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
BadrafC3
A. lagil:lllllal:tionFlllns.rtP
B.AxiiiSacliH-.
F"111ra 1. MRI
IJJ1rt.21Q.
Cl
l.2
r:::Jcj,
C2
C3 C4 C5 C6 C7 CBTl
l.l
LA
LA
r.;:;J ...
G8
II:0::
i
:1!1
0
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!
'67
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
1D. AniBriar ID!ruidal arl8ry 11. Am.ior spinalllllry
cerabllllartary
n:
-
, 2. l'ol18rior spin!. arl8ry
MC
- Ft.tddla canllllll
PCGIII - Po&telior CGIIIIIUliCI!iV PC - Po&telior
cerebnll SC B P -Pontine AIC - Anblriar inl8rior V - Vlltabrll PIC
- Po&telior inl8rior cerabell AS - Anblriar i!Jinal
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
Sulcal aflacemllll
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.