refllllll
• vestibulooochlear response (cold caloric): nonnal = nystagmus fast phase away from cows
stimulated ear Cold
Opposite
• deep tendon reflexes Warm
• plantar reflexes: normal = flexor plantar response :sam.
• tone
• spontaneous involuntary movements
• assess for meningeal irritation, increased temperature
• asses for head injury, Battle's sign, raccoon eyes, skin rashes, and joint abnormalities that
may suggest vasculitis

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 (RAS) or their
connecting fibres
• focal supratentorial lesions do no alter consciousness except by herniation (compression on the
brainstem or on the contralateral hemisphere) or by precipitating seizures
NS36 Nearomrgery 10ronto Nota 2011

Clauificlll:ion
• structural. lesions (tumour. pus, blood, infarction, CSF): 1/3 af comas
• supratentoriallll88slesion -leads to herniation
• infratentoriallesion- compression af or direct damage to the RASor its projections
• metabolic disorders!clitfuse hemispheric damage: 2/3 of comas
• deficiency of essential substrates (e.g. oxygen. glucose. vitamin Bu)
• exogenous tm1ns (e.g. drugs, heavy metals, solvents)
• endogenous toxins/sywtemic metabolic diseases (e.g. uremia, hepatic encephalopathy,
electrolyte imabalances, thyroid stmm)
• infections (meningitis, encephalitis)
• trauma (concussion, diffuse shear uonal damage)

lnvestiglll:ions and Management

• ABCs
• l.ab3: electrolytes, TSH, I.Ffs, Cr, BUN, Ca, Mg, PO" toxin screen, glucose
• Cf/MRI, LP, BEG

Persistent Vegetative State

Definition
• a condition ofcomplete unawareness of the self and the environment accompanied by sleep-
wake cycles with either complete or partial preservation ofhypothalamic and brain5tem
autonomic function
• "awake but not awari'
• fullows comatose state

Etiology/Prognosis
• most commonly caused by cardiac arrest or head Injury
• due to irreversible loss ofcerebral cortical function BUT intact brainstem function
• avenge life expectancy is 2-5 years

Pediatric Neurosurgery
Spinal Dysraphism
---------------------------------
SPINA BIADA OCCULTA

Definition
• congenital absence ofa spinous process and a variable amount aflamina
• no visible exposure ofmeninges or neural tissue

Epidemiology
• 15-2096 ofthe general population; most common at LS or SI
Hair tuft
Etiology
• failure of fusion of the pollterior neural arch

Clinical Felll:ures
• no obvious clinical signs
• presence aflumbosacral cutJLneous abnormalities (dimple, sinus, port-wine stain. or hair tuft)
Figure 27. SpiR Bifillla Occulbl should increase suspiclon ofan underlying anomaly (lipoma. dermoid, diastomatomyella)

Investigations
• plain film - absence ofthe spinous proceas along with minor amounts of the neural arch
• U/S or MRI to exclude spinal anomalies

Tralll:ment
• requires no treal::nlellt

MENINGOCELE (SPINA BIFIDA APERTA)

Definition
• herniation of meningeal tissue and CSF through a defect in the spine, without associated
herniation of neural tissue
'IbroDlo Nota 2011 Pecliatric Neurosurgery Neurosurgery NS37

Etiology
• primary fiillure of neural tube closure

Clinical Features
• most common in lumbosacral area
• usually no disability, low inddence ofassociated anomalies and hydrocephalus

Investigations
• plain film&, cr, MRI, UIS, echo, geniiDurinary (GU) investigations

Treatment
• surgical adsl.on and tissue repair (excellent results)

MYELOMENINGOCELE

Definition
• herniation of meningeal and CNS tissue through a defect in the !pine

Etiology
• same as meningocele
Clinical Features
• sensory and motor changes distal to anatomk level producing varying degrees of weakness
• urinary and fecal incontinence
• 65-8596 of patients with myel.omeniDgocele have hydrocephalus
• most have Type II Chiari malfonnatlon, see NS38
i
Investigations
• plain film&, cr, MRI, UIS, echo, GU investigations
-
."'..
Q

Figu111 21. Myela•aningacela

Treatment
• surgical closure to preserve neurologic status and prevent CNS infections

