Stroke 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
PACS
``` 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 ```
26
Lacunar syndrome (LACS)
``` 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
Posterior circulation syndrome (POCS)
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
What percentage of strokes can be prevented
80%
29
Non modifiable risk factors for stroke
Age Gender (male>female) FH
30
Medical risk factors for stroke
TIA AF Diabetes Fibromuscular dysplasia
31
Modifiable (lifestyle) risk factors for stroke
hypertension - hypecholesterolemia - smoking (tobacco) - obese / overweight - inadequate nutrition - inactivity - excessive alcohol consumption
32
Prognosis : overall
``` General prognosis following stroke - 25% well recovered 25% moderately impaired 25% dependant 25% deceased ``` mortality rate 10% infarction 50% hemorrhagic
33
1 year prognosis for TACS
high mortality, poor functional outcome 60% mortality (40% at 30 days) 35% dependant <5% independant
34
1 year prognosis PACS
fair prognosis, high chance of functional recovery 15% mortality (5% at 30 days) 30 % dependant 55% independant
35
1 year Prognosis LACS
good prognosis 10% dead (5% at 30 days) 30% dependant 60% independant
36
POCS: 1 year prognosis
often good recovery, high reoccurrence 20% dead (<10 at 30 days 20% dependant 60 independant
37
summary
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
Recovery after stroke is affected by what? (4)
- Individual patient characteristics - Type, location and severity of the lesion - Severity of deficits - Environment the patient is exposed to during the recovery periods
39
Poor functional outcomes are linked to
``` prior stroke admission stroke prolonged unconsciousness urinary incontinence >1/52 Cognitive deficits Sensory inattention presence of unilateral spatial neglect ```
40
Degree of motor loss following a stroke
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
list 5 other influences on recovery post stroke
``` age pre-morbid function co-morbidities isolated or difficult social situation patient motivation and attitude ```
42
factors influencing loss of function following stroke
``` 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
Motor impairments - Weakness
most common impairment most significant contributor to reduced function Normally decreased distally >proximally Large variation in nature and distribution of weakness
44
Motor impairments - Spasticity
No relationship found between function and spasticity | No improvement in function has been found following reduction in spasticity
45
Motor impairments - Adaptive features
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
Neuroplasticity definition
the brain's ability to change, remodel and reorganise for purpose of better ability to adapt to a new situation
47
neuroplasticity
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
Neuroplasticity theory
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
Influences on neuroplasticity
enriched or impoverished environments patterns of use or non-use sensory inputs motor skill practice
50
Principle 1 of neuroplasticity and rehab
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
Principle 2
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
principle 3
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
Principle 4
neuroplastic mechanisms can be facilitated - physiotherapists can influence cortical reorganisation after stroke with - rehab techniques sensory stimulation environmental enrichment
54
Motor learning continuum
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
The rehabilitation environment
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
Aims of physiotherapist following stroke (6)
``` prevent secondary complications optimise cardiorespiratory function optimise motor performance increase physical fitness and strength inspire interest and motivation promote mental and physical vigour ```
57
Commencement of intervention
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
Dosage and delivery
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
Maximise practice time
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
Knowledge of expected outcomes
prognosis is dependant on type, location and extent of lesion
61
knowledge of dyscontrol following stroke
70-99% of patients with a motor impairment following stroke will have reduced function weakness is the most common motor impairment
62
Knowledge of recovery mechanisms
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
knowledge of motor skill acquisition
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
optimisation of the rehab environment
commence as soon as patient is medically stable more physio is better type of practice is as important as amount practice ++++ Repetition ++++