Neurology Flashcards
What are the classifications of stroke
Classification
▪ Ischaemic stroke = 85%
• 30 % = Large vessel disease
- Carotid/vertebral/subclavian artery stenosis
- secondary to atherosclerosis →arterial plaque
embolism
• 20% = Cardioembolic
o AF (and other arrhythmias), infective
endocarditis, patent foramen ovale
• 15% = Small vessel disease
o Hypertensive disorders and lipohyalinosis →
occlusion of small penetrating arteries →
lacunar strokes
• 15% = Unknown aetiology
• 5% = Rarer causes
o Hypotension, dissection, venous infarction,
vasculopathy
▪ Haemorrhagic stroke = 10%
▪ Other = 5%
Systematically describe the risk factors for stroke
COMORBIDITIES
- Hypertension
- AF
- Hypercholesterolaemia
- Diabetes
- Carotid stenosis
LESS COMMON RISK FACTORS
Polycythaemia/thrombocytosis/thrombophilia/hyperviscosity • Antiphospholipid syndrome • Oestrogen supplementation • Vasculitis • Migraine with aura • HIV and neurosyphilis • Amphetamine/cocaine use
LIFESTYLE
smoking
alcohol
obesity and inactivity
How does stroke present? (not specific symptoms but what do all strokes have in common)
Most common presentation is the acute onset of focal deficits that are persistent
What investigation would you undertake for stroke within
(a) the first hour
(b) the first 24hrs
or;
(c) if initial investigations are negative
Within 1-hour:
• CT or MRI brain
Often not sensitive for infarction for 24-48 hours
• FBC and BSL
Within 24-hours:
- FBC, BSL, coags, lipids, ESR
- ECG (assess for AF)
- Carotid artery doppler
If unknown cause, consider further investigation:
- CT/MRI angiography
- Echocardiogram
- Telemetry
- Vasculitis, thrombophilia, and antiphospholipid screen
In a systematic manner, describe ACUTE management of stroke
- ABCDE assessment
▪ Assess for thrombolysis eligibility
▪ Brain imaging (CT or MRI non contrast)
Haemorrhage → neurosurgery consultation
No haemorrhage → thrombolysis + aspirin
▪ Admission to stroke unit - Antiplatelet therapy and anticoagulation• Antiplatelet therapyo Initiate 300mg of aspirin per day:
- Straight away if thrombolysis is contraindicated
- After 24-hours if thrombolysis is given
o Switch to clopidogrel after 2-weeks• Anticoagulants
o Anticoagulants (DOACs or warfarin) are
initiated after 2-weeks if the stroke
is of cardioembolic aetiologyo There is a 2-week wait due to risk of haemorrhagic transformation of ischaemic stroke
▪ Decompressive craniectomy (if needed)
- May be performed in cases of massive MCA
stroke causing >50% infarction of the
MCA vascular territory → raised ICP
what kind of a things do they do for a patient in the stroke unit.
