Neurosurgery

Question 1

Treatment of cranial nerve palsies secondary to basilar skull fracture

Answer 1

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

Question 2

Treatment of prolonged leak secondary to basilar skull fracture

Answer 2

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)

Question 3

Diagnosis of cervical spine fracture

Answer 3

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

Question 4

Indication for cervical spine xray

Answer 4

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

Question 5

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

Answer 5

<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

Question 6

What lines should be present in a lateral neck xray

Answer 6

Anterior vertebral line
Posterior vertebral line
Spinolaminar line
Posterior spinous line

Question 7

What is the cause of a C1 or Jefferson fracture

Answer 7

impact or load on back of head causing axial loading

Question 8

What is seen on radiograph with a C1 fracture

Answer 8

odontoid cervical X-ray:

widening space between odontoid process and lateral mass

lateral mass laterally displaced relative to lateral mass of C2

Question 9

When is a C1 fracture considered unstable

Answer 9

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

Question 10

C1 fracture management

Answer 10

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)

Question 11

C2 fracture cause

Answer 11

high force hyperextension

Question 12

C2 fracture radiograph findings

Answer 12

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”

Question 13

Management of C2 fracture

Answer 13

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

Question 14

What causes a flexion teardrop fracture

Answer 14

hyper flexion of neck along with vertical axial compression

Question 15

What are flexion teardrop fractures usually associated with

Answer 15

usually associated with cervical spinal cord injuries

Question 16

Flexion teardrop fracture radiograph findings

Answer 16

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

Question 17

Flexion teardrop fracture management

Answer 17

anterior plate stabilization; surgical fixation stabilization

Question 18

What causes C spine dislocation

Answer 18

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

Question 19

What is C spine dislocation usually associated with

Answer 19

usually associated with spinal cord injury

Question 20

C spine dislocation radiograph findings

Answer 20

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

Question 21

C spine dislocation management

Answer 21

Surgical fixation and stabilization

Question 22

Spinal cord injury clinical presentation

Answer 22

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

Question 23

Spinal shock definition and diagnosis

Answer 23

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

Question 24

What are reflexes tested for for spinal shock

Answer 24

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

Question 25

What is neurogenic shock, its pathophysiology and clinical presentation

Answer 25

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)

Question 26

Neurogenic shock treatment

Answer 26

treated by volume replacement if heart is healthy and strong coupled with sympathomimetic drug (neosynephrine or dopamine) if necessary

