18 - toronto notes 2011 - neurosurgery

5/20/2018 18 - Toronto Notes 2011 - Neurosurgery

1/44

S

eurosurgery

Brian G. Ballioe

Habert

Lee

and

Alireza Mansouri chapter editors

Alaina

Garbens and Modape Oyewwni, associate editors

dam

Gladwish E M editor

Dr.

Todd

Mainpriu

and Dr.

Taufik Valiante

staff

editors

Basic Anatomy Review 2

Differential Diagnoses of Common

Neurosurgical Presentations 4

INTRACRANIAL PATHOLOGY

Intracranial Pressure ICP) Dynamics 4

ICPNolume Relationship

Cerebral Blood Flow CBF)

ICP Measurement

Elevated ICP

Herniation Syndromes 6

Treatment

of

Elevated

ICP

Hydrocephalus , , , 7

Benign Intracranial Hypertension

Pseudotumour Cerebri) . . . . . . . . . . . . . . . . . . 9

Tumour 9

Metastatic Tumours

Astrocytoma

Meningioma

Vestibular Schwannoma Acoustic Neuroma)

Pituitary Adenoma

Pus 14

Cerebral Abscess

Blood 15

Extradural uEpiduraln) Hematoma

Subdural Hematoma

Cerebrovascular Disease 17

Subarachnoid Hemorrhage SAH)

Intracerebral Hemorrhage ICH)

Intracranial Aneurysms

Carotid Stenosis

vascular Malformations 22

Arteriovenous Malformations AVMs)

Cavernous Malformations 23

EXTRACRANIAL PATHOLOGY

Dermatomes/Myotomes , , 24

Approach to Limb/Back Pain , 24

Extradural Lesions . . . . . . . . . . . . . . . . . . . . . 24

Root Compression

Cervical Disc Syndrome

Cervical Stenosis Cervical Spondylosis)

Toronto Notes 2011

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 Malformat ions

Craniosynostosis

Pediatric Brain Tumours

Functional Neurosurgery

4

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

Neurosurgery NS


2/44

NS2 Neuroaursery

n I Func:liaDBI

Bui CIBndamySllftwln

A.

lagil:lllllal:tion

F 111ra 1.

MRI

asic

natomy Review

MRI

Brain

Corpus

calloeiJn

Thlamu.

llypothallmu.

Occipital

lobe

Midblain

Pons

Four1h V8111rida

Cerabllllum

Madl41a

DansofCZ

Spinal cord

BadrafC3

B AxiiiSacli

Flllns rtP

H-.

JJ1rt 21Q

Cl

C2

r J

C3

c j

C4

r ;:;J

C5

...

C6

G

C7

CB

Tl

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

1 oroDio

011

frDnllllloba

Caudltll

nuclau.

Lderllvantricl

ThiiiiiiUI

Occipillllobe

l 2

l.l

L

L

i

I

I

:1 1

:0::

0


3/44

'IbroDloNota

2011

A

2

11

a:

I

0

Arblry

IBgn:

At. -

Antariar

carebral

AcDIII

-

Antariar

CGIIIIIUliCIIilg

n: -

MC - Ft.tddla

canllllll

PCGIII

-

Po&telior CGIIIIIUliCI iV

PC - Po&telior cerebnll

SC -

B

P -Pontine

AIC - Anblriar inl8rior

V - Vlltabrll

PIC - Po&telior inl8rior cerabell

AS -

Anblriari Jinal

B

c

4

7

Buic

Anatomy

Review

Figure

3. s

ly af Bnia.

PIBIIHT 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. Tarritaria af nin and

Bninstam.

Saailbll V'I8W, Sean

Medially

Figure

4. Anallryama

af tfla

Cin:la of

Wllia

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 lrlction. :

7.

P08Uiriar ileriar canbelarartary, 3%

Neumaurgery NS3

1.

Am.iDrcarebralartay

2.

Midcll

centnl

ll'lllry

3.

Postarior

cammlricating

artary

4. Postarior

Clf8bralartay

5. Besilanrtary

6. IC

7.

PIC

8. Var1abrllartary

9.

erabllllartary

1D. AniBriar ID ruidal arl8ry

11.

Am.ior

spinalllllry

,

2.

l'ol18rior

spin .

arl8ry


4/44

NS4

Neurosurgery

,

Mao-KIIIillHypllllli

Vm.

Vlil>od

VcsF

Vlooion

=

v- =

conslllnt

ICPmmHg

100Ll

0

6

-.

..-I

40

,- I

r-

i

I 20 -. 1

I 0 I

I

I

1 Vollda :

I

Wh.n a mass IIICjlllllds Evantualy finl

withilthe slut

small inCielllents

compensatury in voklme

produce

mechanisms initially larger

and

1.-ger

maintain a

nonnaiiCP

increments in ICP

Figure

5. ICP-Volume Curve

Adlpled

lrom

Unduy llW lbl NtwtrJ Jw IIIII

Ne mst6puy

1lu mrrled Copyright 2 4 with parmilliln

lromB18Viar.

Toronto Notes 2011

Differential Diagnoses

of Common

Neurosurgical Presentations

Intracranial Mass Lesions

tumour

metastatic tumours

astrocytoma

meningioma

vestibular schwannoma (acoustic neuroma)

pituitary adenoma

primary CNS lymphoma

pus/inflammation

cerebral abscess, extradural abscess, subdural empyema

encephalitis (see Infectious Diseases, ID7)

tumefactive multiple sclerosis (MS)

blood

extradural (epidural) hematoma

subdural hematoma

ischemic stroke

hemorrhage: subarachnoid hemorrhage (SAH), intracerebral hemorrhage (ICH),

intraventricular hemorrhage (IVH)

C} 5t

Disorders

of the

Spine

extradural

degenerative: disc herniat ion, canal stenosis, spondylolisthesis/spondylolysis

infection/inflammation: osteomyelitis, discitis

ligamentous: ossification

of

posterior longitudinal ligament (OPLL)

trauma: mechanical compression/instability, hematoma

tumours (55

ofall spinal tumours): lymphoma, metastases (lymphoma, lung, breast,

prostate), neurofibroma

intradural extramedullary

vascular: dural arterio-venous fistula, subdural hematoma (especiallyi on anticoagulants)

tumours (40

ofall

spinal tumours): meningioma, schwannoma, neurofibroma

intradural intramedullary

tumours (5

of

all spinal tumours): astrocytomas

and

ependymomasmost common; also

hemangioblastomas and dermoid

syringomyelia (common causes: trauma, congenital, idiopathic)

infectious/inflammatory: TB, sarcoid, transverse myelitis

vascular: AVM, ischemia

Peripheral NeiVe Lesions

neuropathies

traumatic

entrapments

iatrogenic

inflammatory

tumours

INTR CR NI L

PATHOLOGY

Intracranial Pressure ICP)

Dynamics

ICPNoluma Relationship

adult skull is rigid with a const ant 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 compensat ion is exhausted, ICP rises exponentially


5/44

Toronto Notes 2011

Intracranial Pressure (ICP) Dynamics

Cerebral Blood

Flow

CBF)

CBF

depends

on cerebral

perfusion

pressure (CPP)

and

cerebral vascular resistance (CVR)

normal CPP >50

mmHg

n 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

plat eau waves: elevation ofiCP over 50

mmHg

lasting 5-20

min, precursor of urther

deterioration

Elevated I P

Etiology

intracranial space-occupying lesion:

tumour

pus

blood [trauma-+ hematoma

(most common), subarachnoid

hemorrhage]

depressed skull fracture

foreign body

increased intracrani al blood

volume

vasodilatation (increased pC0

2

/decreased p0

2

/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-obstruc tive)

tension

pneumocephalus

(gas

within the

cranial

cavity)

pseudo

umour

cerebri

status epilepticus (chronic seizure resulting

in

brain

edema)

Clinical Features

1.

Acute

Blevated

ICP

headache

HI

A)

- 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 locali zing (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

Neurosurgery

NSS

AulcngtJation: CBF

maidllilad

daspitl

ch111gein CPP

LDw BP or High ICP

Clllllbllll parfusioo prBI Irll

Figura 6.

Carabral

Autoregulation

Curve

Ad1pted fnlm liiiiiiY

et

II. Neii JiogfandNeiiDstlr a

Alsl1rltd. Copyright 2004with pennitlion from

Elsevie

Consider

Monilllring

of

ICP

in

1lle

following

Sitllltians

1.

Patianll

will1an

abnoiiTIIII halld CT

IJid Glngow

Coma Scale

{GCSI

scors of 3 11 8 llfl8r cardiopulmonary

resuscitation.

