Stroke Epidemiology And Patho Flashcards

1
Q

Definition of Stroke by WHO:

A

Rapidly developing signs and focal disturbance of cerebral function, with signs lasting 24hrs or longer, leading to death with no apparent cause other than of vascular origin

Doesn’t include ischaemic attacking or haemorrhage/infarction related to infection or tumour.

Ischaemic = 90%
HAemorrhagic = 10%
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2
Q

Epidemiology of Stroke: In Australia

A

53 000 strokes per year
Second leading killer in Australia [after heart disease]
costs AU $2.4billion
89% of acute stroke patients in Aus are admitted to hospital
Men at 30% greater risk than women early in life, but woman @ greater risk later
Rate of stroke unchanging, although mortality and severity declining slowly.

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3
Q

Epidemiology of Stroke: Risk Factors for Stroke

A
Poor diet
High cholesterol
High BP
Sedentary lifestyle
Smoking
Stress
Drug use 
Family history
Diabetes
Obesity
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4
Q

Epidemiology of Stroke:

A

Risk of stroke increases exponentially with age in adult hood

  • 55-59 years of age: risk increases ~5% a year
  • 80-84 years of age: risk increases ~25% a year

2 out of 10 people die within 1 months of stroke
3 out of 10 die within 1 year
5 out of 10 die within 5 years

Decreasing risk of dying as more time passes following stroke
Subarachnoid or I trace reveal haemorrhage is more likely to cause death than ischaemic stroke

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5
Q

Pathophysiology of Stroke

A

Impaired neurological function occurs from restricted blood supply [ischaemia] or bleeding or pressure injury

Affects multiple systems, depending on area of brain affected - motor and sensory.
The areas of the brain affected by stroke depend on the artery affected: middle cerebral artery [pink], posterior cerebral artery [green], and anterior cerebral artery [blue]

Haemorrhagic strokes caused by blood leaking into the brain [intra-cerebral] or spaces and spinal fluid around brain [subarachnoid]

Ischaemic strokes result form infraction

  • thrombotic = localised thrombus or clot on an atherosclerotic plaque.
  • embolic= material [embolus] from elsewhere concludes blood vessel.
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6
Q

Pathophysiology : What are some signs of haemorrhagic stroke?

What are some signs of ischaemic stroke?

A

Altered level of consciousness
Severe headache
Elevated BP

Some signs of Ischaemic stroke are similar, but cerebral blood flow is the primary marker for assessing [need CT and MRI for diagnosis]

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7
Q

Pathophysiology of Stroke: What are the main arteries?

A

Anterior, middle and posterior cerebral arteries - there are left and right arteries supplying each hemisphere
Cerebellar arteries supply cerebellum

Occlusion to artery on one side will affect the opposite side of the body, as a general rule

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8
Q

Pathophysiology of ACA lesion, Left MCA, Right MCA:

A

ACA lesion:

  • lower limb [LL] hemiparesis
  • upper limb [UL] hemiparesis/paralysis (less severe)
  • hemisensory loss (LL>UL)

Left MCA= withdrawn, anxious, depressed, cautious, disorganised, slow movements.

  • Right hemiparesis (UL>LL)
  • R Hemisensory loss (UL>LL)
  • Expressive and/or receptive aphasia

Right MCA= happy, unconcerned, impulsive, overestimates ability, unpredictable, fast movements.

  • L hemiparesis (UL>LL)
  • L hemisensory loss (UL>LL)
  • denies existence of disability
  • difficult dressing
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9
Q

Functional Consequences: What are some physical and psychological effects

A
  • > 50% develop major depression, and continuation of unhealthy lifestyle increases risk of future stroke
  • Co-morbidities [exist prior to stroke]: obesity, hypertension
  • Secondary conditions [result from the stroke]: increased falls, spasticity, memory loss, aphasia, back pain, social isolation, stress
  • also, hmemiparesis/quadriparesis or paralysis and impaired balance
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10
Q

Functional Consequences of Hemi Neglect?

A

Particularly if right side is damaged:

  • impairment in parietal region, poor coordinate representation of extra-personal space
  • don’t recognise one side of their body
  • needs specific treatment, continued ex training

May set up safe challenges or obstacle course- patient learns to attend the the neglected side.
Patient finds and then uses neglected side to assist in bi manual tasks

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11
Q

Pharmacology:

A

May be using drugs for various conditions.

Blood thinners = increase risk of bruising and bleeding into a joint

Vasodilators = need longer cool down period, increase risk of post exercise hypotension

Antihypertensives = some BP meds cause a decrease HR response, harder to use target HR to determine intensity during cardio training.

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12
Q

Changes seen following Stroke:

A

Suggested that the brain attempts to deal with sudden loss of motor ability by removing inihibition to surrounding areas.

