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Semester 4 - Clinical Neuroscience > 14. The anatomy and physiology of stroke > Flashcards

14. The anatomy and physiology of stroke Flashcards

1
Q

What is a stroke?

A

Serious life threatening condition that occurs when the blood supply to part of the brain is cut off. The symptoms and signs persist for more than 24 hours

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2
Q

What is a TIA?

A

“a transient episode of neurological dysfunction caused by focal brain, spinal cord, or retinal ischemia, without acute infarction.”

Similar clinical features of a stroke but completely resolve within 24 hours

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3
Q

WHat are the different types of strokes? (3)

A
  • Ischaemic (85%)
  • Haemorrhage (10%)
  • Other (15%)
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4
Q

what can cause ischaemic stroke?

A

Thromboembolic

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5
Q

what can cause Haemorrhage stroke?

A
  • Intracerebral (rupture of a vessel in brain parenchyma)

- Subarachnoid

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6
Q

What are other causes of strokes? (3)

A
  • Dissection (separation of walls of artery, can occlude branches)
  • Venous sinus thrombosis (occlusion of veins causes backpressure and ischaemia due to reduced blood flow)
  • Hypoxic brain injury (e.g. post cardiac arrest)
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7
Q

What are the 2 main principles for management of stroke?

A
  • Are they within the window for thrombolysis (<4 hours)?

- Do a CT head to determine if it is a bleed (if bleed cannot proceed with thrombolysis)

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8
Q

What imaging technique are used in acute imaging of stroke?

A
  • CT (most common) - ischaemic area of brain not visible early on, however, bleed will show up as bright white area
  • MRI (Sometimes performed) - Ischaemia shows up as a high signal area
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9
Q

Where is weakness in ACA infarct?

A

Contralateral weakness in lower limb (much worse than in upper limba and face)

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10
Q

Where is sensory loss in ACA infarct?

A

Contralateral - lower limb sensory deficit same pattern as motor deficits (sensory homunculus in similar arrangement as motor homunculus)

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11
Q

What are the other features of ACA infarct?

A
  • urinary incontinence
  • apraxia
  • dysarthria/aphasia (unusual)
  • split brain /alien hand syndrome
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12
Q

Which part of the brain controls urinary continence?

A 
Paracentral lobules (the most medial part of the motor/sensory cortices) and supply the perineal
area
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13
Q

Define apraxia.

A

Inability to complete motor planning (e.g. difficulty dressing oneself even when power is normal)
- often caused by damage to left frontal lobe

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14
Q

What is dysarthria/aphasia?

A

Aphasia occurs when someone has difficulty comprehending speech, while dysarthria is characterized by difficulty controlling the muscles used for speech.
• May be related to frontal lobe damage

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15
Q

What causes split brain/alien hand syndrome in stroke?

A

Caused by involvement of corpus callosum which is normally supplied by the ACA

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16
Q

What is the percentage mortality if the main trunk of the MCA is affected?

A

80% - due to resulting cerebral oedema

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17
Q

What are the 3 main points the MCA can be affected?

A
  • Proximal - all branches of MCA will be affected
  • lenticulostriate arteries
  • distal
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18
Q

What is affected in proximal MCA infarct?

A
  • motor
  • sensory
  • visual fields
  • speech
  • Contralateral neglect/inattention
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19
Q

What is the motor loss in proximal MCA infarct?

A

Contralateral full hemiparesis (face, arm and leg
affected)
- Because the internal capsule has been affected which carries fibres to face, arm and leg so even though the MCA supplies the face and arm area of the motor homunculus, this is irrelevant

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20
Q

What is the sensory loss in proximal MCA infarct?

A

o Contralateral sensory loss
Probably in the distribution of primary sensory cortex supplied by MCA (i.e. face and arm), but could involve larger areas if sensory fibres in internal capsule affected

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21
Q

What is the visual field loss in proximal MCA infarct?

A

Usually contralateral homonymous hemianopia without macular sparing
- destruction of both superior and inferior radiations
- maybe quadrantanopia if more distal infarct as they
run through (superior) temporal and parietal lobes

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22
Q

What type of aphasia results from proximal MCA infarct?

