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