Neurovascular disorders Flashcards
Stroke types and definition
acute onset of neurological deficits lasting more than 24 hours, due to a disturbance in blood supply.
Ischemic (85%): thrombotic (55%) or embolic (30%). Caused by blockage of blood vessel, with embolic having travelled to the brain. Thrombotic can be due to lacunar or large vessel occlusion, while embolic is only due to large vessel occlusion
Haemorrhagic (15%): intracerebral (10%) or subarachnoid (5%)
Stroke risk factors and symptoms
Non-modifiable: age, partial fibrillation, gender, ethnicity, family history.
Modifiable: hypertension, diabetes, hyperlipidemia, smoking, obseity, carotid artery disease.
Headache, seizures, nausea, dysphasia, limb weakness, ataxa, confusion, dizziness, incontinence, etc…
Symptoms will differ depending on the blood vessel blocked, and the brain region most affected.
Lacunar infarction
are very small strokes in penetrating arteries that feed sub-cortical structures. up to 80% are “silent”
Motor hemiplegia syndrome is due to a lacunar infarction in the internal capsule, basal ganglia, and/or pons.
Stroke diagnostic
By CT scan following neurological examination. Harder to see ischaemic stroke on the scan.
Treatments for haemorrhagic and ischaemic strokes
Haemorrhagic stroke: 45% mortality, 30% vasospasms. Pain management and surgery to repair. Lowering blood pressure may help
Ischemic: If within 3 hours, can be treated with alteplase, a plasminogen activator (converts to plasmin, which catalyses the degradation of the fibrin clot). If within 6 hours, thrombectomy to manually remove the block.
Penumbra and what tissue survives.
Tissue that only gets core blood flow will die (<12mL/100g/min)
The penumbra (12-22mL/100g/min) can survive if blood flow is restored in a few hours.
The benign oligemia (>22mL/100g/min) will survive, but will be damaged
Normal blood flow = 50-54mL/100g/min
peri-infarct depolarisations and inflammation
The toxicity can spread in what is known as peri-infarct depolarisations. The imbalance of ion gradients as a result of the stroke causes this. It can mediated excitotoxicity by excessive glutamate release
Inflammation associated with the stroke causes further damage. This is largely mediated by cytokines and leukocytes released by microglia and astrocytes
Vascular mediated cognitive impairment in dementia
The same vascular risk factors for stroke also are seen to increase dementia risk. May share a vascular origin. (50% of AD can be considered cerebrovascular diseases).
In dementia hypoperfusion of the cerebral vasculature is associated with decreased brain blood flow. Can contribute to the microbleeds, lobar/deep haemorrhages, large vessel occlusions (blockages and consequent infarcts), and cerebral amyloid angiopathy.
Also can see enlarged perivascular spaces, which are regions where the CSF should not be. Also white matter hyperintensities, where the damaged blood vessel leads to the leakage and accumulation of products in brain regions.
Most of this can be seen in brain imaging, and as such has been a useful tool in the diagnosis of dementia.