Prognosis
• operative mortality close to 0%, 95% 2-year survival
• 80% have IQ >80 (but most are 80-95), 40-85% ambulatory, 3-10% have normal urinary
continence
• early mortality usually due to Chiari malformation complieuions (respinltory arrest and
aspiration), whereas late mortality is due to shunt malfunction

Intraventricular Hemorrhage (IVH)

• see fedtahjg. P74

Hydrocephalus in Pediatrics
Etiology
• congenital
• aqueductal anomalies, primary aqueductal stenosis in infancy
• secondary gliosis due to intrauterine viral infections (mumps. varicella, TORCH)
• Dandy-Walker malformation (2-4%)
• Chiari malfimnation, especially Type II
• myel.omen1Dgocele
• acquired
• post meningitis
• post hemorrhage {SAH, IVH)
• masses (vascular malformation, neoplastic)

Clinical Features
• symptoms and &igns of hydrocephalus are age related in pediatrics
• increased head circumference (HC), bulging anterior fontanelle. widened cranial sutures
• lrrltabillty,lethargy. poor feeding and vomiting
• "cracked pot" sound on cranial percussion
• scalp vein dilation (increased collateral venous drainage)
• sunset sign - forced downward deviation of eyes
• episodic bradycardia and apnea
NS38 Neuro1urgery 1'oroDio 2011

Investigations
• skull x-ray, U/S, CT, MRI, ICP monitoring

Treatment
• similar to adults (see Hydrocephtdus. NS7)

Dandy-Walker Malformation

Definition
• atresia offoramina ofMagendle and Luschka, resulting in
• complete or Incomplete agenesis of the cerebellar vermia with widely separated. bypoplaat!c
cerebellar hemispheres
• posterior fossa cyBt. enlarged posterior fossa
• dilatation of 4th ventricle (also 3rd and lateral venbicles)
• associated anomalies
• hydrocephalus (9096)
• agenesis ofcarpus callosum (17%)
• ocdpital encephalocele (7%)

Epidemiology
• 2-4% of pediatric hydrocephalus

Clinical Features
• 20% are asymptomatic, seizures occur in 15%
• symptoms and signs of hydrocephalus combined with a prominent occiput in infancy
• ataxia, spasticity, poor fine motor conttol common in childhood

Investigations
•ultresound.CT,MRI

Treatment
• asymptomatic patients require no t:reatment
• associated hydrocephalus :requires surgl.cal treatment
• supratentorial lateral ventricular or cystoperitoneal shunt

Progosis
• 75-10096 survival, 5096 have normal IQ

Chiari Malformations
Definition
• maltbrmations at the medullary-spinal junction

Etiology
• Wldear, llkel.y maldevelopment/dysgenesis during fetal life

Categories
• Type I (cerebellar ectopia)
• definition: cerebellar tonsils lie below the level of the foramen magnum
• epidemiology: average SF at presentation 15 years
• clinical features:
• many are asymptomatic
• scoUosis
• brain compression
• central cord syndrome (6596)
• syr.i.ngomyell.a (50%)
• foramen magnum compression syndrome (2296)
.. •
•
cerebellar syndrome (1196)
hydrocephalUII (1096)
iu • Typell
0 • definition: part of cerebellar vermis, medulla and 4th ventricle extend through the foramen
magnum often to midcervical region
• epidemiology: present in infancy
• cllnical features: findings due to brainstem and lower cranial nerve dysfunction
• syringomyelia, hydrocephalus in >80%
Toronto Notes 2011 Neurosurgery NS39

Investigations
• MRI or CT myelography

Treatment
• indications for surgical decompression
• 'I)rpe 1: symptomatic patients (early surgery recommended; <2 years post symptom onset) -+
suboccipital craniectomy, duraplasty
• 'I)rpe II: neurogenic dysphagia, stridor, apneic spells -+ cervical laminectomy, duraplasty

Craniosynostosis
Definition
• premature closure of the cranial suture(s)

Classification
• sagittal (most common): long narrow head with ridging sagittal suture (scaphocephaly)
• coronal: expansion in superior and lateral direction (brachiocephaly)
• metopic (trigonocephaly)
• lambdoid: least common

