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Neurological Physiotherapy Placement > Stroke > Flashcards

Stroke Flashcards

1
Q

Define a stroke

A
  • A clinical syndrome characterised by rapidly developing
    clinical signs of focal, and at times global disturbance of
    cerebral function
  • Symptoms last > twenty-four hours or cause death
  • No apparent cause other than that of vascular origin
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2
Q

Stroke Types and percentages

A

Ischaemic (85%)
• Thrombotic
• Embolic
• Hypo-perfusion

Hemorrhagic (15%)
• Subarachnoid
• Intracerebral

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3
Q

List of pathogenesis and percentages of ischaemic strokes

A 
Large artery thromboembolism 50%
Small artery disease 20-25%
Embolism associated with cardiac dysfunction 20%
Non atheromatous arterial disease 5%
Blood disease <5%
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4
Q

Pathogenesis of haemorrhagic stroke

A

• Intracerebral haemorrhage activates a nuclear factor
which then perpetuates inflammation
• Inflammation along with oxidative stress leads to
secondary brain damage
• Induction of antioxidative defence components and
inhibition of the nuclear factor protect affected area of
the brain
• Phagocytosis-mediated haematoma clean up also
stimulated, facilitating removal of the haematoma
(source of toxicity and inflammation)

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5
Q

Stroke Classification Bamford Oxfordshire Stroke Classification

A

• TACS: total anterior circulation syndrome (15%)
• PACS: partial anterior circulation syndrome (35%)
• LACS: lacunar syndrome (25%)
• POCS: posterior circulation syndrome (25%)
Once the type of stroke is known (infarct vs haemorrhage)
the letter S is replaced with I or H respectively.

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6
Q

non-modifiable risk factors for stroke

A

• Age (↑ age
 ↑ risk)
• Gender (male > female)
• Family history

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7
Q

Medical Risk factors for stroke

A
  • TIA
  • AF
  • Diabetes
  • Fibromuscular Dysplasia
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8
Q

Modifiable risk factors for stroke

A 
Hypertension
• Hypercholesterolemia
• Smoking (tobacco)
• Obese/ overweight
• Inadequate nutrition
• Inactivity
• Excessive alcohol
consumption
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9
Q

overall prognosis for stroke

A
  • 25% well recovered
  • 25% moderately impaired
  • 25% dependent
  • 25% deceased
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10
Q

mortality rate for infarction vs haemorrhage

A
  • 10% Infarction

* 50% Haemorrhage

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11
Q

1 year prognosis for TACS

A

high mortality, poor functional outcome
• 60% mortality (40% at 30 days)
• 35% dependent
• <5% independent

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12
Q

1 year prognosis for PACS

A

fair prognosis, high chance of functional recovery
• 15% mortality (5% at 30 days)
• 30% dependent
• 55% independent

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13
Q

1 year prognosis for LACS

A

good prognosis
• 10% dead (5% at 30 days)
• 30% dependent
• 60% independent

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14
Q

1 year prognosis for POCS

A

often good recovery, high reoccurrence
• 20% dead (<10% at 30 days
• 20% dependent
• 60% independent

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15
Q

Recovery after stroke is affected by what

A 
• Individual patient characteristics
• Type, location and severity of lesion
• Severity of deficits
• Environment the patient is exposed to during the
recovery period
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16
Q

Poor functional outcomes after stroke are linked to

A
  • Prior stroke
  • Admission severity
  • Prolonged unconsciousness
  • Urinary incontinence > 1/52
  • Cognitive deficits
  • Sensory inattention
  • Presence of unilateral spatial neglect
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17
Q

Weakness in stroke

A
  • Most common impairment
  • Most significant contributor to reduced function
  • Normally decreased distally > proximally
  • Large variation in nature and distribution of weakness
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18
Q

Spasticity in stroke

A

• No relationship found between function and spasticity
• No improvement in function has been found following
reduction in spasticity

