Neurosurgery Flashcards

1
Q

Treatment of cranial nerve palsies secondary to basilar skull fracture

A

most cranial nerve palsies are temporary due to compression or contusion, thus will improve over time as skull fracture heals
cranial nerve palsies can be treated with corticosteroids for faster recovery

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2
Q

Treatment of prolonged leak secondary to basilar skull fracture

A
indication: persistent CSF leak >7 days increases risk of CNS infection especially meningitis
prophylactic antibiotics (Cefazolin or Piperacillin/Tazobactam) and surgery (covering of leak with meninge or replacement tissue)
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3
Q

Diagnosis of cervical spine fracture

A

cervical spine fractures diagnosed first on cervical spine X-rays followed by neck CT for further characterization

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4
Q

Indication for cervical spine xray

A

indication for cervical spine X-ray include any of the following:
1) mental status less than alert (GCS <15)

2) neck pain
3) midline neck tenderness
4) neurologic signs: pain, paresthesia, anesthesia, weakness in extremities
5) injury causing distracting symptoms (painful injuries in extremities)

6) Canadian C-spine rule
patients considered high risk if they have any of the following
age >65 years
paresthesia in extremities
injury mechanism by any of the following
fall >5 steps or >3 feet
axial loading (e.g. diving)
motor vehicle accidents: high speed motor vehicle collision >100km/h or rollover or ejection
accident involving bicycle or recreational motor vehicle involved (e.g. ATVs)

patients with high risk require a cervical spine X-ray

patients considered low risk if they have any of the following:
motor vehicle collision: simple rear ended without roll over, high speed and without being hit by truck or bus
patients in sitting position in emergency department
patients ambulatory at any time after injury
patients with delayed neck pain occurring after injury
no midline tenderness

low risk patients are asked to “rotate their neck left and right as far as they can, stop if any pain or numbness or tingling”

low risk patients who can rotate their neck >45 degrees in both directions actively without pain or numbness or tingling are cleared clinically and do not require C-spine X-ray

low risk patients who cannot rotate their neck >45 degrees in both directions actively require C-spine X-ray

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5
Q

How much soft tissue space should be posterior to the pharynx in a lateral neck xray

A

<1cm at C1

<0.7cm or <1/3 vertebral body width at C2-C4

<2.2cm (in adults) or <1 vertebral body width at C4-C7

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6
Q

What lines should be present in a lateral neck xray

A

Anterior vertebral line
Posterior vertebral line
Spinolaminar line
Posterior spinous line

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7
Q

What is the cause of a C1 or Jefferson fracture

A

impact or load on back of head causing axial loading

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8
Q

What is seen on radiograph with a C1 fracture

A

odontoid cervical X-ray:

widening space between odontoid process and lateral mass

lateral mass laterally displaced relative to lateral mass of C2

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9
Q

When is a C1 fracture considered unstable

A

unstable if interval between atlas and dens is increased or lateral mass extends laterally beyond axis

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10
Q

C1 fracture management

A

if stable, then soft or hard collar immobilization

if unstable (broken transverse ligament), then traction, halo vest or surgical internal fixation (rod or plate from occiput down to C2 to stabilize area)

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11
Q

C2 fracture cause

A

high force hyperextension

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12
Q

C2 fracture radiograph findings

A

3 main types of fractures on odontoid cervical X-ray

1) odontoid fracture: fracture and displacement of odontoid process in odontoid peg fracture
odontoid process fracture:
type 1 = avulsion at tip
type 2 = fracture at base (requiring surgical fusion)
type 3 = fracture extending into body of C2

2) Hangman / traumatic spondylolisthesis of axis: fracture at C2 pedicle and misalignment of C2 / C3 with anterior displacement of C2
3) avulsion of anterior corner of vertebral body of C2 “tear drop”

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13
Q

Management of C2 fracture

A

hard collar or halo vest immobilization until healing occurs (2-3 months)

for unstable, displaced, comminuted or failure to maintain alignment with external immobilization fracture (e.g. type 2 or 3 odontoid fracture): surgical fixation

post intervention, confirm recovery with repeat flexion-extension cervical X-rays

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14
Q

What causes a flexion teardrop fracture

A

hyper flexion of neck along with vertical axial compression

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15
Q

What are flexion teardrop fractures usually associated with

A

usually associated with cervical spinal cord injuries

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16
Q

Flexion teardrop fracture radiograph findings

A

lateral neck X-ray:

hyper-flexion sprain (kyphotic deformity, anterior displacement of vertebral body, widened spinous process)

avulsion fracture “teardrop” of anterior vertebral body

misalignment of spinolaminar alignment

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17
Q

Flexion teardrop fracture management

A

anterior plate stabilization; surgical fixation stabilization

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18
Q

What causes C spine dislocation

A

trauma with perching facet joint preventing bones from returning to normal position

