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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 Differential Diagnoses of Common Neurosurgical Presentations .............. 4 INTRACRANIAL PATHOLOGY Intracranial Pressure (ICP) Dynamics ....... 4 ICPNolume Relationship Cerebral Blood Flow (CBF) ICP Measurement Elevated ICP Herniation Syndromes ................... 6 Treatment of Elevated ICP Hydrocephalus , , , 7 Benign Intracranial Hypertension (Pseudotumour Cerebri) . . . . . . . . . . . . . . . . . . 9 Tumour ................................ 9 Metastatic Tumours Astrocytoma Meningioma Vestibular Schwannoma (Acoustic Neuroma) Pituitary Adenoma Pus .................................. 14 Cerebral Abscess Blood ................................ 15 Extradural (uEpiduraln) Hematoma Subdural Hematoma Cerebrovascular Disease ................ 17 Subarachnoid Hemorrhage (SAH) Intracerebral Hemorrhage (ICH) Intracranial Aneurysms Carotid Stenosis vascular Malformations ................. 22 Arteriovenous Malformations (AVMs) Cavernous Malformations................ 23 EXTRACRANIAL PATHOLOGY Dermatomes/Myotomes , , 24 Approach to Limb/Back Pain , 24 Extradural Lesions . . . . . . . . . . . . . . . . . . . . . 24 Root Compression Cervical Disc Syndrome Cervical Stenosis (Cervical Spondylosis) Lumbar Disc Syndrome Cauda Equina Syndrome Lumbar Spinal Stenosis Neurogenic Claudication Intradural Intramedullary Lesions . . . . . . . . . 28 Syringomyelia Spinal Cord Syndromes ................. 28 Spinal Cord Injuries Peripheral Nerves . . . . . . . . . . . . . . . . . . . . . . 29 SPECIALTY TOPICS Neurotrauma , , 29 Trauma Assessment Head Injury Brain Injury Late Complications of Head/Brain Injury Spinal Cord Injury (SCI) Fractures of the Spine Neurologically Determined Death Altered Level of Consciousness Coma Persistent Vegetative State Pediatric Neurosurgery . . . . . . . . . . . . . . . . . 36 Spinal Dysraphism Intraventricular Hemorrhage (IVH) Hydrocephalus in Pediatrics Dandy-Walker Malformation Chiari Malformations Craniosynostosis Pediatric Brain Tumours Functional Neurosurgery ................ 40 Movement Disorders Neuropsychiatric Disorders Chronic Pain Surgical Management of Epilepsy ......... 41 Neurosurgical Treatment of Epilepsy Surgical Management for Trigeminal Neuralgia ............................. 42 Medical Therapy for Trigeminal Neuralgia Surgical Therapy for Trigeminal Neuralgia Common Medications .................. 43 References . . . . . . . . . . . . . . . . . . . . . . . . . . . . 44

Toronto Notes 2011

Neurosurgery NSI

NS2 Neuroaursery



IBB Func:liaDBI

NBui'CIBndamy Sllftwln

Basic Anatomy Review

MRI Brain

Corpus calloeiJn


Thlamu. llypothallmu.

Caudltll nuclau.
Lderll vantricl

Occipital lobe Midblain Pons Four1h V8111rida



Spinal cord



A. lagil:lllllal:tion


F"111ra 1. MRI






C3 C4 C5 C6 C7 CB




r.;:;J ...




F"111ra 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

... 11

.... 2


1. Am.iDr carebralartay

Arblry IBgn:

At. - Antariar carebral AcDIII - Antariar CGIIIIIUliCIIilg

6. AICA 7. PICA 8. Var1abrllartary


2. 3. 4. 5.

Midcll centnl ll'lllry Postarior cammlricating artary Postarior Clf8bralartay Besilanrtary

1D. AniBriar ID!ruidal arl8ry 11. Am.ior spinalllllry



, 2. l'ol18rior spin!. arl8ry


- 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

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
Figure 3.
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)

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

,, ,
v- = conslllnt
Mao-KIIIill Hypllllli Vm. + Vlil>od + VcsF + Vlooion =

Peripheral NeiVe Lesions neuropathies traumatic entrapments iatrogenic inflammatory tumours


I I 1

40 r-.. . .20 --,-. .

100Ll'-. 60

Intracranial Pressure (ICP) Dynamics




ICPNoluma Relationship
adult skull is rigid with a constant intracranial volume contents (CSF, blood, brain) are incompressible increase in one constituent/space-occupying lesion = increase in ICP however, ICP docs not rise initially due to compensatory mechanisms (autoregulation): immediate: displacement of CSF to lumbar theca, blood delayed: displacement of extracellular fluid (ECF) or intracellular fluid (ICF); displacement of brain tissue into compartments under less pressure (herniation) once compensation is exhausted, ICP rises exponentially



Wh.n a mass IIICjlllllds withilthe slut compensatury mechanisms initially maintain a nonnaiiCP

Evantualy finl& small inCielllents in voklme produce larger and 1.-ger increments in ICP

Adlpled lrom Unduy llW, lbl9 t NtwtrJ1Jw IIIII Ne!mst6puy 1lu.mrrled. Copyright 2004 with parmilliln

Figure 5. ICP-Volume Curve


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 MAP >150 mmHg or MAP <50 mmHg brain injury: e.g. subarachnoid hemorrhage (SAH), severe trauma

AulcngtJation: CBF maidllilad daspitl ch111gein CPP

ICP Measurement
Acute Monitoring
lumbar puncture (LP) (see sidebar) intraventricular catheter/ventriculostomy/external ventricular drain ("gold standard", permits therapeutic drainage of CSF to decrease ICP)
LDw BP or High ICP Clllllbllll parfusioo prBI$Irll

Chronic Monitoring
fibreoptic monitor (intraventricular, intraparenchymal, subdural), subarachnoid bolt (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 severe elevation: increase in mean pressure >40 mmHg waveform: comprised of respiratory and blood pressure pulsations (Traube-Hering waves); the amplitude increases with ICP beta-waves: coarse, variably increased amplitude, frequency Yz-2/min, often related to respiration plateau waves: elevation ofiCP over 50 mmHg lasting 5-20 min, precursor of further deterioration

Figura 6. Carabral Autoregulation Curve

Ad1pted fnlm liiiiiiY et II. Neii!Jiogf and NeiiDstlr,ay Alsl1rltd. Copyright 2004 with pennitlion from Elsevier.



Consider Monilllring of ICP in 1lle following Sitllltians 1. Patianll will1an abnoiiTIIII halld CT IJid Glngow Coma Scale {GCSI scors of 3 111 8 llfl8r cardiopulmonary resuscitation.
2. Patianll will11 noiiTIIII hald CT and 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 Systulic blood pniSIUI'IIIess than 90mmHg 3. Postoperative monitoring 4. Investigation of normal prenura hydrocsphalus {NPHI


Elevated ICP
intracranial space-occupying lesion: tumour


blood [trauma-+ hematoma (most common), subarachnoid hemorrhage] depressed skull fracture foreign body increased intracranial blood volume 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) pseudo tumour cerebri status epilepticus (chronic seizure resulting in brain edema)



Lumbar punctura is contnlindic8tad with known/suspected intracranial mus.



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

!full triad- in ,13 of - 1 1. Hypartansion 2. Bradyclll'dia {late finding) 3. AbnoiiTIIIIrespil'lllllry pllttllm

Cushing's Triad af AcllllllaiiM ICP

NS6 Neuroaursery

lntrac:ranlal Preuure (ICP) Dyaamia/Herniation Syndromes



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

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

Herniation Syndromes
Table1. Hemllllon Syll*ome

Cl1lcal FN1u111

Letalll aurnta*Jriallaaill'l Usualy Wlms af impnling 1nntan1Drial haniatian

I. Sublalcila 2. Cllllni 3. UIICII

DispB;anent ci lesion Small pupila, dilltad. fixed (I'Oitnll clencephalon 11raugh o Diffuse C818b111l tD caudal dataliaration), sapntill flllue of tentDrii!l nab:h o Lata uncal hamimon diancephahn 1111ckla


i 0
: I!