Or

2. Patianll will11 noiiTIIII hald CT and

GCS

liCOr

af

3111

8AND 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

Lumbar

punctura

is contnlindic8tad

with

known/suspected intracranial

mus.

Cushing's Triad

af

AcllllllaiiM ICP

full t r i ad -

in ,13

o 1

1. Hypartansion

2.

Bradyclll dia

{late

finding)

3. AbnoiiTIIIIrespil lllllry

pllttllm


6/44

NS6 Neuroaursery

I. Sublalcila

2. Cllllni

3.

UIICII

S.TDRSillr

F 111ra

1 H1miltian Types- Sua

Tabla

1

or

dascription

hdnll l lof E..,_.ICP:

ICPHEAD

lnllmiB

calm

(sldiiiJ,II:cma

Place .nivParlllylil

ltypemntiltll

Bewle head

AdaqudaBP

Dinlllic (malllilol)

-

I

i

0

lntrac:ranlalPreuure

(ICP) Dyaamia/Herniation Syndromes

1 oroDio 011

2 ChronicElmated ICP

H/A

postural: worsened

by

coughing, straining, bending over

morning/eveningHIA-+

VIUIOdfiatation

due to increasedCOzwith recumbency

visual changes

due to papilledema

enlargedblind spot. i f

dvanced-+

eplsodJ.c

constrictl.ons

ofvisual.

fields ('"grey-outs")

optic atrophy/blindness

differentiate

from

papillitis (usually unilateralwithdecreased visual acuity)

decreased

evel

ofc:onsd.ousness

Investigations

patients

with suspected

elevated ICP

require an urgent

Cf/MRI

ICP

monitoring

where appropriate

Herniation

Syndromes

Table1. Hemllllon

Syll*ome

Cl1lcal FN1u111

o Letalll

aurnta*Jriallaaill'l

Usualy

DispB;anent ci esion

clencephalon

11raugh o Diffuse C818b111l

tentDrii l nab:h o

Lata

uncal

hamimon

Uncus af 8f11)llnll

o Llbnl

sl4)l'llenblrilllaaion

laba

hami1181

down

(oflllll'l)ily

opanding

'llmlgh

IIODrial nab:h

trauiT'IIIIic lllll'llllamll)

CerBJellar Willis

hamiates llnugh

tentDrii l inciBIA

Cerabelltonsis

hemiatell"f'DIQI

funmen011gnum

1 large posterior ossa l1lii5S

(cmman

afta'

VP lhi.IIIRg)

o llinltadorilllaaiiJI

o FltawiJ.I central

tanllrili

heniation

o

Fltawng

LP in

praaance

al

intrlcranial mass IB ian

Treatment

of

levated

I P

Wlms

af

impnling 1nntan1Drial haniatian

Small

pupila, illtad. fixed (I'Oitnll

tD caudal

dataliaration), sapntillflllue

of

diancephahn 1111ckla

Daaaased

l.DC

(nidbrain

EOt.V

aze

iqlaiment yes"):

CaqliiBIIill'l of )l8leCtwn

end

supelill' c*uli

Bninstem IIII ICIIhaga secondaly

: sh111ring af be ilar lrtaryperfa Biing VBSS81s)

llillblti S illlipidus(tractiiJI on pillitaryd and

end-s IQI s9'1

lpslallnii1101H111Ctiva

dilll8d

pupil(estialt,

mast ralllble

sign) +

p&i&tlnl EOM pRy$i&.

plosis (CN II

Daaaased l.DC (nidbrain

1 Contralaleral hemiplegia : : extensor (upgoRg)

plril esponse

: :

ipsilateral

hemiplegia

("Karnallln's

natd( 1 ll&a

lacelizilg aign

re Uiting from pr8&1lll8

from the adga of

tentorium an 1M

cadnllallllll

cerrl:nl

pedurda)

o CII8Jellar

infarct

(sl.pl'ior cerebelar

artery

ISCA) COI11Niian)

Hydf11C8Phakll Cinbnllaquecllct

Neckstiffness

head

tiltftcnsllar

Daaaased

l.DC

(nidbrain

1

Flaccidpnysis

Raapiii1DIV

irra(paritiaa.flll)iratrry IIT8IIt

(CIIII)I'IS&ianof

macklllaly

raspil'llclly

centres)

Blood pr111111 illllllility (camii'BIIIian af

m&GJIII'f

cardDY8SCIBcantras)

Cf or

MRI to

identify

etiology,

assesa formidline

shlft/hemiation

treat primary

cau.se

(ie. remow mass lesioru, ensure adequate ventilation)

i felevated ICP persists following treatmentofprimary cause, consider therapywhen

ICP>20mm.Hg

goals: keep ICP

65

mmHg, MAP

>90 mmHg

General Measures (,CPHEAlY see sidebar)

elevate head ofbed at

30-45, maintain

neckin neutral position ncreases intracranial venous

outflow

prevent hypotension

with

fluid and

vasopressor&,

dopamine, norepinephrinepm

ventilate

to

nonnocarbia (pCOz

35-40mmHg)

-+ prevents

vasodilatation

rn to

maintain

J'02 >60mmHg -+ prevents hypoxic brai n injury


7/44

'IbroDlo

Nota 2011

Herniation

Syndromet/Hydrocephalus

Spec:Hic Mesures

osmolar diuresis (mannitol20% IV solution 1-1.5glkg. then 0.25

glkg

q6h to serum osmolarity

of315-320)

can

give

rapidly,

acts in

30

minutes, mustmaintain 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 m1CSF viaventricles. assess each situation independently

insert external

ventricular

drain ( l facute) or shunt

corticosteroids ...

decrease

edema

over

subsequent days around brain tumour, abscess, blood

no

prawnvalue 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

mglkgaver 30 min, then

1

mglkgq1b continuous infusion)

decreases

mortality,

but

no improvement

in

neurological outcome

decompressive craniectruny is a

last

resort

ydrocephalus

Definition

increased

CSF

volume

Etiology

ob&truction to

CSF

8ow

decreased CSF

absorption

increased CSF production

(rarely) - e.g.

choroid plaus papilloma (0.4-1% of ntracranial

tumours)

Epidemiology

estimated prevalence 1-1.5%;

incidence of

congenital hydrocephalus -1-2/1000 live births

hydrocephalus in

children,

see Pediatric Neurosurgery NS37

Classification

Tllllllle 2. Cl&lllllcatlon ofHydrocephalus

Obllrur:linl

Ciculllliln

blacUd willin

(tm.Cimlllllil:llill) Vldricularsy1l8m pmximal

to the 8111CI IIDid

IJlftllatiJnS

N...OIIIInl:liR

(er.r...lil:ltilg)

CSF absarplian

blac:bd at

l ldnlvmlriculll'

site

=

nchnaid

IJllniJI ian&

Parlisl:8lt

vantric:Uar

dlllalian

il

he

CDI'IIald:

of

IIDIIII1II

CSF pniSSin

Acqund

AIJJeduclal

stenosis

(lllh sians

GU-

Racticxl,

hllllllllhaga)

lnlrllv8nlrii:Ulnians {lllnaurs

e.g. 3nlwnbicle

aJIIaid

cyst.

hemibms)

Vantriclilr ruxinlll

to lilck

o

Periwnbiclilr

hypodensily

lllln8ependymalri{plianl iCSF

mat llo pacal

Sulcal aflacemllll

Mall nariallaniltian,

Vllllric:l& CD11118Uian

Otlllrs: bscaa/

tpllllamas,

aracmaid cysts

AcrJ ductal

S1811asis.

malbmalim

(188 PrMiifllric

NflutDJutgety

NS36)

Post-infactiaus

( 1 C8US1)

meniVfis,

cysticercosis

Post-hemonhegic ( 2 cause)

SAil. MI. tnunatic

Dlamid

1 11111111

papilams

(rm,

c:ausas

ilcraased CSF pmcllctian)

annal

pi8SSU8

hydracephils

All

wnbicles

dilaled

o

ldiapllhic (50%)

o

Enlarged vllllriclaa

withaut

Othe111: lllilereclrlaidlananhllga. incraased pnlfliniiiC8 of

cnbrel

malingitis,

1nlu1111, radiaticD- U:i

iJcU;ed

0 Normal

aging

0 E nllllved venbides and mci

Alzllairnar'a, Crautzlaldt-Jacob Carelnllllqlhy

Diiea a

Neumaurgery NS

1 Clloroid plsxu.

2.

l..lltalllwntricllll

3. Third venlricle

4.

Cerebral aqueduct (Df

5. Four1h vanlrida i

6.

Fo111men l.ulchklland MIQIIIIdie

1

7. Aracmoid

gnmliltions

o

8.