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19
Q

adaptive features in stroke

A

• Arise as a result of the primary impairments
• Develop in response to loss of innervation, immobility
and disuse (e.g. muscle stiffness, muscle shortening,
joint stiffness, shoulder subluxation, pain)
• Increase the overall degree of motor impairment and
often interfere with recovery

20
Q

define neuroplasticity

A

• The brain’s ability to change, remodel and reorganise for

purpose of better ability to adapt to a new situation

21
Q

neuroplasticity theory

A

• Presynaptic cells that provide input to the postsynaptic
cell will have their synaptic connection strengthened
• Connections that are not active will gradually have their
influence weakened
Change in neural function in response to input is the basis
of cellular neuroplasticity

22
Q

Influence on neuroplasticity

A
  • Enriched or impoverished environments
  • Patterns of use or non-use
  • Sensory inputs
  • Motor skill practice
23
Q

Principle 1 of neuroplasticity

A

Body parts can compete for representation in the brain and
use of body part can enhance its representation
• Representation areas increase or decrease depending
on use
• E.g. the cortical representation of the reading finger in
proficient Braille readers is enlarged at the expense of
the representation of other fingers
• E.g. the representation of tibialis anterior is smaller
after the ankle is immobilised in a cast

24
Q

Principle 2 of neuroplasticity

A

The premotor cortex can substitute for the motor cortex to
control movement
• While the primary motor cortex has the largest and most
powerful contribution to the function of the corticospinal
tract, the premotor cortex also contributes

25
Q

Principle 3 of neuroplasticity

A

The intact hemisphere can take over some motor control
• There are ipsilateral corticospinal neural pathways (weak
in humans)
• These pathways innervate many more proximal than
distal muscles
• The transcollosal connections provide another possible
role of the intact hemisphere
• fMRI studies demonstrate that the damaged hemisphere
has increased blood flow when bilateral movements are
made

26
Q

Principle 4 of neuroplasticity

A

Neuroplastic mechanisms can be facilitated
• Physiotherapists can influence cortical reorganisation
after stroke with:
• Rehabilitative techniques
• Sensory stimulation
• Environmental enrichment

27
Q

TIA define

A
  • Neurological deficit of presumed vascular origin lasting less than 24 hours
    • Typically last less than 10 minutes
    • Suggestions to change definition to <1hour
    • Relatively benign in terms of immediate consequences
    as symptoms resolve
    • ‘Warning Stroke’ more appropriate than ‘Mini Stroke’ as it
    is a direct sign that a stroke may potentially occur
    • Important to have investigated
28
Q

ischaemic cascade

A
  • process of stroke injury at cellular level
  • irreversible damage begins immediately at the core
  • the penumbra may viable for up to 6 hrs
  • rapidly initiated within seconds to minutes after the loss of blood flow to a region of the brain
  • comprises a series of subsequent biochemical events that lead to disintegration of cell membranes and neuronal death at the core of the infarction
  • severe focal hypoperfusion leads to excitotoxicity and oxidative damage which in turn causes microvascular injury, BBB dysfunction and initiate inflammation
  • exacerbates initial injury and can lead to permanent cerebral damage
  • amount of permanent damage dependent on : degree and duration of ischaemia and brain’s capability to recover
29
Q

pathogenesis of haemorrhagic stroke

A 
Hypertension
• Acute Hypertension • Alcohol
• Amphetamines etc
Arterial Disease
• Vascular Malformations
Diasthesis (Bleeding Disorders) • Anticoagulants
• Antiplatelets
• Thrombolytic therapy
Trauma
30
Q

pathogenesis of haemorrhagic stroke

A
  • Intracerebral haemorrhage activates a nuclear factor which then perpetuates inflammation
  • Inflammation along with oxidative stress leads to secondary brain damage
  • Induction of antioxidative defence components and inhibition of the nuclear factor protect affected area of the brain
  • Phagocytosis-mediated haematoma clean up also stimulated, facilitating removal of the haematoma (source of toxicity and inflammation)
31
Q

Dominant hemisphere function (usually left)

