L15 & 16 - Stroke Flashcards
What us cerebral stroke?
Blockage or interruption of cerebral artery
Results in death of cells
Symptoms are dependant on location
What is the prevalence of stroke?
250-400 strokes per 100 000 people
3rd cause of death
1st cause of disability
What are the two types of stoke?
Ischemic (80%)
- area deprived of blood
- blood clot (thrombus) or fatty plaque block artery
Haemorrhagic (20%)
- excess pleading due to ruptured blood vessel
- break in blood vessel (aneurysm) due to high blood pressure
Wat is the risk of stroke throughout lifespan?
Childhood strokes - over 400 stroke a year in the UK
1 in 4 strokes occur in working age adults
What are the risk factors of stroke?
Age
Medical conditions - high BP, diabetes, high cholesterol
Lifestyle - smoking, drinking, diet
Family history - related to other risk factors
Specific for women - pregnancy, pill
What are the clinical symptoms of a stroke?
Sudden or gradual onset
One sided limb weakness/paralysis
Confusion, loss of speech
Headache
Loss of consciousness
- Results in dysfunctional cognitive and motor behaviour, determined by size of location of cell loss
How is depression linked to stroke?
Common after stroke
Not a consequence of physical effects
Patients with post-stroke depression often differ from normal depression as they have more cognitive impairment
- irritability, psychomotor slowing, mood liability
What is a transient ischemic attack (TIA)?
Transient episode of neurological dysfunction without acute tissue death (mini stroke)
Disruption of cerebral blood flow
Memory loss/confusion
Risk factor of a subsequent stroke - 10% of strokes are within 90 days of TIA
Silent stroke - no visible symptoms
What is the core and penumbra of an ischemic stroke?
The core = blood flow below critical, cell death
The penumbra = sub-optimal blood flow
Development of the core starts below critical but cell death starts to occur (surrounded by penumbra)
Core damage expands - more cell death, symptoms start
Not always a stable profile of symptoms
Prevent or reduce expansion of the core
What is the pathology of cerebral stroke?
Inflammation
- sodium ions - water, swell, inflammation
- microglia - phagocytic (cell eating)
- blood brain barrier broken down
Cell death
- necrosis, depleted ATP, cellular swelling and membrane breakdown
- apoptosis, trigger cell death, phagocytic from other cells
What is a reperfusion injury?
Hyperperfusion - a major increase in CBF well above metabolic demands
Complications of surgical intervention
Intracranial haemorrhage - mortality 36-63%, 80% patients significantly morbidity
Damage to the blood brain barrier - shows extravasation of contrast agent
What are the types of amino acid transmitters?
Excitatory = glutamate and aspartate
Inhibitory = GABA and glycine
Glutamate and GABA are closely related
What are the two types of glutamate receptors?
Ionotropic - NMDA, AMPA, Kainate
Metabotropic - Many subtypes
Glutamate binds to the receptor and opens the ions gates
Metabotropic is slower
What is a NMDA receptor?
Natural agonist
Magnesium block - cell membrane has to become depolarised to remove magnesium block
What is excitotoxicity?
1957 - Lucas and Newhouse - glutamate caused retinal damage
1969 - only reported that glutamate produced brain damage in neonatal mice
Excess amino acids results in prolonged depolarization of receptive neurons which leads to eventual damage or death
Kainate - specifically affected neurons
Excitotoxic lesions - led to speculation that endogenous amino acids may play a role in the genesis of human neurological conditions