Daaaased l.DC (nidbrain


gaze iqlaiment eyes"): CaqliiBIIill'l of )l8leCtwn end supelill' c*uli

Bninstem IIII!ICIIhaga secondaly 11:1 sh111ring af be&ilar lrtary perfa!Biing VBSS81s) llillblti!S illlipidus (tractiiJI on pillitary d and
end-s!IQI s9'1

F"111ra 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


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
hamiates llnugh tentDrii!l inciBIA

large posterior fossa l1lii5S

(cmman afta' VP lhi.IIIRg)

CII8Jellar infarct (sl.pl'ior cerebelar artery

ISCA) COI11Niian)

Cerabelltonsis hemiatell"f'DIQI funmen011gnum



llinltadorilllaaiiJI FltawiJ.I central tanllrili

Hydf11C8Phakll !Cinbnllaquecllct Neck stiffness head tilt ftcnsllar. ., Daaaased l.DC (nidbrain

Flaccid pnysis

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 ICP>20mm.Hg goals: keep ICP <20 mmHg. CPP >65 mmHg, MAP >90 mmHg General Measures (,CP HEAlY see sidebar) elevate head of bed at 30-45, maintain neck in neutral position

'hdnllllof E..,_.ICP: ICPHEAD lnllmiB

calm (sldiiiJ,II:cma
Place .nivParlllylil
ltypemntiltll Bewle head

increases intracranial venous

AdaqudaBP Dinlllic (malllilol)

prevent hypotension with fluid and vasopressor&, dopamine, norepinephrine pm ventilate to nonnocarbia (pCOz 35-40 mmHg) -+ prevents vasodilatation prn to maintain J'02 >60 mmHg -+ prevents hypoxic brain injury

'IbroDlo Nota 2011

Herniation Syndromet/Hydrocephalus

Neumaurgery NS7

Spec:Hic Mesures

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


increased CSF volume


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


estimated prevalence 1-1.5%; incidence ofcongenital hydrocephalus -1-2/1000 live births hydrocephalus in children, see Pediatric Neurosurgery, NS37
Tllllllle 2. Cl&lllllcatlon of Hydrocephalus Ciculllliln blacUd willin (tm.Cimlllllil:llill) Vldricular sy1l8m pmximal to the 8111CI'IIDid IJlftllatiJnS
1. Clloroid plsxu. 2. l..lltalll wntricllll 3. Third venlricle 4. Cerebral aqueduct (Df
5. Four1h vanlrida

6. Fo111men l.ulchklland MIQIIIIdie


Acqund AIJJeduclal stenosis (lllh!sians !GURacticxl, hllllllllhaga) lnlrllv8nlrii:U lnians {lllnaurs e.g. 3nl wnbicle aJIIaid cyst.


7. Aracmoid gnmliltions

to lilck


8. Subal'lll;l'noid

9. Segilllll sinus


1 of


Periwnbiclilr hypodensily

Sulcal aflacemllll

mat illo

lllln8ependymal ri{plian li CSF

Figure I. 'Ilia Flow of CSF





tnariallaniltian, Vllllric:l& CD11118Uian

ID: vanbiclaa -o

Otlllrs: .. abscaa/ tpllllamas, aracmaid cysts

AcrJ&ductal S1811asis.

CSF prodlad by choroid pillllul. ftOWI of l..uiCI'b (lllll'lll)and MIQardll (medial) ... lblrachnoid spac;e -o ablsofbld by Bl'llchnoid vlflgranuldiona illo ve1111111

malbmalim All wnbicles dilaled

(188 PrMiifllric NflutDJutgety, NS36)


l!ldnlvmlriculll' site = nchnaid IJllniJI!ian&

CSF absarplian blac:bd at

Post-infactiaus (#1 C8US1)

meniVfis, cysticercosis Post-hemonhegic (#2 cause) SAil. MI. tnunatic Dlamid 1)11111111 papilams (rm, c:ausas ilcraased CSF pmcllctian) nannal pi8SSU8 hydracephils

CSF production - CSF l'fllbsorptian -sao mVday i'l nonnalld.llll Normal ml (501 spinal, 5D'Io intracl'llnill -o 25 ml idn.VIIItriculllr. 50 mlaubncl'noid)


Parlisl:8lt vantric:Uar dlllalian il the CDI'IIald: of IIDIIII1II CSF pniSSin

ldiapllhic (50%)
malingitis, 1nlu1111, radiaticDiJcU;ed

Othe111: lllilereclrlaid lananhllga.

Enlarged vllllriclaa withaut incraased pnlfliniiiC8 of cnbrel U:i

AID AlaxiVApiiXia of gait lncantinanca


0 Normal aging Alzllairnar'a, Crautzlaldt-Jacob Diiea&a

E'nllllved venbides and mci Carelnllllqlhy

NS8 Neurosurgery


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

(most common)

Obstruction by choroid plexus Acute hy!Rcephakls Buildup of proteinaceous h:l8iiS8d ICP

accretions, blood, cells (illlaiTII'IIItory or tumour) Infection Di&connaction or dal!lilge

"Silmt series" (plain X-fiVS of

entire shunt that only ruleout discomection. break. tip mi!JIIIion)


Radionuclide "shunto!Jlllf"

lnf8c:tion (3-6%)

s. epidermidis
Gram-negative bacilli

Fever, NN, anorexia, initabiity CBC Meningitis Blood culture Peritonitis Tap shunt for C&S (LP usualy NOT Signs and symptoms of shunt recommended)
obstruction Shunt naplritis NA shunt)


(HI% over 6.5yea11)

Slit ventricle synctoma CIYonic or reculring CTIMRI Collapse of ventricles leading headaches often raliavad to occlusion of shunt ports by when lying down ependymal lining ventricles on imaging Seconday crMiosyno510Sis (childran) Subdural hamillumll A&ymptornatic Collapsing brain tears bridging Headaches, wmiting. veins {especially common in somnolence NPH patients) Apposition and overlapping of Abnormal head shape tha cranial sutures in an infllll following decorqnssion of hy!Rcephakls




Saizun11 (5.5% risk in 151 year, 1.1% attar 3rd year)


...auinal Hamil (1 7% incidence with VP

Increased inlrllperitonaal hguinal swelling. discomfort results in hernia shunt inserted in inflrlcy) becoming apparent skin breakdown over hardware


'IbroDlo Nota 2011

Neumaurgery NS9

Benign Intracranial Hypertension (Pseudotumour Cerebri)

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

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")

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 risk ofblindnes.s is not reliably correlated to symptoms or cl1nica1 course Investigations CT:nonnal CSF studies: normal Treatment
rule out conditions that cause intracranial hypertension



111,.rlanl f'llltura to nubian CT a..t

IIRI(:t cantrMt

MRI: must look fur venous sinus thrombosis

t.e.ia"' (:t ld11111B. nKro.i,, hsmarrhlgs) Midline shifts 1nd h1111ialians Elfat:oment of ventric:lee and aulei (olbln ipllilatn), batal
Single or mLitijlle mebllbllil) implies

discontinue offending medicatioDS, encourage weight loss, fluid/salt R:5triction CSF production), thiazide diuretic or furosemide pharmacotherapy: acetazolamide ifabove fail: serial LPs, shunt optic nerve sheath decompression (if progressive impairment ofvisual acuity) 2-yea.r follow-up with imaging to nde out occult tumour, ophthalmology follow-up

Primary CNS l',mphar.-. npcn11d il 6-201 of HIV inf\lcl8d patienta.

Vllllric...r: CGUDid, chomid prDC81S

pepma. apandymoma.
germiloma. tntoma.

DDx far Rmg (nlllnci.. Laeia1 01 CT wllht:antrAt

hpnllmut.. irrlnr--: lltrDI:Y!Dmt. 1gliobllllluma, aligadlillllllllioma.

Ablcass* blastnma(high .,Ualllracytama)

lnfllrct Contuaion AIDS (lmulplasmosis) DliiiJY'Iinalion IIBIIDiving homlllllma (" 3 mo.t conrnon Dx's)



QMglioma. lymphoma,



craniopharyngioma. apt narva glioma. cyst

MMrySGu- rl



(RCC) 7'!1i 0.

Figura 9. Tuaurs



NSIO Neurosurgery


Toronto Notes 2011



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

Cwr()lc;d'11X11; 14(41:131-43 Patiantt idan1lJid a hiving !ida lnin ma111ta1is oodelgo llliltmlln11hlt inlilde wide liRin

lll'iuw rJ 1helidlnculnd 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

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

ma1lllalis i1 canlidllllld plliiiiMI, iMIMIIDcll

1lllllnlnlllllllt be indiloiludlld. To rda 1111

1llnllll' l'llCU'ItiiC8 fw pl1iants who 11M oodalgont miCii:ln rJ alnilll'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.

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)

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

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 Incidence: 2-&'100,000/y&llr 60% infratentorial >15
80% supratentorial

Astrocytoma (all grades) (511%) Craniophlryn.jiorna (2-5%) Others: pineal region tumours, choroid plexus twnours, ganglioglioma, DNET

Medulloblaslllma (15211%) Ceraballar asbocytoma (15%) Ependymoma{!!%) Brainstem asbocytoma

High IJ!Ide astrocytoma (12-15%. e.g. GBM) Metastasis Metastasis (15-311%, includes infratentorial) Acoustic neuroma (schwannoma) (51II%) 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


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-parietaloccipitallobes (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 multiple 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

Figura 1D. M11tiple Bniin Mlll:astaas (see 111111WS)

medlcal phenymin for seizure prophylaxis ifpatient presents with seizure dexamethasone to reduce edema given with ranitidine chemotherapy (e.g. small cell lung cancer) radiation stereotactic radiosurgery: for discrete. deep-seatc:dJinoperable tumours multiple lesions: use whole brain radiation therapy (WBRT); consider stereotactl.c radiosurgery If<3lesions post-op WBRT 1.1 commonly used surgical single/solitary lesions: use surgery+ radiation
Prognosis median survival without treatment once symptom.at.k is -1 month, with optimal treatment 6-9 months but varies depending on prlmary tumour type

1. HIIIBruganoos conlnlllarll.,callllnt Z. 1-deliled bardn(infltraiM) 3. l'lritumaur adarra 4. CantriiiiiCIIISis 5. CamprvAion of vedricla, me shit

AstrDcyiDma 01 CT

Fiare 11. Hig. Grelle

most common primary intra-uial. brain tumour

'' ,
ICamof*Y lllnlfll c.PIIffGin- 1t1tue Sclll
lldlg Qtlerhl

Tillie 5. Astnlcytuma Grading S.,....

