Stroke Flashcards
Stroke
Consequence of cerebrovascular disease that interrupts blood flow to part of the brain, causing ischemia and hypoxia
Haemorrhagic stroke
Parenchymal- into brain tissue
Subarachnoid- into subarachnoid space
Stroke death
3rd most common cause of death
Stroke symptoms
Numbness/weakness of face, arm or leg, especially on one side
Confusion, trouble understanding or speaking
Trouble seeing in one or both eyes
Dizziness, loss of balance or coordination
Severe headache
Symptoms Pneumonic
FAST Face Arms Speech Time
Types of stroke
TIA
Thrombotic
Embolic
Haemorrhagic
Ischaemic stroke forms
Thrombotic + Embolic
TIA
Confined to area of brain of eye perfused by a specific artery
Release of small emboli from thrombus –> temporarily block downstream vessel then quickly dissolve
TIA Time
Most last seconds to 10 mins
Symptoms more than 1 hour 25%
Resolved within 24 hours
Stroke Diagnosis
Physical exam
Blood test- cholesterol, C reactive protein
CT scan- shows haemorrhage, stroke etc
MRI- shows brain tissue damage
Cerebral thrombosis
Formation of blood clot in cerebral artery, normally at site of atherosclerotic plaque
If surface of plaque breaks open, collagen + TF exposed –> thrombus produced –> blocks blood supply
Thrombotic stroke formation
60% form during sleep
20% form over hours/few days
Arteriosclerosis
Thickening, hardening + loss of elasticity of the walls of arteries
Atherosclerosis
When inside of artery narrows due to build up of plaque
Thrombotic stroke occurrence
Most not due to emboli occur at site of atherosclerosis or arteriosclerosis in brain
Cerebral embolism
Usually occurs during activity
Consciousness usually preserved
Neurological signs develop rapidly
Embolic Stroke
Source of embolism almost always LEFT SIDE OF HEART
AF, MI, defective/ artificial heart valves (especially MV)
Myocardial Infarction
Causes Akinetic region in heart wall
Thrombus can form in immobile region of ventricle
Thrombotic + embolic strokes
85% of all strokes
Haemorrhagic Stroke
Intracerebral haemorrhage- sudden onset of neurological symptoms
Severe headache
Stupor or coma that progress with time
Usually hypertensive
Lacunar stroke
Occlusion of one of arteries that provides blood to the brain’s deep structures instead of cerebral cortex
E.g. basal ganglia, thalamus, pons, cerebellum
Cortical infarct signs (aphasia, neglect, visual field defects) always absent
Lacunar Strokes
15-20% of ischaemic strokes
Motor hemiparesis with dysarthria
Most common lacunar syndrome
33-50%
Infarct in posterior limb of internal capsule
Ataxia + hemiparesis
2nd most common form lacunar stroke
Infarct in posterior limb of internal capsule
Dysarthria + clumsy hand
Infarct in anterior limb of internal capsule
Stroke Risk Factors
Hypertension Atrial Fibrillation Smoking Diabetes Hyperlipidaemia
Hypertension RF
35-50% stroke risk
BP reduction 10mmHg systolic or 5mmHg diastolic reduces risk by 40%
Lowering BP prevents both ischaemic + haemorrhagic strokes
Major RF for athero + arteriosclerosis
Atrial Fibrillation RF
5% a year risk of stroke
Risk higher in those with valvular AF
Diabetes RF
Increases risk by 2 to 3 times
Hypercholesterolaemia (hyperlipidaemia)
Statins reduce stroke risk by 15-20% in those with high LDL cholesterol
Smoking RF
General inflammation of blood vessels
Increased atheroma formation
Hypertension
Obstructive sleep apnoea
Increases risk by up to 3 times
Especially in men
Low diet potassium + hypokalaemia RF
Increase risk
Foods high in K- nuts, potatoes, choc, bananas
Thiazides + loop diuretics RF
Block reabsorption of Na + water upstream from distal tubule
Promotes increased distal tubular K secretion
–> hypokalaemia
MCA
Prone to aneurysms + stroke
Lots of twists
Sodium Pump
Maintains nerve cell size + shape
Removes Na from nerve cells –> water follows
If doesn’t work, brain nerve cells SWELL
Nerve cells
High SA/V ratio
Large SA- more sodium leakage into cells
Swollen brain cells
Brain is contained in rigid box = cranial cavity
Decrease extracellular space
Compresses capillaries + venules–> oedema + swelling
Rise in ICP
Raised ICP
Sign of cerebral hypoxia
Compresses cerebral veins
Loss of blood flow
Worsening hypoxia
Normal Extracellular space in brain cells
20%
Extracellular space in brain cells when swollen
5%
Tonsillar herniation
Rise in ICP
Cerebellar tonsils extrudes through foramen magnum
–> compression of lower brainstem + upper cervical spinal cord
Tonsillar herniation sign
Intractable headache head tilt neck stiffness Decreased consciousness Flaccid paralysis
Glial cells
Maintain homeostasis in brain environment
Remove potassium released into extracellular space by APs
Hypoxic brain- K
Potassium not removed from ECS by glial cells
Increased extracellular K depolarises adjacent cells –> excess neurotransmitter release
ATP levels low, so neurotransmitters not taken up –> remain in synaptic cleft or ECS
Excitotoxicity
Effects of excess release of excitatory neurotransmitter due to increased extracellular K
Glutamate
Main excitatory transmitter
Acts on NMDA + AMPA receptors
Excess NMDA stimulation
After 3-5 mins leads to excess influx of Ca into nerve cells –> fast excitotoxicity
Excess AMPA stimulation
Over several hours
Leads to slow (delayed) excitotoxicity
Excitotoxic Loop
In Hypoxia ATP levels drop + glutamate reuptake fails
Post-synaptic glutamate receptors (especially NMDA) are overstimulated
–> influx of calcium
–> increase in metabolic demand on cell + uses more O2
–> higher demand in absence of O2 leads to free radical formation
–> trigger cell death or apoptosis
Stroke focus
Three regions of brain around it
Internal layer- cells face death
Middle layer- Penumbra region, neurones are hypoxic and/or damaged but survival possible
Outer layer- cells will survive
Penumbra region
Neurones hypoxic and/or damaged
Survival possible
Stroke focus
Stroke treatment strategies
Restore blood flow
Combat excitotoxicity
Combat free radical damage
Stroke treatment goal
Survival of neurones in penumbra region
Restore blood flow
Tissue plasminogen activators (thrombolysis)
Within 3-4 hours for most significant benefit
Intravenous fibrinolytic therapy at cerebral circulation dose
Within first 3 hours of ischemic stroke- substantial benefits
Within 3.5-4.5 hours- Moderate net benefits
Intra-arterial fibrinolytic therapy
In 3-6 hour window offers moderate net benefits
Combat excitotoxicity
NMDA antagonists
AMP antagonists
Delay triggering of apoptotic pathways
NMDA agonists
Cerestat
Block NMDA receptors + fast excitotoxicity
AMP agonists
NBQX
Reduce slow excitotoxicity
Lithium
delay apoptosis
Reduce Free radical damaging
Antioxidants- Vit C + E
Free radical scavenging enzymes- superoxide dismutase
Cool down brain –> reduces O2 demand
Reduce Primary risk
Treat hypertension- ACE inhibitors, AR antagonists
Treat AF- Aspirin <65yo, Warfarin >65yo
Vascular disease- Statins
