NS

NeurosurgeryBrian 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 editorsBasic 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

1'oroDio

2011

n

IBB Func:liaDBI

NBui'CIBndamy Sllftwln

Basic Anatomy ReviewMRI Brain

Corpus calloeiJn

frDnllllloba

Thlamu. llypothallmu.

Caudltll nuclau.Lderll vantricl

Occipital lobe Midblain Pons Four1h V8111rida

CerabllllumMadl41aDansofCZ

ThiiiiiiUI

Spinal cord

Occipillllobe

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F"111ra 1. MRI

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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

A

B

4

... 11a:

.... 2I!

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1. Am.iDr carebralartay

0Arblry IBgn:

cAt. - Antariar carebral AcDIII - Antariar CGIIIIIUliCIIilg

6. AICA 7. PICA 8. Var1abrllartary9.

2. 3. 4. 5.

Midcll centnl ll'lllry Postarior cammlricating artary Postarior Clf8bralartay Besilanrtary

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

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

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

Peripheral NeiVe Lesions neuropathies traumatic entrapments iatrogenic inflammatory tumours

INTRACRANIAL PATHOLOGYICPmmHg80

I I 1

I

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

100Ll'-. 60,-

Intracranial Pressure (ICP) DynamicsiI

...-I

1I

ICPNoluma Relationshipadult 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

0

Vollda

I:I

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

lromB18Viar.

Toronto Notes 2011

Intracranial Pressure (ICP) Dynamics

Neurosurgery NSS

Cerebral Blood Flow (CBF) CBF depends on cerebral perfusion pressure (CPP) and cerebral vascular resistance (CVR) normal CPP >50 mmHg in adults cerebral autoregulation maintains constant CBF by compensating for changes in CPP, unless: high ICP such that CPP 150 mmHg or MAP 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 CurveAd1pted 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

Or

Elevated ICPEtiology intracranial space-occupying lesion: tumour

pus

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 Features1. 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

1'oroDio

2011

2. Chronic Elmated ICP H/A postural: worsened by coughing, straining, bending over morning/evening HIA-+ VIUIOdfiatation due to increased COz with recumbency

visual changes due to papilledema

enlarged blind spot. ifadvanced-+ eplsodJ.c constrictl.ons ofvisual. fields ('"grey-outs") optic atrophy/blindness differentiate from papillitis (usually unilateral with decreased visual acuity) decreased level ofc:onsd.ousness

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

Herniation SyndromesTable1. Hemllllon Syll*ome

Cl1lcal FN1u111o

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

S.TDRSillr

i 0: I!

Daaaased l.DC (nidbrain

EOt.V

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 andend-s!IQI s9'1

F"111ra 1. H1miltian Types- SuaTabla 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 (nidbrain1

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 Willishamiates llnugh tentDrii!l inciBIA

1

large posterior fossa l1lii5S(cmman afta' VP lhi.IIIRg)

o

CII8Jellar infarct (sl.pl'ior cerebelar arteryISCA) COI11Niian)

Cerabelltonsis hemiatell"f'DIQI funmen011gnum

oo

heniationo

llinltadorilllaaiiJI FltawiJ.I central tanllrili

Hydf11C8Phakll !Cinbnllaquecllct Neck stiffness head tilt ftcnsllar. ., Daaaased l.DC (nidbrain1

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 65 mmHg, MAP >90 mmHg General Measures (,CP HEAlY see sidebar) elevate head of bed at 30-45, maintain neck in neutral positionoutflow

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

calm (sldiiiJ,II:cmaPlace .nivParlllylilltypemntiltll 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

HydrocephalusDefinition

increased CSF volumeEtiology

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

Epidemiology

estimated prevalence 1-1.5%; incidence ofcongenital hydrocephalus -1-2/1000 live births hydrocephalus in children, see Pediatric Neurosurgery, NS37ClassificationTllllllle 2. Cl&lllllcatlon of Hydrocephalus Ciculllliln blacUd willin (tm.Cimlllllil:llill) Vldricular sy1l8m pmximal to the 8111CI'IIDid IJlftllatiJnS1. Clloroid plsxu. 2. l..lltalll wntricllll 3. Third venlricle 4. Cerebral aqueduct (Df5. Four1h vanlrida

6. Fo111men l.ulchklland MIQIIIIdie

Obllrur:linl

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

Vantriclilr

7. Aracmoid gnmliltions

to lilck

pruxinlll

8. Subal'lll;l'noid

9. Segilllll sinus

par;

1 ofo

iii

j

o

Periwnbiclilr hypodensily

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mat illo

lllln8ependymal ri{plian li CSF

Figure I. 'Ilia Flow of CSF

spacal

....