T,.al CT.tiiRI FWd1p

1- Pilocytic amocytama

IIIIISS affect. anhanc11111nt

>10 yan. CWBI ps 111111 rasactian

Syaars 1.5-2 yellS

('II.I 100

II- Low (plldr/dilfusa Ill- Anapaslic

IV - GliOOiastoma rrUiimme (GBM)

Mia allact. no anllllranat Cllqllex eManc:ann

Necrosis (rilg emal'll:ef11ID)

12 manlbs, 10% at2 yess


No compeints; no evidanca of diAbla 111 1:11ny on narmlll activity; minor signs or symptoms of di-

NIJIIIIIilldivity with dart; ..,. - . , . Dr symptoms af di-s

Clinical Features epidemiology: most common in 4th_(ilh decades

c.. fw elf: unable 111 carry

on normal activity ur to do lctiva Wllrk

sites: cerebral hemispheres cerebellum. brainstc:m, spinal cord symptoms: recent onset of new/worsening HIA, Ntv; seizure, focal deficits or symptoms of increased ICP
Investigations CT with contrast: va.rl.able appearance depending on grade (see Table 5) tissue biopsy: WHO grade and histology correlates with prognosis, but 25% chance of sampling error due to tumour heterogeneity


Requil88 occuionalllllil1lnce. but ilable 111 Cln for 111011: of



Requiras considlllble 881i111nce 4lld fnlquant medical



Disabled; l'llfJJiras .. care and -illance S8VIlnlly -.blld; missicn is indicltad .U.ough


dflllh not i11111L'11nt V.ry lick; hospital million

ldivB .upportiva 1llltlnBIIt II8C8SWY

Mcriluld; fiiii110C88118 prugllllling lllpidly


NS12 Nearomrgery

10ronto Nota 2011

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)


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

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
1. Homogenous contmt emancement
2. Dui'IIIIIIIBctmmt

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 (10% multiple, likely with lollS ofNF2 gene/22q12 deletion)

3. Dillinc:t margill

Figure 1Z. Meningiam1 on CT

cr with contrast: homogeneouB, densely enhancing. along dural border ("dural tall"), well


drcumsc.ribed (Figure 12} 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

WHO Clluification of Mlnq;.IM


111r iltoltm

Grade 1: low n.k IJf Grada 2: intamedialll risk of NC.-ce Grade 3: high rilk of recul'l'lnce

conservative .management for non-progressive, asymptomatic le8lons surgeryis treatment ofchoice ifsymptomatic or progression on sequential imaging (curative if complete resection)

stereotactic zadiosurgery (SRS) may be an option for lesions <3 em endovascular embolization to facilitate surgery SRS or XRT for recurrent atypical/malignant meningiomas
>90% 5-year survival. recurrence rate variable (often -10-2096} depends on enent of resection (Simpson's classification)



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

Proglllllive ll'lillltlll'lll or sansorineul'lll '-ing loss - acoustic nauroma ll'1li pmvan lltharwi.

'IbroDlo Nota 2011


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

conservative: serlal imaging
radiation: stereotactic radiosurgery is the trea1ment of choice o surgery if: I. lesion >3 em; 2. bn.in8tem compression; 3. edema; 4. hydrocephalus curable ifcomplete resection (almost always possible)

Figure 13.. Vestibular SchwaMJOIII (tumour in ceraballo-pantina angle)

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


bitemporal hemianopsia (compression of optic chiasm) (see NeuroloBf. N21 for details of visual field deficlt) CN m, IY. V 1, V a. VI palsy (compression of cavernous sinus) o endocrine effects hyperprolactinemla (prolactinoma): lnfe:rtlllty, amenorrhea. galactorrhea, deaeased Ubido 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
formal visual :fi.elda, CN testing 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)

A co..-ive adenoma in the pilllibrf wil impair honnone produdion in !hit ardar (i.a. GH-I:nllinv calbl ra mDSI S8IISitivrl tD co,..-.ssiDII}.

OH. ut, FSH. TSII. AC1H. Prollc&l

GD LDak Far ...... AIIIMIH ..._ -

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

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



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 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)


Brain Allscass on CT

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) immunocompmmised: fungi and protozoa: Toxoplasma. Noamlia. Candids a1&iams, Listeria monocytogmes, Mycobacterium and Aspergillus

. , . . _ iii4Zpllillll: ll&tn
.......... Tlillb.ty .... lllrtfy modllyin patinDM!IInil--. .... . , 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!
I (

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

bacterial endocarditis
dental abcess
Clinical Features

penetrating head trauma

Immunosuppression (e,g, AIDS)

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 781 A8. P<D:0011rr l'lllmiiiiMI-'POii!M eocci 1J1M11ian llblcla 1:11lln 111142.3. atlawriiiNspr!Mid ID ba

IIUII:Gn'lrM ....tm:odrGtDihiGII!gCM

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)
with abscess rupture: ventriculitis, meningitis. venous sinus thrombo!ds CSF obstruction transtentorial herniation

c.a.- !knjcll mnamat ICIII'itanTi

iii8CIIIII'BIIId il .. pllildl Mill19*1D

il11111111<2.i 111111 dlllitf-'"1 11'1111. . . il

cocci, lbt{IIIUis il ,.rrran hlwi'cl culln

nnn. 1hlin,nr.wl progllllliiiiDIICilllll wilt

Investigations cr scan often lst test in emergency department MRI imaging of choice apparent diifusion coefficient (ADC) used to differeot:iate abscess (black) from tumour
(white) 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

llldlll'liliriJ...,.IDflill._u llllirmliii11W11Q1111111.

'IbroDlo Nota 2011


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)

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

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

nicHe me.qeal bleed

Good with prorr

!Nota: nspmay ernst e1r1 DCal' from unc:al hamiml)

IISSOCiated with tmuma




Ruptured uan11amid vessels

AQB >50.

No lucid inllML henipsesis, Pupilary chqes

Often lllylqiiDIIllltiC Minar WA. confusion, signs of ilcreased ICP
Sudden onset

Crascen1ic OilS$

Cnriatamy if bleed >1cm

Burr bola to IRil; Cllllliotumy Hreoccurs


Cl111ic SUWanl Ruptured 11....... sdlnclnlid bridgill! vassels Traum11, spmaneous


AQa >50.BOH abusn, antk:ollguilred ega 45


Dopethic, AVMI

m C8888 under

Aae 55-SO

thundan:lap headllcha, signs of inctaad ICP

Hit#J density IDxl (snitivity dacrealas ova"tima)

CIIISIIVlllive: NPO, rl NS, ECG, Foley,

prophylaxis (nlnod'*-); opan vs. llldovascular surgery to repair if rebleed

Paar: 511% mortality

3D% of IUrvMn haw

modnta to IIMr8 cisabiity

11lnDW's, Raclions.

HTN, wsc.-r abnormality,

Aaa >55,

11A-ll8 ..,......,

Hit#J dnity IDxl

ci'ug use (CIICIIile, sip of ilcfelsad ICP BOH, -B1llnila)

Medical: dacnssa BP. cam!ICP Slillil:al: Cnlliotomy

Paar: 44'hlortality dua to c:aralnl hamildion

Extradural (Epidural'") Hematoma

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

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

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

(miclile llhilll

2. Bload

Figura 15. Eatndural Hama1Dm1 usually with


admit, observe, bead elevation mannitol pre-op If elevated ICP!brain herniation craniotDmy to evacuate clot, follow up CT

NS16 Neurosurgery
Calcilm antaganisiJ for aneurysmal subaracllloid haemonhage (Review) Cochrane Review 2008; Issue 3. Introduction: This sbJdy looked to review the evidence in regards as to whether calcium antagonists improve the outcome in patients with aneUJysmal subarachnoid haemonhage. Mathods/Papulation: The review included 3361 patients presenting aneurysmal subarachnoid haemorrhage from 16randomised controlled trials comparing treatment with calcium antagonists vs. control from 1980 ID March 2006. Results: The results were based mainly on one large trial of oral nimodipine, which showed aRR of 0.67(95% Cl 0.551D 0.811 and the evidence for other calcium agonists was not statistically significant Con'*sion: The authors endorse the use of oral nimodipine in patients aneurysmal subarachnoid haemonhage.