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19
Q

What is C spine dislocation usually associated with

A

usually associated with spinal cord injury

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20
Q

C spine dislocation radiograph findings

A

lateral neck X-ray: loss of all spine alignment lines, perching of facets

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21
Q

C spine dislocation management

A

Surgical fixation and stabilization

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22
Q

Spinal cord injury clinical presentation

A

generally, higher up the spinal cord = more severe and debilitating presentation

traumatic spinal cord injury usually have complete spinal cord lesion at spinal cord level, resulting in bilateral paresis and paresthesia below the spinal cord level

spinal cord injury signs: paresthesia, anesthesia, weakness in spinal cord distribution, loss of anal sphincter tone

trauma to spine signs: step deformity on palpation, midline tenderness on palpation of spine

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23
Q

Spinal shock definition and diagnosis

A

spinal shock is short term temporary spinal cord dysfunction resulting in loss of sensation, motor function and reflexes lasting hours to days that will eventually recover

diagnosis of complete spinal cord injury must be made after spinal shock if present

if persistent loss of sensation and paralysis after return of spinal cord reflexes, then the patient does not have spinal shock and can be diagnosed with complete spinal cord injury

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24
Q

What are reflexes tested for for spinal shock

A

normal bulbocavernosus reflex = anal sphincter contracts in response to squeezing glans penis or tugging on indwelling Foley catheter

normal anal wink reflex = anal sphincter contracts upon stroking of skin around anus

normal withdrawal reflex = withdrawal and then relaxation of limb with continued noxious stimulus

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25
Q

What is neurogenic shock, its pathophysiology and clinical presentation

A

neurogenic shock is a distributive shock caused by damage to sympathetic nervous system along cervical - lumbar level

lack of sympathetic nervous stimulation results in unopposed parasympathetic stimulation resulting in bradycardia, vasodilation
vasodilation in peripheral tissue cause pooling of blood in peripheral tissues and hypotension

Clinical presentation: hypotension, bradycardia (due to unopposed parasympathetic) and warm extremities (due to pooling of blood)

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26
Q

Neurogenic shock treatment

A

treated by volume replacement if heart is healthy and strong

coupled with sympathomimetic drug (neosynephrine or dopamine) if necessary

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27
Q

How to clinically assess spinal cord injury

A

assess using ASIA (American Spinal Injury Association) standard neurological classification

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28
Q

What is the neurological level of spinal cord injury

A

neurological level of spinal cord injury is the most caudal (inferior) spinal segment with normal motor and sensation on both sides on motor and sensory testing

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29
Q

What are zones of partial preservation in a spinal cord injury

A

zone of partial preservation are dermatomes and myotomes caudal to neurological level that have partial motor or sensory function

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30
Q

What is considered a complete spinal cord injury

A

complete has no sensory nor motor function in S4-S5

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31
Q

What are the ASIA grades of spinal cord injury

A

categories A-E where A is worse and E is best

A = complete, no sensory or motor function preserved in sacral segments S4-S5
ASIA A suggest no sensory or motor function below level of injury

B = sensory incomplete, only sensory function preserved below neurological level (including S4-S5)

C = motor incomplete, some motor function is preserved under level of injury and majority of key muscles below the level have MRC score <3

D = motor incomplete, motor function preserved below neurological level and majority of key muscles below the level have MRC score >3 (MRC 3 = active movement against gravity, but not resistance)

E = normal, normal motor and sensory function

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32
Q

What is the meaning of the ASIA grade for spinal cord injury

A

ASIA grade gives prognosis

ASIA grade A (complete spinal cord injury) has significant distal recovery rate of 1-2%

ASIA grade B-E (incomplete spinal cord injury) has significant distal recovery rate of 50%

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33
Q

Investigations in spinal cord injury

A

plain X-ray films is a good for screening for any injuries to spine, which is indicated if any pain or neurological deficit on assessment

CT scan is the standard imaging for suspected spine trauma, usually follow up on abnormal or inadequate plain X-ray film
CT good for characterizing fractures

MRI usually not used in acute case of trauma due to time constraint
MRI is best imaging for spinal cord, which can assess hemorrhage, extend of cord edema & injury, traumatic disc herniation

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34
Q

Management of spinal cord injury

A

1) Stabilize patient and ensure ABC
same algorithm as brain injury (see above)
ABC should be done with C-collar on
neurogenic shock treated with fluid resuscitation and vasopressors

2) Steroids
Methylprednisolone IV as bolus then continuous for 1-2 days to reduce inflammation of spinal cord, which is controversial

