Neuro17 - Stroke Flashcards

1
Q

5 stuctures supplied by the ACA and 6 consequences of an ACA infarct

Primary Motor Cortex
Primary Somatosensory Cortex
Paracentral Lobules
Broca's Area
Corpus Callosum 
Apraxia
A
  1. ) Primary Motor Cortex
    - causes contralateral limb weakness
    - lower limb affected > upper limb
  2. ) Primary Somatosensory Cortex
    - causes contralateral sensory changes
    - ACA supplies mainly the lower limb distribution
  3. ) Paracentral Lobules - located in the most medial part of the motor and sensory cortex
    - causes urinary incontinence
  4. ) Broca’s Area
    - causes dysarthria (slurred speech) or aphasia
    - however, this is more associated with MCA infarct
  5. ) Corpus Callosum
    - causes split brain/alien hand syndrome (very rare)
  6. ) Apraxia - left frontal lobe
    - inability to complete motor planning (e.g dressing oneself even when power is normal)
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2
Q

5 structures supplied by the distal MCA and 6 consequences of a distal MCA infarct

Primary Motor Cortex
Broca's Area
Primary Sensory Cortex
Wernicke's Area
Both Optic Radiations
Contralateral Neglect
A
  1. ) Primary Motor Cortex - superior division of MCA
    - causes contralateral face and arm weakness
    - supplies mainly the face and arms distribution
  2. ) Broca’s Area - superior division of MCA
    - causes expressive aphasia if left hemisphere affected
  3. ) Primary Sensory Cortex - inferior division of MCA
    - causes contralateral sensory loss in face and arms
    - supplies mainly the face and arms distribution
    - could involve larger areas if sensory fibres in internal capsule are also affected
  4. ) Wernicke’s Area - inferior division of MCA
    - causes receptive aphasia if left hemisphere affected
    - if superior and inferior divisions are occluded, it can cause global aphasia (cannot understand or articulate)
  5. ) Both Optic Radiations - inferior division of MCA
    - homonymous hemianopia w/out macular sparing
    - more distal occlusions may affect only one radiation causing quadrantanopias
  6. ) Contralateral Neglect - right parietal lobe
    - cannot acknowledge the left side of space
    - visual extinction: e.g. half clock face
    - tactile extinction: if you touch each side at the same time, they do not feel the affected side
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3
Q

What are lacunar infarcts/strokes?

3 types of lacunar infarcts

A

Occlusion of lenticulostriate arteries

  • causes destruction of small areas of the internal capsule and the basal ganglia
  • they do not cause cortical features
  1. ) Pure Motor - contralateral full hemiparesis (face, arm, leg affected equally)
    - damaged motor fibres going through internal capsule
  2. ) Pure Sensory - face, arm, leg affected equally
    - damaged sensory fibres through internal capsule
    - can also be caused by occlusion of the thalamoperforator arteries (deep branch of PCA)
  3. ) Sensorimotor - mixed motor and sensory features
    - infarct occurs somewhere at boundary between motor and sensory fibres
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4
Q

2 structures supplied by the PCA and 2 consequences of a PCA infarct

A
  1. ) Primary Visual Cortex
    - homonymous hemianopia w/ macular sparing
    - PVC contains info from both optic radiations
  2. ) Thalamus - thalamogeniculate, thalamoperforater
    - causes contralateral sensory loss in face, arm and legs
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5
Q

Features of brainstem and cerebellar infarcts

Brainstem x2
Cerebellum x3

A
  1. ) Brainstem
    - contralateral limb weakness w/ ipsilateral CN signs
    - damage to to corticospinal tracts and damage to CN nuclei on the same side
  2. ) Cerebellum - ipsilateral cerebellear signs (DANISH)
    - possible ipsilateral brainstem signs since cerebellar arteries supply the brainstem aswell
    - possible contralateral sensory deficit and ipsilateral Horner’s syndrome
    - symptoms: nausea/vomiting, headache, vertigo
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6
Q

3 features of a basilar artery occlusion

Sudden Death
Distal Occlusion x4
Proximal Occlusion

A

1.) Sudden Death - supplies the brainstem (via pontine arteries) which contains many vital centres

  1. ) Distal Occlusion - pontine arteries spared
    - visual and oculomotor deficits (PCA and CNIII nuclei)
    - behavioural abnormalities
    - somnolence, hallucinations, and dreamlike behaviour (sleep regulation and reticular activating system)
    - motor dysfunction often absent since midbrain gets supply from PCA via the posterior communicating artery
  2. ) Proximal Occlusion - causes locked-in syndrome
    - loss of movement of limbs but preserved ocular movement since midbrain gets supply from PCA
    - preserved consciousness because midbrain and reticular formation is still intact
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7
Q

Bamford Classification for Strokes

Total Anterior Circulation Stroke (TACS)
Partial Anterior Circulation Stroke (PACS)
Posterior Circulation Stroke (POCS)
Lacunar Stroke (LACS)

