Week 2 Flashcards
WHO definition of stroke
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
What is a transient ischaemic attack (TIA)
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
Stroke types (2)
ischaemic (85%)
hemorrhagic (15%)
Types of ischaemic stroke
thrombotic
embolic
hypo-perfusion
Types of hemorrhagic stroke
subarachnoid
intracerebral
Pathogenesis of ischaemic stroke
large artery thromboembolism 50%
small artery disease - 20-25%
embolism associated with cardiac dysfunction 20%
non atheromatous arterial disease 5%
blood disease <5%
Ischaemic cascade
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
ischaemic cascade continued
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
Pathogenesis of haemorrhagic stroke
hypertension - acute hypertension - alcohol -amphetamines arterial disease - vascular malformations
Diasthesis (bleeding disorders)
- Anticoagulants
- Antiplatelets
- Thrombolytic therapy
Trauma
Look up the pathogenesis of hemorrhagic and ischaemic stroke
Kahn’s academy?
Pathogenesis of haemorrhagic stroke cont
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)
Dominant (usually left) hemisphere functions
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
Non dominant (usually right) hemisphere functions
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
Anterior circulation includes
internal carotid artery system
anterior cerebral artery
middle cerebral artery
Posterior circulation includes
vertebrobasilar artery system
vertebral artery posterior inferior cerebellar artery basilar artery anterior inferior cerebellar artery posterior cerebral artery
Symptomology of Middle Cerebral Artery - Right
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
Symptomology middle cerebral artery -Left
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
anterior cerebral artery
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
Posterior cerebral artery
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
Posterior inferior cerebella artery
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
Vertebral artery or branch of vertebral / lower basilar artery
ipsilateral paralysis with atrophy of half the tongue (CN XII)
Contralteral hemiparesis of arm and leg (sparing face)
Contralateral impaired tactile and proprioceptive sense
Stroke classification
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
Bamford oxfordshire stroke classifications
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
TACS
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
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
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
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
What percentage of strokes can be prevented
80%
Non modifiable risk factors for stroke
Age
Gender (male>female)
FH
Medical risk factors for stroke
TIA
AF
Diabetes
Fibromuscular dysplasia
Modifiable (lifestyle) risk factors for stroke
hypertension
- hypecholesterolemia
- smoking (tobacco)
- obese / overweight
- inadequate nutrition
- inactivity
- excessive alcohol consumption
Prognosis : overall
General prognosis following stroke - 25% well recovered 25% moderately impaired 25% dependant 25% deceased
mortality rate
10% infarction
50% hemorrhagic
1 year prognosis for TACS
high mortality, poor functional outcome
60% mortality (40% at 30 days)
35% dependant
<5% independant
1 year prognosis PACS
fair prognosis, high chance of functional recovery
15% mortality (5% at 30 days)
30 % dependant
55% independant
1 year Prognosis LACS
good prognosis
10% dead (5% at 30 days)
30% dependant
60% independant
POCS: 1 year prognosis
often good recovery, high reoccurrence
20% dead (<10 at 30 days
20% dependant
60 independant
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
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
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
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
list 5 other influences on recovery post stroke
age pre-morbid function co-morbidities isolated or difficult social situation patient motivation and attitude
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%)
Motor impairments - Weakness
most common impairment
most significant contributor to reduced function
Normally decreased distally >proximally
Large variation in nature and distribution of weakness
Motor impairments - Spasticity
No relationship found between function and spasticity
No improvement in function has been found following reduction in spasticity
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
Neuroplasticity definition
the brain’s ability to change, remodel and reorganise for purpose of better ability to adapt to a new situation
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
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
Influences on neuroplasticity
enriched or impoverished environments
patterns of use or non-use
sensory inputs
motor skill practice
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
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
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
Principle 4
neuroplastic mechanisms can be facilitated
- physiotherapists can influence cortical reorganisation after stroke with
- rehab techniques
sensory stimulation
environmental enrichment
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
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
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
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
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
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
Knowledge of expected outcomes
prognosis is dependant on type, location and extent of lesion
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
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
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
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 ++++