3) Surgical Decompression
indication: any spine abnormality that may compress on spinal cord
decompression used to relieve pressure, preventing further damage to spinal cord due to increased pressure of compression
decompression = various surgical procedures to relieve pressure or compression of spinal cord and / or spinal nerve roots, including

diskectomy: removing part of vertebral disc to relieve pressure on nearby nerve roots
lamniotomy: removal of lamina of vertebrae to increase size of spinal canal, relieving pressure
foraminotomy: removal of bone or tissue around intervertebral foramen to relieve pressure on spinal nerve roots

osteophyte removal: removal of osteophytes

corpectomy: removal of vertebral body and disc

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35
Q

Branches of the external carotid artery

A

Some Attending Likes Freaking Out Poor Medical Students

(from proximal to distal branches)

Superior thyroid artery
Ascending pharyngeal artery 
Lingual artery
Facial artery
Occipital artery 
Posterior auricular artery
Maxillary artery
Superficial temporal artery
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36
Q

Branches of the internal carotid artery

A

ophthalmic artery before joining into Circle of Willis

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37
Q

What arteries feed into the Circle of Willis

A

left & right internal carotid arteries and basilar artery feeds into circle of willis

internal carotid artery divides into L & R anterior and middle cerebral artery at circle of willis

basilar artery divides divides into L & R posterior cerebral artery at circle of willis

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38
Q

What are the vessels included in the Circle of Willis

A
L &amp; R anterior cerebral artery
anterior communicating artery
L &amp; R middle cerebral artery
posterior communicating artery
L &amp; R posterior cerebral artery

L & R anterior cerebral artery + anterior communicating artery + L & R middle cerebral artery = anterior circulation of circle of willis

L & R posterior cerebral artery + posterior communicating artery = posterior circulation of circle of willis

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39
Q

What does the common carotid artery give rise to

A

L & R CCA (common carotid artery) gives rise to L & R ECA (external carotid artery) and L & R ICA (internal carotid artery), where the L & R ICA feeds into circle of willis near optic chiasm

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40
Q

What do the vertebral arteries give rise to

A

L & R vertebral artery gives rise to single basilar artery, which feeds circle of willis

the L & R vertebral artery also gives branch of L & R PICA (posterior inferior cerebellar artery), which supply the inferior cerebellum

basilar artery also gives branch of AICA (anterior inferior cerebellar artery) and SCA (superior cerebellar artery), which supply the middle and superior cerebellum respectively

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41
Q

Anterior cerebral arteries feed what part of the brain

A

anterior cerebral arteries supply most medial portion of frontal lobe and superior parietal lobe

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42
Q

Posterior cerebral arteries feed what part of the brain

A

posterior cerebral arteries supply:
medial portion of inferior parietal lobe and occipital lobe
posterior aspect of occipital lobe

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43
Q

Middle cerebral arteries feed what part of the brain

A

middle cerebral arteries continue into lateral sulcus, then give branches to supply the lateral cerebral cortex (frontal, parietal and temporal lobes) as well as insular cortex

middle cerebral arteries gives branches of lenticulostriate arteries that supply the basal ganglia and internal capsule on coronal section of brain

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44
Q

What are the origins, names and roles of the 3 cerebellar arteries

A

3 cerebellar arteries supplying cerebellum from superior to inferior

basilar artery -> superior cerebellar artery -> supplies superior half of cerebellum

basilar artery -> anterior inferior cerebellar artery -> supplies anterior inferior quarter of cerebellum

vertebral artery -> posterior inferior cerebellar artery -> supplies posterior inferior quarter of cerebellum

45
Q

What is the origin, location and role of the pontine arteries?

A

pontine arteries are branches from basilar arteries between superior cerebellar artery and the anterior inferior cerebellar artery

role is to feed the pons

46
Q

Definition of stroke (cerebrovascular event)

A

stroke is an acute neurological injury causing loss of brain function due to disturbance of blood supply to the brain

stroke can be caused by lack of brain flow (ischemia) or hemorrhage

47
Q

What causes ischemic stroke

A

ischemic stroke constitute 80% of stroke and is caused by blockage of cerebral blood vessel or systemic hypoperfusion

1) Thrombosis
thrombosis = in-situ obstruction of artery by clot formation
thrombosis can be large vessel or small vessel disease
large vessel disease: stenosis or occlusion of large artery (commonly internal carotid artery, but can also be vertebral or basilar or circle of Willis or proximal intracranial branches)
due to thrombus from atherosclerosis, dissection, arteritis / vasculitis
small vessel disease (aka lacunar stroke): stenosis and occlusion of small cerebral artery branches due to hypertension resulting in lipohyalinosis, fibroid degeneration or
microatheroma

2) Embolism
embolism = clot from elsewhere that traveled in blood vessel to brain, occluding cerebral blood vessels
cardiac embolism = clot from heart embolisms and blocks cerebral artery from atrial fibrillation, rheumatic valve disease, prosthetic heart valve, recent myocardial infarction,
endocarditis and others

