Week 2 Flashcards

1
Q

WHO definition of 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

What is a transient ischaemic attack (TIA)

A

neurological deficit of presumed vascular origin lasting less than 24 hours

  • typically last less than 10 minutes
  • suggestions to change definition definition to <1 hour

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

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3
Q

Stroke types (2)

A

ischaemic (85%)

hemorrhagic (15%)

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4
Q

Types of ischaemic stroke

A

thrombotic
embolic
hypo-perfusion

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5
Q

Types of hemorrhagic stroke

A

subarachnoid

intracerebral

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6
Q

Pathogenesis of ischaemic stroke

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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7
Q

Ischaemic cascade

A

process of stroke injury at the cellular level

irreversible damage begins immediately at the core

the penumbra may be viable for up to 6 hours

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8
Q

ischaemic cascade continued

A

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 cause microvascular injury, BBB dysfunction and initiate inflammation
exacerbates initial injury and can lead to permanent cerebral damage

Amount of permanent damage is dependant on : degree and duration of ischemia and brain’s capability to recover

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9
Q

Pathogenesis of haemorrhagic stroke

A
hypertension 
- acute hypertension 
- alcohol
-amphetamines 
arterial disease
- vascular malformations

Diasthesis (bleeding disorders)

  • Anticoagulants
  • Antiplatelets
  • Thrombolytic therapy

Trauma

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10
Q

Look up the pathogenesis of hemorrhagic and ischaemic stroke

A

Kahn’s academy?

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11
Q

Pathogenesis of haemorrhagic stroke cont

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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12
Q

Dominant (usually left) hemisphere functions

A

language
skilled motor formulation (Praxis)

Arithmetic sequential and analytical calculating skills

musical ability : sequential and analytical skills in trained musicians

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

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13
Q

Non dominant (usually right) hemisphere functions

A

Prosody (emotion conveyed by tone of voice

visual spatial analysis and spatial attention

arithmetic ability to estimate quantity 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

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14
Q

Anterior circulation includes

internal carotid artery system

A

anterior cerebral artery

middle cerebral artery

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15
Q

Posterior circulation includes

vertebrobasilar artery system

A
vertebral artery 
posterior inferior cerebellar artery 
basilar artery 
anterior inferior cerebellar artery 
posterior cerebral artery
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16
Q

Symptomology of Middle Cerebral Artery - Right

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
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17
Q

Symptomology middle cerebral artery -Left

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
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18
Q

anterior cerebral artery

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, apthy 
distractible 
perservation of movement 
notable reduction in speech output 
facial/tongue weakness
grasp/sucking reflex may be present
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19
Q

Posterior cerebral artery

A

homonymous hemianopia (cortical blindness if bilateral lesions)
colour blindness
hemianaesthesia (mild to severe)
verbal dyslexia
memory deficits
poor orientation in space
gerstmann’s syndrome : R/L confusion, finger angosia, acalculia, dysgraphia

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20
Q

Posterior inferior cerebella artery

A

vertigo/nausea/vomiting/nystagmus at rest or with eye movement
ipsilateral loss of pain and temperature to face
contralateral loss of pain and temperature to body
diplopia
hoarseness
dysarthria
dysphagia
transient contralateral hemiparesis
Cerebellar ataxia - falling to side of lesion
Ipsilateral paralysis of muscles of the soft palate, pharynx and larynx causing dysphagia and dysarthria
Horner’s syndrome : ipsilateral small pupil, ptosis, enophthalmos (sunken eye ball), lack of sweating on one side of face

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21
Q

Vertebral artery or branch of vertebral / lower basilar artery

A

ipsilateral paralysis with atrophy of half the tongue (CN XII)
Contralteral hemiparesis of arm and leg (sparing face)
Contralateral impaired tactile and proprioceptive sense

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22
Q

Stroke classification

A

Stoke syndromes are usually divided into
Large vessel stroke within the anterior circulation

large vessel stroke within the posterior circulation

Small vessel disease of either vascular bed

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23
Q

Bamford oxfordshire stroke classifications

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 hemorrhage) the letter S is replaced with I and H respectively

