stroke Flashcards
what is stroke?
consequence of an interruption to blood flow to part of the brain –> hypoxia and ischaemia
what may cause interruption of blood flow to the brain?
o Infarction – blockage of an artery
o Haemorrhage – rupture of an aneurysm
what is haemorragic stroke subdivided into?
o Parenchymal – into brain tissue
o Subarachnoid – into the subarachnoid space
what are symptoms of stroke?
- Numbness or weakness of face, arm or leg, especially on one side of the body
- Confusion, trouble understanding or speaking
- Trouble seeing in one or both eyes
- Dizziness, loss of balance or coordination
- Severe headache with no known cause
what does FAST stand for?
o Face: is loss or tone or weakness in any facial muscles
o Arms: can they raise both their arms equally?
o Speech: any changes e.g. slurring, slowness
o Time: the quicker the person receives help, the more brain function can be preserved
what is transient ischaemic attack?
• Sudden, focal neurologic deficit with clinical symptoms lasting less than an hour but always lasting less than 24 hours, confined to an area of the brain/eye perfused by a specific artery
what causes a TIA?
Result of the release of a small embolus from a thrombus. Blocks a downstream vessel but then quickly dissolves, allowing blood flow to resume
what is a TIA a sign of?
an impending stroke
how long do TIAs last for?
seconds to 10 minutes
what physical exams are used to diagnose stroke?
neurological signs/symptoms; blood pressure; opthalmoscope exam
what blood tests are used to diagnose stroke?
cholesterol, C-reactive protein
what does a CT scan show?
shows a haemorrhage, tumour, stroke and other conditions
what can an mri detect?
can detect brain tissue damaged by an ischaemic stroke and brain haemorrhages
what extra tests can you do for stroke?
- Carotid ultrasound. This test shows presence of plaques and blood flow in your carotid arteries.
- Cerebral angiogram.
- Echocardiogram.
what is cerebral thrombosis?
formation of a blood clot in a cerebral artery, normally at the site of an atherosclerotic plaque
what happens if a plaque breaks open?
collagen and TF are exposed – produces a thrombus that blocks blood supply to the local tissue
why do 60% of thrombotic strokes develop during sleep?
obstructive sleep apnea triggers a sudden rise in BP that ruptures the surface of a plaque
what causes obstructive sleep apnea
caused by obstruction in the upper airway, usually due to soft tissue in the throat collapsing and blocking the airway
how do slow onset strokes present?
20% of thrombotic strokes develop stepwise over several hours/days. Initial neurological deficits appear, followed by a period without further deterioration
define arteriosclerosis
Thickening, hardening and loss of elasticity of the walls of arteries
define arteriolarsclerosis
Thickening, hardening and loss of elasticity of the walls of arterioles
define atherosclerosis
when the inside of an artery narrows due to the build-up of plaque
where do most thrombotic strokes that arent caused by emboli occur?
occur at sites of atherosclerosis or arteriosclerosis in the brain
define embolism
foreign substance that occludes a blood vessel
o Most are blood clots that broke free from a thrombus
o Can also be a mass of bacteria
how do signs develop in cerebral embolisms?
• Neurological signs develop quickly w cerebral embolisms and usually don’t progress
where is the source of the embolism in an embolic stroke?
Source of embolism is almost always the L side of the heart
what heart diseases produce embolisms?
AF, MI, and defective or artificial heart valves, esp the mitral valve
what % of strokes are made up by thrombotic and embolic strokes?
85%
how do neurological symptoms present in intracerebral haemorrhage?
sudden onset (mins to hours)
why is haemorrhagic stroke frequently associated with severe headache?
Possibly due to stretch of the vessel before rupture
what is the cause of haemorrhagic stroke?
often caused by a ruptured aneurysm
what are indicators of haemorrhagic stroke?
nausea, vomiting, intolerance of noise or light
o These patients are usually hypertensive but not always
o Aneurysms and arteriovenous malformations can bleed spontaneously under normal pressure
what are lacunar strokes?
• Type of stroke where there’s occlusion of one of the arteries that provides blood to the brain’s deep structures as opposed to the cerebral cortex e.g. basal ganglia, cerebral white matter, thalamus, pons and cerebellum
what signs are always absent in lacunar strokes?
Cortical infarct signs (aphasia, neglect, and visual field defects) are always absent
what % of ischaemic strokes do lacunar strokes make up?
15-20%
what are common forms of lacunar strokes?
o Motor hemiparesis with dysarthria: most common (33-50%): infarct in posterior limb of internal capsule
o Ataxia & hemiparesis: infarct also in posterior limb of internal capsule
o Dysarthria & clumsy hand: infarct in anterior limb of internal capsule
what are the most important risk factors for stroke?
hypertension, atrial fibrillation, smoking, diabetes and hyperlipidaemia
what is the main cause of all haemorrhagic strokes?
hypertension
how does reducing BP by 10mmHg reduce the risk of stroke?
reduces risk by 40%
what is a major risk factor of atherosclerosis?
hypertension
what drugs are useful for atrial fibrillation?
Anticoagulation with meds such as warfarin, aspirin or other anticoagulants is useful for prevention
how does diabetes mellitus affect the risk of stroke?
increases risk of stroke by 2 to 3 times
how does controlling blood sugar levels affect microvascular and macrovascular complications?