3) Systemic hypoperfusion
systemic hypo perfusion = global decreased blood flow to brain, causing global damage especially watershed areas between major cerebral arterial territories
any shock can cause systemic hypo perfusion, most commonly cardiogenic shock such as cardiac arrest, arrhythmia and myocardial infarction

48
Q

What causes hemorrhagic stroke

A

hemorrhagic stroke constitute 20% of stroke and is caused by rupture of cerebral blood vessel causing bleeding into the brain

1) Intracerebral hemorrhage
intracerebral hemorrhage = bleeding from small arteries of arterioles into the brain, due to rupture of micro aneurysms from hypertension, trauma, amyloid antipathy, vascular
malformation and drug abuse

2) Sub-arachnoid hemorrhage
sub-arachnoid hemorrhage = bleeding into CSF due to rupture of arterial aneurysm at base of brain or vascular malformation

49
Q

What is a transient ischemic attack

A

focal cerebral ischemic event lasting <24 hours followed by full recovery, resulting in no apparent permanent neurological deficit
usually, TIA resolve in minutes to perhaps few hours

50
Q

What is a reversible ischemic neurological deficit (RIND)

A

focal cerebral ischemic event with neurological deficit lasting >24 hours followed by full recovery, so the neurological deficits are temporary and last <3 weeks

51
Q

Presentation of anterior cerebral artery stroke

A

areas of brain affected: frontal lobe

contralateral leg paresis and sensory loss

may have gait disturbance, urinary incontinence

52
Q

Presentation of middle cerebral artery stroke

A

areas of brain affected: posterior frontal lobe, temporal lobe, parietal lobe

contralateral weakness and sensory loss of face and arm
contralateral homonymous hemianopia or quadantanopia

if left hemisphere: aphasia
if right hemisphere: visual-spatial neglect

53
Q

Presentation of posterior cerebral artery stroke

A

areas of brain affected: occipital lobe
contralateral homonymous hemianopia or quadrantanopia
if left hemisphere: alexia without agraphia (cannot read but can write)
if involvement of thalamus: sensory loss, decreased level of consciousness

54
Q

Presentation of basilar artery stroke

A

areas of brain affected: brainstem

locked-in syndrome: quadriparesis or quadriplegia, anarthria or dysarthria, impaired horizontal eye movement

55
Q

Presentation of lacunar infarct

A

areas of brain affected: deep brain structures
pure contralateral hemiparesis or hemisensory loss
ataxia
dysarthria-clumsy hand syndrome: dysarthria, facial weakness, dysphagia, mild hand weakness and clumsiness

56
Q

What area is affected in amaurosis fugax

A

central retinal artery most commonly secondary to embolism from heart (atrial fibrillation) or carotid artery (atherosclerosis)

ophthalmic artery is first branch of internal carotid artery, so embolus into carotid is likely to go to ophthalmic artery to central retinal artery

57
Q

What is amaurosis fugax

A

transient monocular visual loss, classically described as curtain going down blocking vision, which then goes away returning to normal vision

58
Q

Fundoscopy findings in amaurosis fugax

A

pale ischemic fundus with cherry red spot at macula on fundoscopy

59
Q

Next steps after an episode of amaurosis fugax

A

amaurosis fugal usually precede subsequent embolic ischemic strokes, thus is an indication for work-up and addressing underlying cause to prevent ischemic strokes (e.g. carotid
endarterectomy for carotid artery atherosclerosis)

60
Q

Initial assessment and investigations for acute stroke

A

1) Stabilize patient

2) Initial assessment
Hx:
a) onset of symptoms since patient was last awake and free of stroke symptoms
time window for anti-fibrinolytic therapy is 4.5 hours
symptoms of focal neurological deficit
b) rule out other differential diagnosis of stroke
important differential diagnosis of stroke include hypoglycaemia, seizure, migraine and syncope
c) differentiate between ischemic vs. hemorrhagic stroke
hemorrhagic stroke has headache and vomiting

physical exam
full neurological exam for focal neurologic exam
full assessment of neurological deficit using NIH Stroke Scale (NIHSS) which assess severity of stroke
anti-fibrinolytic therapy considered if score >6
inspection for trauma
peripheral vascular exam
cardiac exam and respiratory exam

3) Investigations
non-contrast brain CT
brain CT for all suspected stroke to rule out hemorrhagic stroke, but may also visualize signs of stroke

blood lab test: CBC, electrolytes, blood glucose, INR, aPTT, creatinine, BUN, troponin I
ECG
ECG to screen for myocardial infarction that may cause global ischemic stroke or arrhythmia that may cause ischemic stroke

if sub-arachnoid hemorrhage still suspected based on history (sudden worst headache maximal at onset) despite normal CT, then lumbar puncture

61
Q

Management of hemorrhagic stroke

A

1) blood pressure control to <140mmHg systolic with IV Labetalol
2) immediate interventional radiology for endovascular coiling or neurosurgical consultation for surgical clipping