Epidemiology
• 0.6/1,000 live births, most cases are sporadic; familial incidence is 2% of sagittal and 8% of
coronal synostosis

Clinical Features
• skull deformity, raised ICP, ± hydrocephalus
• ophthalmologic problems due to increased ICP or bony abnormalities of the orbit

Investigations
• plain radiographs, cr scan
Treatment
• parental counseling about nature of deformity, associated neurological symptoms
• surgery for cosmetic purposes, except in cases of elevated ICP sutures involved)

Pediatric Brain Tumours lhHtiVII fnlqnncy Iff 1'811iatric BrUn

TumiDin
• see also Thmour, NS9 Tum-typtl Pwl:ent ('r.l
Altruc:ytDma, 40
Epidemiology Supl'iltentorial (23)
• 20% of all pediatric cancers (second only to leukemia) lnfmentorial (17)
• 60% of pediatric brain tumours are infratentorial MldulloblntDIIII. 20
• pediatric brain tumours arise from various cellular lineages Bn.inst.m gliDI!III 8
• glia: low-grade astrocytoma (supra- or infratentorial), anaplastic astrocytoma, glioblastoma
Ependymoma 8
multiforme (largely supratentorial) (see Astrocytoma, NSll for details)
• primitive nerve cells: supratentorial [primitive neuroectodermal tumour (PNET)] Mllignant glioma 6
• 90% of neonatal brain tumours, infratentorial (medulloblastoma), pineal gland Craniopharyngioma 6
(pineoblastoma) PNET 4
• non-neuronal cells: germ cell tumour, craniopharyngioma, dermoid, meningioma,
Pineal, oemn call tumour 3
neurinoma, pituitary adenoma, others
Other 5
Clinical Features Rlpi1t8d !tom Petflttie cn:s
ri North Alrllrm.
• vomiting, seizure, rn.acrocrania, hydrocephalus Vol44{4L KIN! LE. hill'illxlfn: r:1r1111tngu
• developmental delay, poor feeding, failure to thrive IDidillcfirw,pp.
penrission !tom BIIIVilr.
• often initially escape diagnosis due to expansile cranium and neural plasticity in children
NS40 Neurosurgery Functional Neurosurgery Toronto Notes 2011

Functional Neurosurgery
Movement Disorders
• see Disease, Tremor, Dystonia, and Multiple Sclerosis sections in Neurology, N27, N26, N28, N49, respectively

Tabla 14. Surgical Targets for Monmant Disordars

l'lrldnson'• htractable conlnllateral
D._ stimulation is most comon
Faiure of medical
management (advn:ed
lisease)
Drug-induced dyskinesias
(see dystonia, below)
Dystonia Canirlllallnl primary
(generalized) dystcnias;
cervical and brdive
dyttonias (GI'i)
Cantrlllataral secondary
dyskinasia (i.e.
drug-ilduced: L-dopa,
neuroleptics; STNJ
TIWIDr Canirlllall!ral appendicular
ET (first disorder to be
treated by DBS; DBS i&
viable alternative to Rx)
htention (cerebellar)
tremor (IT] resuking from
demyalination of cerebellar
outflow lnlclll (i.e. in
multiple sclerosis)
Brainstem tremor (Homes
tnrnor)
Simultaneous, biateral surgery/
Parkinson's Disease Rating Scale
Preferred target: anterodorsal
subthalamic nucleus (SlNJ
Other targsts: atellllllactic ablation
(pallidotamyVstimulation of
posteroventral pallidus interna Early intavention may reduce severity,
(GI'i)
Caudalmna incerta
Parkinsonian tremor: sl!reotactic
ablation (thalamotomyVstimulation of
venlnll intermediate (Vim) nucleus of
thalamus
Prefumld targat (primary dystonia):
sterea1actic ablation (pallidDIDmy/
stimulation of posteruvenlnll Gl'i
Secondary dystonia: stimLJation of
anterodorsal S1N
Stimulation of vanlnll poaterior lateral
thalamic nucleus (VPL)
Preferred target: stereotactic ablation
(1halamotomyYstiTIJiation of Vim
nucleus of 1halamus
Other targets: stimulation of caudal mna
incerta
Parkinsonian tremor: slirnulalion of
anterodorsal S1N
39-48% improvament in Unified
( 1%-4%)
(UPDRSJ scores
Reduced dosage rJ medications (STNJ
More effectiwlhan medical management
in advanced PD
Psydliatric: depression, mlllia, anxiety, apathy
course, and pi'OIJ'85Sion rJ disease
Of little benefit for patients with atypical
presentations
Primary dy5tonia: 51% reduction in
Burb-Ftim-Marsden Dystonia Scale
(BFMDS) score
Secondary dystonia: 62·8!1'1.
improvement in dystonias
Delayad efleclll: weala! months
Durable reductions in essential tremor
rating scale (ETRSJ scores
Reduced dosage of medications
Conflictilg data on VOCBl/IBcial tremor
Morbidity
Intracerebral hemanhage, infection. seizure
Paresthesias
Involuntary movements
Cognitive functioning: decreased laxicel fluency,
impaired executive function (STN > GPi)
(SlN > Gl'i)
Intracerebral hemonhage, infection. seizure
(1%--4%)
Minor effects on cognitive functioning (esp.
decreased lexical fluency; SlN > GPi)
Intracerebral hemonhage, infection. seizure
(1%--4%)
ParesthasiiW'pain
Dysarthria
Ataxia
Minor effects on cognitive functioning (esp.
decreased lexical fluency)
Tolerance may develop over time