',

Mall

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 ve1111111lii'IDM.

malbmalim All wnbicles dilaled

(188 PrMiifllric NflutDJutgety, NS36)

N...OIIIInl:liR(er.r...lil:ltilg)

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 hydracephilso

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)

NPH I'NaNAiolo

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

D1111entia

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

0

E'nllllved venbides and mci Carelnllllqlhy

NS8 Neurosurgery

Hydrocephalus

Toronto Notes 2011

Clinical Features (see also Pediatric Neurosurgery, NS36) acute hydrocephalus signs and symptoms of acute raised ICP (see Elevated ICP, NSS) impaired upward gaze ("sunset eyes") and/or CN VI palsy chronic/gradual onset hydrocephalus [i.e. normal pressure hydrocephalus (NPH)] gradual onset of classic triad developing over weeks or months pressure ofventricle on LE motor fibres -+ gait disturbance (ataxia and apraxia usually initial symptoms) pressure on cortical bowc:l/bladder centre -+ urinary incontinence pressure on frontal lobes -+ dementia CSF pressure within clinically "normal" range, but symptoms abate with CSF shunting Investigations CT/MRI periventricular lucency suggests raised CSF pressure ultrasound (through anterior fontanelle in infants) ICP monitoring (e.g. LP) may be used to investigate NPH, test response to shunting (lumbar tap test) radionuclide cisternography can test CSF flow and absorption rate (unreliable) Treatment ventricular drainage surgical removal of obstruction (if possible) or c::xcision of choroid plexus papilloma shunts ventriculoperitoneal (VP) - most common ventriculopleural ventriculo-atrial (VA) - not first choice because of increased infections, shunt emboli lumboperitoneal- for communicating hydrocephalus and pseudotum.our cerebri third ventriculostomy (for obstructive hydrocephalus) via ventriculoscopy LPs [for transient hydrocephalus (e.g. subarachnoid hemorrhage), IVH in premature infants, etc.]

Shunt Compli:ationsTable 3. Shunt ComplicationsComplication Etiolour Clinical Features lnvestiplians

Obstnlction(most common)

Obstruction by choroid plexus Acute hy!Rcephakls Buildup of proteinaceous h:l8iiS8d ICPaccretions, blood, cells (illlaiTII'IIItory or tumour) Infection Di&connaction or dal!lilge

"Silmt series" (plain X-fiVS ofentire shunt that only ruleout discomection. break. tip mi!JIIIion)

CT

Radionuclide "shunto!Jlllf"

lnf8c:tion (3-6%)

s. epidermidis P.ICII8S S.lMR'fiiRl 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)

Ovarsllunting

(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

CT

Clinical

oCT

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

EEG

...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

U/S

'IbroDlo Nota 2011

Neumaurgery NS9

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

Etiology unknown (majority), but aS&Ociated with: lateral venous sinus thrombosis

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

Epidemiology incidence -0.5/100,000 per year usually In 3rd and 4th decade (F>M)

Clinical Features symptoms and signs ofra1secl ICP (HIA in >9096, pulsatile intracranla1 noJse), but NO decreased LOC or diplopia decreased visual acuity. papilledema, visual field defect. optic atrophy (key morbidity) usually self-limited. recurrence is common, chronic In some patientB 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.

TumourVllllric...r: CGUDid, chomid prDC81S

pepma. apandymoma.germiloma. tntoma.

DDx far Rmg (nlllnci.. Laeia1 01 CT wllht:antrAthpnllmut.. irrlnr--: lltrDI:Y!Dmt. 1gliobllllluma, aligadlillllllllioma.

Ablcass* blastnma(high .,Ualllracytama)lnfllrct Contuaion AIDS (lmulplasmosis) DliiiJY'Iinalion IIBIIDiving homlllllma (" 3 mo.t conrnon Dx's)

...,.._..LY!l1111ollll

IUOICALDR

QMglioma. lymphoma,

adnma.

piUtaJy

craniopharyngioma. apt narva glioma. cyst

....MMrySGu- rlTIIIIIIIIS

lu1g8r'llql

44lli

10%(RCC) 7'!1i 0.

Figura 9. Tuaurs

GlMnoma

3%

NSIO Neurosurgery

Tumour

Toronto Notes 2011

.........................:A

..............