Toronto Notes 2011

good with prompt management, as the brain is often not damaged worse prognosis if bilateral Babinski or decerebration pre-op death is usually due to respiratory arrest from uncal herniation (injury to the midbrain)

Subdural Hematoma
rupture of vessels that bridge the subarachnoid space (e.g. cortical artery, large vein, venous sinus) or cerebral laceration

Risk Factors
trauma, anticoagulants, alcohol, cerebral atrophy, infant head trauma (see Pediatrics)

Clinical Features
no lucid period, signs and symptoms can include altered LOC, pupillary irregularity, hemiparesis
CT Density and MRI Appearance of Blood Time Acute (<72hl Subacute 1<4wl Chronic 1>4wl CT Hyper. Iso. Hypo. MRI T1 Grey White Black MRI -T2 Black White Black

CT: high density concave mass, "crescentic" usually less uniform, less dense and more diffuse than extradural hematoma

craniotomy for clinically symptomatic subdural hemorrhage, or subdurals greater than 1 em; optimal if surgery <4 hrs from onset

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


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

CT: hypodense (liquefied clot), crescentic mass

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

Figure 16. Subdural Hematoma on CT

good overall as brain usually undamaged, but may require repeat drainage

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)



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

trauma (most common) spontaneous aneurysms (75-80%) idiopathic (14-22%) AVMs(S%) coagulopathies (iatrogenic or primary), vasculitides, tumours (<5%)

', ,
Grad1 Finding

Normal scan
2 3

<1 mm thick blood

>1 mm thick blood


-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 oral contraceptive pill substance abuse (cigarette smoking, cocaine, alcohol) conditions associated with high incidence of aneurysms (see Intracranial Aneurysms, NS20)

', ,
Huntlmlllus Grade

ar...._ -1 for SAKI



Clinical Features of Spontaneous SAH

sudden onset (seconds} of severe "thunderclap" headache usually following exertion and described as the "worst headache ofmy life" (up to 97% sensitive, 12-25% specific) nausea/vomiting, photophobia meningismus (neck pain/stiffness, positive Kernig's and Brodzinski's sign) decreased WC (due to either raised ICP, ischemia, seizure) focal deficits: cranial nerve palsies (CN III, IV), hemiparesis ocular hemorrhage in 20-40% (due to sudden raised ICP compressing central retinal vein) reactive hypertension sentinel bleeds SAH-like symptoms lasting <1 day ("thunderclap H/ A,) 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

No Sx or mild IVA and/or mild meningismus


Features of 1 + CN palsy Confusiorv1ethlrgy, mild hemiparnil or aphqia

s.-a hemiparnis, mild


GCS <15 but >&,moderate-

Coma (GCS <91. moribund appearanc1

Morblity of Grade 1-2 20%, iiiCI'IIIIslld wilh grads

', ,
World Fedlndion Ill N-ological Surpans Grlllling of SAH

non-contrast CT (Figure 17) 98% sensitive within 12h, 93% within 24h; 100% specificity may be negative if small bleed or presentation delayed several days acute hydrocephalus, IVH, ICH, infarct or large aneurysm may be visible CTA/MRA/ cerebral angiography for localization and treatment planning positive history for SAH with negative CT - MUST do LP to look for blood or xanthochromia (may be negative <12h) lumbar puncture (LP) findings (highly sensitive): elevated opening pressure (> 18 em HzO) bloody initially, xanthochromic supernatant with centrifugation ("yellow") by -12h, lasts 2 weeks RBC count usually> 100,000/mm3 without significant drop from 1st to last tube (in contrast to traumatic tap) elevated protein due to blood breakdown products



Aphuia, llllmiparlllia, ar llllmiphagil



1314 1314

+ +or+or-


1nt11ct anltr{sm

NS18 Neuroaurgery

CerebroYascular DJnase



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 -...



.-ent I CTicen

----+ linb mMm!lnll

Stiff neck Fundi

CSF: clw, cololll'lass, no blood


NBQI1ive fllr blood

I .....-------'----,.

I'DiiiMI fur bllllld ancVor

pllliant chlwsy, uncanacious,

locelizina nuv!Dgicel findinae


CSF: bllllld XWIIhochramil

----+ Flafa'1D NIIUtiU'Qiry

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, decreased 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 cardiac- arrhythmia (>50% have ECG changes), MI, CHF


lri!N H" '"'-PY fvr V.aapum



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 %)

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
<7 mm 7-12mm 13-24mm <!:24 rnn 0% 0%

0% 2.6% 14.5% 40%

2.5% 14.5% 18.4% 50%


It,- rilrior C8111bniV11118rior corrmuriclting 1r1Bry

n.y; MC- middle c8lllbnll nry; K:- inllrnll ci!Oiid llllllry; PC- pnrior cnbmlllllllry; Ff.omm - po6Q

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 overall trend towards better outcome with early surgery or coiling (48-96 hours after SAH) treatment options: surgical placement of clip across aneurysm neck, trapping (clipping of proximal and distal vessels), thrombosing using Gugliemi detachable coils (coiling), wrapping (last resort) choice of surgery vs. coiling not yet well defined, consider location, size, shape, and tortuosity ofthe aneurysm, patient comorbidities, age, and neurological condition. In general: coiling: posterior> anterior circulation, deep/eloquent location, basilar artery bifurcation/apex, older age, presence of comorbidities, presence of vasospasm clipping: superficial > deep, broad aneurysmal base, branching arteries at the aneurysm base, tortuosity/atherosclerosis of afferent vessels, dissection, hematoma, acute brainstem compression unruptured aneurysms average 1% annual risk of rupture: risk dependent on size and location of aneurysm 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%) 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
,._,.. Tlill
CGiq il ZIU l'lliln with .....,_lnlacrllill"--: A....-..d ea..n-nrllh:ll Slniwa, Dlf-llnllll - - 111111............. 11111Ani1J11111 Occbiln 1Mce!2005;36&:D17 Thill randomilld trilllinld endcMac:ullr dellc:l1lbll coiled 1rellment IQiinst nialamy nd rfppinvfor inlrlcllnilll IIIIIUfVIIIII il Pllients who were conside!ld elglile fur eilhel rnoddly ct1herlpr. Canlbin: In pllilnls v.itll rupblfld illrlc!will IIIIIUfVIIIII Utili! fur bcJtb treldJnlrQ, lllikMscull' coing ilmorelklly fD in independent suM1111 1year 'dl111 nUIIUfgiCII cipping; 11i11.1Niw11 bllllfit continUII far Ill lint 7years. The risk af lllllllbB!q il klw. but is

1'IUOIIIViCII clppilg.

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
Sui:CIIIful Clnlid &IIIIIIIII:IDIIJ ill'dlnll MhlltRICIIIINUIIagi:ll lluilonUid C.allll Trill

Cerebrovaac:ular Disease/Vascular Malformations

Toronto Notes 2011

CBC, PTT/INR (hypercoagulable states) fundoscopy: cholesterol emboli in retinal vessels (Hollenhorst plaques) auscultation over carotid bifurcation for bruits carotid duplex Doppler ultrasound: determines size oflumen and blood flow velocity, safest but least accurate, unable to scan above mandible but invasive and 1/200 risk of stroke (not for screening) angiogram: "gold MRA: safer than angiogram, may overestimate stenosis

Llnc:et2004; 363:1491-1502
Slllly: AlympiDnwlic Carotid Sllgary Trill {ACST), a lilldomized, controlled 1rial will 5)WTI. l'llilnll: 3120 asymplomllic pl1ients NUl

111lllllr blllwlan immllilll carotid andulnclmny (CEA) UJ1 indafuitB dafumll ri CEA IIIII \'MII followad for up 1D 5years {maan 3.4 yBIIII. Mlil Oldaml: flirt stroke (incliding flllll or dillblinglc.:llli: In pi!ien1swilh CIIII CI!Qiid QlyQno5ia. immdlbl CfA Nduced the stroke riskflom lllout 1D llbaullft.. lid rltlis5-yalr bnlit iMMd dillbling or fllal Slnla

control ofHTN,lipids, diabetes antiplatelet agents (ASA dipyridamole, clopidogrel) -25% relative risk reduction carotid endarterectomy (generally if symptomatic and >70% stenosis, see Tables 8 and 9) endovascular angioplasty stenting


Table 8. Symptomltic Carotid Stenosis: North American Symptomatic Carotid Endarterectomy Trial (NASCET)
%Stun on Angiogr111

Medal Rx
70-99% 50-6!1%

Medal + Sllf1liCII Rx
!1% over 2years

26% over 2 years

22% over 5years


16% over 5 years 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 MadicaiRx

Risk af Major Strub or Dllllh

11% over 5 yea'S

60-9!1% 70-9!1%

5.1% over 5 years {ACASI

6.4% over 5years {ACSTI

11.8% over 5 years

Vascular Malformations
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


, ..----------------.
1 2

tangle of abnormal vessels/arteriovenous shunts, with no intervening capillary beds or brain parenchyma congenital


0 1 0 1

3.1-6.0 em >6cm
Location Noneloquent Eloquent

prevalence -0.14%, male:female = 2:1, average age at diagnosis= 33 years 15-20% of patients with hereditary hemorrhagic telengiectasia (OslerWeber Rendu syndrome) will have cerebral AVMs

Clinical Features
hemorrhage (40-60%) - small AVMs are more likely to bleed due to direct high pressure AV connections seizures (50%) - more common with larger AVMs mass effect focal neurological signs secondary to ischemia (high :O.ow -+ "steal localized headache:, increased ICP bruit (especially with dural AVMs) may be asymptomatic ("silenn

Deep vwn- dl'lin111

Not prllllent


A'iM gl'llla8 Clbilbld tr;" addirQ tlla 3 inllvidull Spallllr-MI11in Scala -.s 11om Ilia abova table. E.g. A2em 1llnDur in nonaloq.lllnt bcaliDn wilhout daap wnoiJI chinaga Gradel.

