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Sem 3 > stroke/case 5 > Flashcards

stroke/case 5 Flashcards

1
Q

What does the brain use for respiration? what type of respiration?

A

O2 and glucose

aerobic respiration: no lactate build up

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2
Q

What happens with occlusion of the anterior cerebral artery?

A
  • contralateral hemiparesis

- sensory loss of contralateral leg and perineum

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3
Q

What parts of the brain does the middle cerebral artery supply?

A
  • lateral sulcus and travels along lateral surface of frontal, temporal and parietal lobes
  • subcortical areas including internal capsule and neostratium
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4
Q

What happens with occlusion of the middle cerebral artery?

A
  • contralateral hemiparesis
  • sensory loss of contralateral upper limb
  • contralateral homonymous hemianopia
  • aphasia
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5
Q

What happens with occlusion of the posterior cerebral artery?

A

-contralateral homonymous hemianopia with macular sparing
-visual agnosia
(-Weber’s syndrome: branches of the PCA that supply midbrain: ipsilateral CN3 palsy + contralateral weakness of upper and lower extremity)

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6
Q

What parts of the brain does the posterior cerebral artery supply?

A

curves around midbrain to reach medial surface of cerebral hemisphere
–> inferior surface of temporal lobe + occipital lobe

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7
Q

What happens with occlusion of the basilar artery?

A
  • ‘locked-in’ syndrome

- respiratory failure: death

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8
Q

What is a lacunar stroke?

A

type of ischemic stroke that occurs when blood flow to one of the small arteries deep within the brain

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9
Q

What are symptoms of lacunar strokes?
What are the risk factors?
Common sites?

A
  • isolated hemiparesis, hemisensory loss or hemiparesis with limb ataxia
  • strong association with hypertension
  • common sites: basal ganglia, thalamus and internal capsule
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10
Q

What are functional consequences of damage to motor cortex?

A

movement

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11
Q

What are functional consequences of damage to frontal lobe?

A

-Broca’s aphasia
-disinhibition
-perseveration
-anosmia
-inability to generate a list
(judgement, foresight, voluntary movement, smell)

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12
Q

What are functional consequences of damage to temporal lobe?

A
  • Wernicke’s aphasia
  • superior homonymous quadrantonopia
  • auditory agnosia
  • prosopagnosia
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13
Q

What are functional consequences of damage to brainstem?

A

swallowing, breathing, heartbeat, wakefulness centre (+other involuntary functions)

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14
Q

What are functional consequences of damage to cerebellum?

A
  • midline lesions: gait and truncal ataxia

- hemisphere lesions: intention tremor, past pointing, dysdiadokinesis, nystagmus

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15
Q

What are functional consequences of damage to parietal lobe?

A
  • sensory inattention
  • apraxias
  • astereognosis (tactile agnosia)
  • inferior homonymous quadrantanopia
  • Gerstmann’s syndrome (lesion of dominant parietal): alexia, acalculia, finger agnosia and rich/left disorientation)
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16
Q

What are functional consequences of damage to occipital lobe?

A
  • homonymous hemianopia (with macular sparing)
  • cortical blindness
  • visual agnosia
17
Q

What brain areas do the anterior cerebral artery supply?

A

superior and medial surfaces of frontal and parietal lobes

18
Q

What is the WHO definition of stroke?

A

-sudden onset of acute focal ‘occasionally global) neurological deficit probably due to a pathological process in blood vessels

19
Q

What are stroke risk factors?

A
  • BP (especially in haemorrhage strokes)
  • cholesterol
  • blood sugar/diabetes
  • atrial fibrillation
  • obesity
  • smoking
20
Q

What is the FAST test?

A

Face
Arms
Speech
Time

21
Q

What is the percentage of ischemic strokes compared to haemorrhage strokes

A

85%

15%

22
Q

What are causes of ischemic strokes?

