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Sem 4: Nervous System > 10a.) Stroke > Flashcards

10a.) Stroke Flashcards

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1
Q

Define a stroke

A
  • A neurological deficit attributed to an acute focal injury of the central nervous system by a vascular cause, including cerebral infarction, intracerebral haemorrhage and subarachnoid haemorrhage
  • “Serious life-threatening condition in which blood supply to part of brain is cut off. Signs & symptoms persist for more than 24 hours”
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2
Q

Define TIA (transient ischaemic attack)

A
  • A transient episode of neurological dysfunction caused by focal brain, spinal cord or retinal ischaemia without acute infarction
  • “Mini stroke- similar features of a stroke but completely resolve within 24 hours”
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3
Q

State the 3 broad categories of stroke and for each include:

  • Any subdivisions
  • % of strokes that are this category
A
  • Ischaemic (85%)
    • Thromboembolic
  • Haemorrhagic (10%)
    • Intracerebral (rupture of vessel in brain parenchyma)
    • Subarachnoid
  • Other (5%)
    • Dissection (separation of walls of atery which can lead to blood accumulating in the separation and occluding the branches of the artery)
    • Venous sinus thrombosis (occludes veins and causes backpressure & reduced blood flow resulting in ischaemia)
    • Hypoxic brain injury
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4
Q

The emergency management of strokes is based on two main principles; state these two main principles

*NOTE: more stroke teaching later on in unit

A
  • Are they in the window for thrombolysis? (<4hrs)
  • Do a CT head to determine if it is a haemorrhagic or ischaemic stroke (as cannot give thrombolysis if it is a haemorrhagic stroke)
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5
Q

What imaging is preferred in suspected stroke, MRI or CT?

A

CT

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6
Q

Describe the appearance of an ischaemic stroke on CT

A
  • Ischaemic area of brain not visible early on
  • But as the infarct becomes more established ischaemic area will become more hypodense (darker)
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7
Q

Describe the appearance of a haemorrhagic stroke on a CT scan

A
  • Bright white area, maybe with mass effect
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8
Q

Describe the appearance of ischaemia on an MRI

A

High signal area (bright)

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9
Q

What 2 things does the clinical features of a stroke depend on?

A
  • Anterior or posterioc circulation (specifically if was ACA, MCA or PCA)
  • Whether pathology is in the proximal or distal territory
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10
Q

Describe the classical presentation of someone who has had an anterior cerebral artery infarct

*7 points to disucss

A
  • Contralateral weakness in lower limb
    • Homunculus and primary motor cortex
  • Lower limb affected much worse than face
    • Homunculus
  • Contralateral sensory changes in same pattern as motor deficits
    • Homunculus and primay somatosensory cortex
  • Urinary incontinence
    • Paracentral lobules are essentially the most medial part of the motor/sensory cortices and supply the perineal area
  • Apraxia
    • An inability to complete motor planning often caused by damage to left frontal lobe
  • Dysarthria/aphasia
    • Unusual in ACA (in comparison to MCA infarcts where it is common) may be present if damage to frontal lobe
  • Split brain syndrome/alien hand syndrome
    • ACA normally supplies corpus callosum hence may get damage to corpus callosum so hemispheres can’t communicate
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11
Q

MCA infarcts in the main trunk of the MCA have an 80% mortality associated with them; suggest why the mortality is so high for MCA infarcts

A
  • MCA supplies large area of brain (lateral frontal & parietal lobes, superficial temporal lobes, lentiform nucleus, caudate nucleus, internal capsule)
  • If the main trunk of MCA is affected large area of brain will be affected and hence there will be lots of cerebral oedema
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12
Q

Can haemorrhagic transformation occur in a stroke?