Subal'lll;l'noid

par;

j

9. Segilllll sinus o

Figure

I.

Ilia

Flow

of CSF

'

,

CSF prodlad bychoroid pillllul. ftOWI

ID: vanbiclaa o ofl..uiCI'b

(lllll'lll)and

MIQardll

(medial) ...

lblrachnoid spac;e o ablsofbld

by

Bl'llchnoidvlflgranuldiona illove1111111

lii'IDM.

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'NaNAiol

AID

AlaxiVApiiXia of

gait

lncantinanca

D1111entia


8/44

NS8 Neurosurgery Hydrocephalus

Clinical Features (see also Pediatric

Neurosurgery

NS36)

a cute hydrocephalus

signs

and

symptoms ofacute raised

ICP

(seeElevated ICP NSS)

impaired upward gaze ( sunset eyes ) and/or

CN

VI palsy

Toronto

Notes 2011

chronic/g radual onset hydrocephalus [i.e. normal pressure hydrocephalus (NPH)]

gradual onset ofclassic triad developing over weeks or months

pressure ofventricle

on

LE motor fibres -+ gait disturbance (ataxia and apraxia usually

initial symptoms)

pressure

on

cortica l 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

periventricu lar lucency suggests raised CSF pressure

ultrasound

through anterior fontanelle in

infants)

ICP

monitor ing (e.g. LP)

may be

used to investigate

NPH, test

response to

shunting

(lumbar

tap

test)

rad ionuclide 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

ventricu loperitoneal (VP) -

most common

ventriculopleural

ventriculo-atrial (VA) - not first choice because

of

ncreased infections, shunt emboli

lumboperitoneal- for communicating hydrocephalus and pseudotum.our cerebri

third ventriculostomy (for obstructive hydrocephalus)

via

ventriculoscopy

LPs [for transien t hydrocephalus (e.g. subarachno id hemorrha ge), IVH in premature

infants,

etc.]

Shunt

Compli:ations

Table 3.

Shunt Complications

Complication

Etiolour Clinical Features lnvestiplians

Obstnlction

Obstruction

by

choroid plexus Acute

hy Rcephakls

Silmt

series" (plain X-fiVS of

entire shunt

that

only ruleout

discomection.

break. tip

mi JIIIion)

(most common) Buildup of proteinaceous h:l8iiS8d ICP

lnf8c:tion

(3-6 )

Ovarsllunting

(HI over

6.5yea11)

Saizun11

(5.5

risk

in

151

year,

1

attar

3rd year)

...

auinal

Hamil

(1

7

incidence

with VP

shunt inserted in inflrlcy)

skin breakdown over

hardware

accretions,

blood,

cells

(illlaiTII'IIItory or

tumour)

Infection

Di&connaction

or dal lilge

s

epidermidis

S.lMR fiiRl

P ICII8S

Gram-negative

bacilli

Slit ventricle synctoma

Collapse of

ventricles

leading

to

occlusion

of

shunt

ports by

ependymal lining

Seconday

crMiosyno510Sis

(childran)

Subdural hamillumll

Collapsing brain

tears

bridging

veins {especially common

in

NPH

patients)

Apposition and overlapping of

tha cranial sutures in an infllll

following decorqnssion of

hy Rcephakls

Increased inlrllperitonaal

results in

hernia

becoming apparent

CT

Radionuclide

"shunto Jlllf"

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)

CIYonic or reculring CTIMRI

headaches often raliavad

when lying

down

ventricles on imaging

A&ymptornatic

Headaches, wmiting.

somnolence

Abnormal

head

shape

CT

Clinical

oCT

EEG

hguinal

swelling. discomfort

U/S


9/44

IbroDlo Nota 2011

Benign

Intracranial Hypertension

Pseudotumour Cerebri

Definition

rai&ed int:racranial.

pressureandpapilledemawiJ:hout evidenceof any mass lesion,

hydrocephalus,

infection

or

hypertensive encephalopathy (diagnosis

of

exclusion)

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

of

venous sinus thrombosis; similar

to

those for gallstones (' fat,

female,

fertile,

forties )

Epidemiology

incidence -0.5/100,000peryear

usually

In 3rdand4th decade (F>M)

Clinical Features

symptoms and

signs

of a1secl ICP (HIA

in

>9096, pulsatile intracranla1noJse), but NO

decreased

LOC or

diplopia

decreased visual acuity. papilledema, visual field defect.

optic

atrophy (key morbidity)

usually

self-limited. recurrence is common, chronicIn some patientB

risk

ofblindnes.s

is not

reliably

correlated

to

symptoms or cl1nica1

course

Investigations

CT:nonnal

CSF

studies: normal

MRI:must

look

fur

venous sinus thrombosis

Treatment

ruleout

conditions

that

cause intracranial hypertension

discontinue offendingmedicatioDS, encourage weight loss, fluid/salt R:5triction

pharmacotherapy:

acetazolamide

CSF production),thiazide diuretic

or

furosemide

i f

bove 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

Tumour

Vllllric : CGUDid,

chomid prDC81S

pepma.

apandymoma.

germiloma. tntoma.

piUtaJy

adnma.

craniopharyngioma.

apt

narva

glioma. cyst

Figura

9. Tuaurs

hpnl lmut

.

i r r lnr :

lltrDI:Y Dmt.

1gliobllllluma,

aligadlillllllllioma.

QMglioma.

lymphoma,

Neumaurgery

NS

,.----------------

111,.rlanl

llltura

to nubian

CT

a..t

IIRI(:t cantrMt

t.e.ia ' :t ld11111B. nKro.i,,

hsmarrhlgs)

Midline shifts 1nd

h1111ialians

Elfat:oment of

ventric:lee and au

ei

(olbln ipllilatn),

batal

Single

or mLitijlle mplies

mebllbllil)

Primary

CNS

l',mphar.-.

npcn11d i l

6-201 of HIV inf\lcl8d patienta.

DDx

far

Rmg

(nlllnci

Laeia1

01 CT

wllht:antrAt

IUOICALDR

...,.._

Ablcass*

blastnma(high .,Ualllracytama)

lnfllrct

Contuaion

AIDS (lmulplasmosis)

LY l1111ollll

DliiiJY'Iinalion

IIBIIDiving homlllllma

(

3 mo.tconrnon Dx's)

MMrySGu-r l

TIIIIIIIIS

lu1g 44lli

8r llql

10%

RCC)

7' 1i

Gl 0.

Mnoma

3%


10/44

NSIO

Neurosurgery

A

Cwr()lc;d 11X11;

14(41:131-43

Patiantt

idan1lJid

a

hiving ida

lnin

ma111ta1is

oodelgo

llliltmlln11hltinlilde wide

iRin

lldillian

tllapy (WIIRij, 111111ical,..ctian

and

sfnlllcticllldidon..,-, SRSI.

Given

1hlt

conllc:ting

Mlanctlu beln Wplflld

witli 1l5pacl

1D

lhe

best

IPProacli

1D

lilgle brlin rne11st1ses.

he

. . ._cologylli.-

SiQ

Grlql

r-r

Clf'l Onlllio

Progrmn

I:Onlb:tld1 sysllmltic

lll'iuw

rJ

1helidlnculnd

prldi:u

uuidllil8.

c.:lllin:

Surgicalmilion

sllould be

consider8d

fw

IJitiartlwMh pd perfonnlnce

IIIU. or no lll'idiiiCIrJ

ablcmill

cli-.lnd

1 SllllicdyICCeslible

q nlin

maiiSIIsis

amanllila1D

Becue

1rea1ment

il

inglehrail

ma1lllalis

i1

canlidllllld

plliiiiMI,

iMIMIIDcll

1lllllnlnlllllllt

be indiloiludlld.To

rd 111

1llnllll'

'llCU'ItiiC8fw

pl1iants

who

11M

oodalgont

miCii:ln

rJ

a

lnilll lllltiiU.

poslupef1live

W8I T

should be

canlider8d.

As an

llllmiiM

D

u p ii8Ction.

WBI Tfollawld rt

SRS

boost

slwld

be CCIIIIidenid lor

pa1ien1s

wi1h

liJ9a

llllill mallltlliL Tile

Mane& is

ildciant

1D

lllCDIIIrnendSAS

lliorle IS I

llilrlpy.