'IbroDlo Nota 2011

Vucular MalfonnaHona/Cnemoua Malformations

Neurosursery NS23

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

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

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


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

good with surgicallnterventlon

Figure 19. MRI uf CIV8IIIous

A. T2 weighted imaging MRI B. Gradient Echo aaquancing MRI

NS24 Neuro1urgery



,, ,


C2 - Anti of jBw C4 - Colar Df shirt

"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"

..... ,
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

dorsiflaxian and big tDa IIXtlnlion Sl - Planlarflelt f11111


i ...

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


F'11r 20. DanniiiDmas

Approach to Limb/Back Pain

see Orthqpaedics. OR22

RED FLMI fw IHII: 1'1111

Cudlr.rlnl Urilary rvtention or ineontinenc., f8eal incontinanca or loss of anal spiW!ctar tone. IIddie an.U.ia. unLibilllel'll.lea
WAkneWpain. Aga >50, prwiDUI hx of cancer; pain lllr'lliaved by bad rast,. constitutional

Extradural Lesions
Root Compression
Differential Diagnosis herniated disk neoplasm (neurofibroma, schWllllllOinll) synovial c:}'!t. abscess



lnr.:tian. lnCI'IIUtld ESR.. IV drug use. fwlr.

hypertrophic bone/spur

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


Cervical Disc Syndrome

nucleus pulposus herniates through annulus fibrosis and impinges upon nerve root

RED FLAGS fw lladl .....


incontinence) AnNihllillllldlte) Constitutionel symptoms IChronic disease l'lrulhNil AQ1>5Dar<2D IYG'ug uu

Bowel/lllddar ll'llllltion or


most common levels C6-C7 (C7 root) > C5-C6 (C6 root)

Clinical Features
pain down arm in nerve root distribution, worse with neck extension, ipsilateral rotation and lateral flexion (all compress the ipsilateral neural foramen)
LMN signs and symptoms central cervical disc protrusion causes myelopathy as well as nerve root deficits

NIUIIIIIotDr dlficihl

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 activity modiftcation, patient education (reduce sitting, lifting) phys1otherapy. exerd8e programs 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

"',.--------------. ,
Disc hamidions lnpinga tha 111M root
It thaiMI below the illtnpaca (i.e.

C5-ti dise

C& 1111rve 1\!111).

95% improve spontaneously in 4-8 weeks

Tillie 1D. Latenl Cervical Disc Syndrom11

Cl-7 lloGt hdvtMI C7-T1

C5 2\


C8 10%
Rilg fing 5th finger
Digillll flexors, nmsics

Delblid, biceps, tuplllpinlltul

FascicuUI gl'lcilirlcunllllul: joint po.ition. fine txlueh, villnltion Spiullhlllamil: lnll:l: Pain 11'11



No clwlga

llicapl. Bnlclial'lldillis


Fingar jllk (Haffmam's iign)

CGrticaiPilll tract BkiBd movements

Cervical Stenosis (Cervical Spondylosis)

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

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

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

insidiOUII onset of mechanical neck pain exa.cerbated by excess vertebral motion (particularly rotation and lateral bending with a vertical compressive force - Spurling's test). Pain is worse with neck extension. relieved with flenon

Figu111 Z1 A. AliiaI uctian Df Cervical Spine with Vascr Wid 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)

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. intractable pa.ln

FlgUI'II 21 B. Axial secllon of Tbonlcic Spine wilfl Vaacul end fiiiCiional TarritDria

NS26 Neuroaurgery



Lumbar Disc Syndrome

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

Clinical Fntures

leg pain > back pain

Lu..bar Spinu with Vascul and Functloaal Terrllerlea

Figure 21 C. Axial slldion of

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
Functloaal Terrllerlea

Root .......

<10% flllllllllpattam Madill leg Tibillislllllerior (dorlillsxion)

Sciatic patllm


Sciatic palbln


Darsal foot to hab. l..nnlleg

l..a1inll !oat
Gntrocnemius, ealu (pllmr fl&Xian)


Exlnar hal!cia \ballux lllnkln)


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

Onset SpaiDneaus Pain
Sensory Deficit

Suct:!an. blataral Rare. H11111111 usually in pllileum ar thip

IDllal unilateral

Savan, radii:Uar type: in periniJJ11. 1hiP,

legs,IB:k. or bladder

Saddle; bilill2nllllld symmelric; seRIIliV dilaociltion

Sadcle; no sensiiY dissociation; may be unilllarll end asymmetric AsyrrmaiJE; pnsi& IWJI9 mar1cld; lllqlby may be llf8Sid; fascil:ulatians nn

22.. 11-waightad MRI of l.umbllr Disc Humilltion


SVmmalric; pn&i& lass nBkad;

fasciculatians may be IIISR

Dnly lrile jett Bbslft (presEM!d blee jerk)

(bladder elc.)
!mary retEntion end lltlmic -1

Knee end 111kle jllk lllll'f be absent

Sphincter dyWJdian presents IE; impatBnca lass fnlcpn

Autonomic dysfunction,

II'Dftilant 811fv; iq)otanca

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 slow relief with postural changes (sitting >30 min), NOT simply exertion cessation induced by variable degrees of exercise or standing may be elicited with lumbar extension, but may not have any other neurological findings, no signs of vascular compromise (e.g. ulcers, poor capillary refill, etc.)



IC8y fAtu8l uf Neurogenic w.

v-1u CIMit:don

Claudlclltian: denmrtolllll distribution with positional relief accurrilg over minutes. Vacular CIMit:don: sclarotomll distribution with relief accurrilg with
rest owr s1condl.

Investigations 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



Intradural Intramedullary Lesions

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



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


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

....... ,
Compartmentalize spillll cord lllllomil:lllv by loaation.

N4. for spinal cord anatomy

Complete Spinal Cord Lesion bilateral loss of motor/sensory and autonomic function at :M segments below lesion/injury, with
UMNsigns 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)
Tble13. CDmJMriiOn b8tween IIICGIIIplete Spinal Card l..eiiDn Syndrom11
Hemiseetion of card lpsilatinl Lt.lll weakness at tha l11im lpsilatanll UMN waakness bllaw lha l11ian BilatemllMN weakness at the lesioo Bilateml UMN 'ltoelkness belaw the lesion Urillry 1'818nti111 Ipsilateral loss of vibration and pra!Jiacaptian Cormlataralloss of pail111d ta'npnure PmiMIII lii#Jtlauch
Presi!M!d vlnlion and proprioceplion Bilteralloss d pain and lefl1llnlure Presi!M!d lii#Jt tuul:h


A111H Canl

Anterior spinal .my 1:011_.eaion r. occlusim

Celml Card (most commm)

Sytivlmytlia_ tlmaur&, BiiUDI mlltlr Wlllkna&s: spinal Uppa' 1mb W8lkna&s (l.llfi lesion) iniiiY (J8Itsr 1Im LDwer liiD waalcness (UMN lasianl Urillry llllantian
IU!arir. spinal allay

Vllilbla blldsi'IIIIU&pal1dad slll&aly loa Loss d pain and tsiJ'C)III'Era 1han lass of vibl'llian and

P'allllriar Cord


infarction. 'lnUIII

Blalaralloss of vibration. ptapriocaptian. light twch at and balcrN lha !asian

Presi!M!d pail MJd

Figure 24. Spill CaniLBsian


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

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

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

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

Trauma Management (see also 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

Medicine, ER7}

NS30 Neurosurgery


Toronto Notes 2011

Trauma Assessment


INITIAL MANAGEMENT ABC's of Trauma Management see Emeri!=DQ" Medicine. ER8 NEUROLOGICAL ASSESSMENT Mini-History
period of LOC, post traumatic amnesia, loss of sensation/function, type of injury/accident
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Glaqaw Corllll Scale


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, ........