Neuropsychiatric Disorders
• see Syndrome, Obsessive Compulsive Disorder and Depression sections in Neurology, N29 and PSJFchiatry. PSIS, PS7
Table 15. Surgical Targets for Neuropsychiatric Disorders
Disanlar Indications Pro-.ras Outcom• Morbidity
Obleaiva Severe syrl'1l!onns refraclllly to Anterior capsulotamy/stimulatian Currently under investigation lnlnlcerebral hemorrhages (1 %-2%)
Compulsive medical management of the anterior limb of the internal Reportelly 25·75% response rate Mild effects on cognitive functioning
Disanlar (OCD) capsule (IC) Anxiety ± panic disorder
(case report)
Taunrtte"• Syndro1111 S8Vlll8 syrl'1l!onns refreclllly to Stimullltion of midline inlnllaminar Currently under investigation lnlnlcerebral hemorrhages (1 %-2%)
medical management nuclei Ill the thalamus Reportelly >70% reduction in vocal Mild sexual dysfunction
Stimulation of motor and limbic or mDIDr tics + urge
portions rJ GPi
Stimullltion of the antarior limb
of the IC
Major Depl'ellive Severe depression refractory to Stimullltion of the subgenual Currently under investigation lnlnlcerebral hemorrhages (1 %-2%)
Disanler (MDD) medical management and ECT cingulate cortex Reportelly 60% response rate; 35% Pain, headache
remission rate Worsening mood, irritability
Toronto Notes 2011 Functional Neuroaurgery/Surgical Management of EpUepay Neurosurgery NS41

Chronic Pain
Tabla 16. Surgical Targats for Chronic Pain
Dilonl• lndicatio• Pracedur. Oub:ama1 Mlllllillly
Neuropllhic Severe, intractable, Preferred 1Brget: stimLJation 47'l. in Intracerebral hemonhages
Pain organic neuropathic of 1he contralateral ventral pen:eptit11 of pain (1%-2%)
pain (i.e. post-stroke posterior lateral (VPL) and intEnsity Pinesthesia
pain. phaniDm lilt pain. medial (VPM) thalamic Less favourable results Anxiety ± panic disorder
trigemillll neuralgia. nuclei ± periventriruler/ in cenlnll pain syndromes
chronic low-Mck pain. grey matter and poorly localized pain
complex: regional pain (PVGIPAG)
syndrome) Other blrgm: &timulirtion of
the contralatenJIIC
Stimulirtion of the
contralalenll motor cortex
Noc:iceptiva Severe, intractable, Bilateral (most common) Reportedly 63% Intracerebral hemonhages
Pain organic nociceptive pain stimulirtitll of tha PVG,IPAG imiJOVBmanl in (1%-2%)
perceptit11 of pain Pinesthesia
intEnsity Anxiety ± panic disorder