A

language
skilled motor formulation (Praxis)
arithmetic sequential and analytical calculating skills
musical ability : sequential and analyticla skills in trained musicians

sense of direction : following a set of written directions in sequence

32
Q

non-dominant (usually right) hemisphere function

A

prosody (emotion conveyed by tone of voice)
visual spatial analysis and spatial attention
arithmetic : ability to estimate quantity and to correctly line up columns of numbers on the page
musical ability : in untrained musicians, and for complex musical pieces in trained musicians
sense of direction : finding one’s way by overall sense of spatial orientation

33
Q

prognosis : overall

A 
general prognosis 
25% well recovered
25% moderately impaired 
25% dependant 
25% deceased

mortality rate
10% infarction
50% haemorrhage

34
Q

Aims of physiotherapy following stroke

A
  • Prevent secondary complications
  • Optimise cardiorespiratory function
  • Optimise motor performance
  • Increase physical fitness and strength
  • Inspire interest and motivation
  • Promote mental and physical vigour
35
Q

dosage and delivery of physiotherapy intervention

A

evidence shows that more is better
• Type of practice is equality important to amount
• Task-specific/ task-related
• Functional practice
• Context specific
• Must practice in different task and environmental contexts
• Practice ++++++++++
• Learning is directly related to the amount of practice
undertaken
• Repetition ++++++++++
• In both strength training and skill development, repetition is an important aspect of practice
• Let fatigue and quality of movement guide you as to the intensity of the exercise and the number of repetitions to be completed

maximise practice time

36
Q

Benefits of physiotherapy

A

• Prevention of complications (e.g. contracture, subluxation, swelling of extremities, pressure ulcers, falls)
• Management of complications (e.g. fatigue, loss of cardiorespiratory fitness)
• Improved patient positioning and handling by health professionals and family/ carer
• Overcoming learned non-use or compensations through positive movement experiences
• Management of impairments (e.g. weakness, sensory loss, flexibility, tone, spasticity)
• Functional retraining/ restoration of movement
• Teaching new adaptive skills
• Ensuring appropriate aids are issued and used correctly
• Walking aids should not be used in the early stages of management unless they were used prior to the stroke
Positive attitude of patients
• Physiotherapy associated with functional improvement
• Valued by patients because physiotherapy perceived to “keep you moving, keep you going and keep you busy”
• Physiotherapy programs provide structure to day
• Physiotherapists considered as a source of advice, information, faith and hope

37
Q

Physio rehab recommendations - amount and intensity

A
  • Rehabilitation should be structured to provide as much practice as possible within the first six months after stroke
  • As much physical therapy (PT and OT) should be provided as possible with a minimum of one hour active practice/ day at least five days per week
  • Task specific circuit class training or video self modelling should be use to increase the amount of practice
  • Patients should be encouraged to practice skills learnt in therapy throughout the remainder of the day
38
Q

Physio rehab recommendation - timing

A
  • Patients should be mobilised as early and as frequently as possible
  • Upper limb training should commence early
  • Acutely, commence as soon as possible with frequent short sessions out of bed
39
Q

Summary for week 3 - lecture 1

A
  • The earlier that rehabilitation is commenced, the better the outcome for the patient
  • Principles of rehabilitation should be applied in acute and post-acute settings
  • As much physical therapy (PT and OT) should be provided as possible with a minimum of one hour active practice/ day at least five days per week
  • Patients should be mobilised as early and as frequently as possible
  • Physiotherapy for patients with weakness should include progressive exercises and/ or electrical stimulation and/or EMG feedback with conventional therapy
  • Sensory specific training can be provided to stroke survivors who have sensory loss
  • If a visual field deficit is found, refer for comprehensive assessment by relevant health professionals
  • Practising reaching beyond arm’s length, integrated into a functional task, while sitting with supervision/ assistance should be undertaken by people who have difficulty sitting
  • Repetitive task specific training should be undertaken by people who have difficulty in standing up from a chair
  • Task-specific standing practice with feedback can be provided for people who have difficulty standing
  • People with difficulty walking should be given the opportunity to undertake tailored, repetitive practice of walking (or components of walking) as much as possible
  • People with difficulty using their upper limb(s) should be given the opportunity to undertake as much tailored practice of upper limb activity (or components) as possible
  • For people with confirmed apraxia, tailored interventions (e.g. strategy training) can be used to improve ADLs
  • The presence of agnosia should be assessed by appropriately trained personnel and communicated to the stroke team
  • Neglect has deleterious effects on all aspects of ADLs, is a predictor of functional outcome and must be managed
  • Treatment plans must be individualised, problem based and comprehensive
  • Key aspects of treatment plans include functional retraining, strengthening, flexibility, cardiorespiratory fitness and specific impairments
40
Q

