Neurosurgery

Unprotected copy
By: Dr.JKR
Jkr336@hotmail.com
Dr.JKR
NS
Neurosurgery
Stewart Lo, Matt Stacey and Sara Temple, chapter editors
Kathryn Howe and Kim Tsoi, associate editors
Mark Pahuta, EBM editor
Dr. Abhaya Kulkarni and Dr. Taufik Valiante, staff editors
Basic Anatomy Review 2
Differential Diagnoses of Common
Presentions 4
INTRACRANIAL PATHOLOGY
Intracranial Pressure (ICP) Dynamics ...4
ICPNolume Relationship
ICP Measurement
Cerebral Blood Flow (CBF)
Elevated ICP
Herniation Syndromes 6
Subfalcine
Central Tentorial
Lateral Tentorial
Upward
Tonsillar
Treatment of Herniation Syndromes
Hydrocephalus 7
Benign Intracranial Hypertension 8
(Pseudotumour Cerebri)
Tumour 9
Metastatic
Astrocytoma
Meningioma
Vestibular Schwannoma ("Acoustic Neuroma")
Pituitary Adenoma
Pus 12
Cerebral Abscess
Blood 13
Extradural ("Epidural") Hematoma
Subdural Hematoma
Cerebrovascular Disease 15
Subarachnoid Hemorrhage (SAH)
Intracerebral Hemorrhage (ICH)
Intracranial Aneurysms
Carotid Stenosis
Vascular Malformations 20
Arteriovenous Malformations (AVMs)
Cavernous Malformations
EXTRACRANIAL PATHOLOGY
Dermatomes/Myotomes 21
Approach to LimblBack Pain
Extradural Lesion
Intradural Intramedullary Lesion
22
Spinal Cord Syndromes
Brown-Sequard Syndrome
Anterior Cord Syndrome
Central Cord Syndrome
Posterior Cord Syndrome
24
Root Compression
Cervical Disc Syndrome
Lumbar Disc Syndrome
Cauda Equina Syndrome
Lumbar Spinal Stenosis
Neurogenic Claudication
25
Peripheral Nerves
Peripheral Nerve Injury
Nerve Entrapment
27
SPECIALTY TOPICS
Neurotrauma
Trauma Assessment
Head Injury
Brain Injury
Late Complications of Head/Brain Injury
Spine Injury
Neurologically Determined Death
29
Pediatric Neurosurgery
Spinal Dysraphism
Intraventricular Hemorrhage
Hydrocephalus in Pediatrics
Dandy-Walker Malformation
Chiari Malformations
Craniosynostosis
Pediatric BrainTumours
33
Functional Neurosurgery 36
Common Medications 36
Summary Key Questions 37
References 38
Toronto Notes 2008 Neurosurgery N51
Dr.JKR
NS2 Neurosurgery Basic Anatomy Review Toronto Notes 2008
See Functional Neuroanatomy
software
Basic Anatomy Review
MRI Brain
Central sulcus
Frontal lobe \ . Parietal lobe
Cingulate gyrus ' Septum pellucldum
Corpus callosum
Thalamus
Hypothalamus
Occipital lobe
Midbrain
Pons
Fourth ventricle
Cerebellum
Medulla
Dens of C2
Spinal cord
Body of C3
A. Sagittal section
Frontal lobe
Caudate nucleus
Lateral ventricle
Putamen
Internal capsule
Insula
Thalamus
Parietal lobe
Occipital lobe
B. Axial section
Figure 1. MRI Neuroanatomy
From Stewart Pet al. Functional Neuroanatomy (Version 2.1). Health Education Assets Library, 2005.
Dr.JKR
Toronto Notes 2008 Basic Anatomy Review Neurosurgery NS3
Cervical Region
(1
c:J
c:]
(2
CJ
C3
8
d
(4
(5
(6
C7
(8
T1
fJB
Lumbar Region

L3
L4
Figure 2. Relationship of Nerve Roots to Vertebral Level in the Cervical and Lumbar Spine
Note: AP views depict left-sided C4-5 and L4-5 disc herniation, and correlating nerve root impingement
/ anterior communicating artery
/
. anterior cerebral artery
internal carotid artery
middle cerebral artery
posterior communicating artery
posterior cerebral artery
superior cerebellar artery
basilar artery
labyrinthine (internal auditory) artery
anterior inferior cerebellar artery
posterior inferior cerebellar artery
vertebral artery
Figure 3. Circle of Willis
Dr.JKR
NS4 Neurosurgery Differential Diagnoses of Common Presentionsflntracranial Pressure Dynamics Toronto Notes 2008
.....' ,
.)-------------,
Primary eNS lymphoma reported
ill 6-20% of IHIV-infectedl patients.
..... ' ,
.\------------,
Monro-Kellie hypothesis
Vbrain +Vblood +VCSF +Vles;on =
Vskull =constant
ICP mmHg

r-----J :
: 20 ...,---- :
I I
: 0 :
: Volume .. :
When amass expands I
within the skull Eventually further
small increments in
volume produce
mechanisms initially larger and
mam:ain anormal larger increments in
intracranial pressure intracranial
pressure
Figure 4. ICPVolume Curve
Adaptej from Lindsay 'fm, Bone I: Neurology and
Neurosurgery Illustrated. Copyright 2004 with
permission from Elsevier.
Differential Diagnoses of Common
Presentations
Intracranial Mass Lesions
tumour
metastatic tumours
astrocytoma
meningioma
vestibular schwannoma (acoustic neuroma)
pituitary adenoma
primary CNS lymphoma
pus/inflammation
cerebral abscess
cerebritis (i.e. HSV encephalitis)
tumefactive multiple sclerosis (MS)
blood
extradural (epidural) hematoma
subdural hematoma
ischemic stroke
hemorrhage: subarachnoid hemorrhage (SAH), intracerebral hemorrhage
(rCH), intraventricular hemorrhage (rVH)
cyst
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 (onset = minutes
to hours)
tumours (55% of spinal tumours): lymphoma, metastases (lymphoma,
lung, breast, prostate), neurofibroma
intradural extramedullary
vascular: dural arterio-venous fistula, subdural hematoma (anticoagulation)
tumours (40% of spinal tumours): meningioma, schwannoma, neurofibroma
intradural intramedullary:
tumours (5% of spinal tumours): astrocytomas and ependymomas most
common; also hemangioblastomas and dermoid
syringomyelia (common causes: trauma, congenital, idiopathic)
infectious/inflammatory: TB, sarcoid, transverse myelitis
vascular (AVM, ischemia)
Peripheral Nerve Lesions
neuropathies
traumatic
entrapments
iatrogenic
inflammatory
tumours
INTRACRANIAL PATHOLOGY
Intracranial Pressure (lCP) Dynamics
ICPNolume Relationshi
adult skull is rigid with a constant intracranial volume
however, as a lesion expands, rcp does not rise initially due to:
cerebrospinal fluid (CSF), blood, extracellular fluid (ECF) and intracellular fluid
(rCF) displacpd out of the head
brain tissue shifts into compartments under less pressure (herniation)
once compensation is exhausted, rcp rises exponentially
normal rcp <15 mmHg (8-18 cm H
2
0) for adult, 3-7 mmHg (4-9.5 em H
2
0) for
child; varies with patient position
waveform comprised of respiratory and blood pressure pulsations
consider therapy for high rcp when rcp >20-25 rnmHg
Dr.JKR
Toronto Notes 2008 Intracranial Pressure Dynamics
ICP Measurement
lumbar puncture (LP) (contraindicated with known/suspected intracranial mass lesion)
intraventricular catheter/ventriculostomy/external ventricular drain ("gold standard",
permits therapeutic drainage of CSF to decrease rcp; if mass and pressure gradient
present, drainage may increase gradient)
other: fibreoptic monitor (intraventricular, intraparenchymal, subdural), subarachnoid
bolt (Richmond screw), and epidural monitor
Cerebral Blood Flow (CBF)
CBF depends on cerebral perfusion pressure (CPP) and cerebral vascular resistance
normal CPP >50 mmHg in adults
cerebral autoregulation maintains constant CBF by compensating for changes in CPP,
unless:
high rcp such that CPP <60 mmHg
MAP>150 mmHg or MAP <50 mmHg
brain injury: Le. subarachnoid hemorrhage (SAH), severe trauma
Elevated ICP
Etiology of Raised ICP
increased intracranial blood volume
hypoventilation --> increased pCO:Jdecreased paz .-+ vasodilatation
venous outflow obstruction (venous sinus thrombosis, superior vena cava (SVC)
syndrome)
cranial dependency, Valsalva
cerebral edema: vasogenic (vessel damage), cytotoxic (cell death), osmotic (acute
hyponatremia, hepatic encephalopathy)
hydrocephalus
intracranial mass lesion (tumour, pus, blood, depressed skull fracture, foreign body)
tension pneumocephalus
status epilepticus
hypertensive encephalopathy (loss of autoregulation and cerebral edema)
CLINICAL FEATURES
Acute Raised ICP
headache (H/A)
nausea and vomiting (N/V)
decreased level of consciousness (LaC) if rcp =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 next page)
focal signs/symptoms due to lesion
Chronic Raised ICP
H/A
postural: worsened by coughing, straining, bending over (Valsalva)
morning/evening H/A --+ vasodilatation due to increased CO
2
with recumbency
visual changes
due to papilledema
enlarged blind spot, if advanced .-+ episodic constrictions of visual fields
("grey-outs")
optic atrophy/blindness
differentiate from papillitis (usually unilateral with decreased visual acuity)
Neurosurgery NS5
L CPP=MAP-ICP

