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
What are the types of treatment for cerebral stroke?
Pharmacological
Thrombosis
Aspirin
Modifiable risk factor
Physiotherapy
What are drugs and receptors as a treatment?
In the CNS they alter synaptic function
They increase production of dopamine - drugs mimic the precursor of dopamine
Increase activity at dopamine synapse
What are the different types of drugs?
Affect neurotransmitter functioning
- Agonist = increase NT
- Antagonist = decrease NT
Sites of action drugs
- Direct = attaches to NT binding site
- Indirect = binds to alternative site
- Non-competitive binding = does not compete with NT
Drugs
- Direct agonist/antagonist
- Indirect agonist/antagonist
Neuroprotection
- Aim to protect neurons from injury
- Limited by therapeutic time window and effectiveness
NMDA receptor antagonist
- Obvious choice for treating stroke
What are the pharmacological treatments for cerebral stroke?
NMDA receptor antagonist
Proved to be the most successful compounds ever generated to protect against cell death
All other compounds developed have failed
- All clinical trials have failed because of lack of efficacy or toxic side effects
Only 4 drugs that are licenced to give
What is thrombolysis as a treatment?
Tissue Plasminogen Activator
- breaks down blood clots
- only drug licensed in the UK and US
- only effective if given 3 hours after stroke
- not for haemorrhagic stroke
- not useful for when stroke happens into the sleep
What is aspirin as a treatment?
- recommended to high risk patients (after TIA)
- antiplatelet agents
- prevention of recurring strokes
- reduction of severity
- inhibit production of thromboxane
What are the risk factors of a stroke?
High BP
Smoking
Physical Therapy
Obesity
What is physiotherapy as a treatment?
Used or weakness/paralysis
Improve mobility/avoid future injury
Everyday activities
Independent living
Excersise, manipulation, massage and skills ensure repeated use of the muscles
