Stroke Flashcards

1
Q

What is a TIA?

A

TIA = Transient ischaemic attack

  • sudden, focal neurological deficit
  • symptoms usually last <1 hours, and always <24 hours
  • caused by the release of a small emboli from a thrombus
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2
Q

What is a thrombotic stroke?

A

ischaemic stroke resulting from the obstruction of a blood vessel by a blood clot forming locally

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3
Q

What is an embolic stroke?

A

ischaemic stroke resulting from obstruction due to an embolus elsewhere in the body

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4
Q

What is a haemorrhagic stroke?

A

2 main types:

  1. Intracerebral: bleeding within the brain itself (when an artery in the brain bursts, flooding the surrounding tissue with blood), due to either intraparenchymal haemorrhage (bleeding within the brain tissue) or intraventricular haemorrhage (bleeding within the brain’s ventricular system).
  2. Subarachnoid: bleeding that occurs outside of the brain tissue but still within the skull, and precisely between the arachnoid mater and pia mater (the delicate innermost layer of the three layers of the meninges that surround the brain).

haemorrhagic strokes usually cause specific symptoms (for instance, subarachnoid haemorrhage classically causes a severe headache known as a thunderclap headache) or reveal evidence of a previous head injury.

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5
Q

What is a lacunar stroke/infarct?

A

Most common type of ischaemic stroke
Results from the occlusion of the small penetrating arteries that supply the deep brain structures

Cortical signs of infarct, such as aphasia, neglect, visual field defects, are absent

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6
Q

What are the different lacunar syndromes?

A
  1. Pure motor stroke/hemiparesis (most common lacunar syndrome
  2. Ataxic hemiparesis (second most frequent lacunar syndrome)
  3. Dysarthria/clumsy hand
  4. Pure sensory stroke
  5. Mixed sensorimotor stroke
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7
Q

Where do pure motor strokes occur? How do they present?

A

Location:
- posterior limb of the internal capsule, basilar part of pons, corona radiata

Presentation:

  • hemiparesis or hemiplegia that typically affects the face, arm, or leg of the side of the body opposite the location of the infarct
  • dysarthria, dysphagia, and transient sensory symptoms may also be present.
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8
Q

Where do ataxic hemiparesis strokes occur? How do they present?

A

Location:
- posterior limb of the internal capsule, basilar part of pons, and corona radiata, red nucleus, lentiform nucleus, SCA infarcts, ACA infarcts

Presentation:

  • combination of cerebellar and motor symptoms, including weakness and clumsiness, on the ipsilateral side of the body.
  • usually affects the leg more than it does the arm
  • onset of symptoms is often over hours or days
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9
Q

Where do strokes resulting in dysarthria/clumsy hand occur? How do they present?

A

Location:
- basilar part of pons, anterior limb or genu of internal capsule, corona radiata, basal ganglia, thalamus, cerebral peduncle

Presentation:
- dysarthria and clumsiness (i.e., weakness) of the hand –> prominent when pt is writing

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10
Q

Where do pure sensory strokes occur? How do they present?

A

Location:
- contralateral thalamus (VPL), internal capsule, corona radiata, midbrain

Presentation:

  • numbness on one side of the body
  • later develop tingling, pain, burning, or another unpleasant sensation on one side of the body.
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11
Q

Where do mixed sensorimotor strokes occur? How do they present?

A

Location:
- thalamus and adjacent posterior internal capsule, lateral pons

Presentation:
- hemiparesis or hemiplegia (weakness) with sensory impairment in the contralateral side.

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12
Q

What are the risk factors for a stroke?

A
  • HTN
  • AF
  • DM (type 1+2)
  • Hypercholesterolaemia/hyperlipidaemia (lipid accumulation increases the risk of fibrous cap rupture)
  • Diet low in K+
  • Smoking
  • Obstructive sleep apnoea
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13
Q

What happens when the Na+ channel in neurones is removed or defective?

A
  • Water will move into neuroglia by osmosis
  • neuroglia swell and extracellular space reduces
  • cell swelling causes capillaries/venules to compress and this reduced extracellular space even further
  • swollen cells press against each other and this increases the ICP resulting in signs of cerebral hypoxia
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14
Q

What happens to the cerebellum in cases of severely raised ICP? How does this manifest clinically?

A

cerebellum is forced through the foramen magnum = coning/tonsillar herniation

  • leads to compression of brainstem and upper spinal cord
  • signs: intractable headache, head tilt, neck stiffness
  • consciousness declines and this can lead to flaccid paralysis
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15
Q

What is excitotoxicity?

A

the effects of excess excitatory neurotransmitter release (causes cell damage)

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16
Q

Which receptors mediate fast and slow excitotoxicity?

A
Fast = NMDA receptors
Slow = AMPA receptors
17
Q

How are strokes usually treated?

A
  1. restore blood flow
    - tissue plasminogen activators (thrombolysis)
    - converts plasminogen to plasmin
    - administered 3-4 hours after symptoms = most benefit
    - will have moderate benefit when given 3-6 hours from symptom onset
  2. combat excitotoxicity
    - NDMA antagonists (cerestat)
    - AMPA anatagonists (NBQX)
  3. combat free radical damage
    - antioxidant (IV)
    - free radical scavenging enzymes (super oxidase dismutase)
    - cool down brain = reduce O2 demand
18
Q

How can strokes be prevented?

A

Reduce risk factors

- treat HTN, AF, statins for vascular disease