Autoregulation: CSF maintained despite
change in CPP


<60 i>150 mmHg
low BP or high ICP High BP
Cerebral perlusion pressure
Figure 5. Cerebral Autoregulation
Curve
Adapted from Lindsay et al: Neurology and Neurosurgery
Illustrated. Copyright 2004 with permission from Elsevier.
..... ' ,
..)-----------,
Cushing'sTriad of Acute Raised ICP
Full triad seen in 1/3 of cases
1. hypertension
2. bradycardia (late finding)
3. abnormal respiratory pattern
Dr.JKR
NS6 Neurosurgery Herniation Syndromes Toronto Notes 2008
1. Subfalcine
2. Central
3. Uncal
4. Upward
5.Tonsillar
Figure 6. Herniation Types
Herniation Syndromes
Subfalcine (Cingulate) Herniation
definition: cingulate gyrus herniates under falx
etiology: lateral supratentorial lesion
clinical features
usually asymptomatic, pathological/radiological observation
warns of impending transtentorial herniation, risk of ACA compression
Central Tentorial (Axial) Herniation
definition: displacement of diencephalon and midbrain through tentorial notch
etiology: supratentorial midline lesion, diffuse cerebral swelling, late uncal herniation
clinical features:
rostral to caudal deterioration (sequential failure of diencephalon --> medulla)
decreased LOC (midbrain compressed)
EOM/upward gaze impairment ("sunset eyes")
brainstem hemorrhage ("Duret's" secondary to shearing of basilar artery
perforating vessels)
diabetes insipidus (traction on pituitary stalk and hypothalamus) --> end stage sign
Lateral Tentorial (Uncal) Herniation
definition: uncus of temporal lobe herniates down through tentorial notch
etiology: lateral supratentoriallesiun (often rapidly expanding trawnatic hematoma)
clinical features:
ipsilateral non-reactive dilated pupil (earliest, most reliable sign), EOM paralysis
(CN III compressed)
decreased LOC (midbrain compressed)
contralateral hemiplegia, extensor (upgoing) plantar response
"Kernohan's notch": contralateral cerebral peduncle compressed due to shift
of brain -> ipsilateral hemiplegia (a false localizing sign)
Upward Herniation
definition: cerebellar vermis herniates through tentorial incisura, compressing
midbrain
etiology: large posterior fussa mass causing herniation of cerebellum rostrally, common
after VP shunting
clinical features:
superior cerebellar artery (SCA) compression * cerebellar infarct
compression of cerebral aqueduct --> hydrocephalus
Tonsillar Herniation (1IConing")
definition: cerebellar tonsils herniate through foramen magnum
etiology: infratentoriallesion or following central tentorial herniation
clinical features:
compression of cardiovascular and respiratory centers in medulla (rapidly fatal)
may be precipitated by LP in presence of space occupying lesion (particularly in
the posterior fossa)
Treatment of Herniation Syndromes
---------'
goals: keep Iep <20 mmHg, CPP >60-70 mmHg
General Measures
elevate head of bed at 30-45 --> increases intracranial venous outflow
prevent hypotension with fluid and pressors pm
ventilate to normocarbia (pC0
2
35-40 mmHg) --> prevents vasodilatation
oxygen pm to maintain p02 >60 mmHg -> prevents hypoxic brain injury
CT or Mill to identify etiology, assess for midline shift/herniation
Specific Measures (proceed stepwise prn)
mannitol (20% IV solution 1-1.5 glkg, then 0.25 glkg q6h)
can give rapidly, acts in 30 minutes, must maintain sBP >90 mmHg
hyperventiTate to pCO:? 30-35 mmHg
Dr.JKR
Toronto Notes 2008 Herniation Syndromes/Hydrocephalus Neurosurgery NS7
sedation ("light" e.g. codeine --> "heavy" e.g. fentanyl/MgS04 paralysis with
vecuronium --> reduces sympathetic tone, HTN induced by muscle contraction)
corticosteroids
decreases edema over subsequent days around brain tumour, abscess, blood
no proven value in head injury or stroke
surgeryd . 3 5 1CSF' . I h" . d d 1
ram - m VIa ventnc es, assess eac SItuation m epen ent y
remove mass lesion, insert external ventricular drain (if acute) or shunt
decompressive craniectomy is a last resort
Hydrocephalus
Definition
increased CSF volume
Etiology
decreased CSF absorption (majority)
increased CSF production (rarely) - e.g. choroid plexus papilloma
(0.4-1% of intracranial tumours)
Epidemiology
estimated prevalence 1-1.5%; incidence of congenital hydrocephalus -] -2/1000 live births
Classification
1. Obstructive (Non-Communicating) Hydrocephalus
absorption blocked within ventricular system proximal to the arachnoid granulations
acquired causes:
acquired aqueductal stenosis (adhesions following infection, hemorrhage)
intraventricular lesions (tumours - e.g. 3rd ventricle colloid cyst, hematoma)
mass causing tentorial herniation, aqueduct/4th ventricle compression
others: neurosarcoidosis, abscess/granulomas, arachnoid cysts
congenital causes:
aqueductal stenosis, Dandy-Walker malformation, Chiari malformation (see
Pediatric Neurosurgery, NS34)
CT findings:
ventricular enlargement proximal to block
2. Non-Obstructive (Communicating) Hydrocephalus
CSF absorption blocked at extraventricular site = arachnoid granulations
causes:
post-infectious (#1 cause) -... meningitis, cysticercosis
post-hemorrhagic (#2 cause) --> SAH, NH, traumatic
Choroid plexus papilloma (rare, causes l' CSF production)
idiopathic normal pressure hydrocephalus
CT findings:
all ventricles dilated
3. Normal Pressure Hydrocephalus (NPH)
gradual onset of classic triad developing over weeks or months
gait disturbance (ataxia and apraxia usually initial symptoms)
urinary incontinence
dementia
CSF pressure within clinically "normal" range, but symptoms abate with CSF shunting
idiopathic etiology
4. Hydrocephalus Ex Vacuo
enlargement of ventricles and sulci secondary to cerebral atrophy, not hydrocephalus
usually a function of nonnal aging, also in Alzheimer's, Creutzfeldt-Jacob Disease
Clinical Features (see Pediatric Neurosurgery for infant/child, NS34)
Acute Hydrocephalus
signs and symptoms of acute raised ICP (see NS5)
impaired upward gaze ("sunset eyes") and/or CN VI palsy
Chronic Hy'droceEhalus
simIlar to NPH (see above)
Investigations
CT'MRI
. ventricular enlargement, may see prominent temporal horns
periventricular hypodensity (transependymal migration of CSF forced into
extracellular space)
narrow/absent sulci
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 cistemography can test CSF flow and absorption rate (unreliable)
~ [
o
4
5
6
1. Choroid plexus
2. Lateral ventricles
3. Third ventricle
4. Cerebral aqueduct (of Sylvius) ~
5. Fourth ventricle :-::
6. Foramen Luschka and Magendie . ~
7. Arachnoid granulations u::
8. Subarachnoid space ~
9. Sagittal sinus @
Figure 7. The Flow of CSF
..... ' ,
~ } - - - - - - - - - - - - ,
CSF produced by choroid plexuses,
flows to: --t ventricles'" foramina of
Luschka and Magendie ... subarachnoid
space'" absorbed by arachnoid
villi/granulations into venous sinuses.
Luschka =lateral, Magendie =medial
~ ,
NPH Progression "AID" =
Ataxia/Apraxia of gait ... Incontinence
--t Dementia
..... ' ,
~ } - - - - - - - - - - - - ,
CSF production =CSF reabsorption =
- 500mllday in normal adults
Normal CSF volume -150 ml
(50% spinal, 50% intracranial'" 25 cc
intraventricular, 50 cc subarachnoid)
Dr.JKR
NS8 Neurosurgery HydrocephaluslBenign Intracranial Hypertension Toronto Notes 2008
Treatment
surgical removal of obstruction (if possible) or excision of choroid plexus papilloma
shunts:
ventriculoperitoneal (VP) - most common
ventriculo-atrial (VA) - not first choice because of l' infections, shunt emboli
ventriculopleural
lumbopentoneal - for communicating hydrocephalus and pseudotumour cerebri
third ventriculostomy (for obstructive hydrocephalus) via ventricUloscopy
LPs (for transient, IVH in premature infants, etc.)
Shunt Complications
obstruction (most common cause of shunt malfunction)
etiology: obstruction by choroid plexus, buildup of proteinaceous accretions,
blood, cells (inflammatory or tumour), infection, disconnection or damage
clinical features: acute hydrocephalus, increased ICP
investigations: "shunt series" (plain x-rays of entire shunt that only rule-out
disconnection, break, tip migration), CT, radionuclide "shuntogram"
shunt tap and surgical exploration pm
infection (3-6%)
etiology: 5. epidermidis, 5. aureus, P. acnes, Gram-negative bacilli
clinical features: fever, N/V, anorexia, irritability, meningitis, peritonitis, signs
and symptoms of shunt obstruction, shunt nephritis (VA shunt)
investigations: CBC, blood culture, tap shunt for C&S (LP usually NOT
recommended)
overshunting (10% over 6.5 years)
slit ventricle syndrome (collapse of ventricles leading to occlusion of shunt
ports by ependymal lining)
subdural effusion, hematoma (collapsing brain tears bridging veins, especially
in NPH patients)
secondary craniosynostosis (children)
low pressure headache
seizures (5.5% risk in 1st year, 1.1% after 3rd year)
inguinal hernia (17% incidence with VP shunt inserted in infancy), skin breakdown
over hardware
Benign Intracranial Hypertension
(Pseudotumour Cerebri)
Definition
raised intracranial pressure and papilledema without evidence of any mass lesion,
hydrocephalus, infection or hypertensive encephalopathy (a diagnosis of exclusion)
Etiology
unknown (majority), but associated with
lateral venous sinus thrombosis
habitus/diet: obesity, hyper/hypovitaminosis A
endocrine: reproductive age, menstrual irregularities, Addison's/Cushing's
disease, thyroid irregularities
hematological: iron aeficiency anemia, polycythemia vera
drugs: steroid administration or withdrawal, tetracycline, nalidixic acid, etc.
risk factors overlap with those of venous sinus thrombosis and similar to those for
gallstones
Epidemiology
incidence -0.5/100,000/year
usually in 3rd and 4th decade (F>M)
Clinical Features
symptoms and signs of raised ICP (H/A in >90%, pulsatile intracranial noise), but NO
decreased LaC or diplopia
-J, visual acuity, papilledema, visual field defect, optic atrophy (key morbidity,
preventable cause of often pennanent blindness)
usually self-limited, recurrence is common, chronic in some patients
risk of blindness is not reliably correlated to symptoms or clmical course
Investigations
CT: nonnal
CSF studies: nonnal
MRI: must look for venous sinus thrombosis
Treatment
rio conditions that cause intracranial hypertension
D/C offending medications, encourage weight loss, fluid/salt restriction
phannacotherapy: acetazolamide (decreases CSF production), thiazide diuretic or
furosemide
if above fail ---> serial LPs, shunt
optic nerve sheath decompression (if progressive impainnent of visual acuity)
2-year follow-up with imaging to rule out occult tumour, ophthalmology follow-up
Dr.JKR
Toronto Notes 2008 Tumour Neurosurgery NS9
Tumour
Definition
primary vs. 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
Table 1. TumourTypes: Age, Location
Age Supratentorial Infratentorial (posterior fossa)
<15 years . astrocytoma lall grades) 150%1 . medulloblastoma 115-20%)
incidence: 2-51100.000Iyear - craniopharyngioma 15-10%) - cerebellar astrocytoma 115%1
60% infratentorial - others: pineal region tumours, choroid plexus - ependymoma 19%)
tumours, ganglioglioma, DNET - brainstem astrocytoma
>15 years high grade astrocytoma (e.g. glioblastoma - metastasis
80% supratentorial multiforme (GBM) (1215%) - acoustic neuroma Ischwannomal (5-10%)
metastasis 115-30%, includes infratentorial) - hemangioblastoma 12%)
meningioma 115-20%1 - meningioma
- low grade astrocytoma 18%)
- pituitary adenoma 15-8%)
- oligodendroglioma 15%)
- other: colloid cyst, eNS lymphoma,
dermoid/epidermoid cysts
Clinical Features
progressive neurological deficit (70%) - usually motor weakness, CN deficits,
sensory, cognitive, personality, endocrine deficits may localize lesion
HJA (50%) raised ICP (acute or chronic depending on growth rate), H/A
classically worse in am but non-specific (likely hypoventilation during sleep
causing vasodilatation -->1' ICP), also may worsen with bending forwardNalsalva
NN (40%)
seizures (25%)
papilledema, obscured vision
symptoms suggestive of TIA (ictal, post-ictal, or ischemic 2 to "steal phenomenon")
rarely presents with hemorrhage
familial syndromes associated with CNS tumours:
von Hippel-Lindau (hemangiomas)
tuberous sclerosis (astrocytomas)
neurofibromatosis type 1 and 2 (astrocytomas, acoustic neuromas respectively)
Li-Fraumeni (astrocytomas)
Turcot syndrome (GBMs)
multiple endocrine neoplasia type 1 (pituitary adenoma)
Investigations
CT, MRI, stereotactic biopsy (tissue diagnosis), metastatic work-up pm
Treatment
conservative - serial Hx, Px, imaging for slow growinglbenign lesions
medical- corticosteroids to reduce cytotoxic cerebral edema, pharmacological (see
Pituitary Adenoma, NSll)
surgical- total or partial excision (decompressive, palliative), shunt if hydrocephalus
radiotherapy - conventional fractionated radiotherapy (XRT), stereotactic radiosurgery
(Gamma KnifeT
M
)
chemotherapy - e.g. alkylating agents (temozolomide)
MetastaticTumours
most common brain tumour seen clinically
15-30% of cancer patients present with cerebral metastatic tumours
usually spread hematogenously
Location
80% are hemispheric, often at grey-white matter junction or junction of
temporal-parietal-occipital lobes (likely emboli spreading to terminal MCA branches)
OIl'
DDx for ring enhancing lesion
on CT with contrast:
"MAGICAL DR"
'Metastases
'Abscess
'Glioblastoma
(high grade astrocytomal
Infarct
Contusion
AIDS (toxoplasmosisl
Lymphoma
Demyelination
Resolving hematoma
[' by far the 3 most common Ox's]
..... ' ,
~ ) - - - - - - - - - - - - ,
Primary Sources of Metastatic
Brain Tumours
Lung 44%
Breast 10%
Kidney (RCC) 7%
GI 6%
Melanoma 3%
Dr.JKR
NSIO Neurosurgery Tumour Toronto Notes 2008
Investigations
metastatic work-up (OCR, cr chest/abdo, abdominal D/S, bone scan, mammogram)
cr with contrast ~ round, well-circumscribed, often ring enhancing, ++ edema, often
multiple
MRI more sensitive, especially for posterior fossa
consider biopsy in unusual cases
Treatment
medical
phenytoin for seizure prophylaxis if patient presents with seizure
dexamethasone to reduce edema (often Significant cause of symptoms), given
with ranitidine
chemotherapy (small cell lung cancer)
radiation
Figure 8. Multiple Brain Metastases whole brain radiation therapy (WERT) can help reduce symptoms in
inoperable cases (some tumours respond poorly e.g. melanoma), typically the
sole treatment if multiple lesions
post-op WERT is commonly used
stereotactic radiosurgery
multiple lesions:
1. metastatic work-up negative --+ brain biopsy
2. metastatic work-up positive -. biOpsy affected sites other than the brain
surgical
single/solitary lesions ~ surgery + radiation
prognosis: median survival without treatment once symptomatic is -1 month, with
optimal treatment 6-9 months but varies depending on primary
'jt ~ Astrocytom_a _
most common primary intra-axial brain tumour
Table 2. Astrocytoma Grading System (one of many schemes)
World Health Organization (WHO) Typical CTIMRI Findings Survival
1- pilocytic astrocytoma No mass effect, no enhancement >10 years, cure if gross total resection
.. 1
II-low grade/diffuse Mass effect, no enhancement 5years
--- 2 III - anaplastic Complex enhancement 1.5-2 years
IV - glioblastoma multiforme Necrosis (ring enhancement) 9 months
Clinical Features
middle aged, recent onset of new/worsening H/A, N/V, seizure focal
1. heterogenous contrast enhancement
deficits or symptoms of increased ICP
2. ill-defined borders (infiltrativel
3. perilumour edema
Investigations
4. central necrosis
CT with contrast ~ variable appearance depending on grade (see Table 2)
5. compression of ventricles, midline shift
tissue biopsy ~ WHO grade correlates with prognosis, but 25% chance of sampling
Figure 9. High Grade Astrocytoma on error due to tumour heterogeneity
CT
Treatment
low grade astrocytoma:
close follow-up, radiation, chemotherapy, surgery all valid options
surgery: not curative, trend towards better outcomes
radiotherapy alone or post-op prolongs survival (retrospective evidence)
chemotherapy - usually reserved for tumour progression
high grade astrocytomas (comprised of anaplastic astrocytoma and glioblastoma
multiforme (GBM
surgery: gross total removal with radiation to tumour bed WERT is the
standard treatment unless: extensive dominant lobe GBM, Significant bilateral
involvement, end of life near, extensive brainstern involvement
aim to prolong "quality" survival
chemotherapy: -20% response rate
multiple gliomas: WERT chemotherapy
Dr.JKR
Toronto Notes 2008 Tumour Neurosurgery NSll
Meningioma
mostly benign (1% malignant), slow-growing, extra-axial, circumscribed
(non-infiltrative), arise from arachnoid membrane
often cause hyperostosis of adjacent bone, often calcified, classically see Psammoma
bodies on histology
Common Locations
parasagittal convexity or falx (70%), sphenoid wing, tuberculum sellae
Clinical Features
middle aged, symptoms of increased rcp, focal deficits
Investigations
CT with contrast: homogeneous, densely enhancing, along dural border ("dural tail"),
well circumscribed (see Figure 10)
1. homogenous contrast enhancement
contrast enhanced MRI provides better detail
2. dural attachment
angiography: most are supplied by external carotid feeders (meningeal vessels)
3. distinct margins
also assesses venous sinus involvement, "tumour blush" commonly seen
(prolonged contrast image)
Figure 10. Meningioma on CT
Treatment
conservative management for non-progressive, asymptomatic lesions
surgery is treatment of choice if symptomatic or progression on sequential imaging
(curative if complete resection)
stereotactic radiosurgery (SRS) may be an option for lesions <3 em
endovascular embolization to facilitate surgery
SRS or XRT for recurrent atypical/malignant meningiomas
Prognosis
>90% 5-year survival, recurrence rate variable (often -10-20%)
depends on extent of resection (Simpson's classification)
Vestibular Schwannoma e'Acoustic Neuroma")
progressive unilateral or asymmetrical sensorineural hearing loss = acoustic neuroma
until proven otherwise (earliest symptom)
slow-growing (average of 1-10 mm/yr), benign posterior fossa tumour
arises from vestibular component of CN VITI at cerebello-pontine angle (CPA)
if bilateral = neurofibromatosis type II
Clinical Features
compression of structures in CPA, often CN VITI (hearing loss 98%, tinnitus,
dysequilibriurn), then V, then VII
ataxia and raised rcp are late features
Investigations
MRI with gadolinium or T2 FIESTA sequence (>98% sensitive/specific), CT with
Figure 11. Vestibular Schwannoma
contrast 2nd choice
(tumour in cerebella-pontine angle\
audiogram, brainstem auditory evoked potentials, caloric tests
Treatment
conservative: serial imaging
radiation: stereotactic radiosurgery is the treatment of choice
surgery if: 1. lesion >3 em; 2. brainstem compression; 3. edema; 4. hydrocephalus
several routes, curable if complete resection (almost always possible)
operative complications: CN VII, VITI dysfunction (only significant
disability if bilateral), CSF leak
Pituitary Adenoma
o
primarily from anterior pituitary, 3rd-4th decade, M=F
microadenoma <1 em in diameter; macroadenoma ~ 1 em in diameter
may be functional (secretory) or non-functional
Dr.JKR
NSI2 Neurosurgery TumourlPus Toronto Notes 2008
~ ,
Go Look For The Adenoma Please -
GH, LH, FSH,TSH, ACTH, Prolactin
Acompressive adenoma in the pitu-
itary will impair hormone production in
this order (i.e. GH-secreting cells are
most sensitive to compression)
Clinical Features
mass effects
H/A
bitemporal hemianopsia (compression of optic chiasm) (see Neurology, N26
for details of visual field deficit)
CN III, IV, V
v
V'l' VI palsy (compression of cavernous sinus)
endocrine effects
hyperprolactinemia (prolactinoma) ---> infertility, amenorrhea,
galactorrhea, decreased libido
ACTH production -. Cushing's disease, hyperpigmentation
GH production ---> acromegaly/gigantism
panhypopituitarism (hypothyroidism, hypoadrenalism, hypogonadism)
associated MEN I syndrome
diabetes insipidus
pituitary apoplexy
apoplexy (sudden l:'xpansion of mass due to hemorrhage or necrosis)
abrupt onset B/A, visual disturbances, ophthalmoplegia, and reduced
mental status, and panhypopituitarism
CSF rhinorrhea and seizures (rare presenting signs of pituitary tumour)
signs and symptoms of SAH (rare) (see NSI5)
Investigations
formal visual fields, CN testing, endocrine tests (PRL level, TSH, 8 a.m. cortisol, fasting
glucose, FSH/LH, IGF-I), electrolytes, urine electrolytes and osmolarity, imaging (Mill
with and without contrast)
Differential
parasellar tumours (e.g. craniopharyngioma, tuberculum sellae meningioma), carotid
aneurysm
Treatment
medical
rapid corticusteroid ..tdministration surgical decompression for apoplexy
dopamine agonists (e.g. bromocriptine) for prolactinoma
serotonin antagonist (cyproheptadine), inhibition of cortisol production
(ketoconazole) for Cushing's
somatostatin analogue (octreotide) bromocriptine for acromegaly
endocrine replacement therapy
surgical
trans-sphenoidal. transethmoidal, transcranial approaches
Sources of Pus
subdural empyema --> pus in pre-existing space with no capsule barrier thus rapid
expansion is commoll (from sinusitis, mastoiditis - rare, 20% mortality)
meningitis, encephalitis, toxoplasmosis (AIDS)
osteomyelitis of skull (Pott's puffy tumour), usually seen with sinusitis
granuloma (TB, sarcoid)
cerebral abscess (see below)
Cerebral Abscess
Definition
pus in brain substance, surrounded by tissue reaction (capsule formation)
Etiology
modes of spread
hematogenous spread (most common)
adults: chest is #1 source --> lung abscess, bronchiectasis, empyema
children: congenital cyanotic heart disease (CCHO) with R to L shunt
immunosuppression (AIDS - toxoplasmosis)
contiguous spread (adjacent infection)
otitis media, mastoiditis, sinusitis, osteomyelitis, dental abscess
dural disruption
surgery, trauma (especially with continued CSF leak)
congenital defect (e.g. dermal sinus)
Dr.JKR
Toronto Notes 2008 PuslBlood Neurosurgery NS13
pathogens
3
Streptococcus (most common), often anaerobic or microaerophilic
Staphylococcus (penetrating injury)
Gram negatives, anaerobes
immW1ocompromised: Toxoplasma, Nocardia, Candida albicans, Listeria
monocytogmes, Mycobacterium and Aspergillus
Risk Factors
lW1g abnormalities (infection, AV fistulas (especially Osler-Weber-Rendu syndrome))
CCHD
bacterial endocarditis
penetrating head trauma
AIDS
Clinical Features
1. surrounding edema
focal neurological signs and symptoms
2. central low density (pus)
mass effect, increased ICP and sequelae (cranial enlargement in children)
3. ring enhancement
hemiparesis and seizures in 50%
signs of systemic infection (mild fever, leukocytosis)
Figure 12. Brain Abscess on CT
Investigations
WBC/ESR may be normal, blood cultures rarely helpful and LP contraindicated
CT scan often 1st test in emergency department
~ f R l
imaging of choice
diffusion/apparent diffusion coefficient (ADC) used to differentiate abscess
(black) from tumour (white)
Treatment
multiple aspiration excision and send for Gram stain, acid fast bacillus (AFB), C&S,
fungal culture
excision preferable if location suitable
antibiotics
empirically: vancomycin + ceftriaxone + metronidazole or chloramphenicol or
rifampin (6-8 weeks therapy)
revise antibiotics when C&S known
anti-convulsants (1-2 years)
follow up CT is critical (do weekly initially, more frequent if condition deteriorates)
Prognosis
mortality with appropriate therapy -10%, permanent deficits in -50%
Blood
Extradural (6IEpidural") Hematoma
Etiology
temporal-parietal skull fracture ---+ ruptured middle meningeal artery
Epidemiology
young adult, male> female
Clinical Features
classically there is lucid interval between concussion and coma
signs and symptoms depend on severity but can include H/A, N/V, amnesia, altered
LaC
Investigations
CT without contrast ---+ high density biconvex mass against skull, "lenticular-shaped,"
1. compression of ventricles
usually with uniform density and sharp margins, usually limited by suture lines
(midline shift)
Treatment
2. blood
head elevation, mannitol pre-op, craniotomy to evacuate clot
Figure 13. Extradural Hematoma on
Prognosis
CT
good with prompt management, as the brain is often not damaged
Dr.JKR
NS14 Neurosurgery Blood Toronto Notes 2008
CT dInIity IIld III ..,.... of blood
tiiiit CT .. IIIIi
n 12
AMI Hyper. Grey BlICk
72hl
SubIcuIe Iso. White White
4w)
ClvIlIic Hypo. Blaci Blaci
(>4wl
T1: 'George Washington Bridge'
MRH2: 'Oreo' cookie -