• Intensive control of blood sugar has been shown to reduce microvascular complications e.g. nephropathy and retinopathy – hasn’t been shown to reduce macrovascular complications e.g. stroke
how do statins help stroke risk in those with hyperlipidemia?
Statins reduce the risk of stroke by about 15-20% in those with high LDL cholesterol.
how does smoking contribute to stroke risk?
causes general inflammation in blood vessels, increases formation of atheromas, causes hypertension etc.
name lesser risk factors of stroke
- low K+ diet and low K+ blood
- sickle cell disease
name foods high in potassium
nuts, potatoes, chocolate, bananas, orange juice etc
why does sickle cell disease increase the risk of stroke?
increased risk of clotting bc of increased fragility of RBCs
how much extracellular space does the brain?
20%
what organ uses the most ATP and why?
brain - needs it to fuel the Na+ pumps in the membrane
why is sodium important in nerve cells?
• Na+ important in nerve cells to keep the membrane potential intact and to maintain nerve cell size and shape
why are nerve cells so sensitive to swelling?
- Neurons have a high SA:V ratio – small Na+ per unit area = lots of Na+ enters
- When Na+ enters, water follows
- If Na+ pump breaks – nerve cell swells
how does hypoxia lead to an increase in intracranial pressure?
- Hypoxia can cause Na+ pumps to stop working swelling
- Brain is contained in the rigid cranial cavity – swelling cells exert pressure on each other and the amount of extracellular space decreases
- Eventually reduced so much that the cells press against each other – produces a rise in intracranial pressure (ICP)
what is a major sign of cerebral hypoxia
raised ICP
how does a high ICP worsen hypoxia?
High ICP will compress cerebral capillaries and veins, leading to a loss of blood flow –> worsens hypoxia
what is cerebral blood flow determined by?
cerebral perfusion pressure
what is cerebral perfusion pressure?
difference between mean arterial pressure and ICP
what is coning/tonsillar herniation?
ICP rise can cause cerebellum to extrude through foramen magnum
Cerebral tonsils move downwards through FM causing compression of the lower brainstem and upper cervical spinal cord
what are common signs of coning?
intractable headache, head tilt, and neck stiffness
Level of consciousness may decrease – gives rise to flaccid paralysis
what happens to potassium released into the ECS by APs in a healthy brain?
removed by glial cells which maintain the homeostasis of the brain environment
how does hypoxia affect the amount of NTS in the synaptic cleft and how?
K+ isn’t removed. Increased extracellular potassium depolarises adjacent cells and leads to excess NTS release
• NTS are normally taken back up into nerve cells by pumps which use ATP.
o Low ATP means that NTS isn’t taken up and remains in the synaptic cleft
what is excitotoxicity?
effects of excess excitatory NTS
what is glutamate?
a dicarboxylic amino acid; main excitatory NTS in the brain
o Acts on NMDA rand AMPA receptor
how does fast excitotoxicity occur?
Excess stimulation of the NMDA receptor after 3-5mins of anoxia leads to excess influx or Ca2+ ions into nerve cells –> fast excitotoxicity
how does slow excitotoxicity occur?
Excess stimulation of AMPA receptors over several hours leads to slow (delayed) excitotoxicity
explain the excitotoxic loop
- Increased influx of Ca2+ increases metabolic demand on the cell and uses more O2
- High metabolic demand in the absence of oxygen leads to the formation of free radicals which trigger cell death or apoptosis
what are the 3 regions of the brain around a stroke focus?
- area where cells face inevitable death
- penumbra
- area where cells survive
what is the penumbra region?
neurons are hypoxic and/or damaged but survival is possible
what is the main goal of stroke treatment?
max survival of neurones in the penumbra region
what is the median time to presentation of a stroke?
• 13 hours after onset of symptoms is the median time to presentation
what are the main treatment strategies of stroke?
o Restore blood flow
o Combat excitotoxicity
o Combat free radical damage
how can you restore blood flow after a stroke?
• Use of IV tissue plasminogen activators improves outcome after stroke
when should IV tissue plasminogen be used?
until CT has ruled out a brain haemorrhage
what does the efficacy or tissue plasminogen activators depend on?
• Efficacy of treatment depends on how critically soon it’s administered – within 3-4 hours for maximum benefit
how can we combat excitotoxicity and how do these methods work?
- NMDA antagonists e.g. Cerestat – block NMDA receptors and fast excitotoxicity – hasn’t been successful in practice bc it may have been administered late and also has serious side-effects
- AMP antagonists e.g. NBQX – reduces slow excitotoxicity. More hope bc AMPA effects are delayed and drug treatment after 1 hour may be beneficial
- Newer drugs to prevent delayed triggering of apoptotic pathways- ‘programmed cell death’. (e.g. Lithium,)
how can we reduce free radical damage?
• Antioxidants e.g. vitamin C and E given intravenously
o Dietary supplements shown to reduce risk of stroke in vulnerable groups.
• Free radical scavenging enzymes – superoxide dismutase is low in stroke patients
• Cool down the brain – reducing body temp reduces O2 demand and may allow neurones in the penumbra to survive if there’s small O2 supply from collateral BVs
how can we reduce primary risk?
- Treat hypertension – diuretics, ACE inhibitors, AR antagonists, change diet
- Treat AF – give aspirin to healthy patients <65 years. Give warfarin for patients >65 years or having other stroke risk factors.
- Give statins to patients with vascular disease