62
Q

Management of ischemic stroke

A

1) Anti-Fibrinolytic Therapy
if within 4.5 hours of symptom onset and NIHSS >6, patient is candidate for anti-fibrinolytic therapy with IV rtPA (recombinant tissue plasminogen activator)

2) Supportive Therapy

63
Q

Absolute contraindications for rTPA

A

hemorrhagic stroke, which is ruled out with CT or MRI imaging

head trauma or prior stroke in last 3 months, which is ruled out with history

arterial puncture at non-compressible site in last 7 days, which is ruled out with history

any previous intracranial hemorrhage, which is ruled out with history

evidence of active bleeding on physical examination

hypertension >185/110, which should be lowered with beta blocker (IV Labetalol) before initiating antifibrinolytic – antifibrinolytics can be initiated only if blood pressure is <185/110 to limit risk of bleeding complication

if blood pressure >220/120, then initiate IV labetalol to lower pressure

blood dyscrasia which is ruled out with lab test (CBC, INR and aPTT) and includes
platelet <100
heparin use and PTT above upper limit of normal
anticoagulant use and INR >1.7
blood glucose <5, which is ruled out with lab test (blood glucose)

multilobar infarction >1/3 cerebral hemisphere

64
Q

Relative contraindication for rTPA

A

minor or rapidly improving stroke symptoms

seizure at onset

major surgery or serious trauma within previous 2 weeks

recent GI or urinary tract hemorrhage in previous 3 weeks

recent acute myocardial infarction in previous 3 months

65
Q

Options for ischemic stroke if rTPA is contraindicated

A

if rtPA contraindicated, then aspirin 81mg or 325mg chewed
Clopidrogrel or Aggrenox can be used as substitute for aspirin

if rtPA contraindicated, intra-arterial thrombolysis or angioplasty or removal of clot by interventional radiology can be considered

66
Q

Major complications of rTPA

A

rtPA has ~10% risk of hemorrhage

symptomatic intracranial hemorrhage in ~5% cases

systemic bleeding in <1% cases

orolingual angioedema

acute hypotension

67
Q

What is not effective for treating acute ischemic stroke

A

Anticoagulants

68
Q

SAH due to aneurysm rupture management

A

1) Stop source of bleeding
Clipping or coiling by IR
endovascular coiling is the standard and 1st line treatment for most SAH due to aneurysm (less invasive because it avoids craniotomy which is necessary in surgical clipping)

2) Acute Management
lower blood pressure with IV Labetalol to decrease bleeding
external ventricular drain by neurosurgery if continuous deterioration and progressive enlargement of ventricle

3) Short Term Management for Complications
patient hospitalized 1-2 weeks to monitor for and treat any complication
support therapy: oral or NG tube feeding; urinary catheter for fluid balance; benzodiazepine to relieve stress
if new neurological symptoms, transcranial doppler or cerebral angiography to monitor for vasospasm
if hydrocephalus as detected on CT scan, extra ventricular drain

4) Long Term Management
patient followed by MR scanning to evaluate aneurysm to see if it regrew

69
Q

What can be used to decrease vasospasm after SAH

A

nimodipine, a calcium channel blocker used to reduce vasospasm

70
Q

Intracerebral hemorrhage management

A

1) Acute Management
lower blood pressure with IV labetalol to decrease bleeding
external ventricular drain by surgery if continuous deterioration and progressive enlargement of ventricle
if patient is taking anticoagulants, reverse anticoagulation (fresh frozen plasma, Octaplex and vitamin K for Warfarin; fresh frozen plasma for Heparin)
surgical removal or stereotactic aspiration of hemorrhage is controversial

2) Short Term Management for Complications
patient hospitalized 1-2 weeks to monitor for and treat any complication
support therapy: oral or NG tube feeding; urinary catheter for fluid balance; benzodiazepine to relieve stress
if new neurological symptoms, transcranial doppler or cerebral angiography to monitor for vasospasm
nimodipine, a calcium channel blocker used to reduce vasospasm
if hydrocephalus as detected on CT scan, extra ventricular drain
if seizure, benzodiazepine for short term then phenytoin for long term

3) Long Term Management
if patient survives, address risk factors
if patient taking anticoagulant or anti-platelet medication, discontinue medication
if patient is hypertensive, antihypertensive to control hypertension