Subdural Hematoma
ACUTE SUBDURAL HEMATOMA
Etiology
rupture of vessels that bridge the subarachnoid space (e.g. cortical artery, large vein, or
venous sinus) or cerebral laceration
Risk Factors
anticoagulants, EtOH, cerebral atrophy
Clinical Features
no lucid period, signs and symptoms can include altered LOC, pupillary irregularity,
hemiparesis
Investigations
CT - high density concave mass, "crescentic" usually less uniform, less dense and
more diffuse than extradural hematoma
Treatment
craniotomy if causing mass effect, optimal if surgery <4 hrs from onset
Prognosis
poor overall since the brain is often injured
compression of ventricles
midline shift
old blood\
.blood
/
Figure 14. Subdural Hematoma on CT
CHRONIC SUBDURAL HEMATOMA
Etiology
acute subdural with neomembranes, neocapillaries, and liquefaction of clot
recurrent bleeding from the neocapillaries
leads to expansion of the hematoma, increased rcp, herniation, and death
Risk Factors
older, alcoholic, patients with CSF shunts, anticoagulants
Clinical Features
often due to minor injuries or no history of injury
symptoms of raised rcp seizures, progressive dementia, gait problem
obtundation disproportionate to focal deficit; "the great imitator" of dementia, tumours
Investigations
CT --+ hypodense (liquefied clol), crescentic mass
Treatment
burr hole drainage as clot liquefies, craniotomy if recurrent
Prognosis
good overall as brain usually undamaged, but may require repeat drainage
Dr.JKR
Toronto Notes 2008 Cerebrovascular Disease Neurosurgery NS15
Cerebrovascular Disease
Ischemic Cerebral Infarction (80%)
embolic (heart, carotid artery, aorta) or thrombosis of intracerebral arteries (see Carotid
Stenosis section, NSI9, and Neurology. N59)
Intracranial Hemorrhage (20%)
subarachnoid hemorrhage (SAH), spontaneous intracerebral hemorrhage (ICH),
intraventricular hemorrhage (IVH)
Subarachnoid Hemorrhage (SAH)
-,:..----...----
Definition
bleeding into subarachnoid space (intracranial vessels between arachnoid and pia)
Etiology
trauma (most common)
spontaneous
aneurysms (75-80%)
idiopathic (14-22%)
AVMs(5%)
coagulopathies (iatrogenic or primary), vasculitides, tumours (<5%)
Epidemiology
-10-28/100,000 population/year
peak age 55-60, 20% of cases occur under age 45
Risk Factors
hypertension
pregnancy/parturition in patients with pre-existing AVMs, eclampsia
oral contraceptive pill
substance abuse (cigarette smoking, cocaine, alcohol (debatable)
conditions associated with high incidence of aneurysms (see Intracranial Aneurysms
section, NSI8)
Clinical Features of Spontaneous SAH
sudden onset (seconds) severe headache: "worst headache of my life"
(up to 97% sensitive, 12-25% specific)
history of exertion is common (straining, intercourse)
nausea/vomiting, photophobia
meningismus (neck pain/stiffness, positive Kernig's and Brudzinski's sign)
decreased LOC (can include raised ICP, ischemia, seizure)
focal deficits: cranial nerve palsy (e.g. III, IV), hemiparesis
ocular hemorrhage in 20-40% (due to sudden raised ICP compressing
central retinal vein); subhyaloid/pre-retinal hemorrhages
reactive hypertension
sentineVwarningleaks
SAH-like symptoms lasting <1 day ("thunderclap H/A")
may have blood on CT or LP
-50% of patients with full blown SAH giw history suggestive of a warning leak
within past 3 weeks
differential diagnosis of severe HIA, onset within seconds: SAH; thunderclap H/A;
dissection/thrombosis of aneurysm; venous sinus thrombosis; benign exertional H/A
Investigations
non-contrast CT (see Figure 15)
98% sensitive within 12h, 93% within 24h; 100% specificity
may be negative if small bleed or presentation delayed several days
positive history for SAH with negative CT - MUST do LP (may be negative <12h)
acute hydrocephalus, IVH, ICH, infarct or large aneurysm may be visible
CT may also suggest site of aneurysm that has bled
o
..... ' ,
~ } - - - - - - - - - - - ,
Fisher Grade (SAH on CT scan)
Graae finding
1 Normal scan
<1 mm thick blood
>1 mm thick blood
IVH or ICH SAH
,
~ } - - - - - - - - - - - - - ,
Hunt and Hess Grade
(clinical grading scale for SAHI
Grade Description
1 No Sx or mild H/A and/or mild
meningismus
2 Features of 1t CN palsy
3 Confusion/lethargy, mild
hemiparesis or aphasia
4 GCS <15 but>8,
moderate-severe hemiparesis,
mild rigidity
Coma (GCS <9), decerebrate,
moribund appearance
Mortality of Grade 12 20%,
t with grade
.... ' ,
~ I - - - - - - - - - - - - ,
World Federation of Neurological
Surgeons grading of SAH
WFNS
Grade
GCS
Score
Aphasia.
Hemiparesis.
or Hemiphagia
O'
1 15
13-14
13-14
7-'2 tor -
5 3-6 tor -
, Intact aneurysm
Dr.JKR
NS16 Neurosurgery Cerebrovascular Disease Toronto Notes 2008
blood in
blood in blood in
interhemispheric
basal cisterns suprasellar cistern
fissure
,
,
blood on
blood 'in
surface of
sylvian
tentorium fissures
Figure 15. Diagnosis of SAH
lumbar puncture (LP) - findings (highly sensitive):
elevated opening pressure (>18 em H
2
0)
bloody initially, xanthochromic supernatant with centrifugation ("yellow") by
-12h, lasting 2 weeks
spectrophotometry is most sensitive for xanthochromia
RBC count usually>100,000/mm
3
without Significant drop from 1st to last tube
as in traumatic tap
protein elevated due to blood breakdown products
cerebral angiography ("gold standard for aneurysms")
demonstrates source of SAH in 80-85% of cases
"angiogram negative SAH": repeat angiogram in 7-14 days, if negative-+
"perirnesencephalic SAH"
magnetic resonance angiography (MRA) and CT angiography
emerging technologies, sensitivity may be up to 95% for aneurysms
BP
level of consciousness
limb movements
stiff neck
fundi
conscious, alert, no neurological findings.
I CT scan
fundi normal
,-
f
I
[ i ~ b a r puncture I ~ negative I
~ i ~ - e J
clear, colorless.
no microscopic blood
T----
C.;o;;;;-J
CTNMRNangiography
Figure 16. Approach to SAH
Treatment
admit to lCU or NICU
oxygen/ventilation pm
NPO, bed rest, elevate head of bed 300, minimal external stimulation, neurological
vitals qlh
aim to maintain sBP = 120-150 (balance of vasospasm prophylaxis, risk of re-bleed, risk
of hypotension since CBF autoregulation impaired by SAH)
IV NS with 20 mmol KCl/L at 125-150 cclh
phenytoin if seizure or temporal lobe clot
mild sedation pm
nimodipine for vasospasm neuroprotection --> 21 days; may d/c earlier if patient is
clinically well and ready for discharge
Dr.JKR
Toronto Notes 2008 Cerebrovascular Disease Neurosurgery NS17
cardiac rhythm monitor
Foley pm, strict ins & outs
4 vessel angiography, early surgery or coiling to prevent rebleed
Complications
vasospasm
definition: constriction of blood vessels in response to arterial blood clot outside
vessels at the base of the brain
clinical features: confusion, -J., LOC, focal deficit (speech or motor)
onset: 4-14 days post SAH (if deterioration within first 3 days, MUST look
"Triple H"Therapy for Vasospasm
for other cause)
Hypertension
"radiographic" vasospasm in 30-70% of arteriograms performed 7 days
Hypervolemia
following SAH (peak incidence)
Hemodilution
"symptomatic" vasospasm in 20-30% of SAH patients
detect clinically and/or with angiogram or transcranial Doppler (increased
velocity of blood flow), CBC/electrolytes/CT urgently to rio other causes
risk factors: large amount of blood on CT (i.e. high Fisher grade), smoking, l'
age, prior HTN
risk of cerebral infarct and death (biggest cause of morbidity and mortality in
patients who reach hospital)
treatment
"triple H" therapy (hypertension, hypervolemia, hemodilution) using
fluids and pressors (examples: norepinenphrine, phenylephrine)
angioplasty for refractory cases
hydrocephalus (15-20%) - due to blood obstructing arachnoid granulations or
subarachnoid space
can be acute or chronic - requiring intraventricular catheter or shunt
respectively
neurogenic pulmonary edema
hyponatremia - (SIADH, cerebral salt wasting)
diabetes insipidus
cardiac - arrhythmia (>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 moderate - severe disability
a major cause of mortality is rebleeding, for aneurysms:
risk of rebleed: 4% on first day, 15-20% within 2 weeks, 50% by 6 months
if no rebleed by 6 months risk decreases to same incidence of unruptured
aneurysm (2%)
only prevention is early clipping or coiling
rebleed risk for "perimesencephalic SAH" is - same as for general population
Intracerebral Hemorrhage (lCH)
- - ~ - ~ - - - - ~ - - -
Definition
hemorrhage within brain parenchyma, accounts for -10% 01' strokes
can dissect into ventricular system (NH) or through cortical surface (SAH)
Etiology
hypertension (usually 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,
NS20)
venous sinus thrombosis
arteriopathies (cerebral amyloid angiopathy, lipohyalinosis, vasculitis)
tumours (1%) - often malignant (e.g. GBM, lymphoma, metastases)
drugs (amphetamines, cocaine, EtOH, etc.)
coagulopathy (iatrogenic (coumadin, tPA), 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 (carotid endarterectomy, craniotomy)
idiopathic
Dr.JKR
NS18 Neurosurgery
Intemltionll Sublndmoid Aneurysm Trill
(lSAn of IlIUIUIagicII clipping VI. IlldOVIICU-
III coifing in 2143 petienlI with ruplUred
intraCllllilllllturysms: IlindomiZld trill
ILancet 2002; 360:1267-741
InllOduction: This randomized control trial aimed to
compare endovascular detachable coil treatment
against craniotomy and dipping for ruptured
intracranial aneurysms in patients who were consid-
ered eligible for either modality of therapy.
Mat!lods: 2143 patients were randomized to neuro-
surgical dipping In=10701 vs. treatment by endovas-
cular coilln=10731.The primary clinical outcome was
assessment using the modified Rankin scale for a
score of 3-6 (dependellCf or death) at 1year.
Results: Patients in this trial tended to be of good
dillital grade prior to in!mention and amajority of
aneurysms were in the anterior circulatory system.
190 out of 801123.7%1 patients who completed fol-
low up in the endovascular treatment were depend-
ent or dead at 1year compared with 243 of 793
130.6%1 in the neurosurgical treatment group
(p:O,0019j. This showed arelative risk reduction of
22.6% {95% CI8.9-34.21 and an absolute risk reduc-
tion of 6.9 (95 CI2.5-11.3) when comparing endovas-
cular to neurosurgical therapy,
Conclusion: In patients with aruptured intracranial
aneurysm who are suitable for either endovascular
coiling or neurosurgical clipping, the outcome of
dependellCf or death at one year favours the
endovascular coiling therapy. Further neuropsycho-
logical assessment is being planned in subgroups to
allow for subtle outcomes to be detected. Further fol-
low up for dependency death is planned as well.
Cerebrovascular Disease
Epidemiology
12-15 cases/lOO,OOO 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 EtOH use; cocaine, amphetamines
liver disease
Clinical Features
Toronto Notes 2008
rIA-like symptoms often precede ICH, can localize to site of impending hemorrhage
location: basal ganglia/internal capsule (50%), thalamus (15%), cerebral white matter
(15%), cerebellum/brainstem (15%)
gradual onset of symptoms over minutes to hours, usually during activity
H/A, vomiting, decreased LOC are common
specific symptoms/deficits depend on location of ICH
Investigations
high density blood on CT without contrast
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
phenytoin for seizure prophylaxis
follow electrolytes (SIADH common)
angiogram to rio vascular lesion UNLESS >45 yrs, known HTN, and
putamen/thalamic/posterior fossa ICH (yield - 0%)
surgical:
craniotomy with evacuation of clot under direct vision, resection of source of
ICH (Le. AVM, tumour, cavernoma), ventriculostomy to treat hydrocephalus
indications:
symptoms appear related to raised ICP or mass effect
rapid deterioration (especially with signs of brainstem compression)
favourable location, e.g. cerebellar, non-dominant hemisphere
young patient (<50 y.o.)
if tumour, AVM, aneurysm, or cavernoma suspected (resection or clip to
decrease risk of rebleed)
contraindications:
small bleed: minimal symptoms, GCS >10 (not necessary)
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 is 44%, mostly due to cerebral herniation
rebleed rate is 2-6%, higher if HTN poorly controlled
Intracranial Aneurysms
___- - - . . . . I ~ l ~
Epidemiology
prevalence -5% (20% are multiple)
female> male; age 35-65 years
Risk Factors
autosomal dominant polycystic kidney disease (15%)
fibromuscular dysplasia (7-21%)
AVMs
connective tissue diseases (Ehlers-Danlos, Marfan's)
FHx
bacterial endocarditis
Osler-Weber-Rendu syndrome
atherosclerosis and H1N
trauma
Dr.JKR
Toronto Notes ZOOS Cerebrovascular Disease Neurosurgery NS19
Types
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
fusifonn
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
Clinical Presentation
rupture (90%), most often SAH, but 30% ICH, 20% IVH, 3% subdural bleed
sentinel hemorrhage ("thunderclap H/A") ---+ IMMINENT RISK
mass effect (giant aneurysms)
internal carotid or anterior communicating aneurysm may compress:
the pituitary stalk or hypothalamus causing hypopituitarism
the optic nerve or chiasm producing a visual field defect
basilar artery aneurysm may compress midbrain, pons (limb weakness),
or CN III
posterior communicating artery aneurysm may produce CN III palsy
intracavernous aneurysms (CN III, IV, Vv V~ VI)
small infarcts due to distal embolization (amaurosis fugax etc.) IMMINENT RISK
seizures
headache (without hemorrhage)
incidental CT or angiography finding (asymptomatic)
Investigations
CT, magnetic resonance angiography (MRA), angiogram
Treatment
ruptured aneurysms:
overall trend towards better outcome with early surgery or coiling (48-96 hours
afterSAH)
choice of surgery vs. coiling not yet well defined, morphology/location can
aid decision
treatment options: surgical placement of clip across aneurysm neck, trapping
(clipping of proximal and distal vessels), thrombosing using Gugliemi
detachable coils (endovascular technique), wrapping as last resort
unruptured aneurysms:
1% annual risk of rupture: risk dependent on size and location of aneurysm
no clear evidence on when to operate: need to weigh life expectancy
risk of morbidity/mortality of SAH (20%/50%) vs. surgical risk (2%/5%)
generally treat unruptured aneurysms>10 mm
consider treating when aneurysm 7-9 mm in middle-aged, yow1ger patients or
patients with a family history of aneurysms
follow smaller aneurysms with serial angiography
Carotid Stenosis
Definition
narrowing of the internal carotid artery lumen due to atherosclerotic plaque
formation, usually near common carotid bifurcation into internal and external carotids
Risk Factors
for plaque formation: HTN, smoking, OM, cva or CAD, dyslipidemia
Clinical Features
may be asymptomatic
symptomatic stenosis may present as transient ischemic attack (TlA), reversible
ischemic neurologic deficit (RIND), or stroke
retinal insufficiency or infarct due to emboli occluding central retinal artery or
branches permanently or temporarily (amaurosis fugax)
middle cerebral artery (MCA) occlusive symptoms
Prevention of dbabling and fatal strokas by
succeuful carotid endarterectomy in patiants
w ~ h o u t recent neurolGgical symptoms: ran
domised controlled trial. - (lancet 2004;
363:14911502.)
Studr Asymptomatic Carotid Surgery TriaIIACST), a
randomized, controlled trial with followup at 5
years.
Patients: 3120 asymptomatic patienls with signifi
cant carotid artery stenosis were randomized equally
between immediate carotid endarterectomy ICEAI
and indefinite deferral of CEA and were followed for
up to 5years Imean 3.4 yearsl.
Main Outeome: Any stroke lincluding fatal or dis-
abling}.
Results: The risk of stroke or death within 30 days of
CEA was 3.1% (95% CI2.3-4.1). Comparing all
patients randomized to immediate CEA vs. deferral,
the 5-year stroke risks were 3.8% vs. 11% Igain 7.2%
[95% CI 5.0-9.41. p<tl.OOOll. This gain primarily
involved ischemic strokes in the carotid artery territo-
ry 12.7% vs. 9.5%; gain 6.8% [4.8-8.81, p<O.OOOI}, of
which h a ~ were disabling or fatal 11.6% vs. 5.3%;
gain 3.7% [2.1-5.21. p<O.OOOII. Combining the periop-
erative and the non-perioperative strokes, the net 5-
year risks were 6.4% vs. 11.8% for all strokes Igain
5.4% 13.0-7.81. p<D.O001}, 3.5% vs. 6.1% for fatal or
disabling strokes Igain 2.5% [0.8-4.31, p=O.OO4I, and
2.1% vs. 4.2% for fatal strokes Igain 2.1% [0.6-3.61.
p--o.0061.
Cone/u,ion,: In asymptomatic patients with signifi-
taTll talo\\iI .1\ery menosis, immeiliate CEA reduced
the net 5-year stroke risk from about 12% to about
6%. Half of this 5-year benefit involved disabling or
fatal strokes.
Dr.JKR
NS20 Neurosurgery Cerebrovascular DiseaseNascular Malfonnations Toronto Notes 2008
EndIrtmctomy for Asymptomatic Carotid
AI1Iry SlInoIis - (JAMA 1995; 273:14211428.1
Sludy: Asymptomatic Carotid Atherosclerosis
Study (flCASl, aprospective, randomized, multi
centretri.J1.
Patients: 1662 patients with carotid
artery stenosis of 60% or greater were randomized.
Follow-up data are available on 1659. Recognized
ri51: factors for stroke were similar be1ween Ilie two