A

Global if dominant (usually left) hemisphere affected) - broca’s and wernicke’s area affected
• Therefore, cannot understand or articulate words

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23
Q

Damage to which side of the brain usually causes neglect and what is neglect?

A

Right parietal lobe
- Essentially an issue with not ‘acknowledging’ that the usually left side of space or even your own body exists. Visual fields normal

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24
Q

What are other features of neglect?

A
  • Tactile extinction (if touch each side simultaneously doesn’t feel the affected side)
  • Visual extinction (as with half clock face etc.)
  • Anosognosia
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25
Q

What is anosognosia?

A

literally does not acknowledge that they have had a stroke, so will confabulate to explain disability

26
Q

What are lenticulostriate strokes also called and what do cause damage to?

A
  • Lacunar strokes

- destruction of small areas of internal capsule and basal ganglia

27
Q

What is a distinguishing feature of a lenticulostriate stroke compared to other MCA strokes?

A

They do not cause cortical features (e.g. neglect or aphasia)

28
Q

What are the different types of lenticulostriate strokes?

A
  • pure motor
  • pure sensory
  • sensorimotor
  • many other syndromes
29
Q

describe pure motor lenticulostriate strokes

A

face, arm and leg affected equally, caused by damage to motor fibres travelling through internal capsule due to occlusion of lenticulostriate arteries

30
Q

describe pure sensory lenticulostriate strokes

A

face, arm and leg affected equally, caused by damage to sensory fibres travelling through internal capsule
probably due to occlusion of thalamoperforator arteries and maybe also lenticulostriate

31
Q

describe sensorimotor lenticulostriate strokes

A

mixed, caused by infarct occurring somewhere at boundary between motor and sensory fibres

32
Q

What are the divisions of the distal MCA?

A

Superior and inferior divisions

33
Q

What does the superior division of MCA supply?

A

Lateral frontal lobe

• Including primary motor cortex and Broca’s area

34
Q

What does occlusion of the superior division of the MCA cause?

A

• Occlusion will cause contralateral face and arm weakness and expressive aphasia if left hemisphere affected

35
Q

Why are there no sensory deficits with superior division stroke?

A

Collateral supply to the PSC from the inferior division

36
Q

What does the inferior division of the MCA supply?

A

supplies lateral parietal lobe and superior temporal lobe

• Including primary sensory cortex, Wernicke’s area and both optic radiations

37
Q

What does occlusion of the inferior division of the MCA cause?

A

Occlusion will cause contralateral sensory change in face and arm, receptive aphasia if left hemisphere and contralateral visual field defect without macular sparing (often homonymous hemianopia as both radiations damaged)

38
Q

what does Occlusion of branches distal to superior/inferior division cause?

A

even more specific effects, e.g. taking out Broca’s areas specifically with no motor deficit

39
Q

What are the effects of a PCA infarct?

A

Somatosensory and visual dysfunction typical
• Contralateral homonymous hemianopia (with macular sparing due to collateral supply from MCA)
• Contralateral sensory loss due to damage to thalamus

40
Q

why is there macular sparing in PCA infarct but not in MCA infarct

A

in PCA infarct, the collateral supply from MCA is significant enough whereas if MCA is damaged, the supply from PCA is not enough

41
Q

WHat are the symptoms of a cerebellar infarct?

A

• Nausea • Vomiting • Headache • Vertigo / dizziness

42
Q

On which side do cerebellar signs occur?

A

Ipsilateral

43
Q

What are the signs of cerebellar infarct?

A 
DANISH:
Dysdiadochokinesia
Ataxia (gait and posture)
Nystagmus
Intention tremor
Slurred, staccato speech
Hypotonia/Heel-shin test
44
Q

What other signs may also occur in cerebellar infarct?

A

• ipsilateral Brainstem signs - ipsilateral Horner’s syndrome
- since cerebellar arteries supply brainstem as they loop round to the cerebellum
• Contralateral sensory loss due to damage to thalamus

45
Q

What is a typical feature of a brainstem stroke and how is this explained?

A

Contralateral limb weakness is seen with ipsilateral cranial nerve signs
- damage to corticospinal tracts (above decussation of pyramids) and damage to cranial nerve nuclei on same side

46
Q

WHat can occlusion of the basilar artery cause?