Neurological Exam
Glasgow Coma Scale (GCS) head and neck (lacerations, bruises, basal skull fracture signs, facial fractures, foreign bodies) spine (palpable deformity, midline pain/tenderness) 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 record and repeat neurological exam at regular intervals


Assessment of Spl CT/X-ray

IPII'IIAtlittll vilwl

spinal injury precautions (cervical collar) are continued until c-spine is cleared C,T,L-spine x-rays AP,lateral, odontoid views for C-spine (must see from Cl to T1 (swimmer's view if necessary) or CT rarely done: oblique views looking for pars interarticularis fracture ("Scottie dog" sign) CT head and upper C-spine (whole C-spine if patient unconscious) look for fractures, loss of mastoid or sinus air spaces, blood in cisterns, pneumocephalus cross and type, ABG, CBC, drug screen (especially alcohol) chest and pelvic x-ray as indicated

ABCDS Al9mlent (Columns: lllllerior v.n.bnlllin1, portarior vtlrtablllllinl, spinolaminar line, posterior spinou5 tine) IIane (vartebral bodies, facets, spinous
proce5Ses) Cartilqa

Disc (disc space and inbnpinous



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?

Wblch !'dents Need CT Hull or

Tl'llllf1lr to 1 Nlm'DIUf1llcll C.ntrl1

Remains resuscitation aftar

Faclll neurological signs Deterianrtilg

skull fracture indirect signs of basal skull fracture confusion, impaired consciousness focal neurological signs extreme headache, vomiting 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


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 high velocity: highest damage away from missile tract Scalp Injury rich blood supply considerable blood loss (vessels contract poorly when ruptured) minimal risk of infection due to rich vascularity Skull Fractures depressed fractures: double density on skull x-ray (outer table of depressed segment below inner table of skull), CT with bone windows is gold standard simple fractures (closed injury): no need for antibiotics, no surgery compound fractures (open injury}: increased risk of infection, surgical debridement within 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)


,, ,,

WNA (30-55')(,1 Falls (1 >35%1 Gun Shot Wound (S.20'1'ol



U,.rsllf Sclllp

Skin Comective tissue (dense)

Aponeurosis {galea)

Loou connectiw tissu1 Periostllum

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 coup (damage at site ofblow) contre-coup (damage at opposite site ofblow) acute decompression causes cavitation followed by a wave of acute compression

..... ,


AAN Clulliflc:nan Grade I : altered lllllltll status < 15 min Grade 2: altered lllllltll status > 15 min Grad 3: any loss of consciousn111

NS32 Neuro1urgery




'' ,
Exa'ni1115 nin for .,..ill IIIII a1N symptar.-. IIJblm Ia nonnaiii:IMty H lynrml willin 15 nn lllrncrw fnlm activity far

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 ischemia/infarction
raised ICP,lntracranial. HTN

CT or MRI H ar atber IVA


1day, 1hlln - -

>lwaek lllbJm 111 nannalactMly llftlr 3 Em1111n1 DIIIIIIIIIKIIm +


1111 hOlM wi1ll clollfaiOW up M'nUIIIVtip of ,-ttlllotv pa'Sislant abnormlll menlill

Extracranial Conditions


CT or MRI H or atber IVA IP/II1Ihllll fbriefooncussionl<1 ITin),

, waek withatd:syn1fDml


ratum 1o nannalactMly lfllr

f pllllmgad OOI'ICI&Iian I> 1nin), rWim ta nallllll

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)

II:IMtv .nv



loss of cerebral autoregulation leads to decreased CPP, ischemia

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
Direction Df Fun:a

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
Figure ZS. CT Showing Ceep-Contr.Coup InJury

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


Neurosurgery NS33

Spinal Cord Injury (SCI)

see Orthopaedics. OR22 and EmemencyMedidne. ER9

Neurogenic and Spinal Shock 1. neurogenic shock: hypotension that follows SCI (SBP usually S:80 mmHg) caused by
interruption of sympathetics (unopposed parasympathetics) below the level of injury loss of muscle tone due to skeletal muscle paralysis below level of injury -+ venous pooling (relative hypovolemia) blood loss from associated wounds (true hypovolemia) 2. spinal shock: transient loss of all neurologic function below the level of the spinal cord injury, causing flaccid paralysis and areflexia for variable periods

O..RJirillw41waa -.._nlllal11ial ............... card iljnd pllillls?

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Spiii/CII'II2004; lllrodadon: T1'il study YlliS liNd II illllrmning l'lllellierneudogi:IIIM:omewu improved will early 1<24 houll) lliial WV8'Y as C1J1111111Bd 1D lither ID 1>24 hou,.j 11111111V cr

-mMI m-uanart.


Whiplash-Associated Disorders
definition: traumatic injury to the soft tissue structures in the region of the cervical spine due to hyperfle.xion, hyperextension or rotational injury to the neck

Initial Management of SCI

major causes of death in SCI are aspiration and shock the following patients should be treated as having a SCI until proven otherwise: all victims of significant trauma minor trauma patients with decreased LOC or complaints referable to neck or hack pain or SCI (weakness, abdominal breathing, numbness/tingling, priapism)

1683 eligibl& plli8rQ ltnioomic spinal iljuy), 919 lWii irid 764 lWii"" IIIIIIUDgicll dlficit lkill:on wu dltllriied bv' cak:ulltiig the percenblge al pllieniJ Mil senSOIY or molD! r..ction irnprMrnentiiCCOI'ding 1D the FninQI'1 ale. buill: &II;' daCIJII1IIIRion I1UIBd in imp!Md wtcoma COII1llll1d 10 hotllllltand COIII8MtM



Stabilization and Initial Evaluation In the Hospital 1. ABC's

2. immobilization: maintain backboard/head-strap and use log-rolling during transfers mmHg with 3. hypotension: maintain sBP pressors ifnecessary: dopamine is agent of choice (avoid phenylephrine - causes reflex bradycardia) hydration (cautiously to prevent pulmonary edema) atropine (for bradycardia associated with hypotension) 4. oxygenation 5. NG tube to suction: prevents NN, decompresses abdomen to facilitate breathing 6. foley catheter to urometer (to monitor ins and outs) 7. DVT prophylaxis 8. temperature regulation 9. monitor CBC/electrolytes 10. focused history mechanism of injury (hyperflexion, extension, axial loading, etc.) weakness/numbness/tingling in extremities 11. palpate spine for point tenderness a "step-off" deformity widened interspinous space 12. motor level assessment - grade with American Spinal Injury Association (ASIA) Standards skeletal muscle exam rectal exam for voluntary anal sphincter contraction 13. sensory level assessment (grade with ASIA Standards) sensation to pinprick (spinothalamic tract) sensation in face (spinal trigeminal tract can sometimes descend as low as C4) sensation to light touch (anterior spinothalamic tract in anterior cord) proprioception (posterior columns) 14. evaluation of reflexes 15. signs of autonomic dysfunction: altered levels of perspiration, bowel or bladder incontinence, priapism 16. radiographic evaluation 3 view C-spine x-rays (AP,lateral and odontoid) to adequately visualize C1 to C7-Tl junction oblique views to assess integrity of articular masses and lamina flexion-extension views to disclose occult instability scan (bony injuries) MRI (soft tissue injuries)

slides 11Milled .... pllie!O illdQJing nrlv lor incomplll inPv wu homogenous lp>O.IP.iL howeveull iilhar .. lwtaraganaity. Can&bln: Allilllglllllti!ti:lt{ jll1illilirQ. Mil .... lick of pllianl bomOQIIIIIity il T8C8i1l sbilial, tlil anll riCGIIIIiliidaliJn isilatMiugical decompression be considnl as "" optional priCtica liii!JMrG 1l'lllnllic spilllll Cllld ....

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injly. trocal Mlation "' 81Ch of these trillsthe 'If' led tliele din to usess1hellellm lird.iding tlil NASCIS tri*I1D riMYtttlil evidse belind Malhodr,fgpulllion: Acrialllpllli5ll of the dB the NASCIS studies alonill'lilh a lflcl of MP on ICiill spilll injury. buill: Tlilllllhors r1il8 .-1 iau8l l'tilhmh of NASCS land incliding 1111 fltt

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NASCIS I mil blnllill were only obserwd spinll ijlies. NASaS II was awlullad for lick of apilnllion 411 oplirun MP liming Ulng Mlllaikle ID "'llO'' mGtur claiiJIII post-tliellpl' on hotlllhe righl111d
11ft lid1 oftlil body. qgasting lhll ch-.gn in

tlllts1ldisticalanlysis wu



Medical Management Specific to SCI

methylprednisolone (given within 8 hours of injury) decompression in acute, nonpenetrating SCI (Fehlings and Tator, 1999)

tlilliillliingkbill&!itliii'IIUI!s. Odillior sUiies lliled Ill fel)rocb:e 1lie resuls NASC1S. IUdim is11i1 lactDrtllltlllldi Iince NASCIS lim II incUIId r.t' since it was tllrA9t 1D be LMiethiciiiD indMdulls111 aplacdlo111014). CliiCbiu: 1lia Dim conclidalhat basad on U.. mil OIW mlljarcriticilms al tlil NASCIS II mil Ill. nny lilllrougicll depltlmaiitl liM ttopped using MP as alllnillld rwlinl iiiiCIIIIi spinll cord inpy,liid also notetlilt its use is not Cllllllltt IICGIIII'IIndld bythl Food mil Drug Adirinistnltion il111e IXiW SIRs. They111ggest liltliarinvllltigltionis"'*''llllldto-rlhil


