Basic Anatomy Review

Neurosurgery

Unprotected copy By: Dr.JKR

Jkr336@hotmail.com

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

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.

Toronto Notes 2008 Basic Anatomy Review Neurosurgery NS3

Cervical Region

~

_c:J ⁽¹

c:]

⁽²

CJ

^C3

8

d

⁽⁴

(5 (6 C7 (8 T1

fJB

Lumbar Region

~~"""--L2

1\\\1~\"""':'~~-- ^L3

~",,==:=j---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

L~~i-\~::/-l--;--posterior cerebral artery L~~-'.--...!....+-...l_ superior cerebellar artery

basilar artery

labyrinthine (internal auditory) artery anterior inferior cerebellar artery posterior inferior cerebellar artery vertebral artery

Figure 3. Circle of Willis

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

'~f~.):

r---J :

: 20 '~-)^{...,---- :}

I I

: 0 :

: Volume .. :

When a mass expands I

within the skull Eventually further small increments in com~ensatory volume produce

mechanisms initially larger and

mam:ain a normal larger increments in intracranial pressure intracranial pressure

Figure 4. ICP·Volume 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 H20) for adult, 3-7 mmHg (4-9.5 em H20) for child; varies with patient position

• waveform comprised of respiratory and blood pressure pulsations

• consider therapy for high rcp when rcp >20-25 rnmHg

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 CO₂ 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

~j

_{<60 m~Hg}

/~ _i

_{>150 mmHg}

low BP or high ICP High BP Cerebral perlusion pressure IMA~ICPI

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

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 (pC0235-40 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

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 • ram - m 1CSF' VIa ventnc es, assess eac SItuation m epen ent y . I h" . d d 1

• 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)

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

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) (12·15%) - 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)

Metastatic Tumours

• 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%

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

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

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, Vv 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)

Toronto Notes 2008 PuslBlood Neurosurgery NS13

• pathogens

• Streptococcus (most common), often anaerobic or microaerophilic 3

• 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

• ~fRl

• 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

NS14 Neurosurgery Blood Toronto Notes 2008

CT dInIity IIld III ..,....of blood tiiiit ^CT _·n

..

^IIIIi _·12

AMI Hyper. Grey BlICk

«72hl

SubIcuIe Iso. White White

«4w)

ClvIlIic Hypo. Blaci Blaci (>4wl

MR~ T1: 'George Washington Bridge' MRH2: 'Oreo' cookie -

BlackiWh~d1act

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

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 1·2 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

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 H20)

• bloody initially, xanthochromic supernatant with centrifugation ("yellow") by -12h, lasting 2 weeks

• spectrophotometry is most sensitive for xanthochromia

• RBC count usually>100,000/mm³ 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~bar ^puncture I~ ^negative I

~i~-eJ

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

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

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

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~hout recent neurolGgical symptoms: ran·

domised controlled trial. - (lancet 2004;

363:1491·1502.)

Studr Asymptomatic Carotid Surgery TriaIIACST), a randomized, controlled trial with follow·up 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 ha~ 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.