Stroke Flashcards

(21 cards)

1
Q

Stroke

A

Examine this patient’s limbs neurologically and then proceed to examine anything else that you feel is important.

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2
Q

Clinical signs of Stroke

A
  1. Inspection: walking aids, nasogastric tube or PEG tube, posture (flexed upper limbs and extended lower limbs), wasted or oedematous on affected side.
  2. Tone: spastic rigidity, ‘clasp knife’ (resistance to movement, then sudden release). Ankles may demonstrate clonus (>4 beats).
  3. Power: reduced.
  4. Coordination: sometimes reduced. Usually impaired due to weakness but may reflect cerebellar involvement in posterior circulation stroke.
  5. Reflexes: brisk with extensor plantars
    Offer to
  6. Walk the patient if they are able to, to demonstrate the flexed posture of the upper limb and ‘tip toeing’ of the lower limb.
  7. Test sensation (this is tricky and should be avoided if possible!). Proprioception is important for rehabilitation.
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3
Q

Other signs of Stroke

A
  1. Upper motor neurone unilateral facial weakness (spares frontalis due to its dual innervation).
  2. Gag reflex and swallow to minimize aspiration.
  3. Visual fields and higher cortical functions, e.g. neglect helps determine a Bamford classification.
  4. Signs of the Cause: irregular pulse (AF), blood pressure, cardiac murmurs or carotid bruits (anterior circulation stroke).
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4
Q

Medical Research Counsil (MRC) graded muscle strength:

A

0, none
1, flicker (Fasiculation)
2, moves with gravity neutralized (not against gravity)
3, moves against gravity
4, reduced power against resistance
5, normal
Extensors are usually weaker than flexors in the upper limbs and vice versa in the lower limbs.

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5
Q

Definitions of Stroke

A

• Stroke: rapid onset, focal neurological deficit due to a vascular lesion lasting > 24 hours.

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6
Q

Definition of Transient ischaemic attack (TIA):

A

• TIA: focal neurological deficit lasting < 24 hours.

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7
Q

Investigation of Stroke

A
  1. Bloods: FBC, CRP/ESR (young CVA may be due to arteritis), glucose and renal function
  2. ECG: AF or previous infarction
  3. CXR: cardiomegaly or aspiration
  4. CT head: infarct or bleed, territory
  5. Consider
    Echocardiogram,
    Carotid Doppler,
    MRI/A/V (dissection or venous sinus thrombosis in young patient),
    Clotting screen (thrombophilia),
    Vasulitis screen in young CVA
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8
Q

Acute Management of Stroke

A
  1. Thrombolysis with tPA (within 4.5 hours of acute ischaemic stroke)
  2. Clopidogrel (or aspirin + dipyridamole)
  3. Referral to a specialist stroke unit: multidisciplinary approach: physiotherapy, occupational therapy, speech and language therapy and specialist stroke rehabilitation nurses
  4. DVT prophylaxis
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9
Q

Chronic Management of Stroke

A
  1. Carotid endarterectomy in patients who have made a good recovery, e.g. in PACS (if >70% stenosis of the ipsilateral internal carotid artery)
  2. Anticoagulation for cardiac thromboembolism
  3. Address cardiovascular risk factors
  4. Nursing +/− social care.
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10
Q

Bamford classification of stroke (Lancet 1991)

A
  1. Total anterior circulation stroke (TACS)
    • Hemiplegia (contra‐lateral to the lesion)
    • Homonomous hemianopia (contra‐lateral to the lesion)
    • Higher cortical dysfunction, e.g. dysphasia, dyspraxia and neglect
  2. Partial anterior circulation (PACS) • 2/3 of the above
  3. Lacunar (LACS) • Pure hemi‐motor or sensory loss
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11
Q

Prognosis at 1 year (%) for TACS

A
  • Dead 60%
  • Dependent 35%
  • Independent 5%
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12
Q

Prognosis at 1 year (%) for PACS

A
  • Dead 15%
  • Dependent 30%
  • Independent 55%
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13
Q

Prognosis at 1 year (%) for LACS

A
  • Dead 10%
  • Dependent 30%
  • Independent 60%
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14
Q

Dominant parietal‐lobe cortical signs (Stroke)

A
  1. Dysphasia: receptive, expressive or global
  2. Gerstmann’s syndrome
    • ⚬⚬ Dysgraphia, dyslexia and dyscalculia
    • ⚬⚬ L‐R disorientation
    • ⚬⚬ Finger agnosia
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15
Q

Non‐dominant parietal‐lobe signs (Stroke)

A
  1. Dressing and constructional apraxia

2. Spatial neglect

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16
Q

Either parietal‐lobe signs

A
  1. Sensory and visual inattention
  2. Astereognosis
  3. Graphaesthesia
17
Q

The lesion == What is the Visual field defects?

  1. Optic Nerve
  2. Optic Chiasm
  3. Optic Tract
  4. Optic Radiation (Parietal lobe)
  5. Optic Radiation (Temporal lobe)
A

Visual field defects

  1. Optic Nerve => Unilateral field defect
  2. Optic Chiasm => Bitemporal Hemianopia
  3. Optic Tract => Homonymous Hemianopia
  4. Parietal lobe => Inferior Homonymous Quadrantinopia
  5. Temporal lobe => Superior Homonymous Quadrantinopia
18
Q

Lateral medullary (Wallenberg) syndrome

A
  • Most common brainstem vascular syndrome
  • Due to occlusion of posterior inferior cerebellar artery (PICA)
  • Often variable in its presentation
19
Q

Brainstem structures affected by Unilateral lesion of Lateral medullary (Wallenberg) syndrome

A
  1. Vestibular Nucleus
  2. Inferior Cerebellar Peduncle
  3. Descending Sympathetic Tract
  4. CN 5 Descending Spinal Tract
  5. CN 5 Spinal Nucleus
  6. Spinothalamic Tract
  7. Nucleus Tractus Solitarius (CN 7, 9, 10)
  8. Nucleus Ambiguus (CN 9, 10)==> Specific to PICA
20
Q

Clinical consequences of Lateral medullary (Wallenberg) syndrome (PICA) Ipsilateral to lesion (e.g. on right with right‐sided infarction)

A
  1. Nystagmus (Present with vertigo and vomiting) => Vestibular nucleus
  2. Cerebellar signs => Inferior cerebellar peduncle
  3. Horner syndrome => Descending sympathetic tract
  4. Loss of trigeminal pain and temperature sensation => Trigeminal nerve (CN V) spinal nucleus and tract
  5. Palatal paralysis and decreased gag reflex => Nucleus ambiguus (CN IX and X)
21
Q

Clinical consequences of Lateral medullary (Wallenberg) syndrome (PICA) Contralateral to lesion (e.g. on left with right‐sided lesion)

A

Loss of pain and temperature sensation => Spinothalamic tract