71
Q

Secondary prevention of stroke

A
  1. Anti-platelet Therapy
    all patients with ischemic stroke or TIA should be prescribed anti-platelet therapy for secondary prevention of recurrent stroke
    anti-platelet agents can be any of the 3 options
    1) aspirin
    2) aspirin + dipyridamole (Aggrenox)
    3) clopidogrel (plavix)
    no benefit of aspirin + clopidogrel
    note that this does to apply to patients with atrial fibrillation, which is treated with aspirin or anti-coagulant (see below)
  2. Atrial Fibrillation
    if atrial fibrillation, risk stratify for stroke based on CHADS2 score
  3. Hypertension
    treating hypertension result in ~40% reduction of risk of stroke
    hypertension should be treated according to CHEP guidelines (target <140/90 and <130/80 for diabetic patients)
    ACEI or ARB + Thiazide diuretics are recommended as antihypertensives for additional risk reduction compared to other antihypertensives
    ACEI usually Ramipril 10mg daily
  4. Dyslipidemia
    prescribe statin (Atorvastatin (Lipitor) or Rosuvastatin (Crestor))
    statin reduces risk of stroke by 25%
    target should be to lower LDL cholesterol <2
5. Treating Other Comorbidities
glycemic control in diabetes mellitus
treat other cardiovascular disease
Lifestyle Changes
reduce alcohol
quit smoking, which decrease risk of stroke to baseline within 2-5 years
stop hormone supplements if possible
increased physical activity
healthy diet (low fat, low salt)
72
Q

What is the CHADS2 score

A
C = congestive heart failure (1 point)
H = hypertension (1 point)
A = age >75 (1 point)
D = diabetes mellitus (1 point)
S2 = previous stroke or TIA (2 points)

if CHADS2 score = 0, then Aspirin
if CHADS2 score = 1, then Aspirin or anticoagulant (Warfarin, Dabigatran or Rivaroxaban)
if CHADS2 score >2, then anticoagulant (Warfarin, Dabigatran or Rivaroxaban)

73
Q

Carotid arthersclerosis evaluation

A

imaging are required to evaluate stenosis of internal carotid artery, which dictate management

cerebral angiography is gold standard for evaluation of internal carotid artery stenosis, but it is not used clinically due to invasiveness and risk of stroke

non-invasive screening tests include

  1. carotid duplex ultrasound (CDUS)
  2. magnetic resonance angiography (time of flight, contrast enhanced MRA)
  3. computed tomography angiography (CTA)

all screening test have high sensitivity and specificity
CDUS is a cheap and useful screening test to screen for high grade stenosis >50%, which may warrant further imaging (MRA or CTA)

CTA and MRA are used to evaluate carotid stenosis and sufficient for surgical planning

74
Q

Carotid artherosclerosis disease management

A

intervention options = carotid endarterectomy (surgery removal of plaque) by vascular surgery or catheter angioplasty & stenting by interventional radiology

catheter angioplasty and stenting have high risk of peri-operative risk of stroke and death

in all cases, carotid endarterectomy is usually not done if peri-operative risk of stroke and death is >6%

carotid endarterectomy reduces risk of recurrent stroke by 15%

A) asymptomatic carotid artery stenosis
if >70% stenosis based on imaging, then carotid endarterectomy can be considered
if >50% stenosis, then annual CDUS to follow

B) symptomatic stenosis (i.e. TIA, amaurosis fugax or stroke) in proximal carotid artery
if >70% stenosis based on imaging, then carotid endarterectomy
if stenosis 50-70% based on imaging, then carotid endarterectomy can be considered especially for men
if stenosis <50%, then carotid endarterectomy is not indicated and medical management should be initiated (see above for secondary prevention)

if carotid endarterectomy is indicated, best results if treated early, so urgent endarterectomy within 2 weeks

75
Q

What is more common - primary CNS tumour or mets?

A

Mets

76
Q

What are the most common types of primary CNS tumours, benign and malignant?

A

A) Benign tumors

1) meningioma (~34% of all primary brain tumours)
2) acoustic neuroma (~10% of all primary brain tumours)
3) pituitary tutors (~15% of all primary brain tumours)

B) Malignant tumors

1) astrocytoma (including glioblastoma) (~25% of all primary brain tumours)
2) lymphoma (<5% of all primary brain tumors)

77
Q

What is a glioma

A

tumor arising from glial cells, which include ependymomas (arising from ependymal cells), astrocytomas (arising from astrocytes), oligodendroglioma (arising from
oligodendrocytes), brainstem glioma (arising from brain stem), optic nerve glioma (arising from optic nerve), mixed glioma

78
Q

What are the most common malignancies metastasizing to the brain

A

1) lung cancer
2) breast cancer
3) melanoma
4) renal cell carcinoma
5) colorectal cancer
other: testicular cancer, lymphoma, leukemia

79
Q

What is the difference between a tumour that is biologically and histologically malignant

A

histologically malignancy mean tumor that has malignant properties such as uncontrolled proliferation and metastasis

biological malignancy mean tumor is benign (slow growing) but can cause death due to location where its growth will compress nearby structure causing death

80
Q

What is the sequence of herniation that usually occurs in the brain

A

1) sub-falcine herniation where hemisphere herniate through falx cerebri laterally crossing midline compressing on hemisphere on the other side