Classification 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, iMIMIIDcll1lllllnlnlllllllt 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)

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

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

Table 4. Tumour Types: Age, Location10 yan. CWBI ps 111111 rasactianSyaars 1.5-2 yellS

('II.I 100

II- Low (plldr/dilfusa Ill- AnapaslicIV - GliOOiastoma rrUiimme (GBM)

Mia allact. no anllllranat Cllqllex eManc:annNecrosis (rilg emal'll:ef11ID)

12 manlbs, 10% at2 yess

8070

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 carryon 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 ICPInvestigations 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

8050

Requil88 occuionalllllil1lnce. but ilable 111 Cln for 111011: ofhit

needs

Requiras considlllble 881i111nce 4lld fnlquant medicalClQ

4030

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

20100

dflllh not i11111L'11nt V.ry lick; hospital millionldivB .upportiva 1llltlnBIIt II8C8SWY

Mcriluld; fiiii110C88118 prugllllling lllpidly

Delli

NS12 Nearomrgery

10ronto Nota 2011

Tralltment low grade diffuse astrocytoma close follow-up, radl.ation, chemotherapy, surgery all valid options

not curative, trend towards better outcomes

radiotherapy alone or post-op pmlongs survival (retrospective evidence) chemotherapy: usually reaerved for tumour progression high grade astrocytomas (anaplastic astrocytoma and GBM)

surgvy

gross total resection: IDIWmal safe resection + fractionated radiation with 2 em margin + concomitant and adjuvant temozolomide - a.cept: enensive dominant lobe GBM. slgnlfica.nt bllatenl involvement, end ofllfe

near, extensive brainstem involvement stereotactic biopsy ifresection not possible, followed by fractioned radiation with 2 em margin expectant (based on functional impairment - Kamofsk:y score 9896 sensitive/specific), CT with contrast 2nd choice audiogram. bminstem auditory evoked potentials, caloric testll

Treatment conservative: serlal imaging radiation: stereotactic radiosurgery is the trea1ment of choice 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 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

lllllliiiJI!Illenl

11.......

AartalkDiml

Ruptured uan11amid vessels

AQB >50.

No lucid inllML henipsesis, Pupilary chqesOften lllylqiiDIIllltiC Minar WA. confusion, signs of ilcreased ICPSudden onset

Crascen1ic OilS$HypadaiiiBCIIRiCBID: lll8iS

Cnriatamy if bleed >1cmBurr bola to IRil; Cllllliotumy Hreoccurs

Paar

Cl111ic SUWanl Ruptured 11....... sdlnclnlid bridgill! vassels Traum11, spmaneousllllllllllhlge(111811811'11.

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

Good

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% mortality3D% 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'") HematomaEtiology temporal-parietal sJwll fracture: 85% are due to ruptured middle meningeal artery. Remainder ofcaaes are due to bleeding from middle meningeal vein. dural sinus, or bone/diploic veins

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

Clinical Features signs and symptnms depend on severity but can Include H/A. NJV; amnesia. altered WC, HTN and respiratory distress deterioration can talce hours to dayslnvestigtdions 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 dilatation1. Comp1'81Sion of van1ridas

(miclile llhilll

2. Bload

Figura 15. Eatndural Hama1Dm1 usually withDICT

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

NS16 NeurosurgeryCalcilm 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.

BloodPrognosis

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 HematomaACUTE SUBDURAL HEMATOMA Etiology 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, hemiparesisCT Density and MRI Appearance of Blood Time Acute (50% have ECG changes), MI, CHF

we.

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

HyparllnsionHypervolemia

H1111odilution

Prognosis 10-15% mortality before reaching hospital, overall 50% mortality (majority within first 2-3 weeks) 30% of survivors have moderate to severe disability a major cause of mortality is rebleeding, for aneurysms: risk of rebleed: 4% on first day, 15-20% within 2 weeks, 5096 by 6 months if no rebleed by 6 months, risk decreases to same incidence as unruptured aneurysm (296) only prevention is early clipping or coiling of"cold" aneurysm rebleed risk for "perimesencephalic SAH" is approximately same as for general population

Intracerebral Hemorrhage (ICH)

