11. Stroke / Cerebrovascular Accident Flashcards

1
Q

What is a stroke?

A

Focal neurological disorder of abrupt onset due to pathological process in the cerebral blood vessels.

Disruption of blood supply to the brain (infarction) creates an area of brain damage (infarct). –> the brain takes up to 1/5 of the body’s blood supply

Attacks up to 1.9 million brain cells per minute.

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2
Q

How often do strokes occur, what are the effects?

A

1/6 people will have a stroke in their life.
1 stroke every 19 mins
Kills more women than breast cancer and more men than prostate cancer.
30% of stroke patients die within a year of their stroke.

Expected that by 2050, there will be one stroke every 10 minutes, and over 800 000 stroke survivors.

Around 500 000 Australians are living with the effects of stroke.

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3
Q

What are the economic costs of strokes?

A

2020: estimated cost in Australia was $6.2 billion in direct financial impact, and a further $26 billion in mortality and lost wellbeing.

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4
Q

Where in the brain do strokes occur?

A

Can happen anywhere

Strokes in the hind-brain (pons, medulla, cerebellum) are very severe: less likely to survive them, and if you do, neurocognition is not priority

Stokes in the midbrain tend to impact motor function (so neuropsychologists don’t play a big role in this)

The bulk of the brain (forebrain) where most people have strokes impacts cognition (relevant to neuros)

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5
Q

Discuss more neuroanatomy in terms of strokes

A
  • clear lateralization (impacts left or right side) and we tend to see the effects (language skills vs visuospatial skills)
  • distinguish between grey (outside) and white (inside) matter - strokes in white matter tend to be much smaller, show up as little dots on the brain but overtime can cause cognitive deficits
  • white matter important for connectivity and communication (more likely to have slowness, inefficiency, problems with attention and concentration)
  • grey matter: see more cortical deficits (speech, comprehension, memory, movement)
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6
Q

Discuss cerebral circulation - and the two main arteries

A

Cerebral circulation = movement of blood through blood vessels
- internal carotid artery (front of neck)
- vertebral arteries (through the back)

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7
Q

What are the 2 different blood supplies to the brain?

A

Anterior cerebral circulation system: itnernal carotid arteries –> anterior and middle cerebral arteries –> supplies blood to the front part of brain

Posterior cerebral circulation system: vertebral arteries –> basilar and posterior cerebral arteries –> supply blood to occipital lobes, brain stem, cerebellum

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8
Q

What is the role of the posterior communicating arteries?

A

Links the posterior circulation system to the anterior circulation system to create the ‘circle of Willis’

  • engineered redundancy: if there’s an issue with this blood supply in the anterior part of the brain, the blood supplies can still communicate through the circle
  • but only 35% of the population have a circle of Willis - if you don’t, it increases your chances of having negative effects of stroke
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9
Q

What do the vertebral and basilar arteries supply?

A

To the cerebellum, pons, medulla

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10
Q

Where does the anterior cerebral artery supply?

A

Inner parts of frontal lobe, parietal lobe, polar regions (PFC)

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11
Q

Where does the middle cerebral artery supply?

A

Grey matter of the frontal lobe, temporal lobe, and parietal lobe

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12
Q

Where does the posterior cerebral artery supply?

A

Inner parts and lower part of temporal lobe, the occipital lobe, the parietal lobe

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13
Q

What is the acronym for Stroke signs?

A

FAST!
Face (facial asymmetry - eye or mouth drooping)
Arms (motor impairment impacting contralateral side - i.e. left sided stroke = deficits on right side of body) –> ask person to raise both arms

Speech: changes in speech (slurred)

Time: 1.9 million brain cells dying per minute, i.e. call ambulance quickly

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14
Q

What are some other common symptoms

A
  • dizziness
  • loss of vision
  • sensory impairment
  • confusion
  • severe headache
  • difficulty swallowing
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15
Q

Outline a transient ischaemic attack

A
  • relatively small bloodclot gets lodged in small blood vessel
  • until it gets pushed through, it will cause these symptoms
  • symptoms recover, but when the clot comes round again it causes the same symptoms

The build up of this causes damage to the brain - because these symptoms mean that part of your brain is not getting blood supply.