Tumour Toronto

Notes 2011

Classification

primaryvs. metastatic, intra-ax ial (parenchymal) vs. extra-axial, supratentoria l 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

ntracranial tumours

= most

common)

neuroepithelial

glial: astrocytomas, oligodendrogliomas

neuronal: ganglion cell tumours, cerebral neurocytomas/neuroblastomas

poorl y differentiated: glioblastomas, medulloblastomas

other: pineal tumours, ependymomas, choroid plexus papillomas

meningeal: meningiomas

nerve sheath: schwannoma, neurofibroma

blood vessels: hemangioblastomas

germ cells: genninomas, teratomas

pituitary adenomas*

craniopharyngiomas

cysts: epidermoid/dermoid cysts, colloid cysts

local extension: chordomas, glomus jugulare tumours

other: primary CNS lymphomas, metastatic tumours

Clinical Features

progressive neurological deficit (7096) - usually

motor

weakness,

CN

deficits, sensory,

cognitive, personality, endocrine deficits (these

may

localize lesion)

H/A (5096) raised ICP (acute or chronic depending on growth rate), H/A classically worse

in am

but non-specific (likely hypoventilation

during

sleep causing vasodilatation

-+

increased

ICP), may worsen with bending forwardlvalsalva

N/V (4096)

seizures (25%)

papilledema, vision changes

symptoms suggestive

ofTIA

(ictal, post-ictal,

or

ischemic 2

to

steal phenomenonD)

rarely presents with hemorrhage

familial syndromes associatedwith 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

PituitaryAdenoma

NS13)

swgical: total or part ial excision (decompressive, palliative),

shunt

i hydrocephalus

radiotherapy: convent ional fractionated radiotherapy (XRT), stereotactic radiosurgery

(Gamma

Knife

chemotherapy: e.g. alkylating agents (temozolomide)

Table 4. Tumour Types: Age,

Location


11/44

IbroDlo

Nota

2011

Tam.our

Metastatic Tumours

most common brain tumour seen

clinically

15-3QlJ6

of

cancer

patients

presentwith cerebral metastatic twnoUI' I

most common

sites

= lungs, breast

other

sites = kidney, thyroid, stomach.

prostate,

testis,

melanoma

hematogenous spread most common

Location

80% a.re hemispheric, often at grey-white matter junction or junctionof emporal-parietal-

occipitallobes (likely

emboli

spreading to terminal MCA branches)

Investigations

identifyprlmary umour

metastatic work-up (CXR, CT chest/abdo, abdominal U/S, bone scan, mammogram)

crwith

contrut -+ round, well-drcumscrtbed, often ring

enhancing,

++

edema,

often

multiple

MRI more sensitive, especially fur posterior fossa

oonsider

biopsy

in

unusual cases. or fno primary dentified

1- metubrtic

work-up

negative

-+

brain biopsy

2.

metubrtic work-up

p011itive

iopsy

of

affi:cted

lritc:s

other than brain

Treatment

medlcal

phenymin for seizure prophylaxis

i f

patient

presents

with

seizure

dexamethasone

to reduce

edema given

with

ranitidine

chemotherapy e.g. small

cell

lung cancer)

radiation

stereotactic radiosurgery: for discrete.deep-seatc:dJinoperable tumours

multiple lesions: use

whole

brain

radiation

therapy

WBRT); consider stereotactl.c

radiosurgery

If

10yan. CWBIps

rasactian

Syaars

1.5-2

yellS

12 manlbs,

10 at2

yess

sites: cerebral hemispheres cerebellum.

brainstc:m, spinalcord

symptoms:

recent

onsetofnew/worsening IA Ntv; seizure,

focal

deficits

or symptoms of

increasedICP

Investigations

CT

with contrast: va.rl.able appearance

depending

on

grade

(see Table 5)

tissue biopsy: WHO grade and histologycorrelateswith prognosis, but25 chanceof sampling

errordue to tumour heterogeneity

Neurosursery NSl

Figura

1D

M11tiple

Bniin

Mlll:astaas

(see 111111WS)

1.

HIIIBruganoosconlnlllarll.,callllnt

Z

1-deliled

bardn infltraiM)

3. l'lritumaur adarra

4.

CantriiiiiCIIISis

z

3

5.

CamprvAion

of vedricla,m e shit

Fiare

11. Hig. Grelle

AstrDcyiDma 01 CT

,

ICamof*Y

lllnlfll

c .

PIIffGin-1t1tue

Sclll

l l lg Qtlerhl

( II.

I

100

80

70

80

50

No

compeints; no evidanca of

i

Abla 1:11ny

on narmlll

activity;

minorsigns

or symptoms of

i

NIJIIIIIilldivity with

dart;.. .

-. .

Dr symptoms af di s

c

..

w elf: unable carry

on normal

activity

ur to do

lctiva

Wllrk

Requil88 occuionalllllil1lnce.

but ilable Cln for

111011:

of

hit needs

Requirasconsidlllble

881i111nce 4lld

fnlquant

medical

C lQ

40 Disabled; l llfJJiras

.

care

and -il lance

30 S8VIlnlly

-.bl ld;

missicn

s

indicltad

.U.ough

dflllh

not

i11111L'11nt

20

V.ry lick; hospital million

divB upportiva

1llltlnBIIt

II8C8SWY

10

Mcriluld;

fiiii110C88118

prugllllling lllpidly

0

Delli


12/44

NS12 Nearomrgery

1.

omogenouscontmt

emancement

2. Dui'IIIIIIIBctmmt

3. Dillinc:tmargill

Figure 1

Z.

Meningiam1 on CT

,

WHO

Clluification

ofMlnq;.IM

111r

iltoltm

Grade

1

ow n.k Jf

Grada

2: intamedialll

risk

of NC.-ce

Grade3: high rilkof recul'l'lnce

, ,

Proglllllive

l lillltlll lll or

sansorineul'lll ' - ing oss - acoustic

nauroma ll 1li

pmvan lltharwi.

10rontoNota 2011

Tralltment

low

grade

diffuse

astrocytoma

close follow-up, radl.ation, chemotherapy,

surgery

allvalid

options

ot 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

andGBM

surgvy

gross

total

resection: IDIWmal safe resection+

fractionated

radiationwith 2 em margin +

concomitant and

adjuvant temozolomide

- a.cept:

enensive dominant lobe GBM. slgnlfica.nt bllatenl involvement, endofllfe

near, extensive brainstem involvement

stereotacticbiopsy i esection not possible, followedby fractioned radiation with 2 em

margin

expectant

(based on

functional

impairment -

Kamofsk:y score


13/44

'IbroDloNota 2011

Tam.our

Futures

compression

of

structures in

CPA,

often CN

VIII

(hearing loss98%, tinnitus, d}' ICquilibriwn),

then V. then VII

ataxia

and raised ICP are late features

Investigations

MRI

with

gadolinium or T2 FIESTA sequence (>9896 sensitive/specific), CT with contrast2nd

choice

audiogram. bminstem audito ry evoked potentials, caloric

estll

Treatment

conservative: serlal maging

radiation: stereotacticradiosurgery

s the

trea1ment

of

choice

o surgery

if:

I lesion >3 em; 2 bn.in8tem compression;

3. edema;

4 hydrocephalus

curable

i

omplete

resection (almost

always possible)

operative complications:

CN VII, VIII dysfunction

(only sigDificant

dissbility ifbilateral),

CSF

leak

Pituitary

denoma

primarily from anterior pituitary, 3rd-4th decades,M=F

incidence

in

autopsy studies

approximately20

classification

miaoadenoma


14/44

NS14 Neuroaurgery

Brain Allscass

on

CT

. . ._ ii4Zpllillll: l&tn

Tlillb.ty llrtfy

modllyin

patinDM IInil--.