Surgical Management of Epilepsy

Neurosurgical Treatment of Epilepsy
• see Neuroloi)'> N8 for the medical treatment of epilepsy

Indications
• medically refractory seizures, usually defined as seizures resistant to two first line anti-seizure
medications used in succession
• identification of a distinct epileptogenic region through clinical history, EEG, MRI, and
neuropsychological testing. Other localizing investigations include magnetoencephalography,
........
Allandalilld, Clnnlllll Trill If IIQIIy far

NUf21l01; 345:311-8

Thillllldomilld tmnll1rill MlillfR1ba aftic:lcy

SPEer and PET and llflty olnaiiUUQ81Yfor11mpOIIIIalie
• if a distinct epileptogenic region cannot be identified. the patient may be a candidate for a epi811$Y.
palliative procedure such as corpus callosotomy lhllals: II patilll1l Mth poarly Cllll1nllld

ln=-401 or fur mooadn.tn-.nwillantilpiillptic
Procedure drugs (n=401. The PlinarYoulmlewasflliedom
• most commonly flom.m.1bal..-r- ollrllland
• adults: resection of the hippocampus and parahippocampal gyrus for mesial temporal lobe turroundingl pOd all Ylll. Slccnllll'f
oull:urn8l ii:Uiad hquency IIIII -ny al
epilepsy arising from mesial temporal sclerosis
• children: resection of an epileptogenic space-occupying lesion
...-ilr ri 10. diUlq end dedi.
CancUU: In pdents will pocxlf controlled
• hemispherectomy and corpus callosotomy are less common 1Jn1XIIi-labll!il..-y; lllfiiiiY is IUperiar10

Outcomes and Goals
• freedom from seizures
• 41· 79% of adult patients are seizure free for 5 years after temporal lobe resection
• 58· 78% of children are seizure free after surgery
• surgery is associated with improvements in preexisting psychiatric conditions such as
depression and anxiety, a well as improvement in quality of life measures

Morbidity
• 0.4-4% of surgical patients will have partial hemianopsia, aphasia, motor deficit, sensory deficit,
or cranial nerve palsy following anterior mesial temporal lobectomies
• most patients will have some decline in verbal memory following dominant temporal lobectomy
and in visuospatial memory in non-dominant temporal resection
• the degree of memory decline stabilizes after 1-2 years

Predlcton
• positive predictive factors for seizure freedom following anteromedial temporal lobe resection
• hippocampal sclerosis (unilateral)
• focal localization of interictal epileptiform discharges
• absence of preoperative generalized seizures
• twnoural cause
• complete resection of the lesion
NS42 Neurosurgery Surgical Management for 'Iiigeminsl Neuralgia Toronto Notes 2011

Surgical Management for

Trigeminal Neuralgia
Medical Therapy for Trigeminal Neuralgia
• see Neurology. N18 for medical management