Question 27

How to clinically assess spinal cord injury

Answer 27

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

Question 28

What is the neurological level of spinal cord injury

Answer 28

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

Question 29

What are zones of partial preservation in a spinal cord injury

Answer 29

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

Question 30

What is considered a complete spinal cord injury

Answer 30

complete has no sensory nor motor function in S4-S5

Question 31

What are the ASIA grades of spinal cord injury

Answer 31

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

Question 32

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

Answer 32

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%

Question 33

Investigations in spinal cord injury

Answer 33

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

Question 34

Management of spinal cord injury

Answer 34

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

Question 35

Branches of the external carotid artery

Answer 35

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 ```

Question 36

Branches of the internal carotid artery

Answer 36

ophthalmic artery before joining into Circle of Willis

Question 37

What arteries feed into the Circle of Willis

Answer 37

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

Question 38

What are the vessels included in the Circle of Willis

Answer 38

``` L & R anterior cerebral artery anterior communicating artery L & R middle cerebral artery posterior communicating artery L & 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

Question 39

What does the common carotid artery give rise to

Answer 39

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

Question 40

What do the vertebral arteries give rise to

Answer 40

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

Question 41

Anterior cerebral arteries feed what part of the brain

Answer 41

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

Question 42

Posterior cerebral arteries feed what part of the brain

Answer 42

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

Question 43

Middle cerebral arteries feed what part of the brain

Answer 43

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

Question 44

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

Answer 44

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

Question 45

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

Answer 45

pontine arteries are branches from basilar arteries between superior cerebellar artery and the anterior inferior cerebellar artery role is to feed the pons

Question 46

Definition of stroke (cerebrovascular event)

Answer 46

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

Question 47

What causes ischemic stroke

Answer 47

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

Question 48

What causes hemorrhagic stroke

Answer 48

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

Question 49

What is a transient ischemic attack

Answer 49

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

Question 50

What is a reversible ischemic neurological deficit (RIND)

Answer 50

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

Question 51

Presentation of anterior cerebral artery stroke

Answer 51

areas of brain affected: frontal lobe contralateral leg paresis and sensory loss may have gait disturbance, urinary incontinence

Question 52

Presentation of middle cerebral artery stroke

Answer 52

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

Question 53

Presentation of posterior cerebral artery stroke

Answer 53

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

Question 54

Presentation of basilar artery stroke

Answer 54

areas of brain affected: brainstem | locked-in syndrome: quadriparesis or quadriplegia, anarthria or dysarthria, impaired horizontal eye movement

Question 55

Presentation of lacunar infarct

Answer 55

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

Question 56

What area is affected in amaurosis fugax

Answer 56

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

Question 57

What is amaurosis fugax

Answer 57

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

Question 58

Fundoscopy findings in amaurosis fugax

Answer 58

pale ischemic fundus with cherry red spot at macula on fundoscopy

Question 59

Next steps after an episode of amaurosis fugax

Answer 59

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)

Question 60

Initial assessment and investigations for acute stroke

Answer 60

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

Question 61

Management of hemorrhagic stroke

Answer 61

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

Question 62

Management of ischemic stroke

Answer 62

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

Question 63

Absolute contraindications for rTPA

Answer 63

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

Question 64

Relative contraindication for rTPA

Answer 64

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

Question 65

Options for ischemic stroke if rTPA is contraindicated

Answer 65

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

Question 66

Major complications of rTPA

Answer 66

rtPA has ~10% risk of hemorrhage symptomatic intracranial hemorrhage in ~5% cases systemic bleeding in <1% cases orolingual angioedema acute hypotension

Question 67

What is not effective for treating acute ischemic stroke

Answer 67

Anticoagulants

Question 68

SAH due to aneurysm rupture management

Answer 68

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

Question 69

What can be used to decrease vasospasm after SAH

Answer 69

nimodipine, a calcium channel blocker used to reduce vasospasm

Question 70

Intracerebral hemorrhage management

Answer 70

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

Question 71

Secondary prevention of stroke

Answer 71

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) ```

Question 72

What is the CHADS2 score

Answer 72

``` 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)

Question 73

Carotid arthersclerosis evaluation

Answer 73

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

Question 74

Carotid artherosclerosis disease management

Answer 74

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

Question 75

What is more common - primary CNS tumour or mets?

Answer 75

Mets

Question 76

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

Answer 76

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)

Question 77

What is a glioma

Answer 77

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

Question 78

What are the most common malignancies metastasizing to the brain

Answer 78

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

Question 79

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

Answer 79

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

Question 80

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

Answer 80

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

Question 81

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

Answer 81

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

Question 82

Presentation with uncal herniation

Answer 82

blown pupil (CN3 oculomotor palsy)

Question 83

Presentation tonsillar herniation

Answer 83

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

Question 84

What is Cushing's reflex

Answer 84

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

Question 85

Presentation of mass effect in the brain

Answer 85

Herniation --> Cushing reflex

Question 86

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

Answer 86

bitemporal hemianopsia

Question 87

Brain tumour diagnosis

Answer 87

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

Question 88

Astrocytoma epidemiology

Answer 88

most common primary intra-axial brain tumor | common in adults between ages 40-60 years

Question 89

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

Answer 89

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

Question 90

Astrocytoma pathophysiology

Answer 90

tumor arising from astrocytes

Question 91

Astrocytoma usual location

Answer 91

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

Question 92

Astrocytoma CT/MRI with contrast findings

Answer 92

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

Question 93

Astrocytoma management

Answer 93

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)

Question 94

Meningioma epidemiology

Answer 94

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

Question 95

Meningioma pathophysiology and usual location

Answer 95

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

Question 96

Meningioma WHO grading system

Answer 96

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

Question 97

Meningioma on CT/MRI with contrast

Answer 97

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

Question 98

Meningioma management

Answer 98

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

Question 99

Meningioma prognosis

Answer 99

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

Question 100

Pituitary tumour epidemiology

Answer 100

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

Question 101

Pituitary tumour classification/pathophysiology

Answer 101

classification based on size and function micro-adenoma = size <1cm; macro-adenoma = size >1cm functional / secretory = endocrine active tumor non-functional = inactive tumor

Question 102

Pituitary tumour presentation

Answer 102

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

Question 103

Potential complication of pituitary tumour

Answer 103

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

Question 104

Pituitary tumour investigations

Answer 104

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

Question 105

Pituitary tumour management

Answer 105

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

Question 106

Brain metastases epidemiology

Answer 106

15-30% cancer patients present with cerebral metastatic tumours

Question 107

Brain mets pathophysiology/usual location

Answer 107

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

Question 108

Brain mets investigations

Answer 108

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

Question 109

Brain mets management

Answer 109

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)