A
  1. ) TACS - all 3 of:
    - unilateral weakness +/- sensory deficit of FAL
    - homonymous hemianopia w/o macular sparing
    - higher cerebral dysfunction: dysphasia, visuospatial disorder
  2. ) PACS - any 2 of the 3:
    - unilateral weakness +/- sensory deficit of FAL
    - homonymous hemianopia w/o macular sparing
    - higher cerebral dysfunction: dysphasia, visuospatial disorder
  3. ) POCS - one of the following:
    - CN palsy and contralateral motor/sensory deficit
    - bilateral motor/sensory deficit
    - conjugate eye movement disorder
    - cerebellar dysfunction
    - homonymous hemianopia w/ macular sparing
  4. ) LACS - one of the following:
    - pure sensory or motor deficit
    - sensorimotor deficit
    - ataxic hemiparesis
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8
Q

Types of Strokes

Ischaemic
Haemorrhagic
Others

A
  1. ) Ischaemic (85%)
    - TOAST classification used for underlying aetiology:
    - 1: large artery atherosclerosis (embolus/thrombosis)
    - 2: small-vessel occlusion, 3: cardioembolism
    - 4: other aetiology, 5: undetermined aetiology
  2. ) Haemorrhagic (10%) - intracerebral or subarachnoid
    - primary: hypertension, cerebral amyloid angiopathy
    - secondary: trauma, anticoagulation-associated
  3. ) Other (5%)
    - dissection: separation of artery walls –> occlusion
    - venous sinus thrombosis: vein occlusion causes back pressure and ischaemia due to ↓blood flow
    - hypoxic brain injury: e.g post-MI
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9
Q

Transient Ischaemic Attacks (TIAs)

Definition
ABCD2 Score
Investigations
Management

A

1.) Definition - focal neurological deficits due to reduced blood supply to the brain, lasting <24 hours

  1. ) ABCD2 Score - risk assessment tool to predict the short-term risk of a stroke after a TIA
    - uses age, BP, clinical features, duration, diabetes
    - score of 4 and above suggests high risk
    - crescendo TIA (2+ in a week) also seen as high risk
    - high risk should be seen in TIA clinic or seen by a stroke physician
  2. ) Investigations
    - blood tests, carotid USS, CT head, MRI brain
  3. ) Management
    - PO aspirin (300mg) OD started immediately
    - lifestyle modification, control BP and hyperlipidemia
    - carotid endarterectomy if carotid stenosis
    - cannot drive for 1 month (3 months if recurrent)
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10
Q

Stroke

Definition
Assessment Tools
Investigations
Enteral Feeding
Differential Diagnoses
A

1.) Definition - focal neurological deficit lasting >24hrs or w/ imaging evidence of brain damage

  1. ) Assessment Tools
    - Bamford classification: identify the vascular region
    - FAST: quick recognition of stroke in public
    - ROSIER scale: distinguish stroke and stroke mimic
    - NIHSS: measures stroke severity, 15 different criteria
    - CHADS-VASC2: suitability for anticoagulation in AF
    - HAS-BLED: risk of bleeding if on anticoagulation
  2. ) Investigations
    - CT-Head to exclude haemorrhagic stroke: ischaemic area becomes hypodense, bleed glows bright white
    - MRI-Brain: ischaemia shows a high signal area
    - carotid USS to examine carotid stenosis
  3. ) Enteral Feeding - NG or PEG
    - patients with poor swallowing to ↓risk of aspiration
    - aspiration can still occur with enteral feeding
  4. ) Differential Diagnoses
    - seizures, space-occupying lesions, multiple sclerosis
    - hemiplegic migraine, sepsis in pre-existing weakness
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11
Q

Management of Strokes

General Management of Ischaemic Stroke
Carotid Endarterectomy
General Management of Haemorrhagic Stroke
Decompressive Hemicraniectomy

A
  1. ) General Management of Ischaemic Stroke
    - thrombolysis with alteplase if < 4.5hrs of onset
    - contraindications: bleeding disorders, recent trauma, haemorrhage, surgery, acute cerebrovascular event
    - lifestyle modification, control BP and hyperlipidemia
    - cannot drive for 1 month
  2. ) Carotid Endarterectomy - ischaemic stroke or TIA
    - patients with stable neurological symptoms
    - carotid stenosis >50%(NASCET) or >70% (ECST)
    - referred w/in 1wk, treated w/in 2wks of onset of sx
  3. ) General Management of Haemorrhagic Stroke
    - PO aspirin (300mg) (rectal/enterally if dysphagic)
    - aspirin until 2wks after the onset of the stroke
    - reversal of anticoagulation
  4. ) Decompressive Hemicraniectomy - haemorrhagic
    - in severe MCA infarct showing rapid neurological deterioration to prevent malignant MCA syndrome
    - referred w/in 24h, treated w/in 48h of onset of sx
    - <60, NIHSS 15+, infarct >50% of MCA (on CT)
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