Stroke acute care

A

• Acute Care: focus on rapid thorough assessment and
early management
• Principles of rehabilitation should be applied in acute and post-acute settings•

41
Q

Stroke rehabilitation care

A

Rehabilitation: aim is to improve function and/or prevent deterioration of function, and to bring about the highest possible level of independence – physically, psychologically, socially and financially
• Proactive, person-centred and goal-oriented process that should begin the first day after stroke
• Physical recovery + reintegration into community

42
Q

tPA: thrombolysis

A

Intravenous thrombolytic agents (e.g. alteplase (r-tPA), streptokinase, recombinant pro-urokinase and urokinase) promote thrombolysis, degrading clots to relieve ischaemia
• Irreversible damage begins immediately at the ischaemic core, however the penumbra may be viable for up to six hours - early correction of ischaemia may minimise or even prevent any damage to the penumbra
• Recommended as leading treatment for ischaemic stroke
• Evidence that tPA reduces disability, increases recovery rates and independence is unequivocal
• Must be administered within 4.5 hours of symptom onset
• Specific inclusion and exclusion criteria must be satisfied
• Access to t-PA is low (~7% in Australia) and has stalled In Australia, only 26% of appropriate patients received thrombolysis within 60 minutes of hospital admission (USA 43%, UK 56%)
• Requires appropriate infrastructure (MDT with expert knowledge, pathways and protocols, immediate access to imaging facilities)

43
Q

look up medical mgmt

A

lecture 3-2

44
Q

R MCA infarct

A
  • L hemiplegia; upper limb affected more than lower limb
  • L hemianaesthesia
  • L hemianopia / quadrantopia
  • Gaze palsy
  • Dysarthria
  • Unilateral neglect / inattention
  • Agnosognosia
  • Autopagnosia
  • Motor impersistence
  • Disinterest / poor motivation / apathy
  • Impulsiveness
  • Dyspraxia – constructional / dressing
  • Impaired ability to judge distance
  • Astereognosis
  • Verticality problems
  • Coma – depending on extent of lesion
45
Q

L MCA

A
  • R hemiplegia; upper limb affected more than lower limb
  • R hemianaesthesis
  • R hemianopia / quadrantopia
  • Dysphasia – receptive and/or expressive
  • Anomia
  • Dyspraxia – ideomotor / ideational
  • Gerstmann’s syndrome: R/L confusion, finger agnosia, acalculia, dysgraphia
  • Coma – depending on extent of lesion
46
Q

ACA

A
  • Contralateral hemiplegia – lower limb affected more than upper limb
  • Cortical sensory loss to leg and foot
  • Urinary incontinence
  • Dyspraxia of left limbs
  • Abulia
  • Slow to respond to commands; decreased mental quickness
  • Flat affect, lack of spontaneity, apathy
  • Distractible
  • Perseveration of movement
  • Notable reduction in speech output
  • Facial/ tongue weakness
  • Grasp/ sucking reflex may be apparent
47
Q

PCA

A
  • Homonymous hemianopia (cortical blindness if bilateral lesions)
  • Colour blindness
  • Hemianaesthesia (mild to severe)
  • Verbal dyslexia
  • Memory defects
  • Poor orientation in space
  • Gerstmann’s syndrome: R/L confusion, finger agnosia, acalculia, dysgraphia

Neurological Physiotherapy Placement (16 decks)

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