A

Yes, idea that is was initially an ischaemic stroke however the vessels in the infarcted area break down and it becomes a heamorrhagic stroke

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13
Q

The MCA can become occluded, and result in a stroke, in 3 places; state and describe the position of these 3 places

A
  • Proximal (after where it branches/continues off the ICA and before the lenticulostriate arteries)
  • Lenticulostriate artery/arteries
  • Superior or inferior division
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14
Q

Describe the classical presentation of someone who has had a proximal MCA occlusion/stroke

A

All branches of MCA willbe affected:

  • Contralateral full hemiparesis (in which face, arm and leg are affected)
    • Homunculus would make us think only face and arms affected however because MCA supplies internal capsule and the IC carries fibres to face, arm AND leg the leg is affected
  • Contralateral sensory loss in face and arm
    • Most likely face and arm due to homunculus however if sensory fibres in IC capsule affected may be larger area
  • Visual field defects
    • Destruction of both superior & inferior optic radiations which would lead to contralateral homonymous hemianopia without macular sparing. NOTE: more distal occlusions may only affect one radiation causing quandrantanopia
  • Aphasia
    • Global if the dominant hemisphere affected (remember dominant hemisphere is usually left)- can’t understand or express words (Wernicke’s & Broca’s aphasia)
  • Contralateral neglect
    • Usually occurs if lesion in right parietal lobe. Don’t acknowledge left side of space, or even own body, exists
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15
Q

Describe neglect, include:

  • What is is
  • Where lesion usually is
  • Other features
A
  • Don’t acknowledge left side of space or even own body exists despite visual fields being normal
  • Lesion usually in right parietal lobe
  • Other features:
    • Tactile extinction: if touch either side simultaneously doesn’t feel the affected side
    • Visual extinction: if ask to draw clock face will only put numbers on the right side
    • Anosognosia: does not acknowledge that they have had a stroke so will confabulate (fabricate imaginary experinces) to explain disability
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16
Q

What is anosognosia?

A

Lack of understanding, awareness, or acceptance that you have a medical condition

*In relation to stroke, it happens as a feature of neglect; person does not belive they have had a stroke and will confabulate (make up imaginary experiences) to explain their disability

17
Q

If a lenticulostriate artery/arteries are occluded, what kind of stroke do we call this?

A

Lacunar stroke

18
Q

Describe the differnt types of lacunar stroke and describe the typical presentation for each

A

Lacunar stroke means lenticulostriate artery/arteries are affected. LS arteries supply internal capsule, lentiform nuclues and caudate nucleus. Since there are numerous lenticulostriate arteries you can have different types of lacunar strokes:

  • Pure motor
    • Face, arm, leg affected equaly due to damage to motor fibres travelling in IC
  • Pure sensory
    • Face, arm, leg affected equally due to damage to snesory fibres travelling in IC and proabably due occlusion of thalmaoperforator arteries and maybe also lenticulostriate
  • Sensorimotor
    • Mixed motor & sensory due to infarct somewhere at boundary between motor & sensory fibres
  • Other (don’t need to worry about)
19
Q

Why could an occlusion of thalamoperforator arteries lead to pure sensory stroke?

A

Thalamus is the ‘hub’ to relay sensory information to the cortex

20
Q

What feature, of the presentation, allows you to distinguish a lacunar stroke from say a proximal MCA infarct?

A

Lacunar stroke= NO CORTICAL FEATURES

Proximal MCA= CORTICAL FEATURES

21
Q

Distally, the MCA splits into superior and inferior division. Describe the classical presentation of someone who has an occlusion in the superior division

A

Superior division essentially supplies lateral frontal lobe including primary motor cortex & Broca’s area hence occlusion will cause:

  • Contralteral face and arm weakness
  • Expressive aphasia (if left hemisphere affected)
22
Q

Distally the MCA splits into superior and inferior divisions. Describe the classical presentation of an occlusion in the inferior divison

A

Inferior divisoin essentially supplies the lateral parietal lobe and superior temporal lobe hence it supplies primary sensory cortex, Wernicke’s area and both optic radiations. Hence will present with:

  • Contralateral sensory changes in face and arm
  • Receptive aphasia (if left hemisphere)

Contralateral visual field defect without macular sparing (often contralateral homonymous hemianopia as both radiations damaged)

23
Q

MCA splits into superior and inferior divisions; state which area each division supplies

A
  • Superior divison: lateral frontal lobe
  • Inferior division: lateral parietal and superior temporal
24
Q

If you occluded branches distal to the superior and inferior divisions of MCA what kind of presentation would you get?