A
  • blood clot causing occlusion: carotid atherosclerosis (carotid bifurcation), embolism of plate rich clot further i cerebral vessel
  • atrial fibrillation
23
Q

What must be looked at in terms of blood diffusion:perfusion for treatment via thrombolysis?

A

it mismatch (perfusion loss but not much diffusion loss) then brain tissue can be salvaged

24
Q

What is the neurovascular unit and what does it consist of?

A
  • close interaction of brain cells with the brain endothelium and the extracellular matrix contributes to the maintenance of brain homeostasis and functions
  • consists of :
  • ->astrocytes, microglia, neurones
  • -> endothelial cells and pericytes
  • -> extracellular matrix
25
Q

What are the different post stroke complications?

A
  • paralysis/motor control
  • sensory disturbances
  • dysphagia
  • language problems
  • memory impairments
  • depression/anxiety
  • fatigue
26
Q

What is the initial damage in stroke? When does it take place?

A

energy failure, excitatoxicity, depolarisation, necrosis, oxidative stress (causing mitochondrial damage)
-within minutes to hours

27
Q

What happens in secondary damage in stroke? When does it happen?

A

inflammation, programmed cell death

hours to days

28
Q

What is excitotoxicity?

A

over activation of NMDA receptors by glutamate allowing excess calcium into cell causing it to swell and rupture
(inhibitory cells die quite quickly)

29
Q

How would you describe progression of injury between the tissue and the MRI scan?

A
  • upon presentation: no perfusion of tissue (doesn’t show in brain tissue but it shows in MRI scan)
  • one day after presentation: loss of brain tissue
  • 6 days after presentation: not much difference n MRI but more tissue loss
30
Q

What do you measure stroke severity with?

A

-National Institute of stroke scale

the higher the scale, the more severe the stroke

31
Q

What is the initial treatment of ischemic stroke? What are the complications

A
  1. -thrombolysis: tissue plasminogen activator (alteplase) by IV bolus (10%) plus 1 hour infusion (90%) with 4.5h
    - complications: haemorrhage, anaphylaxis
  2. endovascular thrombectomy: removal of clot
    BUT time dependent benefit: within 6 hours of onset
32
Q

What treatment do you give if the patient presents with haemorrhagic stroke?

A
  • PCC (prothrombin complex concentrates) to reverse bleeding
  • management of BP
  • lower blood pressure: beta blockers and GTN
  • sometimes minimally invasive surgery
33
Q

What is secondary treatment for stroke?

A
  • blood pressure
  • aspirin 300 mg 14days then clopidogrel 75mg
  • exclude AF (if have AF: anticoagulants)
  • statins
  • exclude DM
  • exclude carotid stenosis (if have stenosis more than 50% can get carotid endarterectomy)
  • speech and language therapy (dysarthria + swallowing)
  • physiotherapy
  • occupational therapy
  • pschomotor
34
Q

How do you diagnose stroke?

A

MRI
CT
signs (ROSIER and National Institute of Stroke scale, FAST)

35
Q

What are the different types of aphasia?

A
  • Wernicke’s (receptive) aphasia
  • Broca’s (expressive) aphasia
  • conductive aphasia
  • global aphasia
36
Q

What happens in Wernicke’s (receptive) aphasia?

A
  • due to lesion of superior temporal gyrus
  • comprehension is impaired
  • sentences that make no sense, word substitution and neologisms but speech remains fluent
37
Q

What happens in Broca’s (expressive) aphasia?

A
  • due to lesion of the inferior frontal gyrus
  • speech is non-fluent, laboured, and halting
  • comprehension is normal
38
Q

What happens in conductive aphasia?

A
  • ususally due to stroke affecting arcuate fasciculus (connection between Wernicke’s and Broca’s area)
  • speech fluent but repetition is poor
  • aware of errors they are making
  • comprehension is normal
39
Q

What happens in global aphasia?

A

large lesion affecting all 3 of the areas (Wernicke’s, Broca’s and arcuate fascicles)
–> severe expressive and receptive aphasia

Sem 3 (20 decks)

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