2) trans tentorial herniation where the innermost part of temporal lobe (uncus) herniate through tentorium cerebelli inferiorly compressing on brainstem especially midbrain
trans tentorial herniation usually present with blown pupil due to CN3 (oculomotor) palsy

3) tonsillar herniation where cerebellar tonsil herniate through foramen magnum inferiorly compressing lower brainstem (pons and medulla)
compression of medulla disrupt cardiovascular and respiratory centres, usually resulting in brain death

81
Q

What is the usual pattern of metastasis for a primary CNS tumour

A

malignant CNS tumor commonly disseminates via CSF to other parts of brain

malignant CNS tumor tend not to spread by blood, so it rarely causes systemic metastases to other parts of body

82
Q

Presentation with uncal herniation

A

blown pupil (CN3 oculomotor palsy)

83
Q

Presentation tonsillar herniation

A

loss of corneal reflex (CN5 & 7), loss of gag reflex (CN 9 & 10), respiratory & cardiovascular collapse -> death

84
Q

What is Cushing’s reflex

A

brainstem compression cause Cushing reflex (hypertension, bradycardia, then respiratory depression), which is an ominous sign of impending death and require
urgent intervention to lower intracranial pressure

85
Q

Presentation of mass effect in the brain

A

Herniation –> Cushing reflex

86
Q

Presentation of tumor related compression of optic chiasm (commonly pituitary tutors)

A

bitemporal hemianopsia

87
Q

Brain tumour diagnosis

A

1) Imaging
A) brain imaging
imaging test = head CT or MRI with contrast, where MRI with Gadolinium contrast is best test for characterization of brain tumours
brain imaging can differentiate mass versus other lesion such as hemorrhage or hematoma or abscess or stroke

B) body imaging
body imaging may be done for brain metastases to look for primary malignancy, as guided by history and physical exam
most common body imagings for primary source of brain metastases include
chest X-ray followed by chest CT for lung cancer
abdomen & pelvis CT for colon cancer
mammogram for breast cancer

2) Biopsy
biopsy of brain required for definitive diagnosis based on pathology for primary brain tumor
procedure = stereotactic biopsy or open neurosurgery
biopsy of brain is not indicated for brain metastases

88
Q

Astrocytoma epidemiology

A

most common primary intra-axial brain tumor

common in adults between ages 40-60 years

89
Q

Astrocytoma WHO grading system, typical CT/MRI findings and survival

A

I - Pilocytic astrocytoma
CT/MRI +/- mass effect, +/- enhancement
Survival >10y, cure if gross total resection

II - Low grade/diffuse
CT/MRI mass effect, no enhancement
Survival 5 year

III - Anaplastic
CT/MRI complex enhancement
Survival 1.5-2y

IV - Glioblastoma multiforme (GBM)
CT/MRI necrosis (ring enhancement)
Survival 12 mo, 10% at 2 year

90
Q

Astrocytoma pathophysiology

A

tumor arising from astrocytes

91
Q

Astrocytoma usual location

A

most common sties: most commonly at cerebral hemispheres, but may occur at cerebellum, brainstem or spinal cord

92
Q

Astrocytoma CT/MRI with contrast findings

A
  1. Heterogenous contrast enhancement
  2. Ill-defined borders (infiltrative)
  3. Peritumoural edema
  4. Central necrosis
  5. Compression of ventricles, midline shift
93
Q

Astrocytoma management

A

1) Low grade diffuse astrocytoma
options include close observation, radiation, chemotherapy, neurosurgery
neurosurgery = surgical resection of tumor, which is not curative but trend towards better outcomes
radiotherapy = external beam radiotherapy, which alone or post-op can prolong survival
chemotherapy usually for tumour progression

2) High grade diffuse astrocytoma (anaplastic astrocytoma and glioblastoma multiforme GBM)
management to improve quality of life, not necessarily to prolong life
1st line = gross total surgical resection = maximal safe surgical resection + fractionated radiation within 2cm margin + concomitant & adjuvant chemotherapy (Temozolomide)
contraindication: extensive dominant lobe GBM, significant bilateral involvement, end of life, extensive brainstem involvement
Temozolomide is agent of choice for astrocytoma (20% response rate) with better response for patients with MGMT gene hypermethylation

2nd line = stereotactic biopsy + fractioned radiation with 2cm margin

3rd line = whole brain radiotherapy +/- chemotherapy (Temozolomide)

94
Q

Meningioma epidemiology

A

common in middle aged adults
3 females : 2 males ratio
genetic mutation: loss of NF2 gene, 22q12 deletion

95
Q

Meningioma pathophysiology and usual location

A

tumor arising from meningothelial cells in arachnoid membrane, typically benign, slow-growing and circumscribed (non-infiltrative)

