Neurosurgery Flashcards
Treatment of cranial nerve palsies secondary to basilar skull fracture
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
Treatment of prolonged leak secondary to basilar skull fracture
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)
Diagnosis of cervical spine fracture
cervical spine fractures diagnosed first on cervical spine X-rays followed by neck CT for further characterization
Indication for cervical spine xray
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
How much soft tissue space should be posterior to the pharynx in a lateral neck xray
<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
What lines should be present in a lateral neck xray
Anterior vertebral line
Posterior vertebral line
Spinolaminar line
Posterior spinous line
What is the cause of a C1 or Jefferson fracture
impact or load on back of head causing axial loading
What is seen on radiograph with a C1 fracture
odontoid cervical X-ray:
widening space between odontoid process and lateral mass
lateral mass laterally displaced relative to lateral mass of C2
When is a C1 fracture considered unstable
unstable if interval between atlas and dens is increased or lateral mass extends laterally beyond axis
C1 fracture management
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)
C2 fracture cause
high force hyperextension
C2 fracture radiograph findings
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”
Management of C2 fracture
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
What causes a flexion teardrop fracture
hyper flexion of neck along with vertical axial compression
What are flexion teardrop fractures usually associated with
usually associated with cervical spinal cord injuries
Flexion teardrop fracture radiograph findings
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
Flexion teardrop fracture management
anterior plate stabilization; surgical fixation stabilization
What causes C spine dislocation
trauma with perching facet joint preventing bones from returning to normal position
What is C spine dislocation usually associated with
usually associated with spinal cord injury
C spine dislocation radiograph findings
lateral neck X-ray: loss of all spine alignment lines, perching of facets
C spine dislocation management
Surgical fixation and stabilization
Spinal cord injury clinical presentation
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
Spinal shock definition and diagnosis
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
What are reflexes tested for for spinal shock
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
What is neurogenic shock, its pathophysiology and clinical presentation
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)
Neurogenic shock treatment
treated by volume replacement if heart is healthy and strong
coupled with sympathomimetic drug (neosynephrine or dopamine) if necessary
How to clinically assess spinal cord injury
assess using ASIA (American Spinal Injury Association) standard neurological classification
What is the neurological level of spinal cord injury
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
What are zones of partial preservation in a spinal cord injury
zone of partial preservation are dermatomes and myotomes caudal to neurological level that have partial motor or sensory function
What is considered a complete spinal cord injury
complete has no sensory nor motor function in S4-S5
What are the ASIA grades of spinal cord injury
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
What is the meaning of the ASIA grade for spinal cord injury
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%
Investigations in spinal cord injury
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
Management of spinal cord injury
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
Branches of the external carotid artery
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
Branches of the internal carotid artery
ophthalmic artery before joining into Circle of Willis
What arteries feed into the Circle of Willis
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
What are the vessels included in the Circle of Willis
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
What does the common carotid artery give rise to
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
What do the vertebral arteries give rise to
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
Anterior cerebral arteries feed what part of the brain
anterior cerebral arteries supply most medial portion of frontal lobe and superior parietal lobe
Posterior cerebral arteries feed what part of the brain
posterior cerebral arteries supply:
medial portion of inferior parietal lobe and occipital lobe
posterior aspect of occipital lobe
Middle cerebral arteries feed what part of the brain
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
What are the origins, names and roles of the 3 cerebellar arteries
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
What is the origin, location and role of the pontine arteries?