Surgical Therapy for Trigeminal Neuralgia

• reserved for cases refractory to medical management

Surgical Options
• trigeminal nerve branch procedures
• local blocks (phenol, alcohol)
• neurectomy ofthe trigeminal branch
• nerve branches
• V1 at the supraorbital, supratrochlear or infraorbital nerves
• V2 at the foramen rotundum
• V3 block at the foramen ovale
• percutaneous trigeminal rhizotomy
• glycerol injection
• mechanotrauma via catheter balloon
• injection of sterile boiling water
• radiofrequency thermocoagulation
• microvascular decompression
• posterior fossa craniotomy with microsurgical exploration of the root entry zone,
displacement of the vessel impinging on the nerve with placement of a non-absorbable
Teflon felt
Toronto Notes 2011
Common Medications
The folowing are ONLY; follow clinical judgment and
to adults unless otherwise specified
Tabla n. Common Medications
Dnlg Nama Doling Schadule
lariZipam 4 mg IV over 2minutes, q1 0-15
milutes (do not axcaad
8 m!V'I2hr)
cublmmpina Trigeminal neuralgia (tic
{TegnltuPJ douloureux): 100 bid,
increase by 200 day up to
a maximum of 1,200 mQI'day
200 mgtid
Seizures: 200 mg PO bid.
increase by 200 mg (inpatient:
q3 days; outpatient q7 clays)
until tharapeutic lewl achievad
(usual opti'lllm dosege:
800-1,200 mQI'day; range:
60()..2,000 mQI'day]
ph•ytain Seizures: Loading dose:
(Dilanti..) 18 mg./kg &low IV or 300-600 mg Status apilepticus
PO/day divided bid/lid
Maintenance: 201J..500 mg
W/day (max. rate:
<41J..50 mQI'min or 300 mg PO
average mainlllnance
ose: 300 mQI'day PO
Status epilepticus: 200 mg W
over 30 miootes (-20 miVlcu;
not taking 11111ularly), or 500 mg
Wover 10m1nutes
(if alraedy on phenytoin)
dllliiii1IIIIIISIIII Loading dose: 10-20 mg IV;
Maintenance: 4-6 mg W/day secondlry to 1urnour,
divided qid (may be PO)
man1itol 1-1.5 wkg Wrapid i'lusion
(350 ml of 20% solution]
w
followed by 0.25 glkg q6h
nimclllpila 60 mg PD/NG q4h X 21
started within 96 hours of AH
Common Medications Neurosurgery NS43
prescription reconmendlllions i1 practice; dosages refer
lndic:lltians Side Effacts Cammon lniBI'II:ticm Canlrlinllcatians Cammllllll
Status apilepticus Drowsin111s. sedation OtharCNS S1lrt phenytoin
depressants, loading
digoxin (increaSIII simultaneously
digoxin levels)
Trigeminal neuralgia Worsening of Lithium (increases Hypersensitivity to TCAs. Monitor CBC
Seizures seizures, heart failure, lithium toxicity), MAOI previous bone marrow (potential
anhytllnias, Other meds may suppression, MAOI in hematological
AV block. increase past 14 days toxicity)
aplastic anemia. carbammpine II!Vllb
agranulocytosis, ortlave decreased
tlrorDiocytopenia, ella
hepatitis, erythema
multifurme, Stuwns-
Johnson syndrome
Seizures Thrombocytopenia, Other meds may Bradylrrhythmias, Important to give
leukopenia, incree&e phenytoil heart block IMII' time to pllMint
agl'lll.llocytosis, levels and toxicity causing a cardiac
pancytopenia, or have decreesad arrest
toxic llepatilis, effects
StiMIIIS-
Johnson syndrome,
toxic epidermal
necrolysis
Cerebral edema (e.g. Psaudotumour cerebri, Aminogkrtethimide, Systamic fungal No longer used in
seizures, heart failure, antidiabetics,I>SA, infl!ctions, acute spinal cord
head injury, anhytllnias, NSAIDs, balbituata&, immun05Uppressive injury
pseudotumour cerebri) tlromboembolism, phenytoin, rifampin, dose with live
Preoperative pancreatitis, acute cardiac glycosides, virus vaccines
preparation for adfl!lllll insufficiency; cyclosporine,
patients with avoid abrupt ephedrine, oral
increased ICP withdrawal
secondlry to brain potassium-
neoplasms drugs.
selicytates,
skin-tasting antigens,
toxoicls, vaccines
Raised ICP Seizures, heart failure Lillium (increases Anuria, severe pulmonary Effect occurs in
excretion of lithium) congestion, fnd 1-5 mins, maximal Ill
edema. severe
eart failure, severe Often altemllled with
dehydration, metabolic furosemide 1()..20 mg
edema, progressive renal Wq6h
di&asse or dysfunction, Indwelling urnry
active intracranial bleeding catheter to measure
except during craniotomy ins and outs
Vasospasm in SAH Decraased blood Antihypertansives Nona known Causes vasodilation
pressure, tachycardia, (may increase Only calcium channel
dyspnea hypotansive elfacts], blocker (CCB]1hat
CCB (may ilcreese crosses BBB (blood
ellec:b), cimetidine brain berrier]
(increases nimodipine Use half the nonnal
bioavailability] dose for liver failure;
monitor BP always
NS44 Neurosurgery References Toronto Notes 2011

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