90% solitary tumor, 10% multiple tumors

most common extra-axial tumor most commonly at para-sagittal convexity or falx (70% cases), sphenoid wing, tubercular sellae, foramen magnum, olfactory groove

history: classically Psommoma bodies on pathology

96
Q

Meningioma WHO grading system

A

WHO grading system based on histology, which correlate with risk of recurrence
grade 1 = low risk of recurrence
grade 2 = intermediate risk of recurrence
grade 3 = high risk of recurrence

97
Q

Meningioma on CT/MRI with contrast

A
  1. extra-axial mass
  2. classically well circumscribed
  3. homogeneous densely enhancing mass
  4. along dural border
98
Q

Meningioma management

A

1) Conservative management
indication: non-progressive and asymptomatic meningioma
follow up with repeat imaging

2) Neurosurgery
indication: progressive or symptomatic lesion
pre-operative endovascular embolization may be used to facilitate surgery

if meningioma <3cm, then stereotactic radiosurgery
if meningioma >3cm, then open neurosurgery to excise

if recurrent atypical or malignant meningioma, then stereotactic radio surgery or external beam radiotherapy

in most cases, neurosurgery with complete resection is curative

99
Q

Meningioma prognosis

A

excellent prognosis with >90% 5-years survival with recurrence rate of ~10-20%, which depend on extent of resection

100
Q

Pituitary tumour epidemiology

A

common in age 30-40 years, male = female ratio

101
Q

Pituitary tumour classification/pathophysiology

A

classification based on size and function
micro-adenoma = size <1cm; macro-adenoma = size >1cm

functional / secretory = endocrine active tumor
non-functional = inactive tumor

102
Q

Pituitary tumour presentation

A

increased ICP: headache, nausea, vomiting

focal symptoms: bitemporal hemianopsia, CN3, 4, 5 (V1, V2), 6 palsy (compression of cavernous sinus)

endocrine effects for secretory tumor depending on hormones secreted

A) secretory hormones
hyperprolactinemia from prolactinoma: galactorrhea, amenorrhea, infertility, decreased libido

ACTH: Cushing’s disease, hyperpigmentation

GH production: acromegaly, gigantism

B) suppression of hormones
pan-hypopituitarism: hypothyroidism, hypoadrenalism, hypogonadism

hypothyroidism

decreased ADH: diabetes insipidus

103
Q

Potential complication of pituitary tumour

A

pituitary apoplexy (sudden mass expansion due to hemorrhage or necrosis), which present with abrupt onset headache, visual disturbance, ophthalmoplegia, reduced mental status, panhypopituitarism, CSF leak (rhinorrhea), seizure, subarachnoid hemorrhage

104
Q

Pituitary tumour investigations

A

visual field: formal visual field test, cranial nerve test
endocrine test: prolactin level, TSH, 8AM cortisol (to measure ACTH), fasting glucose & IGF-1 (to measure GH), FSH/LF
head MRI with contrast: pituitary tumor

105
Q

Pituitary tumour management

A

1) Surgery
indication: non-secreting symptomatic adenoma (causing mass effect), adenoma secreting ACTH or GH
procedure = trans-sphenoidal, trans-ethmoidal or trans-cranial surgical resection of pituitary tumor

2) Medical management
pituitary apoplexy: rapid corticosteroid administration +/- surgical decompression

prolactinoma: doptamine agonist (Bromocriptine)

Cushing: serotonin antagonist (Cyproheptadine), inhibition of cortisol production (Ketoconazole)

acromegaly: somatostatin analogue (Octeotide), Bromocriptine

decreased hormone production: endocrine replacement therapy

106
Q

Brain metastases epidemiology

A

15-30% cancer patients present with cerebral metastatic tumours

107
Q

Brain mets pathophysiology/usual location

A

usually hematogenous spread to brain, classically at cerebral hemisphere (80% cases) at grey-white matter function or junction of temporal-parietal-occipital lobes

usually appear as multifocal masses

108
Q

Brain mets investigations

A

identification of primary tumour (metastatic work-up), usually consisting of chest X-ray, CT chest & abdomen, abdominal U/S, bone scan, mammogram if no symptoms or signs

if primary tumor found in metastatic work-up, biopsy of primary tumor site for diagnosis

if primary tumor not found in metastatic work-up then consider brain biopsy for diagnosis

head CT or MRI with contrast: multifocal round, well-circumscribed ring enhancing lesion with peri-tumor edema

109
Q

Brain mets management

A

1) Treat underlying cause
treatment of underlying primary cancer, based on appropriate guidelines
consider chemotherapy and / or radiotherapy for brain metastases to slow progression

2) Treat complications of brain metastases
seizure prophylaxis for patients presenting with seizure due to brain metastases Phenytoin or Levetiracetam

corticosteroids Dexamethasone (with Ranitidine) to reduce cerebral edema to reduce mass effect associated symptoms (headache, nausea, vomiting)