-Thromboembolism prophylaxis (aspirin → clopidogrel)
• Swallowing assessment
• Assessment and management of medical complications
o Infection, hyper/hypoglycaemia, AF
• Assessment and management of risk factors
• Initiate secondary prophylaxis and give lifestyle advice
• MDT management with physiotherapy, OT, and speech therapy
what are the eligibility criteria for thrombolysis in a pt coming in with acute stroke
ELIGIBILITY
- Pt with persistent neurological deficit diagnosed as stroke by an experienced medical team
- Haemorrhagic stroke excluded by CT
- Onset of stroke is well established
- thrombolysis can occur within 4.5 hrs
what are the exclusion criteria/contraindications for thrombolysis in a pt presenting with acute stroke
There are historical, clinical and laboratory exclusion criteria for stroke
HISTORY
- stroke or trauma in the last 3 months
- any ICH in the past
- major surgery within 2 weeks
- GI or GU bleed in last 3 weeks
- arterial puncture in a non compressible site in the last 7 days
- LP in last 7 days
CLINICAL
- rapidly improving neuro signs
- isolated and minor neuro signs
- seizure at the time of stroke if residual symptoms are due to post ictal phenomena
- symptoms suggestive of SAH even if CT is negative
- persistently high BP >185/110
- active bleeding or acute trauma
LABORATORY
- Platelets <100 000
- INR >1.3 on warfarin
- PTT elevated on heparin
- BSL = <2.8 or >26.2
List and briefly describe secondary stroke prevention after an acute stroke
▪ Antihypertensive therapy
• There is often a transient compensatory rise in BP following a stroke
• BP should be lowered gradually to prevent hypotensive-hypoperfusion
▪ Hypercholesterolaemia management
• Atorvastatin 40mg → aim for total cholesterol <4mmom/L
▪ Lifestyle changes
• Smoking/alcohol cessation, diet change, exercise, weight loss,
▪ Surgery
• Carotid endarterectomy should be performed within 2-week if there is 70-99%
stenosis
▪ Rehabilitation
• Early physiotherapy → relieve spasticity and prevent contractures; assess
eligibility for walking aids
• Speech therapy and further assessment of swallowing
• Psychological support
what is the prognosis for a stroke
Prognosis
▪ 25% die within 2-years; 10% within 1-month
• Higher for haemorrhage vs. stroke
▪ Improvement of symptoms usually peaks ~12-months post-stroke
Which arteries make up the anterior circulation
MCA, ACA, Internal carotid, lenticulostriate arteries
what are expected presentations of the anterior circulation strokes. List them separately
Anterior Circulation Infarcts
Anterior circulation = ACA, MCA, and ophthalmic arteries
Complete MCA stroke (most common)
• Contralateral hemiplegia and facial weakness (arms > legs)
• Hemianopia
• Parietal lobe involvement
o Hemisensory loss
o Neglect syndromes (if non-dominant side
affected)
o Aphasia
Complete ACA stroke • Hemiparesis (leg > arm) • Frontal lobe defects (apathy, apraxia) ▪ Internal carotid artery occlusion • Presents similarly to MCA stroke, but more likely to only have partial signs due to anastomoses
What is medial medullary syndrome?
Which types of stroke causes them?
What neurological structures are affected
What are the resulting deficits
Medial Medullary Syndrome
• Pathology of the PICA or vertebral artery → damaged hypoglossal nerve,
corticospinal tract, and dorsal column
• Ipsilateral tongue palsy, contralateral hemiparesis, and contralateral impaired
proprioception
what presentation would you expect in a Posterior cerebral artery stroke?
Homonymous hemianopia (unilateral) or cortical blindness (bilateral) • Thalamus and temporal lobe involvement → confusion and memory impairment
Expected presentation in a brainstem infarct
Brainstem Infarct
• Variable presentation depending on the affected CN nuclei and spinal cord tracts
• E.g hemiparesis (corticospinal tract), sensory loss (dorsal column/spinothalamic
tracts), facial numbness/weakness, nystagmus, dysarthria/dysphagia (CN
involvement), Horner’s syndrome (sympathetic fibres), coma (reticular formation)
what presentation would you expect in a cerebellar infarct?
Cerebellar Infarcts
• Can occur by itself or with brainstem involvement
• Ataxia, dysmetria, dysarthria
what is the difference between the brain stem and the cerebellum ?
The key difference between brainstem and cerebellum is that brainstem is the region of the brain that connects the brain to the spinal cord, while the cerebellum is the middle part of the brain that helps in motor learning, motor coordination, and equilibrium.
what syndrome results from basillar artery thrombosis?
Locked in syndrome
what are lacunar strokes and what major sign on presentation differentiates them from larger artery strokes?
Mostly occur due to ischaemic aetiology, with hypertension being the number one risk
factor
▪ Most common = posterior internal capsule infarction
▪ Usually present without cortical signs (hemispatial neglect, aphasia, visual field change, etc.)