A

More specific effects e.g. you might just damage Broca’s area hence have expressive dysphasia but with no motor deficit

25
Q

Describe the typcial presentation of a PCA infarct

A

PCA supplies occipital lobe, inferior temporal lobe, thalamus (via thalamoperforator & thalamogeniculate arteries) and the midbrain hence will present with:

  • Contralateral sensory loss due to damage to thalamus
  • Contralateral homonymous hemianopia WITH macular sparing (due to collateral supply from MCA)
26
Q

Explain why occlusion of proximal MCA results in no macular sparing whereas occlusion in PCA results in macular sparing

A
  • Occlusion in proximal MCA: although the visual cortex has a collateral supply from PCA, if you occlude MCA you will damage both optic radiations hence macular will not be spared (even though you could have collateral blood supply no information can get there on that side)
  • Occlusion in PCA: collateral supply from MCA and optic radiations intact
27
Q

Describe the classical presenation of a cerebellar infarct (include both symptoms and signs- for signs think DANISH)

A

Symptoms

  • Nausea
  • Vomitting
  • Headache
  • Vertigo/dizziness

Signs

  • Ipsilateral cerebellar signs:
    • Dysdiadochokinesis
    • Ataxia
    • Nystagmus
    • Intention tremor
    • Slurred speech (dysarthria)
    • Hypotonia
  • Possible ipsilateral brainstem signs since cerebellar arteries also supply brainstem as they loop round to get to cerebellum
  • Possible contralateral snesory deficit/ipsilateral Horner’s due to brainstem involvement
28
Q

Explain why you can get ipsilateral Horner’s syndrome in PCA occlusion

A
29
Q

State, and explain, the two typical features of brainstem strokes

A
  • Contralateral limb weakness: damage to lateral coricospinal tracts before they decussate in medulla
  • Ipsilateral cranial nerve signs: due to damange to cranial nerve nuclei on ispsilateral side
30
Q

Why can occlusions of basilar artery cause sudden death?

A

Basilar artery gives rise to cerebellar arteries which also supply brainstem; brainstem contians many vital centres hence if blood supply to these areas is interupted it can cause sudden death

31
Q

Describe what we mean by an occlusion of the:

  • Distal (superior) basillar artery
  • Proximal basillar artery
A
  • Distal: after the pontine branches
  • Proximal: level of pontine branches
32
Q

Describe the classical presentation of an occlusion in the distal (superior) basillar artery

A
  • Visual defects
    • Occlusion may prevent blood flow through PCAs which supply occipital lobe
  • Occulomotor defects
    • Basilar artery sends branches to the midbrain (in particular superior cerebellar artery which could be affected by a distal basillar artery occlusion)
  • Behavioural abnormalities
  • Somnolence (sleepy/drowsy), hallucinations & dream like behaviour
    • Brainstem contains centres for sleep regulation
33
Q

Explain why motor dysfunction is often absent in PCA occlusions

A

If cerebral peduncles (contain ascending sensory & descending nerve tracts going to cortex) can get blood from the PCAs which are being filled by the posterior communicating arteries then motor dysfunction will be absent

34
Q

Describe the classical presentation of a proximal basilar artery occlusion

A
  • Locked in syndrome
    • Complete loss of movement of limbs but have preserved ocular movement
    • Preserved consciousness
35
Q

Explain why ocular movement is preserved in locked in syndrome

Suggest why consciousness may be preserved

A
  • Midbrain is getting supply from PCAs which are being filled by posterior communicating arteries
  • Midbrain contains cranial nerve nuclei 3 and 4 which both have important roles in eye movement
  • Consciousness may be preserved because the midbrain reticular formation is still intact
36
Q

State the 4 categories in the Bamford/Oxford stroke classification

A
37
Q

Where are the paracentral lobules and what is their role?

A
  • Think of them as the most medial parts of the primary motor and somatosensory cortex
  • Have role in motor and sensory to lower limb including the perineal area

Sem 4: Nervous System (21 decks)

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