This CORTICAL INHIBITION is seen in a perilesional intracortical and intercortical capacity.
Motor cortex disinhibition is a phenomenon seen following stroke - weeks
Commonly know as ‘unmasking’, it referees to a loss of inhibitory interneurone input.

Loss of inhibition is temporary: important function implications
Think of this as ‘rebooting’ the system, which places us in a unique position
The lack of inhibitory input gives formerly ‘silent’ synapses the opportunity to influence the connected neurones
Gives us ability to change the motor homunculus - new connections and networks allows us to learn ‘new’ tasks without damaged brain tissue

Significant increases in spasticity and muscle tone
The flexed adducted posture is probably due to reflex activity, excessive motor neurone excitability and abnormal descending drive onto the motor neurone pool
Amplitudes of PICs may not be excessive, but enhanced reflex gain causing synaptic drive may be.

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13
Q

Importance of Exercise in Stroke patients?

A

Help to integrate back into community, reduce depression, improve social inclusiveness
Increases learning of visual and auditory tasks and improved association of shapes and figures
Improves fatigue resistance to allow to return to work
Minimise weight gain and accumulation of cardiac risk factors
INCREASED SYNAPTIC PLASTICITY- strong evidence that ex + learning is more effective than learning alone - BDNF and GDNF

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14
Q

Exercise Testing for Stroke Patients

A

Stroke patients should be screened by a physician before commencement of testing/training, and complete PAR-Q
Requires fasting blood draw, resting ECG, resting HR, BP [standing, seated, supind] and basal temp
Graded exercise test should follow before other testing

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15
Q

Exercise Testing for Stroke Patients: Endurance

A

Normally they have lower VO2 due to hemiparalysis/paresis and loss of muscle mass
A symptom limited test can be performed on treadmill, bike, arm ergo, etc.
If graded ex test showed no irregularities, there is no reason for staged test with continuous BP monitoring

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16
Q

Exercise Testing for Stroke Patients: Strength

A

Strength assessed using standard machines, free weights or dynamometers
Need variety of tests to measure function in different areas of body - compare ‘normal’ with hemiparetic side
Proper instruction on technique important- remember patients have hearing, comprehension, language or learning difficulties
Strapping may be required
Standard progression, specificity,etc applies

17
Q

Exercise Testing for Stroke Patients: Flexibility/body comp

A

Flexibility about the spine and shoulder areas can be affected by hemiparesis
Modified sit & reach tests, and shoulder flexibility are useful
Other joints/muscle groups should be monitored continuously
Obesity a key problem - may use girths, skin folds, and BMI to track body comp.

18
Q

Exercise Prescription for Stroke patients: Aerobic

A

May need to monitor BP during ex - walking up stairs associated with higher HR and BP, so may not use it for some patients
Otherwise standard protocols are possible
Consider aquatic activities, under supervision
Use of HR to set loads might be problematic:
- if patient is on medication
- muscle fatigue in working limb may occur before significant rise in HR and O2 because smaller muscle mass use in hemiparetic patients

19
Q

Exercise Prescription for Stroke patients: Strength

A

May have hemiparesis or spasticity, so program accordingly
Strength of knee extensors, ankle plantarflexors and hip flexors correlated with gait performance in stroke patients
Low strength increases risks of falls
Should progress slowly to reduce DOMS and minimise BP increases
Learn proper technique without Valsalva manoeuvre - may use BP feedback during learning

Isometric and water resistance ex a good start
Good evidence that ST significantly improves gait re-training in stroke patients

20
Q

Exercise Prescription for Stroke patients: Flexibility and Balance

A

Target upper and lower body groups
Stretch prior to session may help ROM and movement capacity, although it might reduce max strength in muscles
Particular emphasis on spastic muscle groups - finger and wrist ext, elbow flex, shoulder add, hip flex, knee flex, and plantarflexors

Hold stretches for up to 20min for contractures
Balance and stability a key issue - progress to unstable surface under supervision

21
Q

Exercise Prescription for Stroke patients: General Guidelines/Considerations

A

HR monitors worn at all sessions
BP monitored before and after training, also several times during sessions
Good to record all training and response so no major changes occur in program that might elicit unexpected responses
Psychological interventions [for depression], goal setting, social environments, may help ex adherence
Think about accessibility

22
Q

Neuroplasticity - Edward Taub [synaptic plasticity]

A

Dendrite sprouting - growth of remaining neurones
Collateral sprouting - nearby axons innervate synaptic sites that have lost their connections
Unmasking of previously inactive synapses
Synaptogenesis - new synapses develop

Changes occur soon after stroke and persist
Constraint induced therapy