Transient ischaemic attacks are predictors for a big upcoming stroke - i.e. should go to hospital

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16
Q

What are some risk factors for stroke that you cannot control:

A

Age: >55, each decade your chance of stroke doubles

Sex: men are more likely to have a stroke at any one time, but at the end of life, more common in women

Family history: certain genetic mutations predispose someone to having more strokes (e.g. cadasil)

Race: people from Japan and Africa have higher likelihood of stroke

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17
Q

What are some controllable risk factors (lifestyle risk)

A

Hypertension / high blood pressure: puts more pressure on the blood vessel walls

Hypercholesterolaemia –> fatty deposits stick to the walls of the blood vessels and cause pathology

Cigarettes - increases blood pressure and releases chemicals which stick to the walls

Obesity - increases cholesterol, diabetes, blood pressure risk

Excessive alcohol consumption - increases blood pressure

18
Q

What are some medical risk factors of strokes?

A

Cardiovascular disease: more likely to have the same type of disease in your brain

Atrial fibrillation - the chambers of the heart vibrating instead of beating rhythmically

Diabetes - the brain will be deprived of adequate sugar and oxygen (if not well managed)

Previous stroke or transient ischaemic attacks increase chances of having a stroke

19
Q

What is atherosclerosis?

A

Pathological thickening and hardening of your arteries due to build up of fatty deposits in artery walls
- as you get older, they become thinner, rigid, hardened
- high blood pressure puts more pressure on these already compromised vessels

20
Q

What are the 2 mechanisms of stroke:

A

Ischemia (deficient blood flow)

Haemorrhage (bleed)

21
Q

Outline Ischaemia

A

Blood flow is deficient / absent due to obstruction in vessel (blood clot)

80% of strokes

Major risk factors = diabetes, hypercholesterolaemia, ischemic heart disease

22
Q

What are the main causes of ischemic stroke?

A

Thrombus: clot formed in brain

Embolus: clot formed in body

23
Q

What is a thrombotic stroke?

A

Most common cause of ischemia - blood clot formed in the brain!

Thrombus accumulates and becomes lodged in artery causing ischemia - may take hours to fully develop.

Thrombus in small arteries in white matter results in lacunar stroke - where you don’t see symptoms, but many will cause deficits.
But if its happening in grey matter in big blood vessels, there will be symptoms.

24
Q

What is an embolic stroke?

A

Less common form of ischemia - accounting for only 20-30%.

Blood clot formed in the body that travels to the brain - usually originating from the heart. Becomes lodged in a cerebral artery causing ischemia.

Abrupt presentation (as clot is already formed)

25
Q

Outline haemorrhage strokes

A

Account for 20% of strokes
Bleeding within the brain tissue (intracerebral haemorrhage) or on the surface of the brain (subarachnoid haemorrhages).

Usually abrupt, high mortality rate (die within a month).
Bleeding destroys tissue, causes ischemia, surrounding oedema (swelling) and puts pressure on the brain. - i.e. causing both a haemorrhagic stroke and ischaemic stroke

Risk factor: hypertension

Causes:
- hypertension
- aneurysm (abnormal blood filled bulge on vessel wall that ruptures)
- arteriovenous malformation (AVM) (abnormal connection of blood vessels that are weak and susceptible to leakage)
- tumours and other bleeding pathology

26
Q

Prevention of strokes (reducing risk factors)

A
  • lower blood pressure through lifestyle changes and medication
  • lower cholesterol (dietary changes)
  • smoking cessation
  • dietary changes, regular exercise, weight management
  • better management of diabetes and cardiovascular disease
  • carotid endarectomy (remove plaque from vessels)
  • anithrombotic (blood thinning) medication
27
Q

Treatment (acute stage) for stroke

A

Immediate hospital admission to figure out what type of stroke

Ischaemic stroke:
- dissolve the clot (medication = tPA - within 3 hours)
- endovascular procedures (mechanical removal of clot through femeral artery)

Haemorrhagic stroke
- no effective targeted treatment
- manage hypertension
- control of bleeding and pressure on the brain

28
Q

What is the role of the neuropsychologist in managing stroke sequalae??

A
  • document degree of impairment (estimate premorbid level and compare performance, modify standardized administration in the consideration of fatigue, headaches, etc)
  • assess patient’s judgements on their personal functioning (will they make risky decisions)
  • document presence of emotional / behavioural disturbance
  • contribute to prognosis + rehab planning (will they ever get back to pre-morbid levels)
  • educational / occupational planning
  • assess recovery over time
29
Q

Motor and sensory sequelae

A

assessed by a medical doctor
- more common after right hemisphere infarct
- contralateral sensorimotor impairment (hemiparesis - i.e. if stroke is right sided, it will impact left side of the body)
- ipsilateral deficits in motor integration and fine motor control (but major motor will be contralateral)
- apraxia: inability to perform purposive movements
- homonymous hemianopia: visual field loss on the same side of both eyes (sensory deficits usually visual)

30
Q

What are the cognitive sequalae?