→ pure motor or sensory strokes, unilateral ataxia, dysarthria…
Define TIA and what are common signs on presentation
Definition
▪ Sudden loss of function that usually only lasts for several minutes, with complete recovery
and no associated findings on neural imaging
▪ Presentation is varied, but the most common signs are hemiparesis and aphasia, and
sometime amaurosis fugax (transient loss of vision in one eye)
▪ Consciousness is usually preserved
A pt comes in having had a TIA what are potential complications you are worried about
Complications
▪ The main complication is the increased risk of vascular event in the future:
• 30% will have a stroke within 5-years (10% in 1-year)
• 15% will have an MI within 5-years
• Highest risk period for having is a stroke is the 2-week period after TIA
o
How would you stratify risk of stroke in a patient coming in with TIA
Risk stratification and investigations ▪ Risk stratification = ABCD2 score (high-risk for stroke within 48-hours if >6) • A = Age >60 (1 point) • B = BP >140/90 (1 point) • C = Clinical features o Unilateral weakness (2 points) o Isolated change in speech (1 point) • D = Duration of symptoms o >60 minutes (2 points) o <60 minutes (1 point) • D = Diabetes mellitus (1 point)
What investigations would you undertake for a patient you suspect has a TIA
Within 1-hour:
• CT or MRI brain
Often not sensitive for infarction for 24-48 hours
• FBC and BSL
Within 24-hours:
- FBC, BSL, coags, lipids, ESR
- ECG (assess for AF)
- Carotid artery doppler
If unknown cause, consider further investigation:
- CT/MRI angiography
- Echocardiogram
- Telemetry
- Vasculitis, thrombophilia, and antiphospholipid screen
Management of TIA?
Management
▪ Assess and manage risk factors
▪ Medical therapy
• 300mg aspirin initially → 100mg ongoing
• Consider statin therapy and anti-hypertensives
▪ Carotid artery stenting/endarterectomy if severe stenosis
Intracerebral haemorrhage 1. Definition 2. aetiology 3. presentation reflect on how these 3 aspects differ from stroke
Intracerebral Haemorrhage
▪ Definition
• Haemorrhage into the brain parenchyma, usually arising from rupture of small
arteries perfusing the basal ganglia, thalamus, and brainstem
▪ Aetiology
• Most common cause = hypertension
• Other causes = amyloidosis, haemorrhagic conversion of ischaemic stroke, AVM,
drug-use-associated, cancer-related, trauma-related
▪ Presentation
• Sudden-onset focal neurological deficit in the context of headaches and
hypertension
Mx of intracerebral haemorrhage
Management
• ABCDE
• Admit to stroke unit
• Investigations = FBC, BSL, and brain CT
• Cease anticoagulants/anti-platelets
• Maintain systolic BP <140 +/- mannitol to decrease ICP
o Nicardipine or nimodipine drip
• Neurosurgical consult → haematoma evacuation +/- ventricular drain
• Monitor for hyponatraemia (cerebral salt wasting and SIADH)
Define a SAH
Definition
• Haemorrhage into the subarachnoid space +/- intraparenchymal haemorrhage
What are the brain layers from top to bottom
- skull
- dura mater
- arachnoid mater
- pia mater
- brain parenchyma
Aetiology SAH
Aetiology • Berry aneurysm of larger cerebral arteries (70%) o PcommA + ICA junction (causes painful CN 3 palsy) o AcommA + ACA junction o MCA trifurcation 91 • AVM (10%) • Unknown/other (20%)
Presentation of SAH
Presentation
• As opposed to intra-cerebral haemorrhage, focal neurological deficits are less
common and are not the sentinel finding
• Severe thunderclap headache, possibly preceded by a sentinel headache several
days/weeks earlier
• Neck stiffness, photophobia and possible focal neurology
What investigations would you consider in a subarachnoid haemorrhage and what findings would you expect@
CT non-contrast → ‘chicken sign’
•
LP → yellow CSF (xanthochromia secondary to bilirubin in CSF)
Treatment of SAH
Initial work-up and management as per ICH
• Unruptured → endovascular coiling or clipping
• Associated hydrocephalus → ventricular drain
• Maintain BP <140 systolic with nimodipine
• Monitor for hyponatraemia (cerebral salt wasting and SIADH)
• Consider haematoma evacuation
• Consider anti-epileptic prophylaxis if high-risk
Subdural haemorrhage aetiology and presentation
Aetiology
• Rupture of bridging veins in the subdural space, usually secondary to minor trauma
in people with risk factors
• Older age and alcohol → cortical atrophy → increased exposure of bridging veins →
more prone to trauma
• Alcohol and falls-risk → increased risk of bridging vein trauma
• Alcohol and anticoagulants → increased bleeding risk
Presentation
• Usually gradual onset over weeks-months with headaches, drowsiness, confusion →
possible focal neurology → coma/death
management and investigation of subdural haemorrhage
Investigations
• CT brain → concave (banana-shaped) bleed
Management
• May be managed with ongoing monitoring and serial imaging; even large collections
can resolve spontaneously
aetiology and presentation of extradural haemorrhage
Aetiology
• Rupture of the middle meningeal artery, usually secondary to trauma at the pterion
▪ Presentation
• Initial loss of consciousness → lucid interval → decline in function
o Stupor, ipsilateral pupil dilation, contralateral hemiparesis
• Signs of raised ICP and coning
what investigations are done in an extradural haemorrhage
Investigations
• CT or MRI → convex (lemon-shaped) bleed that does not cross suture lines
What is the management of in an Extradural Haemorrhage?