A

As this vessel supplies the brainstem (which contains many vital centres), occlusion can sometimes cause sudden death

47
Q

What are the effects of a distal (superior) basilar artery stroke?

A
  • Visual and oculomotor deficits
  • Behavioural abnormalities
  • Somnolence, hallucinations and dreamlike behaviour (as brainstem contains important centres for sleep regulation - reticular activating system etc.)
  • Motor dysfunction often absent
48
Q

Why is there visual and oculomotor deficits in distal basilar artery occlusion?

A

As basilar sends some branches to midbrain which contains oculomotor nuclei. Also, occlusion at this site can prevent blood flowing into PCAs affecting occipital lobes

49
Q

WHy is motor dysfunction usually absent in distal basilar occclusion?

A

if the cerebral peduncles can get blood from the PCAs which in turn are being filled by the posterior communicating arteries

50
Q

At what level are proximal basilar occlusion?

A

In region of pontine arteries - Embolus in basilar artery can occlude pontine branches on each side

51
Q

What can a proximal basilar occlusion cause?

A
  • Can cause locked in syndrome
  • Complete loss of movement of limbs however preserved ocular movement. Eyes still move because midbrain is getting supply from PCAs via posterior communicating arteries
  • Preserved consciousness (maybe because midbrain reticular formation is still intact)
52
Q

WHat are the different bamford/oxford classifications of strokes?

A
  • TACS (Total Anterior Circulation Stroke)
  • PACS (Partial Anterior Circulation Stroke)
  • POCS (Posterior Circulation Stroke)
  • LACS (lacunar syndrome)
53
Q

What is required for diagnosis of TACS?

A
  1. Unilateral weakness (+/- sensory deficit) of the face, arm and leg
  2. Homonymous hemianopia
  3. Higher cerebral dysfunction
    • Dysphasia / aphasia
    • Visuospatial disorder
54
Q

What is required for diagnosis of PACS?

A 
Only 2 of:
1. Unilateral weakness (+/- sensory deficit) of the face, arm and leg
2. Homonymous hemianopia
3. Higher cerebral dysfunction
• Dysphasia / aphasia
• Visuospatial disorder
55
Q

What is required for diagnosis of POCS?

A

One of:
• Cranial nerve palsy and contralateral motor/sensory deficit
• Bilateral motor/sensory deficit
• Conjugate eye movement disorder
• Cerebellar dysfunction
• Isolated homonymous hemianopia (with macular sparing)

56
Q

What is required for diagnosis of LACS?

A 
One of the following:
• Pure sensory deficit
• Pure motor deficit
• Senori-motor deficit
• Ataxic hemiparesis
57
Q

What is rule 1 of rule of 4s for brainstem?

A

4 cranial nerves from above the pons (including 2 from the midbrain), 4 from the pons, and 4 from the medulla oblongata

58
Q

What is rule 2 for brainstem?

A

4 cranial nerve motor nuclei that are in the mid-line (actually paramedian) are those that divide equally into 12 (3, 4, 6, 12)

59
Q

Which cranial nerve motor nuclei are medial and which are lateral in the brainstem?

A

Paramedian: 3,4,6 (in pons), 12 (in medulla)
Lateral: 5 (pons), 7, 9, 10, 11 (medulla)

60
Q

What is rule 3 for brainstem?

A

There are 4 ‘mid-line’ (i.e. medial, but actually paramedian) structures beginning with ‘m’:

  • Motor pathway (corticospinal tract)
  • Medial lemniscus (dorsal columns)
  • Medial longitudinal fasciculus
  • Motor nuclei (but only 3,4,6,12 - see rule 2)
61
Q

What is rule 4 for brainstem?

A

There are 4 ‘side’ (i.e. lateral) structures beginning with ‘s’:

  • Spinocerebellar pathway
  • Spinothalamic pathway
  • Sensory nucleus (mainly 5)
  • Sympathetics
62
Q

what is the key rule for brainstem pathology?

A 
Ipsilateral cranial nerve signs
\+
Contralateral sensory and motor tract deficits
=
Brainstem pathology

Semester 4 - Clinical Neuroscience (19 decks)

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