pontine arteries are branches from basilar arteries between superior cerebellar artery and the anterior inferior cerebellar artery
role is to feed the pons
Definition of stroke (cerebrovascular event)
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
What causes ischemic stroke
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
What causes hemorrhagic stroke
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
What is a transient ischemic attack
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
What is a reversible ischemic neurological deficit (RIND)
focal cerebral ischemic event with neurological deficit lasting >24 hours followed by full recovery, so the neurological deficits are temporary and last <3 weeks
Presentation of anterior cerebral artery stroke
areas of brain affected: frontal lobe
contralateral leg paresis and sensory loss
may have gait disturbance, urinary incontinence
Presentation of middle cerebral artery stroke
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
Presentation of posterior cerebral artery stroke
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
Presentation of basilar artery stroke
areas of brain affected: brainstem
locked-in syndrome: quadriparesis or quadriplegia, anarthria or dysarthria, impaired horizontal eye movement
Presentation of lacunar infarct
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
What area is affected in amaurosis fugax
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
What is amaurosis fugax
transient monocular visual loss, classically described as curtain going down blocking vision, which then goes away returning to normal vision
Fundoscopy findings in amaurosis fugax
pale ischemic fundus with cherry red spot at macula on fundoscopy
Next steps after an episode of amaurosis fugax
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)
Initial assessment and investigations for acute stroke
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
Management of hemorrhagic stroke
1) blood pressure control to <140mmHg systolic with IV Labetalol
2) immediate interventional radiology for endovascular coiling or neurosurgical consultation for surgical clipping
Management of ischemic stroke
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
Absolute contraindications for rTPA
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
Relative contraindication for rTPA
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
Options for ischemic stroke if rTPA is contraindicated
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
Major complications of rTPA
rtPA has ~10% risk of hemorrhage
symptomatic intracranial hemorrhage in ~5% cases
systemic bleeding in <1% cases
orolingual angioedema
acute hypotension
What is not effective for treating acute ischemic stroke
Anticoagulants
SAH due to aneurysm rupture management
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
What can be used to decrease vasospasm after SAH
nimodipine, a calcium channel blocker used to reduce vasospasm
Intracerebral hemorrhage management
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
Secondary prevention of stroke
- 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) - Atrial Fibrillation
if atrial fibrillation, risk stratify for stroke based on CHADS2 score - 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 - 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)
What is the CHADS2 score
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)
Carotid arthersclerosis evaluation
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
- carotid duplex ultrasound (CDUS)
- magnetic resonance angiography (time of flight, contrast enhanced MRA)
- 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
Carotid artherosclerosis disease management
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
What is more common - primary CNS tumour or mets?
Mets
What are the most common types of primary CNS tumours, benign and malignant?
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)
What is a glioma
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
What are the most common malignancies metastasizing to the brain
1) lung cancer
2) breast cancer
3) melanoma
4) renal cell carcinoma
5) colorectal cancer
other: testicular cancer, lymphoma, leukemia
What is the difference between a tumour that is biologically and histologically malignant
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
What is the sequence of herniation that usually occurs in the brain
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
What is the usual pattern of metastasis for a primary CNS tumour
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
Presentation with uncal herniation
blown pupil (CN3 oculomotor palsy)
Presentation tonsillar herniation
loss of corneal reflex (CN5 & 7), loss of gag reflex (CN 9 & 10), respiratory & cardiovascular collapse -> death
What is Cushing’s reflex
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
Presentation of mass effect in the brain
Herniation –> Cushing reflex
Presentation of tumor related compression of optic chiasm (commonly pituitary tutors)
bitemporal hemianopsia
Brain tumour diagnosis
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
Astrocytoma epidemiology
most common primary intra-axial brain tumor
common in adults between ages 40-60 years
Astrocytoma WHO grading system, typical CT/MRI findings and survival
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
Astrocytoma pathophysiology
tumor arising from astrocytes
Astrocytoma usual location
most common sties: most commonly at cerebral hemispheres, but may occur at cerebellum, brainstem or spinal cord
Astrocytoma CT/MRI with contrast findings
- Heterogenous contrast enhancement
- Ill-defined borders (infiltrative)
- Peritumoural edema
- Central necrosis
- Compression of ventricles, midline shift
Astrocytoma management
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)
Meningioma epidemiology
common in middle aged adults
3 females : 2 males ratio
genetic mutation: loss of NF2 gene, 22q12 deletion
Meningioma pathophysiology and usual location
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
Meningioma WHO grading system
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
Meningioma on CT/MRI with contrast
- extra-axial mass
- classically well circumscribed
- homogeneous densely enhancing mass
- along dural border
Meningioma management
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
Meningioma prognosis
excellent prognosis with >90% 5-years survival with recurrence rate of ~10-20%, which depend on extent of resection
Pituitary tumour epidemiology
common in age 30-40 years, male = female ratio
Pituitary tumour classification/pathophysiology
classification based on size and function
micro-adenoma = size <1cm; macro-adenoma = size >1cm
functional / secretory = endocrine active tumor
non-functional = inactive tumor
Pituitary tumour presentation
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
Potential complication of pituitary tumour
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
Pituitary tumour investigations
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
Pituitary tumour management
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
Brain metastases epidemiology
15-30% cancer patients present with cerebral metastatic tumours
Brain mets pathophysiology/usual location
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
Brain mets investigations
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
Brain mets management
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)