.Daily aspirin administration and
medical ri51: factor management for all patients and
carotid endarterectomy for patients randomized to
SlJrgery.
IIIin 0IIfl:0mI: TlA or cerebral infarction occurring
in the carotid artery territory and any TIA, stroke, or
dealli occurring in the perioperative period.
IIauIII:The risil for ipsilateral stroke and any peri
operative stroke or death based on a5-year follow
up lmedian of 2.7 yearsl was estimated to be 5.1%
for surgical patients and 11.0% for patients treated
medically (aggregate risk reduction of 53% (95%
CI=2272%1),
CencIuaIotlI: Patients with asymptomatic carotid
artery of 60% or greater that are good can
didates for elective surgery will have areduced 5-
year risl: of ipsilaterai stroke if carotid endarterecto-
my is perlormed in addition to aggressive manage-
ment of modifiable risl: factors.
Investigations
CBC, PIT, INR (hypercoagulable/hyperviscous states)
fundoscopy > cholesterol emboli in retinal vessels (Hollenhorst plaques)
auscultation over carotid bifurcation for bruits
carotid duplex Doppler ultrasound: determines size of lumen and blood flow
velocity, safest but least accurate, unable to scan above mandible
angiogram: "gold standard", 1/200 risk of stroke
MRA: safer than angiogram, may overestimate stenosis
CT angiogram (CTA)
Treatment
control of HTN, lipids, diabetes (risk factor management)
antiplatelet agents (ASA dipyridamole, clopidogrel) -25% relative risk reduction
carotid endarterectomy (generally if symptomatic and >70% stenosis, see Prognosis)
endovascular angioplasty stenting (utility being evaluated)
Prognosis
Table 3. Symptomatic Carotid Stenosis: North American Symptomatic Carotid
EndarterectomyTrial (NASCET)
% Stenosis on Angiogram Risk of Major Stroke or Death
Medical Rx Medical +Surgical Rx
70-99 % 26% over 2years 9% over 2years
50-69% 22% over 5years 16% over 5years
<50% Surgery has no benefit with 5% complication rate
Table 4. Asymptomatic Carotid Stenosis: Asymptomatic Carotic Atherosclerosis Study
(ACAS) and Asymptomatic Carotid SurgeryTrial (ACsn
% Stenosis on Angiogram Risk of Major Stroke or Death
Medical Rx Medical + Surgical Rx
60-99% 11% over 5years 5.1% over 5years (ACASl
70-99% 11.8% over 5years 6.4% over 5years (ACSn
.... ,
.)---------,
Spetzler-Mertin AVM
Grading Scale
Item Score
Size
D-3cm
3.1-6.0 cm
>6cm
Location
Noneloquent
Eloquent 1
Deep venous dreinage
Not present 0
Present 1
AVM grades calcu/aled by adding 1Ile 3individual
SpetzIer-Manin Scale scores from 1Ile above table.
Vascular Malformations
Types
arteriovenous malformations (AVMs)
cavernous malformations (cavernoma, cavernous hemangioma/angioma)
venous angioma
capillary telangiectasias
arterio-venous fistula (AVF) (carotid-cavernous fistula, dural AVF, vein of Galen
aneurysm)
"angiographically occult vascular malformations" (any type, 10% of malformations)
clinical Significance:
principally AVMs and cavernous malformations produce intracranial
hemorrhages and seizures
Arteriovenous Malformations (AVMs)