. I (

' II patiaJDiamlhl

Nalilnll

TIMan

Lllivnty fiDsPtalwara rl'liiMid

rWIId

f(a) aloc-.t

ln il pmlCirjmlllllillwilt

rq t .amrt

brconlrllt rM

nti lantr I'MRIIIIII

bl

-_. wilt tIIIII I l)llliliull*Kid

1:11hnt,

,_1M

1:11luw

IllirCnlclnDIIIIIIBBI

rrhilab.rJIIIIhlirDII:rinllilianiUJIIIIIIi g

lninabtcMI42(tlllllle.1111111111 '41

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

o...:an. ko1e

IOOSI

M

IDrUwtnnDI

Wth VIIIIiiDicslurlllllllt4Mib.

llldmilioa- primlld11111iens

>tS IIII

in

- -

dimBIIL

,._..:A1ullli I

llllr:Grnl:

13 44,411 hid

ful

_. - 42

I2SAI

hid

rrildRill,3'l

Pllimlhid

Il l

ll:ll:llnl,

Hlild

lhGIPII anl13

hldl i i i iBD

dllblly,

AJIMrill

loil1ic Nllll"iln lhllwld in'fiiNIIM:omll

..:illalMil

bqii'IIIIIIIUR

Ul, P=O:Im),

tmJJ CS >IZ OR .20. P=O.OII),

OR

781

A8. P


15/44

IbroDlo

Nota

2011

PwiBlood

Neurosursery NSlS

Treatment

aspiration excision and send for

Gram

stain, acid fast bacillus

(AFB),

C&S,

fu.ngul

culture

exdsl.on preferable lflocation

suitable

antibiotics

empirically: vancomycin +ceftriaxone+ metroniduole or chloramphenl.rol or rifiunpin

(6-8

weeks

therapy)

revise antibiotics when C&S known

anti-convulsants (1-2 years)

follow up

cr

scritical (doweekly initially,more frequent i condition deteriorates)

Prognosis

mortalitywithappropriate therapy

-10%,

permanent defidts in -50%

Blood

Tllllla

&. Cum)lllrisun

uf Epi..........,. EtiDIDIIf Ill ntnn:rasial

BIDIIds

Tna

of EtiDIDar EpidamiCIIDgy Clnical FtlbJIII

CT

Fllllnl

fpanllallluma

SkYI

fraellnc:ausing M > F la

(4:1) lucid inllMI

bafonl LOC

Lanticlilr

DIISS

nicHe

me.qeal

bleed

AartalkDiml Ruptured AQB >50. No lucid inllML Crascen1ic OilS

uan11amid

IISSOCiated

with

henipsesis,

vessels

tmuma

Pupilarychqes

Cl111icSUWanl

Ruptured

AQa

>50.BOH

Often lllylqiiDIIllltiC HypadaiiiB

sdlnclnlid abusn,

Minar

WA

confusion,

CIIRiCBID:

lll8iS

bridgill

vassels

antk:ollguilred signs of ilcreased

ICP

raum11, spmaneous

Aae

55-SO

Sudden onset Hit#J

density

IDxl

llllllllllhlge (111811811'11.

m C8888 under thundan:lap headllcha, (snitivitydacrealas

Dopethic, AVMI

ega

45

signs of

inctaad ICP ova"tima)

HTN,wsc.-r

Aaa

>55, 11A-ll8 ..,......, Hit#J dnity IDxl

abnormality,

ci'ug use

(CIICIIile, s ip

of ilcfelsad ICP

11lnDW's,

Raclions.

BOH, -B1llnila

xtradural

(Epidural' )

Hematoma

Etiology

Good

with prorr

lllllliiiJI Illenl

Nota:

nspmay

ernst e1r1

DCal' rom

unc:al

hamiml)

Cnriatamy ifbleed

Paar

>1cm

Burr

bola to

IRil; Good

Cllllliotumy

Heoccurs

CIIISIIVlllive:

NPO, rl NS, ECG,

Foley,

prophylaxis(nlnod *-);

opanvs.

llldovascular

surgery to repair if rebleed

Paar:

511%

mortality

3D of IUrvMnhaw

modnta to

IIMr8

cisabiity

Medical: dacnssa

BP. Paar:

44'hlortality dua to

cam ICP c:aralnl

hamildion

Slillil:al:

Cnlliotomy

temporal-parietal sJwll fracture:

85%

are due

to

rupturedmiddle meningeal

artery.

Remainder

of

caaes are due to bleedingfrom middle meningeal vein. dural sinus,

or

bone/diploic veins

Epidemiology

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

Clinical Features

in

6096, there

s

lucid intervalofseveral houn between conCI158ion and coma

then, obtundation. hemlpareals, .ip6Jlateralpupillary dilatation

signs and symptnms depend on severity

but

can Include

H/

A.

NJV;

amnesia.

altered

WC

HTN

and respiratory distress

deterioration can talce hours to days

lnvestigtdions

CTwithout contrast: high densitybiconvex mass against skull, usually with

unlfonn

density

and sharp margins. usually im:iJ:ed bysuture

Unes

Treatment

admit,

observe, bead elevation

mannitol pre-op

I f

elevated ICP brain herniation

craniotDmy to evacuate

clot, follow up

CT

1.

Comp1'81Sion

of

van1ridas

(miclile

llhilll

2. Bload

Figura 15. Eatndural Hama1Dm1

DICT


16/44

NS16 Neurosurgery

Calcilm antaganisiJ for

aneurysmal

subaracllloid haemonhage (Review)

ochraneReview 2008; Issue 3.

Introduction:

This

sb dy

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 16random ised 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

a

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.

CT

Density

and MRI Appearance of

Blood

Time CT MRI

MRI

T1

-T2

Acute

Hyper.

Grey

Black


17/44

Toronto Notes 2011 Cerebrovascular Disease

Cerebrovascular Disease

Ischemic Cerebral Infarction (80 )

embolic (heart, carot id

artery,

aorta) or thrombosis of ntracerebral arteries

(see arotid

Stenosis

NS21 and Neurology. N45)

Intracranial Hemorrhage {20 )

subarachnoid hemorrhage (SAH), spontaneous intracerebral hemorrhage (ICH),

intraventricular hemorrhage (IVH)

Subarachnoid emorrhage

SAH)

Definition

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

Etiology

trauma (most common)

spontaneous

aneurysms (75-80%)

idiopathic (14-22%)

AVMs(S%)

coagulopathies (iatrogenic

or

primary),

vasculitides,

tumours

(


18/44

NS18 Neuroaurgery

CerebroYascular

DJnase 1'oroDio 011

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

demonstrates source

of SAH

in 80-8596

of

cases

"angiogram

negative

SAH": repeat angiogram in 7-14 days, i negative - perimesencepbalic

SAH

magnetic resonELilce

angiography

(MRA) andcr

angiography

sensitivity maybe

up

to 95% for aneurysms

F"IJara

1'1.

DiaiJDalia

af

SAH

HiiiDry af..W.n da... BP

l OC

. ent

---- inb mMm lnll

+

NBQI1ive fllr blood

I Stiff neck

Fundi

CTicen

I

+

I'DiiiMI fur bllllld anc or

pllliant

chlwsy, uncanacious,

locelizina

nuv Dgicel findinae

uncture

I

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

CSF:

clw, cololll'lass,

CSF: bllllld

---- Flafa'1D NIIUtiU'Qiry

no

mic ie

blood

XWIIhochramil

DIC heme

f IJIFI 18. Appraacii1D

SAH

Treatment

admit to

ICU

r

NICU

oxygenlventilation pm

NPO, bed rest, elevute head ofbed

30D, minimal external

stimulation, neurologicalvitals qlh

aim

to maintain sBP

=

120-150 (balance ofvasospasm prophylaxis, riskof e-bleed, riskof

hypotension since

CBF

autoregulation impaired

by

SAH

cardiac rhythm monitor

Foley

pm, strict

monitoring

of

ns

and

outs

IV NS

with 20

mmol

KClJL

at

125-150

cclb.

phenytoin i

eizure

r emporal lobe clot

mild

sedation

pm

nimodipine fur

vasospum

neuroprotection for 21

day5;

may discontinue earlier i patient

s

clinkally

well


19/44


Complications

vasospasm - vessel constriction

in

response to extravascular blood irritation

clinical features: confusion, decreasedwe focal deficit (speech

or

motor)

onset

4-14 days post-SAH (deterioration within first 3 days is NOT caused by vasospasm)

risk factors: large

amount ofblood on

CT

(high

Fisher grade), smoking, increased age,

HTN

symptomatic vasospasm

in

20-3096

ofSAH

patients

radiographic vasospasm in 30-70% of arteriograms performed7 days following SAH (peak

incidence)

diagnosed clinically, and/or with transcranial Doppler (increased velocityof blood flow)

risk of cerebral infarct and death

treatment

triple

W

therapy using fluids

and

pressors (examples: norepinenphrine, phenylephrine)

angioplasty

for

refractory cases

hydrocephalus (15-20%} - due to

blood

obstructing CSF drainage

c n

be acute or chronic, requires extraventricular

dr in

(EVD) or shunt, respectively

neurogenic pulmonary edema

hyponatremia - SIADH, cerebral salt wasting

diabetes insipidus

cardiac- arrhythmi a (>50%have ECG changes), MI, CHF

Prognosis

10-15% mortality before reaching hospital, overall 50% mortality (majority within

first

2-3 weeks)

30%

of

survivors have mode rate to severe disability

a major cause

of

mortality

is

rebleeding, for aneurysms:

risk of rebleed: 4% on first day, 15-20% withi n 2 weeks,

5096

by 6 months

i fno

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

emorrhage ICH)

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

Definition

hemorrhage within brain parenchyma, accounts for -10 of strokes

c n

dissect into ventricular system (IVH) or through cortical surface (SAH)

Etiology

hypertension (usually causes bleeds

at putamen,

thalamus, pons

nd

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 (amphetami nes, 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 populat ion/year