Urgent surgical decompression
What is the Aetiology/pathogenesis in Venous Sinus Thrombosis?
- Thrombosis of the venous sinuses within the brain
- Associated with risks for hypercoagulability (female, OCP, pregnancy, obesity, dehydration, thrombophilia), though can occur idiopathically or secondary to trauma
What is the Presentation in Venous Sinus Thrombosis?
- Cortical veins involvement → venous infarct → focal neurology
- Dural veins involvement → raised ICP → headache, papilloedema, eye pain, fever, seizures, coma
What are the Investigations in Venous Sinus Thrombosis?
MRI or CT with contrast in the venous phase
What is the Management in Venous Sinus Thrombosis?
Initial LMWH therapy → conversion to DOAC or warfarin therapy for 6-months
What are the Diagnostic Criteria for Dementia?
o Acquired loss of mental function affecting 2 or more cognitive domains, including:
▪ Episodic memory (acquisition of new information)
▪ Language function
▪ Frontal executive function (ability to make decisions)
▪ Visuospatial function
▪ Apraxia (impaired movement)
o Must cause significant social or occupational impairment
o Must not be better explained by another pathology
▪ Especially delirium, which is typically acute and fluctuating)
What is the Epidemiology for Dementia?
> 20% of people aged >80 years are affected
What is the Assessment in Dementia?
o Bedside cognitive assessments to screen for dementia
▪ Mini-Mental State Examination (MMSE)
• Considered positive if <25
▪ Montreal Cognitive Assessment (MOCA)
• Testing of memory, visuospatial ability (drawing a clock), executive function, attention, language, abstraction, recall, and orientation to time, person, and place
• Positive if <26
▪ Addenbrooke’s Cognitive Examination (ACE)
• Best done as a supplement to the MMSE
o Detailed neuropsychiatric assessment
▪ Performed by a specialist physician, usually a Geriatrician
▪ Depression is a common cause of dementia-like symptoms, and depression also commonly occurs secondary to dementia
o Physical examination to assess for comorbidities and differential diagnoses
▪ Thorough neurological assessment to screen for possible Parkinson’s, brain lesions, delirium, raised ICP, etc.
o Assessment of functional ability
▪ Assessment of the patient alongside a collateral history to determine the severity of their condition and their ability to complete ADLs
▪ Are they a danger to themselves (can they drive, cook, wash themselves, ambulate?)
▪ Are they a danger to others (are they prone to bursts of aggression/violence?)
o Assessment for polypharmacy and substance use
What are the Investigations in Dementia?
Investigation of dementia is largely aimed at ruling out differential diagnoses and assessing for reversible causes
o FBC – infection
o Vitamin B12 and thiamine levels
o BSL - hypoglycaemia → dementia-like syndromes
o LFTs – hepatic encephalopathy
o CMP and UECs – electrolyte derangements (especially sodium and calcium)
o TFTs – hypothyroidism can cause cognitive impairment
o HIV serology
o Syphilis serology – assessment for tertiary syphilis
o CT/MRI – assessment of structural lesions or hydrocephalus
▪ Alzheimer’s is associated with hippocampal atrophy, and FTLD is associated with temporal/frontal lobe atrophy
o CSF – assessment for specific proteins or infective aetiology
o EEG
What are the types of Dementia?
o Alzheimer’s Disease (64%)
▪ Most common form of dementia
▪ Typical features include:
• Marked reduction in day-to-day memory and ability to learn new things.