NS34 Neuroaurgery




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 '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

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


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


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 vestibulooochlear response (cold caloric): nonnal = nystagmus fast phase away from stimulated ear deep tendon reflexes plantar reflexes: normal = flexor plantar response 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

Clleric Refllllll

Cold Opposite Warm


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

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

Persistent Vegetative State

a condition ofcomplete unawareness of the self and the environment accompanied by sleepwake 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


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

failure of fusion of the pollterior neural arch

Clinical Felll:ures
no obvious clinical signs

Figure 27. SpiR Bifillla Occulbl

presence aflumbosacral cutJLneous abnormalities (dimple, sinus, port-wine stain. or hair tuft) 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

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

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)

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
Investigations plain film&, cr, MRI, UIS, echo, GU investigations Treatment

Figu111 21. Myelaaningacela

."' ..

surgical closure to preserve neurologic status and prevent CNS infections


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

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

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
Investigations skull x-ray, U/S, CT, MRI, ICP monitoring Treatment similar to adults (see Hydrocephtdus. NS7)



Dandy-Walker Malformation

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%)


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

i u


scoUosis brain compression central cord syndrome (6596) syr.i.ngomyell.a (50%) foramen magnum compression syndrome (2296) cerebellar syndrome (1196) hydrocephalUII (1096)


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

MRI or CT myelography

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

premature closure of the cranial suture(s)

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

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

plain radiographs,

cr scan

parental counseling about nature of deformity, associated neurological symptoms sutures involved) surgery for cosmetic purposes, except in cases of elevated ICP

Pediatric Brain Tumours

see also Thmour, NS9

lhHtiVII fnlqnncy Iff 1'811iatric BrUn TumiDin Tum-typtl

Pwl:ent ('r.l
40 (23) (17)

Epidemiology 20% of all pediatric cancers (second only to leukemia)

60% of pediatric brain tumours are infratentorial pediatric brain tumours arise from various cellular lineages glia: low-grade astrocytoma (supra- or infratentorial), anaplastic astrocytoma, glioblastoma multiforme (largely supratentorial) (see Astrocytoma, NSll for details) primitive nerve cells: supratentorial [primitive neuroectodermal tumour (PNET)] 90% of neonatal brain tumours, infratentorial (medulloblastoma), pineal gland (pineoblastoma) non-neuronal cells: germ cell tumour, craniopharyngioma, dermoid, meningioma, neurinoma, pituitary adenoma, others

Altruc:ytDma, Supl'iltentorial lnfmentorial

MldulloblntDIIII. Bn.inst.m gliDI!III

8 8

Mllignant glioma Craniopharyngioma

6 6

Pineal, oemn call tumour Other


Clinical Features
vomiting, seizure, rn.acrocrania, hydrocephalus developmental delay, poor feeding, failure to thrive often initially escape diagnosis due to expansile cranium and neural plasticity in children

Rlpi1t8d !tom Petflttie ri North Alrllrm. Vol44{4L KIN! LE. hill'illxlfn: r:1r1111tngu IDidillcfirw,pp. penrission !tom BIIIVilr.


NS40 Neurosurgery

Functional Neurosurgery

Toronto Notes 2011

Functional Neurosurgery
Movement Disorders
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._ Faiure of medical management (advn:ed lisease) Drug-induced dyskinesias (see dystonia, below)

Simultaneous, biateral surgery/ stimulation is most comon Preferred target: anterodorsal subthalamic nucleus (SlNJ Other targsts: atellllllactic ablation (pallidotamyVstimulation of posteroventral pallidus interna (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

39-48% improvament in Unified Parkinson's Disease Rating Scale (UPDRSJ scores Reduced dosage rJ medications (STNJ More effectiwlhan medical management in advanced PD Early intavention may reduce severity, course, and pi'OIJ'85Sion rJ disease Of little benefit for patients with atypical

Intracerebral hemanhage, infection. seizure ( 1%-4%) Paresthesias Involuntary movements Cognitive functioning: decreased laxicel fluency, impaired executive function (STN > GPi) Psydliatric: depression, mlllia, anxiety, apathy (SlN > Gl'i)



Canirlllallnl primary (generalized) dystcnias; cervical and brdive dyttonias (GI'i) Cantrlllataral secondary dyskinasia (i.e. drug-ilduced: L-dopa, neuroleptics; STNJ 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)

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

Primary dy5tonia: 51% reduction in Burb-Ftim-Marsden Dystonia Scale (BFMDS) score Secondary dystonia: 628!1'1. improvement in dystonias Delayad efleclll: weala! months

Intracerebral hemonhage, infection. seizure (1%--4%) Minor effects on cognitive functioning (esp. decreased lexical fluency; SlN > GPi)


Durable reductions in essential tremor rating scale (ETRSJ scores Reduced dosage of medications Conflictilg data on VOCBl/IBcial tremor

anterodorsal S1N

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
Disanlar Obleaiva Compulsive Disanlar (OCD) Taunrtte" Syndro1111

Syndrome, Obsessive Compulsive Disorder and Depression sections in Neurology, N29 and PSJFchiatry. PSIS, PS7
Anterior capsulotamy/stimulatian of the anterior limb of the internal capsule (IC)

Table 15. Surgical Targets for Neuropsychiatric Disorders Indications Severe syrl'1l!onns refraclllly to medical management Outcom Currently under investigation Reportelly 2575% response rate Morbidity lnlnlcerebral hemorrhages (1 %-2%) Mild effects on cognitive functioning Anxiety panic disorder (case report) lnlnlcerebral hemorrhages (1 %-2%) Mild sexual dysfunction

S8Vlll8 syrl'1l!onns refreclllly to medical management

Stimullltion of midline inlnllaminar Currently under investigation nuclei Ill the thalamus Reportelly >70% reduction in vocal Stimulation of motor and limbic or mDIDr tics + urge portions rJ GPi Stimullltion of the antarior limb of the IC Stimullltion of the subgenual cingulate cortex Currently under investigation Reportelly 60% response rate; 35% remission rate

Major Depl'ellive Disanler (MDD)

Severe depression refractory to medical management and ECT

lnlnlcerebral hemorrhages (1 %-2%) Pain, headache Worsening mood, irritability

Toronto Notes 2011

Functional Neuroaurgery/Surgical Management of EpUepay

Neurosurgery NS41

Chronic Pain
Tabla 16. Surgical Targats for Chronic Pain

Neuropllhic Pain




Mlllllillly Intracerebral hemonhages


Severe, intractable, Preferred 1Brget: stimLJation organic neuropathic of 1he contralateral ventral pain (i.e. post-stroke posterior lateral (VPL) and pain. phaniDm lilt pain. medial (VPM) thalamic trigemillll neuralgia. nuclei periventriruler/ chronic low-Mck pain. grey matter complex: regional pain (PVGIPAG) syndrome) Other blrgm: &timulirtion of the contralatenJIIC Stimulirtion of the contralalenll motor cortex Severe, intractable, organic nociceptive pain Bilateral (most common) stimulirtitll of tha PVG,IPAG

47'l. in pen:eptit11 of pain intEnsity Less favourable results in cenlnll pain syndromes and poorly localized pain

Pinesthesia Anxiety panic disorder

Noc:iceptiva Pain

Reportedly 63% imiJOVBmanl in perceptit11 of pain intEnsity

Intracerebral hemonhages

Pinesthesia 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, SPEer and PET if a distinct epileptogenic region cannot be identified. the patient may be a candidate for a palliative procedure such as corpus callosotomy Procedure most commonly adults: resection of the hippocampus and parahippocampal gyrus for mesial temporal lobe epilepsy arising from mesial temporal sclerosis children: resection of an epileptogenic space-occupying lesion hemispherectomy and corpus callosotomy are less common 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


Allandalilld, Clnnlllll Trill If IIQIIy far

NUf21l01; 345:311-8 Thillllldomilld tmnll1rill MlillfR1ba aftic:lcy and llflty olnaiiUUQ81Yfor11mpOIIIIalie

epi811$Y. lhllals: II patilll1l Mth poarly Cllll1nllld

flom.m.1bal..-r- ollrllland

ln=-401 or fur mooadn.tn-.nwillantilpiillptic drugs (n=401. The PlinarYoulmlewasflliedom

turroundingl pOd all Ylll. Slccnllll'f oull:urn8l ii:Uiad hquency IIIII -ny al

...-ilr ri 10. diUlq end dedi.