Risk actors

increasing

age (mainly >55 years)

male gender

hypertension

Black/Asian > Caucasian

previous CVAofany type (23x risk)

both

acute

and

chronic heavy alcohol use; cocaine, amphetamines

liver disease

anticoagulants

Neurosurgery NSH

l r i N

H

' '-PY fvr

V aapum

Hyparllnsion

Hypervolemia

H odilution


20/44

NS2 Neurosurgery

Cerebrovascular Disease Toronto Notes 2 11

linical Features

TIA-like symptoms often precede ICH,

can

localize to site of mpending 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 and decreasedWC are common

specific symptoms/deficits depend on location ofiCH

Investigations

hyperdense blood on noncontrastcr

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 ynamics section, NS4)

phenytoin for s izur 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 ofclot. treatment of source of ICH {i.e. VM tumour,

cavernoma), ventriculostomy to treat hydrocephalus

indications

symptoms of raised ICP or mass effect

rapid deterioration (especially if signs ofbra instem 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

i f

iTN

poorly controlled

Intracranial neurysms

Epidemiology

prevalence 1-4

(20

have multiple)

female > male; age 35-65 years

Risk

Factors

autosomal dominant polycystic

kidney

disease (15 )

fibromuscular dysplasia (7-21 )

VMB

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


21/44


Table 7.

5-year Cumulative

Rupture Risk in

Unruptured Aneurysms

Based

on

Size and

Location

Cmlmo111 Cuolid

ACJMCIIC V.llllbmbuillrJPC./PCIIIIIII


22/44

NS22

Neurosurgery

,..__of IIQqllldFIIII._IIJ

Sui:CIIIful Clnlid &IIIIIIIII:IDIIJ ill'dlnll

MhlltRICIIIINUIIagi:ll

lluilonUid

C.alll lTrill

Llnc:et2004; 363:1491-1502

Slllly:

AlympiDnwlic Carotid

Sllgary Trill {ACST),

a illdomized, controlled 1rial

will

5)WTI.

l'llilnll:

3120

asymplomllicpl1ients NUl

111lllllr blllwlan immllilll carotid andulnclmny

(CEA) UJ1

indafuitB

dafumll ri

CEA

IIIII

\'MII

followad

for

up D 5 ears

{maan

3.4yBIIII.

Mlil

Oldaml:

lirt stroke (incliding

flllllor

dillblingl-

c.:l l l i:

n

i ien1swilh

CII I I

CI Qiid QlyQno5ia. immdlbl

CfA

Nduced the

nets..,. stroke

riskflom lllout

1D

llbaullft.. lid ltlis5-yalr bnlit MMd

dillbling or

fllal

Slnla

..._. ,

.

----------------.

Spetzler-M1rtin

AVM

Grading Scale

I am

Sc:ere

Size

0-3cm

1

3.1-6.0 em

2

>6cm

3

Location

Noneloquent

0

Eloquent

1

Deep vwn- dl'lin111

Not prllllent

0

Present

1

A'iM gl'llla8 Clbilbld

tr; addirQ

tlla 3 nllvidull

Spallllr-MI11in Scala . s

om

Ilia abova table.

E.g. A2 m

1llnDur

in nonaloq.lllntbcaliDn wilhout

daap

wnoiJI chinaga

Gradel.

Cerebrovaac:ularDisease/Vascular Malformations

Toronto

Notes2011

Investigations

CBC, PTT/INR (hypercoagulable states)

fundoscopy: cholesterol emboli

in

retinal vessels (Hol lenhorst 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

angiogram: gold but invasive and 1/200 risk of stroke (not for screening)

MRA: safer

than

angiogram, may overestimate stenosis

Treatment

control

ofHTN,lipids, diabetes

antiplat elet agents (ASA dipyridamole, clopidogrel) -25% relative risk reduction

carotid endarterectom y (generally i f ymptomatic and > 0% stenosis, see Tables 8 and 9)

endovascular angioplasty stenting

Prognosis

Table

8. Symptomltic Carotid Stenosis:

North

American Symptomatic Carotid Endarterectomy Trial

(NASCET)

Stunon

Angiogr111

Medal

Rx

26% over 2years

22% over 5

years

Medal +Sllf1liCII Rx

1%

over

2years

1 % over 5years

70-99

50-6 1%


23/44

'IbroDlo

Nota 2011

Vucular

MalfonnaHona/Cnemo ua Malformations

Investigations

MRI

Bowvoid),MRA

angiography

(7

will

also have one

or

more associated aneurysms)

Tnatment

decreases

risk

of

uture hemorrhage and

seizure

surgical

excision

is reatment

of

choice

stereotactic radiosurgery (SRS)

is

preferred

for

small {


24/44

NS24 Neuro1urgery

,,

,

IIIIIOIWII

Dlrlllll1181

IIIII

.. ...._

C2- nti

of

Bw

C4-

Colar Df

shirt

"C3A.5

lileP11hl diaplnam

alive"

T4 - Nippla line

T6-Xiphoid

TIO-lnbiliCIII

l12-S..,apubil:

'1.3 abava lha knaa"

"S2,3,4 -

Klllpl YIU'

s1Dol olf 111 flw

.....

,

Mvnnl

C5

-

Sho Mir abductioNellow fllllion

Cl - Wrist

IXIInsors

C7 - Bbow IDdlnlion

ca

-Squ-

hand

T1

- Abduct

fiiG ers

12-8

-lntlrcolllal

(Abdominal n . l

Tt-10 -

Upperlbclomillll

Tll-12-I.Jiwar abdominall

l2-Fiax.hip

L3 -

Hip

addulrtion

L4 -Knaa IDIIIInlliDII

and BJtla

L5 orsiflaxian and

big tDa

IIXtlnlion

Sl -

Planlarflelt

IIIIIIIDa

1, 2 tia

my

shoe -> S1-2 Anlda

jerk

3.

4

kidt he door-> LJ-4 ICMe

5,

I

pick up sticks -o C5-l Bicaps/

Brac:lioradilli

7, Slay

hem

-ight -> C7-8 Triclpl

RED FLMI fw IHII: 1 1111

Cudlr.rlnl

Urilary

rvtention

or neontinenc., f8eal

incontinanca or

oss

of anal spiW ctar

tone.

IIddie

an.U.ia.unLibilllel'll.lea

WAkneWpain.

....,

Aga >50,

prwiDUI

hx

of

cancer;

pain

lllr'lliaved by

bad

rast,.

constitutional

fYI I1P1DmL

lnr.:tian.

lnCI'IIUtld ESR.. IV drug

use.

wlr.

c.....-.nfrlcb,.

Aga

>SO.Irlllna.

prolonged

hroidu.a.

J

RED FLAGS fw lladl .....

BACK PAIN

Bowel/lllddar ll'llllltion or

incontinence)

AnNihllillllldlte)

Constitutionel

symptoms

IChronicdisease

l'lrulhNil

AQ1>5DarC5-C6 (C6

root)

Clinical Features

pain

down

arm

in

nerve

root

distribution, worse

with

neckextension, ipsilateralrotation and

lateral flexion (all compress the ipsilateralneuralforamen)

LMN

signs and symptoms

central cervicaldisc

protrusion

causes myelopathy as wellas

nerve

root deficits

Investigations

I f ed flags: C-splnex-ray,

CT,

MRI

(imaging

of choice)

consider EMG,

nerve conduction

studies If iagnosis

uncertain


25/44

IbroDlo Nota 2011

JW:radural Leal.ODI

Treatment

conservative

no bedrest: unless severe radicular

symptoms

activity modiftcation, patient education (reduce sitting,

lifting)

phys1otherapy. exerd8e programs

analgesl.cs, collar, tractl.on

mayhelp

surgical indications

in:tnu:table

pain

despite

adequate

conservative treatment for

>3

months

progreMM:

neurological

deficit

llll12rior cervical discectomy s usual ru.rgical choice

Prognosis

95 mprovespontaneously in 4-8 weeks

Tillie

1

D. Latenl Cervical Disc Syndrom11

lloGt

hdvtMI

C5 C

2\

SIIJuldar

Delblid, biceps,

tuplllpinlltul

Cl-7

No

clwlga

llicapl. Bnlclial'lldillis

Triceps

C7-T1

C8

10%

Rilg

fing

5th finger

Digillll

flexors,

nmsics

Fingar

llk

Haffmam's

ign)

Cervical Stenosis Cervical Spondylosis)

Definition

cervical

spondylosis is chronic disc degenerationand usodated facet arthropathy

resultant syndromes include mechanical neck pain. radiculopathy

root

compreasion),

myelopathy

(spinal

cord compression)and combinations

Epidemiology

typicallybegins at age 40-50,

men

>women, most commonlyat

he

C5-C6

>

C6-C7levels

Pathogenesis

with

neck

atenslon

the

c:ervical.

cord spinched. With neck

flalon. the

canal

dimensions

increase

slightly

to relieve

pressure on the

cervical

cord

Fetdures

insidiOUII

onset

of

mechanical neck pain exa.cerbated byexcessvertebral motion (particularly

rotation and ateralbending with a vertical compressive force - Spurling's test). Pain s worse

with

neck

extension.

relieved

with

flenon

ocdpltal headache

is common

radiculopathymay Involve 1or more roots, and symptoms include neck. shoul&W and arm

pain,

paresthesias and numbness

cervical

myelopathy

maybe characterized

by

weakness upper

>

ower

extremity),

decreased

derterityand sensorychanga.