----------------------------

Definition hemorrhage within brain parenchyma, accounts for -10% of strokes can dissect into ventricular system (IVH) or through cortical surface (SAH) Etiology hypertension (usually causes bleeds at putamen, thalamus, pons and cerebellum) hemorrhagic transformation (reperfusion post stroke, surgery, strenuous exercise, etc.) vascular anomalies aneurysm, AVMs and other vascular malformations (see Vascular Malformations, NS22) venous sinus thrombosis arteriopathies (cerebral amyloid angiopathy, lipohyalinosis, vasculitis) tumours (1%}- often malignant (e.g. GBM,lymphoma, metastases) drugs (amphetamines, cocaine, alcohol, anticoagulants, etc.) coagulopathy (iatrogenic, leukemia, TTP, aplastic anemia) CNS infections (fungal, granulomas, herpes simplex encephalitis) post trauma (immediate or delayed, frontal and temporal lobes most commonly injured via coup/contre-coup mechanism) eclampsia post-operative (post-carotid endarterectomy cerebral reperfusion, craniotomy) idiopathic Epidemiology 12-15 cases/100,000 population/year

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

NS20 Neurosurgery

Cerebrovascular Disease

Toronto Notes 2011

Clinical Features TIA-like symptoms often precede ICH, can localize to site of impending hemorrhage location: basal ganglia/internal capsule (50%), thalamus (15%), cerebral white matter (15%), cerebellumlbrainstem- usually pons {15%} gradual onset of symptoms over minutes-hours, usually during activity HJA, NN and decreased WC are common specific symptoms/deficits depend on location ofiCH Investigations hyperdense blood on noncontrast cr Treatment medical decrease BP to pre-morbid level or by -20%; check PTT/INR, and correct coagulopathy (stop anticoagulation for 1-2 weeks) control raised ICP (see Intracranial Pressure Dynamics section, NS4) phenytoin for seizure prophylaxis follow electrolytes (SIADH common) angiogram to r/o vascular lesion unless >45 yrs, known HTN, and putamen/thalamid posterior fossa ICH (yield - 0%) surgical craniotomy with evacuation of clot. treatment of source of ICH {i.e. AVM, tumour, cavernoma), ventriculostomy to treat hydrocephalus indications symptoms of raised ICP or mass effect rapid deterioration (especially if signs ofbrainstem compression) favourable location, e.g. cerebellar, non-dominant hemisphere young patient (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 AneurysmsEpidemiology prevalence 1-4% (20% have multiple) female > male; age 35-65 years Risk Factors autosomal dominant polycystic kidney disease ( 15%) fibromuscular dysplasia (7-21 %) AVMB

connective tissue diseases (Ehlers-Danlos, Marfan's) family history bacterial endocarditis Osler-Weber-Rendu syndrome (hereditary hemorrhagic telangiectasia) atherosclerosis and HTN trauma

Types (Figure 4, NS3) saccular (berry) most common type located at branch points of major cerebral arteries (Circle of Willis) 85-95% in carotid system, 5-15% in vertebrobasilar circulation fusiform atherosclerotic more common in vertebrobasilar system, rarely rupture mycotic secondary to any infection of vessel walL 20% multiple 60% Streptococcus and Staphylococcus 3-15% of patients with SBE

Toronto Notes 2011

Cerebrovascular Disease

Neurosurgery NS21

Table 7. 5-year Cumulative Rupture Risk in Unruptured Aneurysms Based on Size and Location

Cmlmo111 Cuolid N47 and OP37) middle cerebral artery (MCA) occlusive symptoms

NS22 Neurosurgery,..__of!IIQqllldFIIII._IIJSui:CIIIful Clnlid &IIIIIIIII:IDIIJ ill'dlnll MhlltRICIIIINUIIagi:ll lluilonUid C.allll Trill

Cerebrovaac:ular Disease/Vascular Malformations

Toronto Notes 2011

InvestigationsCBC, 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; 363:1491-1502Slllly: 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

Treatment 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

nets..,.

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

Medal Rx70-99% 50-6!1%

Medal + Sllf1liCII Rx!1% over 2years

26% over 2 years22% over 5years

50, prwiDUI hx of cancer; pain lllr'lliaved by bad rast,. constitutional

Extradural LesionsRoot CompressionDifferential Diagnosis herniated disk neoplasm (neurofibroma, schWllllllOinll) synovial c:}'!t. abscess

.......,

fYI'I1P1DmL

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

hypertrophic bone/spur

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

c.....-.nfrlcb,.

Cervical Disc SyndromeEtiology nucleus pulposus herniates through annulus fibrosis and impinges upon nerve root

J

RED FLAGS fw lladl .....