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24
Q

TACS

A

large cortical and subcortical stroke in MCA/ACA
high mortality, poor functional outcome (long term dependancy)

symptoms include all three of the following 
Higher cerebral dysfunction 
- neglect (right hemisphere) 
-Aphasia (L hemisphere) 
-Apraxia 

Homonymous hemianopia
motor sensory deficit
>2/3 face + arm + leg

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25
Q

PACS

A
cortical stroke in MCA branch 
fair prognosis, high chance of functional recovery 
symptoms at maximum deficit include two of the following 
-higher cerebral dysfunction 
-homonymous hemianopia 
-motor sensory deficit
or
-higher cerebral dysfunction 
or 
-limited motor/sensory deficit
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26
Q

Lacunar syndrome (LACS)

A
subcortical stroke in deep perforating artery
good prognosis
Symptoms include on of the following 
- sensori-motor stroke
- pure sensory stroke
-pure motor stroke 
-ataxic hemiparesis 
no evidence of higher cerebral or visuospatial or hemianopia or vertebrobasilar dysfunction
27
Q

Posterior circulation syndrome (POCS)

A

lesion in posterior cerebral hemisphere, brainstem or cerebellum
often good recovery, high reoccurrence
symptoms at maximum deficit include one of the following
- cerebellar or brainstem syndromes
cranial nerve palsy with contralateral motor/sensory deficit
loss of consciousness
isolated homonymous hemianopia

28
Q

What percentage of strokes can be prevented

A

80%

29
Q

Non modifiable risk factors for stroke

A

Age
Gender (male>female)
FH

30
Q

Medical risk factors for stroke

A

TIA
AF
Diabetes
Fibromuscular dysplasia

31
Q

Modifiable (lifestyle) risk factors for stroke

A

hypertension

  • hypecholesterolemia
  • smoking (tobacco)
  • obese / overweight
  • inadequate nutrition
  • inactivity
  • excessive alcohol consumption
32
Q

Prognosis : overall

A
General prognosis following stroke 
- 25% well recovered
25% moderately impaired 
25% dependant 
25% deceased 

mortality rate
10% infarction
50% hemorrhagic

33
Q

1 year prognosis for TACS

A

high mortality, poor functional outcome
60% mortality (40% at 30 days)
35% dependant
<5% independant

34
Q

1 year prognosis PACS

A

fair prognosis, high chance of functional recovery
15% mortality (5% at 30 days)
30 % dependant
55% independant

35
Q

1 year Prognosis LACS

A

good prognosis
10% dead (5% at 30 days)
30% dependant
60% independant

36
Q

POCS: 1 year prognosis

A

often good recovery, high reoccurrence
20% dead (<10 at 30 days
20% dependant
60 independant

37
Q

summary

A

A stroke is a clinical syndrome characterised by rapidly
developing clinical signs of focal, and at times global
disturbance of cerebral function
• Immediate damage occurs due to ischaemia/ haemorrhage
with secondary damage resulting from cellular processes
including inflammation, excitotoxicity and oxidative stress
• Clinical signs and symptoms are dependent of location and
extent of lesion
• Stroke is one of Australia’s biggest killers and a leading cause
of disability
• More than 80% of strokes can be prevented
• Prognosis is dependent on type, location and extent of lesion

38
Q

Recovery after stroke is affected by what? (4)

A
  • Individual patient characteristics
  • Type, location and severity of the lesion
  • Severity of deficits
  • Environment the patient is exposed to during the recovery periods
39
Q

Poor functional outcomes are linked to

A
prior stroke 
admission stroke 
prolonged unconsciousness
urinary incontinence >1/52
Cognitive deficits 
Sensory inattention 
presence of unilateral spatial neglect
40
Q

Degree of motor loss following a stroke

A

important factor influencing outcome after stroke
10 times more likely to recover function if motor deficit is mild
initial lack of sitting balance correlated with dependant gait at 6/52