UMN

findings suchashyperreflexia,clonw and Babinslri

reflex

may

be

present

1he

mostworrisomecmnplaint is l wex extremityweakneM (corticospinal tracts)

myelopathymay

be

associated

with

funicular paiD. characterizedbyburning 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. strengtheningand range ofmotion exercises, analgesics.

cervical

collar,

cervical

traction

surgical indications: myelopathy with motor impairment, progressive neurologl.c impairment.

intractable pa.ln

Neurosursery NS25

' ,

Disc

hamidions lnpinga tha 111M root

t haiMI below the illtnpaca

(i.e.

C5-ti

dise

1111rve

1\ 111)

rrFibras

FascicuUI

gl'lcilirlcunllllul:joint

po.ition.

fine

txlueh,

villnltion

Spiullhlllamil: lnll:l:

Pain 11'11

tampemn

CGrticaiPilll

tract

BkiBd movements

Figu111

Z1 A. Alii

a

uctian

Df

Cervical Spine with

Vascr Wid

Functional

Terltlclrlll

FlgUI II 21B. Axial

secllon

of

Tbonlcic Spine wilflVaacul end

fiiiCiional TarritDria


26/44

NS26 Neuroaurgery

Figure

21C. Axial

slldion

of

Lu..bar

Spinu

with Vasculand

Functloaal

Terrllerlea

Figure

21D.

AKial semion

of

S111:111l

Spinewltll

Ya&cular aad

Functloaal

Terrllerlea

22..

11-waightad

MRI of

l.umbllr

Disc

Humilltion

1 oroDio

011

Lumbar isc Syndrome

Etiology

laterally

herniated

lumbar disc compre&lleS nerve root, central hernilllion

caUIIes cauda

equinaor lumbar stenosis (neurogenic claudication)

Epidemiology

common

(>95%

of

herniated lumbardisks) -

L5

andSl roots

Clinical

Fntures

leg

pain

>back

pain

limited

back

movement

(especiallyforward flexion) due to

pain

motor weakness. dermatomalsensory changes, reflex changes

exacerbation with coughing. sneezingor straining. Relief with flexing the knee or

thigh

nerve root tension signs

straight leg raise (SLR:

Lasegue's

test) or aossed SLR

(pain should

occurat

less than 60

degrees) suggests

LS,

Sl root ilivolvement

femoral

stretch test suggests

L2,

L3

or

L4

root

involvement

Investigations

x-ray spine only o rule out

other

esions), Cf, MRI

myelogram and post-myelogram

cr

(onlyi MRI 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

Root

. . . . . . . L4 L5

llcidaiC8


27/44

Toronto otes 2011

Extradural

Lesions

auda quina Syndrome

Etiology

compression or irritation oflumbosacral nerve roots below conus medullaris below L2level)

decreased space in the vertebral canal below

1.2

common causes: herniated disk

spinal stenosis, vertebral fracture and tumour

Clinical Features

usually acute develops in less than 24 hours); rarely subacute or chronic

motor LMN signs)

weakness/paraparesis in multiple root distribution

reduced deep tendon reflexes knee or ankle)

autonomic

urinary retention or overflow incontinence) and/or fecal incontinence due to loss ofanal

sphincter tone

sensory

low back pain radiating to legs sciatica) aggravated

by Valsalva maneuver and by sitting;

relieved by lying down

bilateral sensory loss or pain: depends on the level affected

saddle area S2-S5) anesthesia

sexual dysfunction late finding)

Treatment

urgent investigation and decompression

30

min),

NOT simply exertion cessation

induced

by

variable degrees ofexercise or standing

may be elicited with lumbar extension, but may not have any other neurological findings, no

signs ofvascular compromise

e.g.

ulcers, poor capillary

refill

etc.)

Investigations

bicycle test may help distinguish neurogenic claudication NC) from vascular claudication the

waist-flexed individuals on the bicycle with NC can last longer)

Treatment

same as for lumbar spinal stenosis

Neurosurgery NS27

IC y

fAtu8l

uf Neurogenic w.

v 1 u

CIMit:don

Claudlclltian: denmrtolllll

distribution

with

positional relief

accurrilg

over

minutes.

Vacular CIMit:don: sclarotomll

distribution

with

relief accurrilg

with

rest owr s1condl.


28/44

NS28 Neuro1urgery

Flg1re Z3.

T1 WelgMid

IIIRI of

SyringDmyalil

,

Compartmentalize

spillll cord

lllllomil:lllv by loaation.

I

1i

B

I

Figure 24. Spil l

CaniLBsian

Spdi'DIIIIIS

Intradural

Intramedullary

Lai.ODI/Spinal

Cord

1'oroDio

011

Intradural

Intramedullary Lesions

Syringomyelia

Definition

cystic cavitation

of

he

spin81

cord

presentation ishighly

variable,

usuallyprogresses over months to years

initiallypain and weakness; later atrophy and loss

ofpain

and temperature sensation

Etiology

7096 are associated with ChiariI malfoi'IIl8tion

post-traumatic

tumour

Clinical Features

nonspecific features for any intramedullary

spin81

oord pathology:

sensory

loss

similar

to

central

cord

syndrome

pain and temperature losswithpreserved touchand joint position sensein a cape-like

distribution

at

levelofcervical

syrinx

dysesthetic pain often occurs in the distrlbution of he eDllory .o a

LMN

arm/hand

weakness

orwasting

painless arthropathles (Charcot's joints),especially in the shoulder and neck dueto loss of

pain

and temperature sensation (seen in less than 5%)

Investigations

MRI is bestmethod,myelogram

with

dela}'M CT

Treatment

treat

underlying cause

(e.g.

posterior fossa decompression for

Chiarl

I.

surgical

removal

of

tumour i ausing a syrinx)

Spinal

ord Syndromes

Spinal ord njuries

4.

for

spinal cordanatomy

Complete

Spinal Cord Lesion

bilateral loss

of

motor/sensory and autonomic function at

:M

segments below

lesion/injury,with

UMNsigns

about

396 ofpatients with

complete

in:jurie& will

develop some

recoverywithin 4

hours,

beyond

24 hours,

no dlstaJ.

function will recover

Incomplete

Spinal

Cord

Lesion

any residual function

at 2:4

segments below lesion

signs include

sensory/motor

function

in lower

i mbs

and sacral

sparing (perianal

sensation,

voluntary rectal sphincter contraction)

Tble13. CDmJMriiOn b8tween IIICGIIIplete Spinal

Card l..eiiDn

Syndrom11

Hemiseetion

ofcard

lpsilatinl

Lt.lll

weakness Ipsilateral loss of vibration

and

pra Jiacaptian

at

tha

l11im Cormlataralloss

ofpail111dta'npnure

lpsilatanll

UMN waakness PmiMIII lii#Jtlauch

bllaw

lha l ian

A111H Canl Anteriorspinal .my BilatemllMN

weakness

1:011_.

eaion r. at the

lesioo

occlusim Bilateml UMN

ltoelkness

belawthe lesion

Urillry 1'818nti111

CelmlCard Sytivlmytlia_ tlmaur&, BiiUDI mlltlrWlllkna&s:

(most

commm) spinal

Uppa'

mb

W8lkna&s

(l.llfi

lesion)

iniiiY (J8Itsr

1Im

LDwer

liiD

waalcness (UMN lasianl

Urillry llllantian

P'allllriar

Cord

IU arir.

spinal allay PmiMIII

infarction. lnUIII

Presi M d vlnlion

and

proprioceplion

Bilteralloss d pain and lefl1llnlure

Presi M d lii#Jt uul:h

Vllilbla blldsi'IIIIU pal1dad

slll&aly

loa

Loss

d

pain

and

tsiJ'C)III'Era han lass

of

vibl'llian

and

Blalaralloss

ofvibration.