Amnesia for more recent events is far more affected than events in the distant past
• Difficulty with finding the right words and naming of objects
• Impaired frontal executive function
• Impaired skilled motor movements
o Normal walking is intact very late into disease progression; hence patients often go wandering and get lost
• Personality change is usually not seen until very late stages (in contrast to other types of dementia)
• Late stage features → myoclonus, reversed sleep-wake cycles, impaired swallowing
▪ Associated with atrophy of the temporal lobe and hippocampus on MRI
▪ Definitive diagnosis can only be made post-mortem with the presence of betaamyloid depositions in the cerebrum
o Vascular Dementia (17%)
▪ Dementia that occurs via multiple aetiologies that ultimately result in neurological impairment secondary to multiple small strokes
▪ Risk factors for vascular disease are usually present
▪ Features of apraxia, pyramidal signs, and urinary incontinence are common
o Mixed Dementia (10%)
▪ Mix of multiple forms of dementia, most commonly Alzheimer’s and vascular dementia
o Dementia with Lewy Bodies (4%)
▪ Dementia occurring secondary to deposition of alpha-synuclein-containing Lewy bodies throughout the brain
▪ Associated with early disorders of REM sleep, visual hallucinations, and Parkinsonism – changes in memory usually appear later
o Frontotemporal Lobe Dementia (2%)
▪ Presents in various ways depending on whether the frontal or temporal lobe is more affected
▪ Frontal lobe involvement → personality change, emotional dysregulation/blunting, apathy, disinhibition, and usually preserved memory
▪ Temporal lobe involvement → progressive aphasia (usually Wernicke’s aphasia/receptive aphasia)
▪ Can be diagnosed with asymmetric involvement of the frontal and/or temporal lobes on MRI
▪ More commonly seen in adults <65-years
What is the Management for Dementia?
o MDT management
▪ GP, geriatrician, social supports, aged-care nursing, family and patient education
o Assessment and management of reversible/contributory causes
▪ Hormonal/vitamin/electrolyte anomalies, polypharmacy, substance use
o Cholinesterase inhibitors (donepezil or rivastigmine)
▪ Alzheimer’s disease is associated with an ACh deficit in the CNS
▪ Increased neural ACh → improved function
▪ Not effective in FTLD or vascular dementia
o NMDA receptor antagonists (Memantine)
▪ If cholinesterase inhibitors are not effective
o Antipsychotics and antidepressants
▪ Antidepressants should be trialed if depression is present
▪ Anti-psychotics may be necessary in later-stages of disease due to agitation and patient distress
o Advanced care planning
What are the Differentials for Dementia?
In addition to the causes mentioned above
o Normal pressure hydrocephalus
▪ Idiopathic hydrocephalus → triad of dementia, urinary incontinence, and gait abnormalities
• “weird, wet, and wobbly”
o Wernicke-Korsakoff Syndrome
▪ Permanent progression from Wernicke’s encephalopathy occurring secondary to thiamine deficiency, usually in chronic alcoholics
▪ Causes severe anterograde and retrograde amnesia, with some confusion, but otherwise intact cognition
o Pseudodementia
▪ Dementia-like symptoms associated with severe major depression
What is the Pathogenesis/pathology of Multiple Sclerosis?
▪ T-cell-mediated inflammation of the CNS → CNS demyelination and plaque formation → broad spectrum of clinical manifestations presenting over time
▪ Plaques occur secondary to inflammatory-mediated axonal destruction and oligodendrocyte atrophy
▪ Plaques can occur anywhere in the CNS, but over-represented sites include the optic chiasm, periventricular area, corpus callosum, and brainstem connections
What is the Aetiology of Multiple Sclerosis?
▪ Unknown, but there is a suspected genetic susceptibility and an association with EBV and HHV-6 infection
▪ Risk factors = low vitamin D, smoking, and obesity
What is the Epidemiology of Multiple Sclerosis?