Definition
tangle of abnormal vessels/arteriovenous shunts, with no intervening capillary beds or
brain parenchyma
congenital, tend to enlarge with increasing pressures and with age
Epidemiology
prevalence -0.2%, male:female = 2:1, average age at diagnosis = 33 years
Clinical Features
hemorrhage (40-60%) - small AVMs have more direct high pressure AV connections
-> bleed more
seizures (50%) - more common with larger AVMs
mass effect
focal neurological signs secondary to ischemia (high flow -> "steal phenomena")
localized headache, increased ICP
bruit (especially with dural AVMs)
may be asymptomatic ("silent")
Dr.JKR
Toronto Notes 2008 Vascular Malformations/DermatomesIMyotomes Neurosurgery NS21
Investigations
MRl (flow void), MRA
angiography (7% will also have an aneurysm)
Treatment
decreases risk of future hemorrhage and seizure
surgical excision is treatment of choice for grade I and II lesions
endovascular embolization (glue, balloon) can facilitate surgery or stereotactic
radiosurgery (SRS) for suitable grade II to V lesiono:;
SRS is treatment of choice for small (-S3 em in diameter) grade I and II lesions
surgery alone is unsuitable for grade IV and V lesions
conservative (e.g. palliative embolization, seizure control if necessary)
Prognosis
10% mortality, 30-50% morbidity (serious neurological deficit) per bleed
risk of major bleed: 2-4% per year (untreated AVMs)
Cavernous Malformations
Definition
benign vascular hamartoma consisting of irregular sinusoidal vascular channels
located within the brain
Epidemiology
0.1-0.2%, both sporadic and hereditary forms described
Clinical Features
seizures (60%), progressive neurological deficit (50%), hemorrhage (20%), H/A
hemorrhage risk less than AVM, usually minor bleeds
Investigations
MRl (non-enhancing)
usually not seen witb angiography
Treatment
surgical excision - depending on presentation and location (supratentorial lesions
are less likely to bleed than infratentoriallesions)
EXTRACRANIAL PATHOLOGY
Dermatomes/Myotomes

-1J;II; L2
L3
L4
L5
L1
L4 L2
'L3
L5 L4
/ L5
"'-, ,

Important Dermatomes and
Myotomes
C2 - angle of jaw
C4 - collar of shirt
"C3,4.5 keeps the diaphragm alive"
T4 - nipple line
T6- xiphoid
Tl0 - umbilical
T12 - suprapubic
"L3 above the knee"
"$2,3,4 - keeps your stool off the floor"
Figure 17. Dermatomes
Dr.JKR
NS22 Neurosurgery
.... ' ,
9)------------,
Myotom..
C5 - Shoulder abduction/elbow flexion
C6 - Wrist extensors
C7 - Elbow extension
C8 - Squeeze hand
T1 - Abduct fingers
T2-9 -Intercostal (Abdominal reflexesl
T9-10 - Upper abdominals
T1112 - Lower abdominals
L2 - Flex hip
L3 - Hip adduction
l4 - Knee extension
l5 - Dorsiflex ankle
Sl - Plantarflex fool

Reflexes
1,2 tie my shoe. 512 Ankle jerit
3, 4kid. the door >l3-4 Knee
5, 6pick up sticks. C56 Biceps/Brachioradialis
7. Slay them straight> C7STrieeps
DermatomeslMyotomes/Approach to LimblBack Pain
Table 5. Myotomal Distribution of Nerve Roots
Roots
C14
C3, 4, 5
C5,6
C5,6
C6,7
C7,8
ca,Tl
ca,Tl
T2-9
T9.10
T11,12
Lt, 2. 3
L2,3,4
L4,5
L5, 51, 52
L5,51
51,52
52,3,4
Movement/action
Neck flexion, extension, rotation
Inspiration,lV, FEV, VC
Abduct arm
Flex and supinate forearm
Wrist extension
Forearm extension
Grasp
Abduct/adduct fingers
Hip flexion
Leg extension
Ankle dorsiflexion
Leg flexion
Great toe extension
Foot plantar flexion
Clamp down during rectal exam
Reflex
Biceps, brachioradialis
Supinator
Triceps
Finger jerk
Abdominal cutaneous reflex
Abdominal cutaneous reflex
Cremasteric
Knee jerk
Medial hamstring
Achilles tendon
(ankle jerkl
Anal cutaneous
Nerve
Cervical
Phrenic
Axillary
Musculocutaneous
Radial
Radial
Anterior interosseus
Ulnar
Intercostal
Upper abdominals
Lower abdominaIs
Femoral
Femoral
Deep peroneal
Sciatic
Deep peroneal
Tibial
Pudendal
Toronto Notes 2008
Muscle
Deep neck
Diaphragm
Deltoid
Biceps brachii, brachioradialis
Extensor carpi radialis
Triceps brachii
Flexor digitorum profundus
Interossei
Intercostals
Iliopsoas
Quadriceps
Medial hamstring, tibialis anterior
Biceps femoris, semitendinosus,
semimembranosus
Extensor hallucis longus
Soleus, gastrocnemius
Bladder, lower bowel, anal sphincter
Approach to LimblBack Pain
I
Pain
I
Back pain
(above gluteal fold)
I Neuropathy r
(below gluteal foldl
OR2t
--r L..'''i' I see Orthopaedics
(any limb)
With exertion or
sustained position

