Stroke Flashcards
Define a 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
Stroke Types and percentages
Ischaemic (85%)
• Thrombotic
• Embolic
• Hypo-perfusion
Hemorrhagic (15%)
• Subarachnoid
• Intracerebral
List of pathogenesis and percentages of ischaemic strokes
Large artery thromboembolism 50% Small artery disease 20-25% Embolism associated with cardiac dysfunction 20% Non atheromatous arterial disease 5% Blood disease <5%
Pathogenesis of haemorrhagic stroke
• 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)
Stroke Classification Bamford Oxfordshire Stroke Classification
• 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.
non-modifiable risk factors for stroke
• Age (↑ age
↑ risk)
• Gender (male > female)
• Family history
Medical Risk factors for stroke
- TIA
- AF
- Diabetes
- Fibromuscular Dysplasia
Modifiable risk factors for stroke
Hypertension • Hypercholesterolemia • Smoking (tobacco) • Obese/ overweight • Inadequate nutrition • Inactivity • Excessive alcohol consumption
overall prognosis for stroke
- 25% well recovered
- 25% moderately impaired
- 25% dependent
- 25% deceased
mortality rate for infarction vs haemorrhage
- 10% Infarction
* 50% Haemorrhage
1 year prognosis for TACS
high mortality, poor functional outcome
• 60% mortality (40% at 30 days)
• 35% dependent
• <5% independent
1 year prognosis for PACS
fair prognosis, high chance of functional recovery
• 15% mortality (5% at 30 days)
• 30% dependent
• 55% independent
1 year prognosis for LACS
good prognosis
• 10% dead (5% at 30 days)
• 30% dependent
• 60% independent
1 year prognosis for POCS
often good recovery, high reoccurrence
• 20% dead (<10% at 30 days
• 20% dependent
• 60% independent
Recovery after stroke is affected by what
• Individual patient characteristics • Type, location and severity of lesion • Severity of deficits • Environment the patient is exposed to during the recovery period
Poor functional outcomes after stroke are linked to
- Prior stroke
- Admission severity
- Prolonged unconsciousness
- Urinary incontinence > 1/52
- Cognitive deficits
- Sensory inattention
- Presence of unilateral spatial neglect
Weakness in stroke
- Most common impairment
- Most significant contributor to reduced function
- Normally decreased distally > proximally
- Large variation in nature and distribution of weakness
Spasticity in stroke
• No relationship found between function and spasticity
• No improvement in function has been found following
reduction in spasticity
adaptive features in stroke
• 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
define neuroplasticity
• The brain’s ability to change, remodel and reorganise for
purpose of better ability to adapt to a new situation
neuroplasticity theory
• 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
Influence on neuroplasticity
- Enriched or impoverished environments
- Patterns of use or non-use
- Sensory inputs
- Motor skill practice
Principle 1 of neuroplasticity
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
Principle 2 of neuroplasticity
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 of neuroplasticity
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
Principle 4 of neuroplasticity
Neuroplastic mechanisms can be facilitated
• Physiotherapists can influence cortical reorganisation
after stroke with:
• Rehabilitative techniques
• Sensory stimulation
• Environmental enrichment
TIA define
- 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
ischaemic cascade
- 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
pathogenesis of haemorrhagic stroke
Hypertension • Acute Hypertension • Alcohol • Amphetamines etc Arterial Disease • Vascular Malformations Diasthesis (Bleeding Disorders) • Anticoagulants • Antiplatelets • Thrombolytic therapy Trauma
pathogenesis of haemorrhagic stroke
- 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 hemisphere function (usually left)
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
non-dominant (usually right) hemisphere function
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
prognosis : overall
general prognosis 25% well recovered 25% moderately impaired 25% dependant 25% deceased
mortality rate
10% infarction
50% haemorrhage
Aims of physiotherapy following stroke
- Prevent secondary complications
- Optimise cardiorespiratory function
- Optimise motor performance
- Increase physical fitness and strength
- Inspire interest and motivation
- Promote mental and physical vigour
dosage and delivery of physiotherapy intervention
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
Benefits of physiotherapy
• 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
Physio rehab recommendations - amount and intensity
- 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
Physio rehab recommendation - timing
- 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
Summary for week 3 - lecture 1
- 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
Stroke acute care
• Acute Care: focus on rapid thorough assessment and
early management
• Principles of rehabilitation should be applied in acute and post-acute settings•
Stroke rehabilitation care
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
tPA: thrombolysis
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)
look up medical mgmt
lecture 3-2
R MCA infarct
- 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
L MCA
- 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
ACA
- 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
PCA
- 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