▪ Increased prevalence in women and Caucasians
▪ Peak onset between ages 20-40
What are the Classification of presentations in Multiple Sclerosis?
There are various clinical courses that MS can follow, and the courses can change between each other
▪ Relapsing-Remitting = 85%
• MS with acute flares in which there is a decrease in function, but return to baseline (or close to baseline) upon resolution before the next attack
• Progresses into secondary progressive MS in 75% of cases
▪ Secondary Progressive
• Initial relapsing-remitting MS that deteriorates such that there is no return of function back to baseline, and functionality deteriorates continuously with time
▪ Primary Progressive = 10-15%
• Deterioration of function with time from the onset of symptoms
▪ Relapsing Progressive = <5%
• As per primary progressive, but with acute episodes of deteriorating function dispersed throughout
What is Multiple Sclerosis
- what are common manifestations (no need to describe clinical course)
Highly variable presentation of MS between people. The disease is characterised but neurological signs and loss of function that occurs with time and follows one of the above
clinical courses
▪ Optic neuritis (common; often earliest finding)
• Inflammation of the optic nerve → blurred vision, visual field defects, and pain with eye movement
▪ Brainstem involvement
• Cranial nerve palsies, usually 1-8 → facial numbness/weakness, diplopia, vertigo, nystagmus, dysarthria, dysphagia, etc.
• Internuclear Ophthalmoplegia
o Lesion of the medial longitudinal fasciculus → impaired conjugate lateral gaze
o Able to adduct both eyes with convergence (looking at your nose), but unable to adduct the eye ipsilateral to the lesion when looking towards the contralateral direction (the abducting eye will usually have nystagmus)
▪ Spinal cord involvement
• Dorsal column → impaired vibration, fine touch, and proprioception, usually asymmetrical
o Usually the first sensory sign observed in MS
• Corticospinal tract → spasticity and hyper-reflexia +/- Babinski
▪ Cerebellum involvement
• Scanning speech (individual syllables over-pronounced)
• Nystagmus
• Intention tremor
▪ Autonomic involvement
• Bowel and bladder incontinence/retention, and impaired sexual activity
▪ Memory deficits, altered concentration and depression
• Relatively late signs
▪ Other
• Lhermitte’s sign = shooting electrical pain down the spine with neck flexion
• Uhthoff’s phenomenon = temporary exacerbation of neurological symptoms with heat exposure (exercise, fever, hot shower, etc.)
• Pseudobulbar palsy = UMN lesion of CNs 9, 10, and 12 → spasticity of associated muscles and labile emotions
What are the Diagnosis/Investigations of Multiple Sclerosis?
▪ Gold standard = Brain and spine MRI → plaque visualization
• Usually periventricular
- Investigations to rule out differentials
• B12, SLE, thyroid pathology, sarcoidosis, HIV, etc.
▪ Diagnosis may be made clinically with multiple lesions separated by space (CNS location) and time
▪ CSF electrophoresis → oligoclonal IgG bands
• Relatively non-specific; associated with a poorer prognosis
What is the pharmaceutical medical management of Multiple Sclerosis?
▪ Medical Management
• Acute exacerbation
o High-dose glucocorticoids (500-100 mg/day IV methylprednisolone)
• Maintenance therapy
o Initial induction therapy with strong immunosuppressants →
o Glatiramer, interferon-beta therapy, or natalizumab
What is the Prognosis of Multiple Sclerosis?
▪ Very variable depending on age of presentation and specific clinical course
▪ Decreased life expectancy by 7-years on average
▪ Average time to being wheelchair dependent = ~25-years
What is the definition of Motor Neurone Disease (MND)?
o MND is an umbrella term for a disease that causes progressive deterioration of UMNs and LMNs with sparing of sensory neurons
o The most common form of MND is Amyotrophic Lateral Sclerosis (ALS)
o Second most common cause = progressive bulbar or pseudobulbar palsy
▪ Spasticity of CNs 7-12 with associated emotional lability (PPP)
Who is more likely to hae MND and what is the peak age of onset?
o Men > women
o Peak age = 50-75