A

Cog impairment varies from 11-56% of patients - most recovery occurring within 6 months, may continue 2yrs

Deficits depend on: extent and location of damage, and individual differences in brain organisation

Lateralisation of deficits:
- left (dominant) hemisphere infarct = greater impairment in verbal skills (aphasia: language impairment)
- right (non-dominant) hemisphere infarct = greater impairment in nonverbal skills, constructional apraxia (purposeful movements)

31
Q

Cognitive sequelae - attention and processing speed

A

Most common area of impairment
- determine of these deficits should be based on formal testing and qualitative observation
- deficits in immediate attention span, sustained attention, divided attention, processing speed

You see very quick recovery, but least likely to get back to premorbid baselines

32
Q

Cognitive sequelae - language

A

Commonly impaired following LEFT hemisphere infarct, especially following left MCA ischaemic stroke

1/3 stroke patients have aphasia - 85% of aphasia caused by stroke

Deficits include:
- expressive language impairment (Broca’s)
- receptive language impairment (Wernicke’s)
- dysarthria: disorder of motor control of speech
- speech apraxia; defective sequencing of muscle movements required for speech - might move around the syllables in the word

Significant improvement in first year post stroke, but mild deficits may persist

33
Q

Cognitive sequelae - visuospatial skills

A

Vision may not be affected - but brain may have difficulty interpreting

Often following posterior right hemisphere infarct
- Agnosia = difficulty recognising objects
- difficulty understanding spatial relationships
- may get lost / disoriented in familiar places
- visuospatial / hemispatial neglect: failure to respond / attend to stimuli in visual space contralateral to the infarct (often occurring following posterior RH infarct, resulting in neglect of left side / space)

34
Q

Cognitive sequelae - memory

A

13-50% of stroke patients have memory problems in first few weeks

Amnestic syndromes:
- PCA (posterior cerebral artery) occlusion (supplies the temporal lobe - hippocampi - causing the brain tissue to die off)
- thalamic infarction (severe memory problems, can impact communications between hemispheres)

Lateralisation is present:
- left (dom) infarct - impaired verbal memory
- right (non-dom) hemi infarct - impaired visual memory

Common symptoms: difficulties with new learning, difficulty applying previously learned info to new situations, repetitive, forgetful, misplacing items, confabulation, confusion

35
Q

Cognitive sequelae - executive function

A
  • impaired reasoning and problem solving
  • difficulty with abstract reasoning
  • cognitive rigidity
  • difficulties with planning and organisation
  • poor self-monitoring

Area most likely to be impacted, less localised as frontal lobe communicates with all other parts of the brain.

36
Q

Behaviour sequelae of strokes

A

Behavioural and personality change
- difficulties with initiation and cessation
- poor motivation
- apathy (lack of interest)
- reduced insight
- perseveration (response repetition)
- impulsivity
- inappropriate social conduct (disinhibition)
- personality change: social withdrawal, loss of independence, irritability, lack of empathy, egocentric, demanding and uncompromising, jealous, impatient

37
Q

Emotional sequelae

A
  • emotional lability: inappropriate laughing / crying
  • euphoria
  • frustration and outbursts of anger
  • anxiety
  • distress
  • lateralisation is present:
    left (dom) stroke - preponderance of initial depression and catastrophic reactions (i.e. having more insight);
    right (non-dom) stroke - initial apathy and indifference (lack insight)
  • depression is common regardless of stroke hemispheres
38
Q

Left dominant hemisphere - emotional sequelae

A
  • insight
  • catastrophic reactions when presented with own limitations
  • greater incidence of depression early on
  • anxiety
  • agitation
  • tearfulness
  • exaggeration of disability
39
Q

Right (non-dominant) hemisphere stroke

A
  • inability to discern emotional features of stimuli
  • decreased emotional responsivity
  • can have distinct impairments in facial expression, prosody, humour

Early stages: indifference reaction
- apathy
- not upset by own limitations
- reduced awareness, denial and dismissal of deficits
- risk taking

Late stages: poor psychosocial adaptation
- reduced social skills

40
Q

Emotional sequelae: depression after stroke

A
  • Common regardless of stroke hemisphere
  • LH: increased incidence of depression 2-6 months post stroke (related to awareness of deficits)
  • RH: increased incidence of depression > 6 months post stroke (lack of awareness of deficits spares them from initial depression, but is more chronic and debilitating, more resistant to treatment)

-50% of patients report significant levels of depression 1-2 years post stroke
- elderly are more vulnerable
- leads to poorer functional recovery and outcome
- higher mortality at 10 year follow up

41
Q
A