dependent

/ t -----..
Vascular claudicetion
Perip/leral nerve
Neurogenic Cord Root
- sclerotomal pain and
lperipherel neuropathy)
claudication (myelopathy) (radiculopathy)
sensory deficit
- non-dermatomaV
- dermatomal pain - LMN signs! -LMN signs!
- reproduced by fixed
myotomal
and sensory deficit symptoms symptoms
amount of exercise
- sclerotomal
- exercise or posture - UMN signs!
- immediately relieved
- autonomic
induced symptoms
with
dysfunction
- prolonged reliefl below lesion
rest or standing
posture dependent
- signs of poor vascular
(need to sitl
supply to limb
Figure 18. Approach to Limb/Back Pain
Dr.JKR
Toronto Notes 2008 Approach to LimbfBack Pain
Clinical Features
local pain at site of lesion
radiculopathy (LMN)
fascieulations, atrophy
motor: flaccid, weakness, decreased deep tendon reflex in root distribution
sensory: dermatomal .J,. pinprick sensation, numbness, paresthesia, pain
trophic changes: e.g. dry skin (if long-standing radieulopathy)
myelopathy
LMN signs/symptoms at level of lesion
UMN signs/symptoms below lesion
arms flexed, legs extended
motor: proximal weakness and spasticity of lower extremities, increased
reflexes, clonus, Babinski sign (extensor plantar response), l-:loffman's
sign (cervical), sphincter disturbance (decreased tone/sensation)
sensory: findings may be minimal (reduced vibration, proprioception),
Lhermitte sign (shock sensation radiating down arms or legs with
neck flexion)
Investigations
plain x-ray of spine, CT, MRl, myelogram, electromyography (EMG),
electrophysiology
Extradural Lesion
Cervical Stenosis (Cervical Spondylosis)
etiology: combination of factors
congenital spinal stenosis, degenerative disc process leading to osteophytes and
central disc herniation
hypertrophy of lamina/dura/facets/ligaments
subluxation, increased mobility, loss of normal spinal eurvature
epidemiology: increasing age (usually >50)
clinical features:
radieulopathy (at level of lesion)
AND/OR myelopathy (usually if >30% canal stenosis, below level of lesion)
AND/OR pain/paresthesia in neck/head/shoulders
investigations: x-ray of cervical spine flexion/extension views, MRl, CT/
myelogram
treatment:
analgesics, collar
surgery - indications: myelopathy, progressive neurologic impairment,
intractable pain, <1 year since presentation
prognosis:
myelopathy - 48% improve if treated within 1 year, 16% after 1 year
radieulopathy - variable, but better results than myelopathy
Intradural Intramedullary Lesion
Syringomyelia
definition: "syrinx", cavitation of spinal cord substance
etiology: congenital, neoplastic, post-traumatic
congenital craniovertebral anomalies (e.g. Chiari malformation,
myelomeningocele, tethered cord)
intramedullary tumours
arachnoiditis (traumatic)
clinical features:
suspended, dissociated sensory loss
pain and temperature loss in a cape-like distribution at level of cervical syrinx
preserved light touch and other modalities
LMN arm/hand weakness or wasting
may have spastic weakness of legs
may have hydrocephalus, often asymptomatic
painless arthropathies (Charcot's joints)
investigations: MRI is best method, myelogram with delayed CT
treahnent:
conservative if NOT progressing
treat underlying cause (e.g. posterior fossa decompression for Chiari 1, surgical
removal of tumour if causing a syrinx)
prognosis: progressive deterioration in>1/3 despite therapy
Neurosurgery NS23
RED FLAGS for back pain -
"BACK PAIN":
Bowel/bladder dysfunction
Anesthesia (saddle)
Constitutional symptoms (fever,
night sweat, chills, weight loss)
IKlhronic disease
Paresthesia
Age >50
IV drug use
Neuromotor deficits
Figure 19. T, weighted
MRI of Syringomyelia
Dr.JKR
NS24 Neurosurgery Spinal Cord Syndromes Toronto Notes 2008
... '
.l--------------,
,
Compartmentalize spinII cord ayncIromM
anatomically by location.
o
o
~ ) .
~ ,
The pattern of impairment in
Central Cord Syndrome is
uMUO":
Motor> sensory loss
Upper> lower extremity
Distal> proximal
Spinal Cord Syndromes
see Neurology. N2 for Spinal Cord Anatomy
Complete Spinal Cord Lesion
bilateral loss of motor/sensory and autonomic function at ;::4 segments below
lesion/injury, with UMN signs
Incomplete Spinal Cord Lesion
any residual function at ;::4 segments below lesion
signs include sensory/motor fimction in lower limbs and "sacral sparing" (perianal
sensation, voluntary rectal sphincter contraction)
syndromes include Brown-Sequard's, central cord, anterior cord and posterior cord
Brown-Sequard Syndrome
hemisection of spinal cord (lateral compression of one half of spinal cord)
common causes:
trauma, tumour (extrinsic compression)
Signs and Symptoms
motor
ipsilateral loss of voluntary motor function below level of lesion with UMN signs
ipsilateral LMN signs at level of lesion
sensory
ipsilateral loss of vibration and proprioception; contralateral loss of pain
and temperature below level of lesion; "suspended" ipsilateral deficits (deficits
are 1 to 2 levels below injury - Lissauer's tract)
preserved light touch
prognosis
best prognosis of cord injuries (90% ambulate independently and have good
sphincter control)
Anterior Cord Syndrome
common causes
anterior spinal artery territory compression or occlusion (anterior spinal artery
supplies anterior 2/3 of cord)
Signs and Symptoms
motor
bilateral paraplegia (UMN below and LMN at level of lesion)
sphincter dysfunction (urinary retention)
sensory
bilateral loss of pain and temperature below level of lesion with preserved light
touch, vibration and proprioception (dissociated sensory loss)
Central Cord Syndrome
most common incomplete spinal cord injury syndrome
common causes:
syringomyelia (progressive central cord cavitation), central tumours, spinal
extension injuries
Signs and Symptoms
motor
bilateral motor paresis; upper (LMN lesion) > lower (UMN lesion) extremities;
more pronounced in the hands
sensory
variable bilateral suspended sensory loss (dissociated sensory loss - pain and
temperature loss greater than vibration and proprioception loss)
intact sensation aoove and below affected dermatomes; sacral sparing
other
bowel and/or bladder dysfunction is usually a late manifestation
prognosis
50% recover enough lower extremity function to ambulate, 90% ambulate
within 5 days, hand recovery variable
Dr.JKR
Toronto Notes 2008 Spinal Cord SyndromesfRoot Compression Neurosurgery S25
Posterior Cord S ndrome
[
o
common causes
posterior spinal artery infarction, trauma
Signs and Symptoms
motor
preserved motor function
sensory
bilateral loss of vibration and proprioception below level of lesion
preserved pain and temperature
prognosis
more favourable than anterior cord syndrome
Root Compression
Differential Diagnosis
herniated disk
neoplasm (neurofibroma, schwannoma)
synovial cyst, abscess
hypertrophic bone/spur
Cervical Disc Syndrome
Etiology
nucleus pulposus herniates through annulus fibrosis and impinges upon nerve root
Epidemiology
most common levels C6-C7 (C7 root) > C5-C6 (C6 root)
Clinical Features
pain down arm in nerve root distribution, worse with neck extension, ipsilateral
rotation and lateral flexion (all compress the ipsilateral neural foramen)
LMN signs/symptoms
..... ' ,
central cervical disc protrusion causes myelopathy as well as nerve root deficits
.\-----------,
Investigations Disc herniations impinge the nerve
C-spine x-ray, CT, MRl (procedure of choice), EMG, nerve conduction studies root at the level below the inter-
space in the cervical spine (i.e. C5-
Treatment
6 disc affects the C6 nerve root)
conservative
no bedrest unless severe radicular symptoms
activity modification, patient education (reduce sitting, lifting)
physiotherapy (PT), exercise programs
analgesics; collar, traction may help
surgical indications
intractable pain despite adequate conservative treatment for >3 months
progressive neurological deficit
anterior cervical discectomy is usual surgical choice
Prognosis
95% improve spontaneously in 4 to 8 weeks
Table 6. lateral Cervical Disc Syndromes
C4-5 C5-6 C6-7 C7-T1
Root Involved C5 C6 C7 C8
Incidence 2% 19% 69% 10%
Sensory Shoulder Thumb Middle finger Ring finger, 5th finger
Motor Deltoid, biceps, Biceps Triceps Digital flexors,
supraspinatus intrinsics
Reflex No change Biceps, Triceps Finger jerk
Brachioradialis
Dr.JKR
----------------
NS26 Neurosurgery Root Compression Toronto Notes 2008
[uml)ar Disc Syn(lrome
o
Figure 20. T
2
-weighted MRI of
Lumbar Disc Herniation
Etiology
same as cervical disease (laterally: compressing nerve root, centrally: cauda equina)
Epidemiology
common (>95% of herniated lumbar disks) - L5 and S1 roots
Clinical Features
leg pain> back pain
limited back movement (especially forward flexion) due to pain
symptoms and signs of radiculopathy (LMN)
reflex paravertebral muscle spasm (functional scoliosis, loss of lordosis)
nerve root tension signs:
straight leg raise (SLR: Lasegue's test), crossed SLR ---+ LS, Sl roots
femoral stretch ---+ L4 root
Investigations
x-ray spine (only to rule out other lesions), CT, MRl
myelogram and post-myelogram CT (if surgery contemplated and plain CT not
conclusive)
Treatment
conservative (same as cervical disc disease)
surgical indications
same as cervical disc + cauda equina syndrome
Prognosis
95% improve spontaneously within 4 to 8 weeks
Table 7. Lateral Lumbar Disc Syndromes
1.34 L4-5 L5-S1
Root Involved L4 L5 S1
Incidence <10% 45% 45%
Pain Femoral pattern Sciatic pattern Sciatic pattern
Sensory Medial leg Dorsal foot to hallux Lateral foot
lateral leg
Motor Tibialis anterior (dorsiflexion) Extensor hallucis longus Gastrocnemius, soleus
(hallux extension) (plantar flexion)
Reflex Knee jerk Medial hamstrings Ankle jerk
Cauda Equina Syndrome
-----------------'
Etiology
compression of lumbosacral nerve roots below conus medullaris
large central herniated disc (L4-5 or L5-S1) spinal stenosis, extrinsic mass
Clinical Features
motor (LMN signs)
weakness/paraparesis in multiple root distribution
reduced deep tendon reflexes (knee and ankle)
sphincter disturbance (urinary retention and fecal incontinence due to loss of
anal sphincter tone)
sensory
pain in back radiating to legs
bilateral sensory loss or pain: involving multiple dermatomes
saddle anesthesia (most common sensory deficit)
sexual dysfunction (late finding)
Treatment
requires urgent investigation and decompression 48 hrs) to preserve bowel and
bladder function
Dr.JKR
--------------
Toronto Notes 2008 Root Compression/Peripheral Nerves Neurosurgery NS27
___________~ _ ~ _ - - l
Lumbar SRinal Stenosis
Etiology
congenital narrowing of spinal canal combined with degenerative changes
(herniated disk, hypertrophied facet joints and ligaments)
Clinical Features
neurogenic claudication - 60% sensitive
neurologic exam may be normal, including straight leg raise test
often absent Achilles reflexes and diminished knee jerks
symptoms relieved only by changing position (leaning forward, sitting down)
Investigations
spine x-ray, CT, MRl, myelogram
Treatment
conservative - NSAIDs, analgesia
surgical -laminectomy with root decompression
enic Claudication
Etiology
ischemia of lumbosacral nerve roots secondary to vascular compromise and
increased demand from exertion, often associated with lumbar stenosis
Clinical Features
dermatomal pain/paresthesia/weakness of buttock, hip, thigh, or leg initiated by
standing or walking
slow relief with postural changes (sitting >30 min), NOT simply exertion cessation
induced by variable degree of exercise or standing
may be elicited with lumbar extension, but may not have any other neurological
findings, no signs of vascular compromise (e.g. ulcers, poor capillary refill, etc.)
Investigations
bicycle test may help distinguish neurogenic claudication (NC) from vascular
claudication (with the waist flexed individuals with NC can last longer)
Treatment
same as for lumbar spinal stenosis
Peripheral Nerves
Clinical Features
peripheral polyneuropathy vs. peripheral nerve injury (entrapment/trauma)
sclerotomal distribution (non-dermatomallmyotomal)
loss of sensation, paraesthesia
sensory deficits often symmetric, glove and stocking
motor weakness
trophic changes: cold extremities, cutaneous hair loss, brittle nails
autonomic changes: local vasoconstriction (hypohidrosis) --> edema --> vasodilation
(hyperhidrosis)
Peripheral Nerve Inju
Classification and Clinical Course
neuropraxia: nerve intact but fails to function, recovery within hours to months
axonotmesis: axon disrupted but nerve sheath intact --> Wallerian degeneration (of
axon segment distal to injury) --> recovery -1 mm/day
neurotmesis: nerve completely severed, need surgical repair for recovery
Investigations
radiologic (C-spine, chest/bone x-rays, myelogram, CT, MRl), bloodwork (CSF)
electrophysiological studies (EMG, nerve conduction velocities (NCV)) may be helpful
in assessing nerve integrity
Treatment
surgical repair of nerve sheath unless known to be intact (suture nerve sheaths or
nerve graft)
.... ' ,
."l----------,
Spinal cord ends at L1-2; dura
ends at 51-2
.... ' ,
.}--------------..,
Key Features of Neurogenic vs.
V.scular Claudication
Neurogenic Claudication: der-
matomal distribution with positional
relief occurring over minutes
Vascul.r Claudication: sclerotomal
distribution with relief occurring with
rest over seconds
.,;.
Differential Diagnosis for Peripheral
Neuropathy - "DANG THERAPIST"
Diabetes or Drugs
Alcohol or AIDS
Nutritional (8'2 deficiency)
Guillain-8arre Syndrome
Traumatic
Hereditary (Refsum's)
Endocrine or Entrapment
Renalluremia)
Amyloid
Porphyria
Infectious
Sarcoid
Toxins
Dr.JKR
NS28 Neurosurgery Peripheral Nerves Toronto Notes 2008
L
o
if sharp transection may consider primary repair
most cases are dealt with in a delayed fashion
conditions for ideal healing/regeneration
nerve transected sharply
clean wound
optimal surgical facilities
optimal cell metabolism
possible spontaneous recovery/regeneration
delay surgical repair for a few weeks if first 3 conditions are not met
Nerve Entrapment
definition: nerve compressed by nearby anatomic structures, often secondary to
localized, repetitive mechanical trauma with additional vascular injury to nerve
clinical features: sensory loss in nerve distribution (often discriminative touch lost
first)
Carpal Tunnel Syndrome (CTS)
see Plastic Surgery. PL17
Ulnar Nerve Entrapment at Elbow
etiology: may be entrapped at several locations:
behind medial epicondyle
at medial intermuscular septum
distal to elbow at cubital tunnel
epidemiology: second most common entrapment neuropathy
clinical features
sensory: pain, numbness in ulnar 1.5 fingers
wasting of interossei (especially first dorsal interosseous)
weakness (especially abduction of index finger) - Wartenberg's sign
claw hand
Tiner's sign from percussion of elbow (does not localize site of entrapment)
dislocation of ulnar nerve may be palpated at medial epicondyle with elbow
flexion/extension
investigations: NCV ---> conduction delay across elbow
treatment
conservative: prevent repeated minor trauma (e.g. leaning on elbow or sleeping
with hand under head), elbow pads, NSAIDs
surgical: nerve decompression and transposition anterior to medial epicondyle
Less Common Entrapments
Brachial plexus
Erb's palsy ("Bellhop's tip position"): C5-6 injury; arm hangs at side, internally
rotated, extension at elbow
Klumpky's palsy: C8-Tl injury; clawed hand and wasting of small muscles of
hand, flexed elbow
Thoracic outlet syndrome
compression of the lower portion of the brachial plexus (which supplies the
ulnar nerve) as it emerges from the axilla, through a narrow passage beneath the
clavicle and between the anterior and middle scalene muscles, while resting on
the first rib
CXR to rule out Pancoast tumour (associated with Homer's syndrome) as this
may mimic thoracic outlet syndrome, congenital cervical rib
Radial nerve ("Saturday Night Palsy")
more often a pressure palsy (compression of axilla)
weakness of wrist and finger extensors (normal triceps)
Motor branch of ulnar nerve at wrist (Guyon's canal)
same as ulnar nerve entrapment but no sensory deficit on dorsum of hand
Common peroneal nerve
superficial and fixed behind fibular neck (sensitive to trauma, e.g. fracture)
motor: decreased foot and toe extension ("foot drop"), decreased ankle eversion
sensory: decreased lateral foot and dorsum (less common)
Lateral cutaneous femoral nerve of the thigh ("meralgia paraesthetica")
pain over anterior/lateral aspect of thigh
common in obese people, patients post-iliac bone grafts
Posterior tibial nerve ("tarsal tunnel")
pain/paresthesia in toes and sole of foot clawing of toes (Tiner's sign over
medial malleolus)
Dr.JKR
Toronto Notes 200S Neurotrauma
SPECIALTV TOPICS
Neurotrauma
Trauma Management (see also Emergenc;y Medicine. ER6)
Trauma Assessment
INITIAL MANAGEMENT
ABC's of trauma management take priority
see Emergenc;y Medicine. ER2
NEUROLOGICAL ASSESSMENT
Mini-History
period of LOC, post traumatic amnesia, loss of sensation/function, type of injury/
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)
brainstern (breathing pattern, CN palsies)
cranial nerve exam
motor exam, sensory exam (only if GCS is 15), reflexes
sphincter tone
record and repeat neurological exam at regular intervals
Investigations
CT,L-spine x-rays
AP, lateral, odontoid views for C-spine (must see from Cl to T1
(swimmer's view if necessary)) or CT
oblique views looking for pars interarticularis fracture ("Scottie dog" sign)
CT head and upper C-spine (whole C-spine if patient unconscious) look for fractures,
loss of mastoid or sinus air spaces, blood in cisterns, pneumocephalus
Type and cross-match, ABG, CBC, drug screen (especially alcohol)
chest and pelvic x-ray as indicated
TREATMENT
Treatment for Minor Head Injury
see also Canadian CT Head Rule sidebar, Emerenc;y Medicine. ER8)
observation over 24-48 hours
wake every hour
judicious use of sedatives or pain killers during this monitoring period
Treatment for Severe Head Injury (GCS :::;8)
clear airway and ensure breathing (intubate if necessary)
secure C-spine
maintain adequate BP
monitor to detect complications (GCS, CT, ICP)
monitor and manage increased ICP if present (see Herniation, NS6)
pharmacotherapy: anticonvulsants x 7 days, calcium channel blocker (CCB) for adult
cases only
repair dural tears (>7 days)
Treatment of Spinal Injury
reduce dislocation if present by traction or surgery
stabilize spine if unstable (halo vest, fusion, etc.)
MRJ if neurological deficit is present to rule out cord compression
Neurosurgery NS29
"" ' ,
.}-------------,
Glasgow Coma Scale
Eye IlIIponse VerbIIIItesponse Motor IlIIponse
4spontaneous 5oriented 6obeys commands
3opens eyes to 4confused 510calires to pain
voioe 3inappropliate words4 withdraws from
2opens eye to 2incomprehensible pain
pain soonds 3flexion to pain
1no eye opening 1no response (decorticate
posturingl
2e x t e n ~ o n t o
pain (decerebrate
posturingl
1no response
"'.
Assessment of Spine CTlXray
(parasagittal view) - "ABCDS
Alignment (Columns: anterior vertebral
line, posterior vertebral line, spinolami-
nar line, posterior spinous line)
Bone (vertebral bodies, facets, spinous
processes)
Cartilage
Disc (disc space and interspinous space)
Soft tissues
Dr.JKR
NS30 Neurosurgery
Vl/hich patients need CT head or
transfer to aneurosurgical center?
remains unconscious after resuscitation
focal neurological signs
deteriorating
It'
Layer. of Scalp - "SCALP"
Skin
Connective tissue (dense)
Aponeurosis (galea)
Loose connective tissue
Periosteum
Neurotrauma Toronto Notes 2008
emergent surgical decompression and/or fusion if necessary (i.e. patient with
neurological deterioration)
more likely to be beneficial in incomplete cord injury
emergent surgery contraindicated for: complete spinal cord injury >8 hours,
medically unstable patient, and central cord syndrome
urinary catheter, shifting in bed q2h, physiotherapy long-term
high dose methylprednisolone (controversial)
Which patients should be admitted to hospital?
skull fracture
indirect signs of basal skull fracture
confusion, impaired consciousness
focal neurological signs
extreme headache, vomiting
seizures
concussion with >5 minutes amnesia
unstable spine
use of alcohol
poor social support (i.e. no friend/relative to monitor for next 24 hours)
if there is any doubt, especially with children
KEY POINTS
never do lumbar puncture in head injury
all patients with head injury have C-spine injury until proven otherwise
don't blame coma on alcohol- 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)
Head Injury
-""--------------------_.....-
Scalp Injury
rich blood supply
considerable blood loss (vessels contract poorly when ruptured)
minimal risk of infection due to rich vascularity
Skull Fractures ~
depressed fractures ---> double density on skull x-ray (outer table of depressed segment
below inner table of skull), CT with bone windows is gold standard
simple fractures (closed injury) ---> no need for antibiotics, no surgery
compound fractures (open injury) ---> increased risk of infection, surgical debridement
within 24 hours is necessary
internal fractures into sinus ---> meningitis, pneumocephalus, risk of operative
bleed may limit treatment to antibiotics
basal skull fractures ---> not readily seen on x-ray, rely on clinical signs
retroauricular ecchymoses (Battle's sign)
periorbital ecchymoses (raccoon eyes)
hemotympanum
CSF rhinorrhea, otorrhea (suspect CSF if halo or target sign present)
suspect with Lefort II or ill midface fracture (seen on imaging)
Cranial Nerve Injury
most traumatic causes of cranial nerve injury do not warrant intervention and have
at least minimal improvement
surgical intervention:
CN II -local eye/orbit injury
CN ill, IV, VI - if herniation secondary to mass
CN VIII - repair of ossicles
CN injuries that improve:
CN I - recovery may occur in a few months; most do not improve
CN ill, IV, VI - majority recover
CN VII - recovery with delayed lesions
CN VITI - vestibular symptoms improve over weeks, deafness usually
permanent (except when resulting from hemotympanum)
Dr.JKR
Toronto Notes 2008 Neurolraurna
Arterial Injury
e.g. carotid-cavernous (C-C) fistula, carotid/vertebral artery dissection
Intracranial Bleeding
(see Blood, NS13 and Cerebrovascular Disease, NSI5)
Brain Injury
Primary Impact Injury
mechanism of injury determines pathology: penetrating injuries, gunshot wounds
low local damage
high velocity -. distant damage possible (due to wave of compression),
concussion
American Academy of Neurology (AAN) definition of concussion: "a trauma-induced
alteration in mental status that mayor may not involve loss of consciousness"
AAN Classification:
Grade 1: altered mental status <15 min
Grade 2: altered mental status>15 min
Grade 3: any loss of consciousness
no parenchymal abnormalities on CT
coup (damage at site of blow)
contre-coup (damage at opposite site of blow)
acute decompression causes cavitation followed by a wave of acute compression
contusion (hemorrhagic)
high density areas on CT mass effect
commonly occurs with brain impact on bony prominences (inferior frontal lobe,
pole of temporal lobe)
diffuse axonal injury/shearing
may tear blood vessels ---> hemorrhagic foci
wide variety of damage results
all brain injury causes shear
often the cause of decreased LOC if no space occupying lesion on CT
Secondary Pathologic Processes
1/3 of in-hospital mortalities following head injury were able to talk after the injury
delayed and progressive injury to the brain due to:
edema
intracranial hemorrhages
ischemia/infarction
raised rcp
Extracranial Conditions
hypoxemia
trauma: chest, upper airway, brainstem
exceptionally damaging to traumatized brain cells
leads to ischemia, raised rcp
hypercarbia
leads to raised rcp (secondary to vasodilation)
systemic hypotension
caused by blood loss, not by head injury (e.g. ruptured spleen)
cerebral autoregulation lost in trauma
leads to decreased CPP, ischemia
hyperpyrexia
leads to increased brain metabolic demands ---> ischemia
fluid and electrolyte imbalance
iatrogenic (most common)
syndrome of inappropriate antidiuretic hormone (SlADH) secretion (from head
injury)
diabetes insipidus (Dr) from head injury
may lead to cerebral edema and raised rcp
coagulopathy
Intracranial Conditions
raised rcp due to traumatic cerebral edema OR traumatic intracranial hemorrhage
Neurosurgery NS31
... ' ,
9}-----------,
AAN Classification
Grade 1: altered mental status <15 min
Grade 2: altered mental status> 15 min
Grade 3: any loss of consciousness
Management Associated AAN Concussion
Grades
AANGrede Management Options
1 Examine 15min for amnesia and other
symptoms
Return to normal activity it symptoms
clear within 15mins
Remove from activity for 1day, then
reexamine
CT or MRI if HlA or other symptoms
worsen or last>1week
Return to normal activity after 1week
without symptoms
Emergent neuro exam t imaging
If initial exam is normal, may go
home with close follow up
Admit if any signs of pathology or
persistent abnormal mental status
CT or MRI if H/A or other symptoms
If brief concussion 1(1 mini, return to
normal activity after 1week without
symptoms
If prolonged concussion 1>1 min),
return to normal activity only after 2
weeks wnhout symptoms
Coup