Epidemiology

incontinence) AnNihllillllldlte) Constitutionel symptoms IChronic disease l'lrulhNil AQ1>5Dar 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

Investigations Ifred flags: C-splne x-ray, CT, MRI (imaging of choice) consider EMG, nerve conduction studies Ifdiagnosis uncertain

'IbroDlo Nota 2011

JW:radural Leal.ODI

Neurosursery NS25

Treatment conservative no bedrest: unless severe radicular symptoms 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 rootIt thaiMI below the illtnpaca (i.e.

C5-ti dise

C& 1111rve 1\!111).

Prognosis 95% improve spontaneously in 4-8 weeks

Tillie 1D. Latenl Cervical Disc Syndrom11Cl-7 lloGt hdvtMI C7-T1

C5 2\

C&

C8 10%Rilg fing 5th fingerDigillll flexors, nmsics

SIIJuldarDelblid, biceps, tuplllpinlltul

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

rrFibras

tampemn

No clwlga

llicapl. Bnlclial'lldillis

Triceps

Fingar jllk (Haffmam's iign)

CGrticaiPilll tract BkiBd movements

Cervical Stenosis (Cervical Spondylosis)Definition cervical spondylosis is chronic disc degeneration and usodated facet arthropathy

resultant syndromes include mechanical neck pain. radiculopathy (root compreasion), myelopathy (spinal cord compression) and combinations

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

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

Fetdures insidiOUII onset of mechanical neck pain exa.cerbated by excess vertebral motion (particularly 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)

lnvutlgatlona x-ray of cervical spine flmOD!emnslon or oblique views (studied for changes in LU8chka and fe.cet: joints, osteophytes and disc space narrowing), MRI, cr, EMG Treatment NSAIDS, moist heat. strengthening and range of motion exercises, analgesics. cervical collar, cervical traction surgical indications: myelopathy with motor impairment, progressive neurologl.c impairment. intractable pa.ln

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

NS26 Neuroaurgery

1'oroDio

2011

Lumbar Disc SyndromeEtiology 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 aadFunctloaal Terrllerlea

Root .......llcidaiC8

L4O.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 ....

......,..,,...had ......

............ hllmnliiiCIDipi..

. . . . dnugllt

7lit Spiil.lrunl/2006; 6:335-343 lllrodlllliln: BIQng in lhlla 70's irid tliraugb1DU.eerly ID's tlil Nltilll'lll Awtl Spinll CGnl ..jlly SWes INASCISI were Clllluclld in tlir8e llrgt lliidomillld conlrolled trilll,liid lium tiiCIIelriillthei'IICIIIIIIiilllllltion1Dgivepltients

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

m ofthl

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 righl111d11ft lid1 oftlil body. qgasting lhll ch-.gn in

tlllts1ldisticalanlysis wu

onlv

cr

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

tJjeStionCOIIcUsNeiy.

NS34 Neuroaurgery

Neurotrauma

1'oroDio

2011

Fractures of the SpineFractures 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 ligamentsTypes 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)

Clasalllcatlo

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 fractureImaging

avulsion of spinous process, usually C7

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

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

Toronto Notes 2011

Neurotrauma

Neurosurgery NS35

Neurologically Determined Death

------------------

Definition irreversible and diffuse brain injury resulting in absence of clinical brain function cardiovascular activity may persist for up to two weeks Criteria of Diagnosis prerequisites: no CNS depressant drugs/neuromuscular blocking agents, no drug intoxication/ poisoning, temperature >32C, 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 ConsciousnessEvaluation 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

cowsCold Opposite Warm

:sam.

ComaDefinition an unrousable state in which patients show no meaningful response to environmental stimuli Pathophysiology lesions affecting the cerebral cortex bilaterally, the reticular activating system (RAS) or their connecting fibres focal supratentorial lesions do no alter consciousness except by herniation (compression on the brainstem or on the contralateral hemisphere) or by precipitating seizures

NS36 Nearomrgery

10ronto Nota 2011

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

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

Persistent Vegetative State a condition ofcomplete unawareness of the self and the environment accompanied by sleepwake cycles with either complete or partial preservation ofhypothalamic and brain5temautonomic function

Definition

"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 NeurosurgerySpinal DysraphismSPINA BIADA OCCULTA

---------------------------------

Definition congenital absence ofa spinous process and a variable amount aflamina no visible exposure ofmeninges or neural tissue Epidemiology 15-2096 ofthe general population; most common at LS or SIHair tuft