41
Q

list 5 other influences on recovery post stroke

A
age 
pre-morbid function
co-morbidities 
isolated or difficult social situation 
patient motivation and attitude
42
Q

factors influencing loss of function following stroke

A
motor impairment (70-99%) 
sensory impairment (66%) 
Visual inattention (58%) 
Neglect (43%) 
Apraxia (39%) 
Aphasia (33%) 
Dysphagia (38%) 
Dysarthria (35%) 
Visual disturbances (35%) 
Cognitive dysfunction(21%)
43
Q

Motor impairments - Weakness

A

most common impairment
most significant contributor to reduced function
Normally decreased distally >proximally
Large variation in nature and distribution of weakness

44
Q

Motor impairments - Spasticity

A

No relationship found between function and spasticity

No improvement in function has been found following reduction in spasticity

45
Q

Motor impairments - Adaptive features

A

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

46
Q

Neuroplasticity definition

A

the brain’s ability to change, remodel and reorganise for purpose of better ability to adapt to a new situation

47
Q

neuroplasticity

A

the brain’s ability to reorganise itself by forming new neural connections throughout life

allows neurones to compensate for injury and disease and to adjust their activity in response to new situations or changes in environment

how we adapt to changing conditions, learn new facts and develop new skills

describe changes in neural system at many levels
- molecular, morphological, synaptic, cortical, functional

48
Q

Neuroplasticity theory

A

presynaptic cells that provide input to the postsynaptic cell will have their synaptic connections 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

49
Q

Influences on neuroplasticity

A

enriched or impoverished environments
patterns of use or non-use
sensory inputs
motor skill practice

50
Q

Principle 1 of neuroplasticity and rehab

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

In the case of a stroke that damages a body part’s representation in the primary motor cortex, plasticity permits some reorganisations that will restore a representation

the process must be competitive with all other body parts

51
Q

Principle 2

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

52
Q

principle 3

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
MRI studies demonstrate that the damaged hemisphere has increased blood flow when bilateral movements are made

53
Q

Principle 4

A

neuroplastic mechanisms can be facilitated

  • physiotherapists can influence cortical reorganisation after stroke with
  • rehab techniques
    sensory stimulation
    environmental enrichment
54
Q

Motor learning continuum

A

learner gains a basic idea of movement pattern

the movement pattern is adapted to real word tasks

performance becomes more consistent, efficient and automatic

55
Q

The rehabilitation environment

A

very important in optimising functional recovery

patients in stroke units more likely to be alive, independent and living at home one year after stroke

56
Q

Aims of physiotherapist following stroke (6)

A
prevent secondary complications 
optimise cardiorespiratory function 
optimise motor performance 
increase physical fitness and strength 
inspire interest and motivation 
promote mental and physical vigour
57
Q

Commencement of intervention

A

immediate start providing the patient is medically stable
patients who receive early intervention are more likely to walk independently, are discharged earlier and are more likely to return home
care needs to be taken not to place extreme demands on the affected limbs in the early stages

58
Q

Dosage and delivery

A

evidence that more is better
type of practice is equally 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

59
Q

Maximise practice time

A

only a small percentage of a patient’s daily time is spent with a physio
exercise classes and circuit training
independant practice outside of therapy time (alone, with family or physio assistant

maximise participation in ADLs and mobility with nursing and care staff
mental practice can produce positive effects in performance

60
Q

Knowledge of expected outcomes

A

prognosis is dependant on type, location and extent of lesion

61
Q

knowledge of dyscontrol following stroke

A

70-99% of patients with a motor impairment following stroke will have reduced function
weakness is the most common motor impairment

62
Q

Knowledge of recovery mechanisms

A

neuroplasticity is the brain’s ability to change, remodel and reorganise for purpose of better ability to adapt to a new situation

body parts can compete for representation in the brain and use of body part can enhance its representation

the premotor can substitute for the motor cortex to control movement

the intact hemisphere can take over some motor control
neurplastic mechanisms can be facilitated

63
Q

knowledge of motor skill acquisition

A

patient must be actively involved in rehab
practice practice practice
practice must be task orientated
goals must be meaningful to the patient so that they have the motivation to persevere

64
Q

optimisation of the rehab environment

A

commence as soon as patient is medically stable
more physio is better
type of practice is as important as amount
practice ++++
Repetition ++++