Figure 21. CT Showing
Coup-Contre-Coup Injury
... ,,
9}-----------,
SIAOH -> hyponatremia,
01-> hypernatremia
Dr.JKR
NS32 Neurosurgery
.....
Type 2 I \
, I
0
Hidenori Miyagawa 2006
Figure 22. Odontoid Fracture
Classification D-,r
Neurotrauma Toronto Notes 200S
Late of HeadIBrain
seizures
5% of head injury patients develop seizures
incidence related to severity and location of injury -> increased with local brain
damage or intracranial hemorrhage
post-traumatic seizure may be immediate, early, or late
presence of early (within first week) post-traumatic seizure raises incidence of
late seizures to 25%
meningitis: associated with CSF leak from nose or ear
hydrocephalus: acute hydrocephalus or delayed normal pressure hydrocephalus (NPH)
see Orthopaedics. ORlO and Emergency Medicine. ER9
Vertebral Column (See Assessment of Spine sidebar, NS29)
stable fracture
compression fracturf'
unstable fracture
burst fracture (note: not all burst fractures are unstable)
dislocation, locked facets
"special" fractures
odontoid (Type I, II, III): Type 11/111 unstable; II requires fixation
Jefferson (fractures in ring of CI): due to axial loading
hangman's (fractured C2 pedicles at pars interarticularis, spondylolisthesis of
the axis): due to hyperextension
clay shoveler's fracture (avulsion of spinous process, usually C7)
assess ligamentous instability using flexion/extension x-ray views of C-spine MRI
thoracolumbar spine unstable if 4/6 segments disrupted (3 columns divided into left
and right)
anterior column: anterior half of vertebral body, disc and anterior longitudinal
ligament
middle column: posterior half of vertebral body, disc and posterior longitudinal
ligament
posterior column: posterior arch, facet joints, and ligaments
Spinal Cord
cord injury with initial bony or ligamentous trauma or after moving an unstable
vertebral column
complete: no preservation of sensory/motor function below lesion, no recovery
incomplete lesions (see Spinal Cord Syndromes, NS24)
Nerve Roots
avulsion (e.g. bracrual plexus in motorcycle accident)
Neurologically Determined Deatli ________--11
Definition
irreversible and diffuse brain injury resulting in absence of clinical brain function
cardiovascular activity may persist for up to two weeks
Criteria of Diagnosis
prerequisites: no CNS depressant drugs/neuromuscular blocking agents, no drug
intoxication/poisoning, temperature >32"C, no electrolyte/acid-base/endocrine
disturbance
absent brainstem reflexes:
absent pupillary light reflex
absentcornealreflpxes
absent oculocephalic response
absent caloric responses (i.e. no deviation of eyes to irrigation of each ear
with 50cc of ice water - allow 1 min after injection, 5 min between sides)
absent pharyngeal and tracheal reflexes
absent cough with tracheal suctioning
absent respiratory drive at PaC0
2
>60mmHg or >20mmHg above baseline
(apnea test)
2 evaluations separated by time, usually performed by two specialists
(e.g. neurologist, anesthetist, neurosurgeon)
confirmatory testing: flat EEG, absent perfusion assessed with cerebral angiogram
Dr.JKR
Toronto Notes 2008 Pediatric Neurosurgery Neurosurgery NS33
Pediatric Neurosurgery
Spinal Dysraphism
Spina Bifida Occulta
definition:
congenital absence of a spinous process and variable amounts of lamina
no visible exposure of meninges or neural tissue
epidemiology: 15-20% of the general population; most common at L5 or Sl
etiology: failure of fusion of the posterior neural arch
clinical features:
no obvious clinical signs
presence of lumbosacral cutaneous abnormalities (dimple, sinus, port-wine
stain, or hair tuft) should increase suspicion of an underlying anomaly (lipoma,
dermoid, diastomatomyelia)
investigations: Figure 23. Spina Bifida Occulta
plain film - absence of the spinous process along with minor amounts of the
neural arch
DIS or MRI to exclude spinal anomalies
treatment: requires no treatment
Meningocele (Spina Bifida Aperta)
definition: a defect consisting of a herniation of meningeal tissue and CSF through a
defect in the spine, but not neural tissue
etiology: 2 theories:
1) primary failure of neural tube closure
2) rupture of a previously closed neural tube due to overdistention (Gardner;
unpopular theory)
clinical features:
most common in lumbosacral area
usually no disability, low incidence of associated anomalies and hydrocephalus
investigations: plain films, CT, MRI, DIS, echo, genitourinary (GD) investigations
treatment: surgical excision and tissue repair (excellent results)
Figure 24. Meningocele
Myelomeningocele
definition: a defect consisting of a herniation of meningeal tissue and CNS tissue
through a defect in the spine
etiology: same as meningocele
clinical features:
sensory and motor changes distal to anatomic level producing varying degrees
of weakness
spinal
urine and fecal incontinence
65-85% of patients with myelomeningocele have hydrocephalus
: : : ~ ~ ~ ~ I J - - cord
most have Type II Chiari malformation roots
investigations: plain films, CT, MRI, DIS, echo, GD investigations
treatment: surgical closure
g:
indications: preserve neurologic status, prevent CNS infections
~