Etiology 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::nlelltMENINGOCELE (SPINA BIFIDA APERTA)

herniation of meningeal tissue and CSF through a defect in the spine, without associated herniation of neural tissue

Definition

'IbroDlo Nota 2011

Pecliatric Neurosurgery

Neurosurgery NS37

Etiology primary fiillure of neural tube closure

Clinical Features most common in lumbosacral area usually no disability, low inddence ofassociated anomalies and hydrocephalusInvestigations plain film&, cr, MRI, UIS, echo, geniiDurinary (GU) investigations Treatment surgical adsl.on and tissue repair (excellent results)

MYELOMENINGOCELEDefinition 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 NS38Investigations plain film&, cr, MRI, UIS, echo, GU investigations Treatment

iFigu111 21. Myelaaningacela

."' ..Q

-

surgical closure to preserve neurologic status and prevent CNS infectionsPrognosis

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 urinarycontinence

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 PediatricsEtiology congenital aqueductal anomalies, primary aqueductal stenosis in infancy secondary gliosis due to intrauterine viral infections (mumps. varicella, TORCH) Dandy-Walker malformation (2-4%) Chiari malfimnation, especially Type II myel.omen1Dgocele

acquired post meningitis post hemorrhage {SAH, IVH) masses (vascular malformation, neoplastic) Clinical Features symptoms and &igns of hydrocephalus are age related in pediatrics increased head circumference (HC), bulging anterior fontanelle. widened cranial sutures lrrltabillty,lethargy. poor feeding and vomiting "cracked pot" sound on cranial percussion scalp vein dilation (increased collateral venous drainage) sunset sign - forced downward deviation of eyes episodic bradycardia and apnea

NS38 Neuro1urgeryInvestigations skull x-ray, U/S, CT, MRI, ICP monitoring Treatment similar to adults (see Hydrocephtdus. NS7)

1'oroDio

2011

Dandy-Walker MalformationDefinition

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

Epidemiology

2-4% of pediatric hydrocephalusClinical 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 childhoodInvestigations ultresound.CT,MRI Treatment

asymptomatic patients require no t:reatment associated hydrocephalus :requires surgl.cal treatment supratentorial lateral ventricular or cystoperitoneal shuntProgosis 75-10096 survival, 5096 have normal IQ

Chiari MalformationsDefinition 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)

Typell

0

definition: part of cerebellar vermis, medulla and 4th ventricle extend through the foramen magnum often to midcervical region epidemiology: present in infancy cllnical features: findings due to brainstem and lower cranial nerve dysfunction syringomyelia, hydrocephalus in >80%

Toronto Notes 2011

Neurosurgery NS39

Investigations MRI or CT myelography

Treatment indications for surgical decompression 'I)rpe 1: symptomatic patients (early surgery recommended; GPi) Psydliatric: depression, mlllia, anxiety, apathy (SlN > Gl'i)

presentations

Dystonia

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 S1NStimulation 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)

TIWIDr

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 seeDisanlar Obleaiva Compulsive Disanlar (OCD) Taunrtte" Syndro1111

Syndrome, Obsessive Compulsive Disorder and Depression sections in Neurology, N29 and PSJFchiatry. PSIS, PS7Pro-.rasAnterior 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 PainTabla 16. Surgical Targats for Chronic Pain

DilonlNeuropllhic Pain

lndicatio

Pracedur.

Oub:ama1

Mlllllillly Intracerebral hemonhages(1%-2%)

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(1%-2%)

Pinesthesia Anxiety panic disorder

Surgical Management of EpilepsyNeurosurgical 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 olnaiiUUQ81Yfor11mpOIIIIalieepi811$Y. lhllals: II patilll1l Mth poarly Cllll1nllld

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

ln=-401 or fur mooadn.tn-.nwillantilpiillptic drugs (n=401. The PlinarYoulmlewasflliedomturroundingl 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 NeuralgiaMedical Therapy for Trigeminal Neuralgia see Neurology. N18 for medical management

Surgical Therapy for Trigeminal Neuralgia reserved for cases refractory to medical managementSurgical 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 MedicationsThe folowing are ONLY; follow clinical judgment and to adults unless otherwise specified prescription reconmendlllions i1 practice; dosages refer

Tabla

n. Common MedicationsDoling 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 simultaneouslyMonitor CBC(potential

{TegnltuPJ

cublmmpina

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: 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

man1itol

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

Raised ICP

Seizures, heart failure

w

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

nimclllpila

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

References

Toronto Notes 2011

ReferencesAhn 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.