ptapriocaptian.

light

twch

at and

balcrN lha

asian

Presi M d pailMJd


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Toronto Notes 2011

Peripheral Nerves/Neurotrauma

Peripheral erves

see

Neurology; N30

Classification and Clinical Course

neurapraxia: axon intact but fails to function, recovery

within hours

to

months

nerve entrapment: nerve compressed

by

nearby

anatomi c structures, often

secondary

to

localized, repetitive mechanica l trauma

with

additional vascular injury to nerve - sensory loss

in nerve distribu tion (often discriminativetouch lost first)

axonotmesis: axon disrupted but nerve sheath

intact

-+ Wallerian degeneration ofaxon segment

distal to injury- axonal recovery

of

I em/month, max at 1-2 years

neurotmesis: nerve completely severed,

need

surgical repair for recovery

Investigations

neurological

exam

(power, sensation, reflexes), localization

via

Tinel's sign (paresthesia& elicited

by

tapping

along

the course of a nerve}

electrophysiological studies (EMG, nerve

conduction

study) may be helpful in assessing nerve

integrity

and monitoring

recovery; not helpful unti12-3 weeks post-inju ry

labs: bloodwork,

CSF

imaging:

C-spine, chest/bone

x-rays

myelogram, CT,

MRI

"neurography" to

rule out

cerebral/

spinal

cord

lesions, identify etiology

angiogram i vascular damage

is

suspected

Treatment

early neurosurgical consultation i njury is suspected

entrapment

conservative: prevent repeated stress/injury, physiotherapy, NSAIDs, local anaesthesia

steroid injection

surgical:

nerve

decompression transposition for progressive deficits, muscle weakness/

atrophy, failure of medical management

stretch/ contusion

follow-up clinically for recovery; exploration i

no

recovery in 3

months

axonotmesis

i

no

evidence of recovery, resect

damaged

segment

prompt

physical therapy

and

rehabilitation to increase muscle function, main tain joint range

of motion, and maximize return

of

useful function

recovery usually incomplete

neurotmesis

surgical repair

of

nerve sheath unless

known

to

be

intact [suture nerve sheaths directly i

ends

approximate or nerve graft (usually sural nerve)]

clean laceration: early exploration and repair

contamination or associated injuries: ta g initially

with

nonabsorbable suture, reapproach

within 10 days

Complications

neuropath ic pain:

with neuroma

formation

complex regional pain syndrome: with sympathetic nervous system involvement

SPECI LTY TOPICS

eurotrauma

Trauma Management (see also edicine, ER7}

Indications

or

Intubation

in

Trauma

1

depressedW (patient cannot

protect

airway): usually GCS

2.

need

for hyperventilation

3. severe maxillofacial trauma: patency of airway

s

doubtful

4. need for pharm acologic paralysis for evaluation or

management

i basal skull fracture suspected, use orotracheal instead of nasotracheal intubation

note: intubation prevents patient's ability to verbalize for determining GCS

Neurosurgery NS29


30/44

NS30 Neurosurgery

,

Glaqaw

Corllll Scale

4

. . . . . . . .

5orinlld

lOIDI II

400lhslil

Z-1 1111 3lllllnldii MIIII 4lllllnllflllnlllll

Plil

1noeyeopllilg 3lelionl0poil

..

pa UiiQ

, ...... 2lllllm0110poil

It'

,....... .

ln

Assessment of

Spl CT/X-ray

IPII'IIAtlittll vilwl

ABCDS

Al9mlent (Columns: lllllerior

v.n.bnlllin1, portarior vtlrtablllllinl,

spinolaminar line, posterior

spinou5

tine)

IIane (vartebral bodies,

facets, spinous

proce5Ses)

Cartilqa

Disc

(disc

space and inbnpinous

spiC8)

Softtissun

Wblch 'dents Need T Hull or

Tl'llllf1lrto 1

Nlm'DIUf1llcll

C.ntrl1

Remains

aftar

resuscitation

Faclll neurological signs

Deterianrtilg

Neurotrauma

Trauma ssessment

INITIAL MANAGEMENT

ABC s of Trauma Management

see Emeri =DQ" Medicine. ER8

NEUROLOGICAL ASSESSMENT

Mini-History

Toronto Notes 2011

period

of

LOC, post

traumatic

amnesia, loss

of

sensation/function, type of njury/accident

Neurological Exam

Glasgow

Coma

Scale (GCS)

head and neck

(lacerations, bruises, basal

skull

fracture signs, facial fractures, foreign bodies)

spine

(palpable deformity, midline pain/tenderness)

eyes (pupillary size

and

reactivity)

brainstem

(breathing

pattern, CN

palsies)

cranial nerve exam

motor exam, sensory exam

(only i fGCS is

15), reflexes

sphincter

tone

record

and repeat neurological

exam at

regular intervals

Investigations

spinal injury

precautions (cervical collar)

are continued

until c-spine is cleared

C,T,L-spine

x-rays

AP,lateral,

odontoid

views

for

C-spine

(must

see

from

Cl

to T1 (swimmer's

view

if

necessary)

or

CT

rarely done: oblique views

looking for pars

interarticularis fracture ("Scottie dog"

sign)

CT head and

upper

C-spine (whole C-spine

i fpatient

unconscious)

look for

fractures, loss

of

mastoid

or sinus

air

spaces,

blood

in cisterns, pneumocephalu s

cross and

type, ABG,

CBC, drug

screen (especially alcohol)

chest and

pelvic x-ray as indicated

TREATMENT

Treatment for Minor Head lniury

see

Canadian CT Head

Rule sidebar, Emer.senc:y Medicine. ER8

observation

over

24-48

hours

wake everyhour

judicious

use of

sedatives

or

pain

killers

during monitoring

period

Treatment

for

Severe Head

lniury (GCS

s8)

clear airway

and

ensure breathing

if

GCS sa, intubate)

secure

C-spine

maintain

adequate BP

monitor

to

detect complications (GCS, CT, ICP)

monitor

and

manage increased

ICP

i f

present

(see erniation Syndromes NS6)

Which patients should be

admitted to

hospital?

skull fracture

indirect

signs

ofbasal skull

fracture

confusion,

impaired

consciousness

focal neurological signs

extreme

headache,

vomiting

seizures

concussion

with

>5

minutes

amnesia

unstable spine

use of

alcohol

poor social

support

(i.e.

no

friend/relative to

monitor for next

24

hours)

i f

here

is any

doubt, especially

with

children

KEY POINTS

never

do lumbar puncture in head injury unless increased

ICP

has been ruled out

all

patients

with

head

injuryhave C-spine

injury

until proven otherwise

alcohol

may not be the

cause

of

coma

-

there may

also

be

a

hematoma

low BP

after

head injury means

injury

elsewhere

must

clear

spine both

radiologically

AND

clinically

will

require re-assessment if/when

patient

improves clinically)


31/44

Toronto Notes

2011 Neurotrauma

ead

Injury

Epidemiology

male

to

female: 2-3:1

Pathogenesis

acceleration/deceleration: contusions, subdural hematoma. axon and vessel shearing/

mesencephalic hematoma

impact: skull fracture, concussion, epidural hematoma

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

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

high velocity: highest damage away from missile tract

Scalp Injury

rich blood supply

considerable blood loss (vessels contract poorly when ruptured)

minimal risk of nfection due to rich vascularity

Skull Fractures

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

table of skull), CT with bone windows is gold standard

simple fractures (closed injury):

no

need for antibiotics, no surgery

compound fractures (open injury}: increased

risk

of

nfection, surgical debridement within

24 hours is necessary

internal fractures into sinus may lead to meningitis, pneumocephalus

risk of operative bleed may limit treatment to antibiotics

basal skullfractures: not readily seen on x-ray, rely on clinical signs

retroauricular ecchymoses (Battle s sign)

periorbital ecchymoses (raccoon eyes)

hemotympanum

CSF

rhinorrhea. otorrhea (suspect

CSF

ifhalo or target sign present); suspect with Lefort

II/

III midface fracture

Cranial Nerve Injury

most traumatic causes ofcranial nerve injury do not warrant surgical intervention

surgical intervention

CN II local eye/orbit injury

CN

III IY

V ifherniation secondary to mass

CN

VIII -

repair

of

ossicles

CN injuries that improve

CN I - recovery may occur in a few months; most do not improve

CN

III IY

VI

-

majority recover

CN VII - recovery with delayed lesions

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

when resulting from hemotympanum)

Arterial Injury

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

Intracranial Bleeding

(see

Blood NS15

and Cerebrovascular Disease NS17)

rain

Injury

Primary Impact

18 - toronto notes 2011 - neurosurgery

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