prognosis:
:/ ~
operative mortality close to 0%, 95% 2-year survival
@
80% have IQ >80 (but most are 80-95), 40-85% ambulatory, 3-10% have Figure 25. Myelomeningocele
normal urinary continence
most common cause of early mortality are complications from Chiari
malformation (respiratory arrest and aspiration), whereas late mortality is due
to shunt malfunction
Intraventricular Hemorrhage (lVH)
see Pediatrics. P71
Dr.JKR
NS34 Neurosurgery Pediatric Neurosurgery Toronto Notes 2008
I.
o
o
Hydrocephalus in Pediatrics
Etiology
congenital
aqueductal anomalies, primary aqueductal stenosis in infancy
secondary gliosis due to intrauterine viral infections (mumps, varicella,
TORCH)
Dandy-Walker malformation (2-4%)
Chiari malformation, especially Type II
myelomeningocele
acquired
post meningitis
post hemorrhage (SAH, IVH)
masses (vascular malformation, neoplastic)
Clinical Features
symptoms and signs of hydrocephalus are age related in pediatrics
increased head circumference (HC), bulging anterior fontanelle, widened cranial
sutures
irritability, 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
Investigations
skull x-ray, DIS, CT, }"IRI, ICP monitoring
Treatment
similar to adults (see Hydrocephalus, NS7)
Definition
atresia of foramina of Magendie and Luschka, resulting in:
complete or incomplete agenesis of the cerebellar vermis with widely separated,
hypoplastic cerebellar hemisphere
posterior fossa cyst, enlarged posterior fossa
dilatation of 4th ventricle (also 3rd and lateral ventricles)
associated anomalies
hydrocephalus (90%)
agenesis of corpus callosum (17%)
occipital encephalocele (7%)
Epidemiology
2-4% of pediatric hydrocephalus
Clinical Features
20% are asymptomatic, seizures occur in 15%
symptoms and signs of hydrocephalus combined with a prominent occiput in infancy
ataxia, spasticity, poor fine motor control common in childhood
Investigations
skull x-ray, CT
Treatment
asymptomatic patients require no treatment
associated hydrocephalus requires surgical treatment
supratentorial lateral ventricular or cystoperitoneal shunt
Prognosis: 75-100% survival, 50% have normal IQ
Dr.JKR
Toronto Notes 2008 Pediatric Neurosurgery Neurosurgery !lJS35
Chiari Malformations
o
Definition
malformations at the medullary-spinal junction
Etiology
unclear, likely maldevelopment/dysgenesis during fetal life
Categories
Type I (cerebellar ectopia):
definition: cerebellar tonsils lie below the level of the foramen magnum
epidemiology: average age at presentation 41 years
clinical features:
many are asymptomatic
scoliosis
brain compression
central cord syndrome (65%)
syringomyelia (50%)
foramen magnum compression syndrome (22%)
cerebellar syndrome (11%)
hydrocephalus (10%)
Type II:
definition: part of cerebellar vermis, medulla and 4th ventricle extend
Figure 26. Chiari Malformations
through the foramen magnum often to midcervical region
epidemiology: present in infancy
clinical features: findings due to brainstem and lower cranial nerve dysfunction
syringomyelia, hydrocephalus in >80%
Investigations
MRI or CT myelography
Treatment
indications for surgical decompression:
Type I: symptomatic patients (early surgery recommended; <2 years post
symptom onset) -> suboccipital craniectomy, duroplasty
Type II: neurogenic dysphagia, stridor, apneic spells ---> cervical laminectomy,
duraplasty
Craniosynostosis
o
Definition
premature closure of the cranial suture(s)
Classification
sagittal (most common): long narrow head with ridging sagittal suture
(scaphocephaly)
coronal: expansion in superior and lateral direction (brachiocephaly)
lambdoid: least common
Epidemiology
0.6/1,000 live births, most cases are sporadic, familial incidence is 2% of sagittal and
8% of coronal synostosis
Clinical Features
skull deformity, raised ICP, hydrocephalus
ophthalmologic problems due to increased ICP or bony abnormalities of the orbit
Investigations
plain radiographs, CT scan
Treatment
parental counseling about nature of deformity, difficulty growing up as "cone head",
associated neurological symptoms
surgery for cosmetic purposes, except in cases of elevated ICP ( ~ sutures involved)
Dr.JKR
NS36 Neurosurgery Pediatric NeurosurgerylFunctional Neurosurgery/Common Medications Toronto Notes 2008
Pediatric BrainTumours
Relative frequency of pediatric
see also Tumour, NS9
brain tumours
Tumour type Percent
Epidemiology
20% of all pediatric cancers (second only to leukemia)
Astrocytoma, low-grade 40
60% of pediatric tumours are infratentorial
Supratentorial (23)
pediatric brain tumours arise from various cellular lineages:
Infratentorial (17)
Medulloblastoma 20
glia: low-grade astrocytoma (supra- or infratentorial), anaplastic astrocytoma,
Brainstem glioma 8
glioblastoma multiforme (largely supratentorial) (see NSlO for details)
Ependymoma 8
primitive nerve cells: supratentorial (primitive neuroectodermal tumour,
Malignant glioma 6 PNET), infratentorial (medulloblastoma), pineal gland (pineoblastoma)
Craniopharyngioma 6 non-neuronal cells: germ cell tumour, craniopharyngioma, dermoid,
PNET 4 meningioma, neurinoma, pituitary adenoma, others
Pineal, germ cell tumour 3
Other 5 Clinical Features
vomiting, seizure, macrocrania, hydrocephalus
Reprinted from Pediatric Clinics of North
America, Vol, 44(41, Kun LE, Brain Tumors: chal-
developmental delay, poor feeding, failure to thrive
lenges and directions, pp. 907-17. Copyright
1997, with permission from Elsevier.
Functional Neurosurgery
Surgical Treatment of the following disorders (see Neurology for details)
Parkinson's disease and tremor, N32 and N34
spasticity (including dystonias), N36
surgical management of pain, N51
Common Medications
The following are guidelines ONLY: follow clinical jUdgment and up-to-date prescription recommendations in practice: dosages refer to adults unless otherwise specified
Table 8. Common Medications
Drug Name Dosing Schedule Indications Side Effects Contnlincications Comments
lorazepam IAtivan"l 4mg IV over 2minutes, Statusepilepticus drowsiness, sedation other CNS depressants, start phenytoin loading
ql()'15 minutes digoxin lincreases simuhaneously
ldo not exceed 8mg/12hr) digoxin levelsl
ClIIbamazep'me lTegtelol") rIC douloureux (Trigeminal neuralgial: Tic douloureux worsening of seizures, lithium lincreases lithium hypersensnivity toTCAs, monnor CSC (potential
100 mg PO bid, increase by 200 mg/day ITrigeminal neuralgial heart failure, arrhythmias, toxicity!. MAOI previous bone marrow hematological toxidtyl
up 10 amaximum of 1,200 mg/day AV blad, aplastic anemia, other meds may increase suppression, MAOI in
200 mg tidl agranulocytosis, carbamazepine levels or past 14 days
Seizures: 200 mg PO bid, increase by thrombocytopenia, have decreased effects
200 mg (inpatient q3 days: hepatnis, erythema
outpatient q7 daysj until therapeutic muhrrorme, Stevens-Johnson
level achieved lusual optimum syndrome
dosage: 8O()'1,200 mg/day:
range: 600-2,000 mg/dayl
phenytoin (Dilantin") Seizures: Loading dose: 18m!Jl<g Seizures thrombocytopenia, other meds may increase bradyarrhythmias, heart blod< important to give over time to
slow IV or 3O().600 mg PO/day Statusepilepticus leukopenia, phenytoin levels and prevent causing acardiac arrest
divided bitl'tid, agranulocytosis, toxicity or have decreased
Maintenance: 2O().500 mg IV/day pancytopenia, toxic effects
[max. rate: (4().50 mg/min or hepatitis,Stevens-
300 mg PO q4hl: Johnson syndrome,
average maintenance dose: toxic epidermal
300 mg/day PO necrolysis
Status epilepticus: 200 mg IV
over 30 minutes 1- 20 m!Jl<g:
regularly),or
500 mg IV over 10 minutes
(if already on phenytoinl
dexameltlasone loading dose: 1()'20 mg IV: Cerebral edema le.g. pseudotumour cerebri, 'aminoglutethimide, systemic fungal infections, no longer used in acute spinal C()rd
IDecadron"\ Maintenance: 4- mg IV/day secondary to tumour, seizures, heart failure, antidiabetics, /!.SA, immunosuppressive dose injury
divided qid (may be POI head injury, arrhythmias, NSAlDs, barbiluates, with live virus vaccines
pseudotumour cerebri) thromboembolism, phenytoin, rifampin,
Preoperative preparation pancrealitis, acute adrenal cardiac glycosides,
for patients with insufficiency; avoid cyclosporine, ephedrine,
increased ICP abrupt withdrawal oral anticoagulants,
secondary to brain potassium-depleting
neoplasms drugs, salicylates,
skin-testing antigens,
toxoids, vacdnes
Dr.JKR
Toronto Notes 2008 Common Medications/Summary Key Questions
Table 8. Common Medications (continued)
DNg Name Dosing Schedule Indications Side Effeots Corrvnon Interactions
mannitol 1-1.5 g/lg IV rapid infusion Raised ICP seizures, heart failure lithium (increases
(350 mL of 10% solutionl excretion of lithium)
followed by 0.15 glkg IV q6h
mimodipine INimotop'"l 60 mg PO/NG q4h x11 days Vasospasm in SAH decreased blood antihypertensives (may
within 96 hours of SAH pressure, tachycardia, increase hypotensive effects),
dyspnea CCB (may increase effects!.
cimetidine (increases nimodipine
bioavailabilityl
Summary Key Questions
Questions Answers
1. What are the contraindications to lumbar puncture? Uncorrected coagulopathy
Known or suspected intracranial mass lesion
Non-communicating hydrocephalus
Skin infections near site of puncture
2. What is the most common CNS neoplasm in adults? Metastasis
3. What is the most common CNS neoplasm in children? Astrocytoma
4. What is the clinical features of acute raised ICP? Headache, nausea, vomiting, decreased LOC, papilledema
retinal hemorrhage, abnormal extra-ocular movements,
herniation syndromes, focal deficits due to lesion
5. What is the likely source of bleeding causing an Middle meningeal artery tear
epidural hematoma?
6. What are the risk factors for subdural hematoma? Alcohol, anticoagulants, cerebral atrophy
7. What is the most common site for an intracranial aneurysm? Anterior artery
8. What are the symptoms of subarachnoid hemorrhage? "Worst headache of my life", nausea/vomiting, photophobia,
meningismus, sleepiness, focal deficits
9. What are the top three etiologies for a neoplasm, GBM, abscess
rim-enhancing intraparenchymal lesion?
lO.ln asevere, unstable stroke patient, what do Intubate
you do before sending them to CT?
11. If apatient had increased ICP, what position do you not Trendelenberg
want them in?
12.60 year-old man has aseizure for the first time. Space-occupying lesion !tumour)
What's the most likely cause?
13. Ahockey player gets hit in the head and becomes Epidural hematoma
unconscious for afew minutes. He wakes up after afew
minutes. Next day: drowsy and headache.
What could be the cause of these symptoms?
14. What is the GCS of apatient who can open their 3+4+6=13
eyes to voice, obeys commands, and has confused speech?
15. L4/L5 herniated disc, what motor effects may be observed? Foot Drop
16. Best test to investigate subarachnoid hemorrhage? CT Scan
17. Would rupture of an intracranial artery cause an No, it would cause asubarachnoid hemorrhage
epidural hematoma?
18. Loss of plantar re1\ex, what level would you expect the lesion? L5-S1
19. If C5-6 disk herniation, which root affected? C6
20. What are the early signs and symptoms of increased ICP? Headache, nausea, papilledema
Contraindications
anuria, severe pulmonary
frank pulmonary
edema, severe heart failure,
severe dehydration, metabolic
edema, progressive renal
disease or dysfunction,
active intracranial bleeding
except during craniotomy
none known
Neurosurgery NS37
Comments
effect OCC\lrs in 1-5mins,
maximal at 1D-OO mins
often altemated with furosemide
10-10 mg IV q6h
indwelling urinary catheter to
measure ins and outs
causes vasodilation
only calcium channel blader ICCBI
to cross BBB (blood brain bamerl
use half the normal dose for liver
failure; monitor BP always
Dr.JKR
NS38 Neurosurgery Summary Key PointslReferences Toronto Notes 2008
Questions Answers
21. What are the 3divisions of the brain stem? Midbrain, pons, medulla
22. What region olthe bram governs comprehension of speech? Wernicke's area, dominanttemporallobe
Which lobe is it located?
23. What is the normal cerebral perfusion pressure? >50 mm Hg
24. Which sensory level corresponds to the shoulders? C4
25. What name is given to cn C2? Cl =Atlas, C2 =Axis
26. How many cervical vertebrae are there? Cervical nerve roots? 7 cervical vertebrae, 8cervical nerve roots
27. What is the most common cervical disc herniation? C6fl
28. What physical findings would you expect from aC7 radiculopathy? Triceps muscle weakness, decreased triceps reflex
29. What is the usual treatment of acervical disc herniation? Watchful waiting, over 95% heal spontaneously
30. What is the most likely position of alesion leading to Left frontal lobe
expressive dysphasia and mild arm weakness?
31. What nerve root exits between L4 &L5? L4 nerve root
32. What root is usually affected with an L415 disc herniation? L5
33. Can an L4 disc ever impinge on an L4 nerve root? Yes. With afar lateral disc herniation
34. What is sciatica? Pain traveling down the leg associated with nerve root
impingement
35. What are 3main signs of an Sl radiculopathy? Weak plantar flexion of foot
Decreased sensation over lateral foot
Decreased ankle jerk
36. What are the most common presentations of brain tumours? Progressive neurologic deficit, headache, seizure
37. Pituitary tumours are most commonly associated MENI
with what endocrine syndrome?
38. What are the most common metastases to the brain? Lung>Breast>RenaI>GI>Melanoma
39. What nerve is trapped in carpal tunnel syndrome Median nerve
References
Ahn NU, Ahn UM, Nallamshetty L, et al. Cauda equina syndrome in ankylosing spondylitis (the CES-AS syndrome): meta-analysis of
outcomes after medical and surgical treatments. Journal of Spinal Disorders 2001;14:427-33.
Aids to the examination of the peripheral nervous system. London, UK: BalliereTindall, 1986.
AI-Shahi R, Warlow CP Interventions for treating brain arteriovenous malformations in aduhs. The Cochrane Library 2004;Volume 2.
Barker FG 2
0d
, Ogilvy CS. Efficacy of prophylactic nimodipine for delayed ischemic deficit after subarachnoid hemorrhage: ametaanaly-
sis. Journal of Neurosurgery 1996;84:405-14.
Barnett H, Taylor W, Eliasziw M, et al. Benefit of carotid endarterectomy in patients with symptomatic moderate or severe stenosis.
NEJM 1998;339:1415-25.
Bracken MB, Shepard MJ, HolfordTR, et al. Methylprednisolone or tirilazad mesylate administration after acute spinal cord injury: 1-
year follow up. Results of the third National Acute Spinal Cord Injury randomized controlled trial. Journal of Neurosurgery 1998;89:699-
706.
Crossman AR, Neary D. Neuroanatomy: an illustrated colour text. Toronto, ON: Churchill Livingston, 1998.
Edlow J, Caplan L. Avoiding pitfalls in the diagnosis of subarachnoid hemorrhage. NEJM. 2000;342(11:29-36.
Executive Committee for the Asymptomatic Carotid Atherosclerosis Study IACAS). Endarterectomy for asymptomatic carotid artery
stenosis. JAMA 1995;273:1421-28.
Fitzgerald MJ1 Neuranatomy: basic and clinica/13rd edition). Philadelphia: WB Saunders, 1997.
Goetz CG, Pappert EJ. Textbook of clinical neurology 11 st edition). Toronto, ON: WB Saunders, 1999.
Greenberg MS. Handbook of neurosurgery 15th edition). NewYork:Thieme, 2001.
Kun, LE. Brain Tumours: Challenges and Directions. Pediatric Clinics of North America. 1997; Vol 44141:907-17.
Lindsay KW, Bone I. Neurology and neurosurgery illustrated. NewYork: Churchill Livingstone, 2004.
MRC Asymptomatic Carotid SurgeryTrial (ACSTI Collaborative Group. Prevention of disabling and fatal strokes by successful carotid
endarterectomy in patients without recent neurological symptoms: randomised controlled trial. Lancet 2004;363:1491-502.
Nieuwenhuys R, Voagd J, van Huijzen C. The human central nervous system 13rd edition). NewYork: Springer-Verlag, 1988.
Nursing 2004 Drug Handbookl24th editianl. New York, NY: Springhouse LippincottWiliiams &Wilkins, 2004.
Ogilvy CS, Stieg PE, Awad I., et al. Recommendations for the management of intracranial arteriovenous malformations. Circulation
2001 ;103:2644-57.
Porter PJ, Willinsky RA, HarperW, et al. Cerebral cavernous malformations: natural history and prognosis after clinical deterioration
with or without hemorrhage. Journal of Neurosurgery 1997;87:190-7.
Saal JS, Saal JA,Yurth EF. Nonoperative management of herniated cervical intervertebral disc with radiculopathy, Spine. 21(161:1877-83,
1996.
Shapiro S. Medical realities of cauda equina syndrome secondary to lumbar disc herniation. Spine. 25(3):348-51; discussion 352, 2000.
Shemie S, Doig C, Dickens B, et al. Severe brain injury to neurological determination of Death: Canadian forum recommendations.
CMAJ 2006; 174(6): SI-30.
Short OJ, EI Masry WS, Jones PW. High dose methylprednisolone in the management of acute spinal cord injury - asystematic review
from aclinical perspective. Spinal Cord 2000;38:273-86.
Spetzler RF. Martin NA. A proposed grading system for arteriovenous malformations. Journal of Neurosurgery 1986;65:476-83.
The North American Symptomatic Carotid EndarterectomyTrial INASCET). Beneficial effects of carotid endarterectomy in symptomatic
patients with high-grade carotid stenosis. NEJM 1991;325:445-53.
Dr.JKR