1Jn1XIIi-labll!il..-y; lllfiiiiY is IUperiar10

CancUU: In pdents will pocxlf controlled

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

Neurosurgery NS43

Common Medications
The folowing are ONLY; follow clinical judgment and to adults unless otherwise specified prescription reconmendlllions i1 practice; dosages refer


n. Common Medications
Doling Schadule 4 mg IV over 2minutes, q1 0-15 milutes (do not axcaad 8 m!V'I2hr) Trigeminal neuralgia (tic 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 q clays) 7 until tharapeutic lewl achievad (usual opti'lllm dosege: 800-1,200 mQI'day; range: 60()..2,000 mQI'day] lndic:lltians Status apilepticus Side Effacts Cammon lniBI'II:ticm Canlrlinllcatians Cammllllll Drowsin111s. sedation OtharCNS depressants, digoxin (increaSIII digoxin levels) Worsening of seizures, heart failure, anhytllnias, AV block. aplastic anemia. agranulocytosis, tlrorDiocytopenia, hepatitis, erythema multifurme, StuwnsJohnson syndrome Lithium (increases lithium toxicity), MAOI Other meds may increase carbammpine II!Vllb ortlave decreased ella Hypersensitivity to TCAs. previous bone marrow suppression, MAOI in past 14 days

Dnlg Nama lariZipam

S1lrt phenytoin loading simultaneously

Monitor CBC



Trigeminal neuralgia Seizures

hematological toxicity)

phytain (Dilanti..)

Seizures: Loading dose: Seizures 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) Cerebral edema (e.g. secondlry to 1urnour, head injury, pseudotumour cerebri) Preoperative preparation for patients with increased ICP secondlry to brain neoplasms

Thrombocytopenia, leukopenia, agl'lll.llocytosis, pancytopenia, toxic llepatilis,


Other meds may incree&e phenytoil levels and toxicity or have decreesad effects

Bradylrrhythmias, heart block

Important to give IMII' time to pllMint causing a cardiac


Johnson syndrome, toxic epidermal necrolysis

dllliiii1IIIIIISIIII Loading dose: 10-20 mg IV; Maintenance: 4-6 mg W/day divided qid (may be PO)

Psaudotumour cerebri, seizures, heart failure, anhytllnias, tlromboembolism, pancreatitis, acute adfl!lllll insufficiency; avoid abrupt withdrawal

Aminogkrtethimide, antidiabetics,I>SA, NSAIDs, balbituata&, phenytoin, rifampin, cardiac glycosides, cyclosporine, ephedrine, oral potassiumdrugs. selicytates, skin-tasting antigens, toxoicls, vaccines

Systamic fungal infl!ctions, immun05Uppressive dose with live virus vaccines

No longer used in acute spinal cord injury


1-1.5 wkg Wrapid i'lusion (350 ml of 20% solution] followed by 0.25 glkg q6h

Raised ICP

Seizures, heart failure

Lillium (increases excretion of lithium)

Anuria, severe pulmonary congestion, fnd edema. severe eart failure, severe dehydration, metabolic edema, progressive renal di&asse or dysfunction, active intracranial bleeding except during craniotomy Nona known

Effect occurs in 1-5 mins, maximal Ill Often altemllled with furosemide 1()..20 mg Wq6h Indwelling urnry catheter to measure ins and outs Causes vasodilation Only calcium channel blocker (CCB]1hat crosses BBB (blood brain berrier] Use half the nonnal dose for liver failure; monitor BP always


60 mg PD/NG q4h X 21 started within 96 hours of AH

Vasospasm in SAH

Decraased blood Antihypertansives pressure, tachycardia, (may increase dyspnea hypotansive elfacts], CCB (may ilcreese ellec:b), cimetidine (increases nimodipine bioavailability]

NS44 Neurosurgery


Toronto Notes 2011

Ahn NU, Ahn UM. Nalllmshltly L. at II. Cauda equina in ankyb!ilg spondylitis {tha CES-AS syndroma): mlll-tnalylis af outcomnllfllr medical and Jcunll af Spinal Dilorder$ 2001;14:427-33. .Aids to the exlriiidiln af1he neJWUS sys1eut Loll don, UK: Baliele fmdll. 1986. AI.Shahi 11. WllllrN 111t8JW11tions brain WIBriownDIJI malformations in IIU1s. lba Co::hrana Librl!y 2004;Voklma 2. lllrbr FG 2nd, Ogilvy CS. Bliclcy cl pruphytlctie nimodipine fur dellyed ischemic Iller U.rachnaid hemonhlge: 1 melunlttsis. Joumal of Neurougery 1996;84:40514. Bamaa H. TaylorW,Iillsziw M. atal.lllnafitafCIRIIid 111dartaractDmyinpatiantJwith symptmnatic modarata or aera stJmosis. NEJM 1198;339:141!i-25. llrlc:lc8n MB, Sheperd MJ. Holford Tll, at II. ortirilmd adninislllti0111fter aculll spinal cord injury: 1-'IIIIT follow up. Rasulls of !he lllinl National AcuiB Spinal Cord lnpy r111dorniz&d eon!nllad 1rial. Joumal of NIIUUSUrgary 1988;89:69!1-706. CnMisman AA, Nelly D. Neuroanatomv: an iiUtrided cclculell!. Toronto, ON: lhirdillivings1an, 1998. EdlawJ, Caplin L. Awiding pitfalls in tha diagnosis ohubllllclhnoid hnarrhlga. NEJM. 2000;342{1):2S-36. Elalcl.rlive CPrittaa for tha A5ymptomatic Clrotid Alherosclarosis Study IACAS). ciTDiilartaryatanosis. JAMA 19!15;Z73:14Z128. Fahlilgs MG. Tllllr Cit. An INilanca-illlad raviiM' of surgical dacomprallirm for ICUI8 spinal cord injury: lllionala, indicatiDns,and timing besad on axparimBnlll and clinical sludies. J. Neu111111rg. 1991;91{1 Sllppij:1-11. Fi1zgnld MJT. Nllnnatorny: basic 111d cirical {3rd edition). Philldalphia: WB S111ndars, 1997. Goltz CG,I'IIppart EJ. Tllldbook af clinicalllllllllagy {1st edition). Tomnto, ON: WB Saundars, 1119. Gr8riarg MS. H111dbook af neurosurgery {5th New 'fait: Thiama, 2001. lluv M. Guy Nlil Kill: han. Clinical Naurolagy l1ld Naurollll'QIIY. Thama Madical Publishers. 2003 Klrl, LE. Brain Clllllsngasand Cliniesti NorthAmsrica. 1997; Vol44{4):90711. Lildsay KW, Bone LNlulllagy l1ld illusbi11d. New York: Chun:hill Livilgslone. 2004. MRC AartmPtomatic Ceratid Surgary Trial {ACST) Cdlabonllivl Pnrvllltion of dillbling and fatal rlrDkas by SUCCIIslul CIIDiid and...racmmv in palilllll withaut reeent neUJDiogical randomisad eontrollad trial. Lancet 2004;363:1491502. Nieuwerh.rjs R, Voogd J. VIII C. The human central nervrNS system 13rd edibl. New Yart: Springer.lJerllg, 1988. Nlfting 2004lllug lllndbaok {24th Naw YoR. NY: SpringhoUI8 Lippincott Williams &Wilkinl. 2004. Ogilvy CS. Stieg PE, Awlld 1., et aL Recammllldlliollsfor the managemem of irtlai:ruial nriiMinous malurmations. Cin:ulation 2001;103:2644-57. 1'Dr1111JfRK.lipton RB. Fall\' KM.Illlckpail in tha cm:BTpatian1: An algori1hmfurMklltion and Nluq. 37:134-8, 1987. l'orllr PJ. Wilir.ky RA.IIIrpar W, at al. Cnlnl CMI1IIIUI nlfonnations: 1llbnl hirbly and pognDiislfter clinical datarioridiln rr without t.nlmhage. Joumsl af NIUIDSUiglly 1987;87:1107. SIIIJS, Sui JA. Yurth IF. Nonopmtive henil11d c:eMcal imverlllnl disc v.i1h radi:uiopl1hy. Spine. 21 {16):1877-83, 1996. Shapiro S. Medical cularnl'flldromaii8CDndaryto llmbrrlile humiation. Spila. 25{3):34&-51; ci6C1111ion 352, 2000. Shemie S, Doig C,llckens B. elal. Sevn brlin injury ta neurollgieal determination of Dlilth: Canadian forum recammendations. CMAJ 2006; 174{6): Sl-30. DJ, 8 MillY WS. Jon11 F'W. High dole mlllhy1pradnisol011a in tha K111111!1illl cord injury -a sysiBml1ic nMiw IJDm a clnical parspectiva. Cord 2000;38:273-86. Spancar S. L !Means ti epilepsy llllliiiV in &dulls 111d cilldran. Llllcet Nuol. 2008 Jun;7{6):525-37. Spatzlar RF. Marlin NA. Apoposad grading flySIBm for 1118riovenous malorrrltions. Journal of Naurolurgary 1118&;65:476-81 Tha Narlh Amaricln Syrrlmltic CanJiid Elldlntnclrrrl!' TriaiiNASCET). llllnulicial affaell cl carotid andlllllnletamy il symptomatic pdiardl v.i1h high-pia carotid s11Dis. NEJM 1991;325:44&-53.