Stroke Pathology Flashcards Preview

MD2- Neuroscience Block > Stroke Pathology > Flashcards

Flashcards in Stroke Pathology Deck (26):

define stroke

development of a focal or global neurological deficit due to a vascular events.

warnings signs:
transient clinical events may also occur due to a vascular event.
Silent vascular events may occur.


what is the most common pathological event behind a stroke? second most? third most?

Infarction (75%)

Haemorrhage (25%)

Subarachnoid haemorrhage (5%)
-more related to pathology large vessels in subarachnoid space, rather than trauam


prevalence of stroke related mortality?

third leading cause of death. 10% of all deaths attributable to stroke.


Risk factors for cerebral infarction?

aging, hypertension, cardiac disease (atrial fibrillation), hyperlipidaemia, diabetes mellitus, hypercoagulable states (antiphospholipid antibody syndrome), obesity, smoking


what is a cerebral infarction?

necrosis of cerebral tissue in a particular vascular distribution in response to vessel occlusion or severe hypo-perfusion.
-->usually related to arterial obstruction, but may also be at level of arterioles, veins, and heart.


mechanisms of infarction?

-inadequate supply of blood to tissues due to pump failure.
-inadequate supply of blood due to narrowed vessel lumen (due to atherosclerosis, thrombosis, hypertensive vessel thickening, diabetes, amyloid angiopathy).
-vessel occlusion by embolus (most common)


what is the most common cause of infarction? and thus stroke?

vessel occlusion by embolus


cardiac cause of cerebral infarction?

from thrombi built up in valves or recent infarct site in myocardium


T/F - in pathogenesis of cerebral infarction, the most common cause of large and small vessel occlusion is thrombosis (not emboli).

TRUE. Thrombosis is much more common. Except in the posterior circulation, where emboli are more commonly the cause of occlusion.


T/F thrombosis is the most common cause of venous occlusion leading to cerebral infarction?



how might a probe-patent interatrial septum result in thrombosis potentially causing cerebral infarct?

this is a congenital condition where valve flaps have not fully fused, leaving a potential opening. 1/3 of people have this.
clot thrombotic material could pass from Rt atrium to Lt atrium in situation where right atrial pressure is raised
-->right sided thrombi could develop in the legs
----->more likely in younger patients than older.


what are most common sites of athersclerosis in the cerebral circulation?

circle of willis and associated vessels:
-basilar artery
-junction of vertebral arteries


3 risks of atherosclerosis?



what gross/histological features would be present 36hrs after cerebral infarction?

loss of definition b/w gray and white matter; ventricles have narrowed with midline shift at falx cerebri, sulci obliteration.

nerve cell and glial nuclei would appear shrunken, pyknotic.


what gross/histological features would be present days/weeks after cerebral infarction?

liquefactive necrosis

-lots of neutrophils and cellular debris


what gross/histological features would be present months/years after cerebral infarction?

crater in the brain left behind, with gliosis (scarring) in the margins


how are cerebral micro aneurysms caused?

hyaline arteriosclerosis of tiny vessels deep in the brain substance.
-diabetes (and other conditions) may cause these vessels to thicken, allowing thrombus to develop and causing either burst or stricture.


what causes death following cerebral infarction?

infarction of brain stem (and adversely affected vital areas),
cerebral swelling,
cardiovascular disease,
pulmonary thromboembolism


what are possible effects of raised intracranial pressure?

transtentorial herniation; brainstem hemorrhages


most common cause of intracerebral haemorrhage?

hypertensive small vessel disease


what are the causes of intracerebral haemorrhage?

hypertensive small vessel disease,
congophilic (amyloid) angiopathy,
blood disorder,
vascular malformation,


which regions of the cerebrum are most susceptible to hypertensive haemorrhage ?

-basal ganglia/thalamus,
-lobar white matter,

NB: characterized by presence of small vessel disease! (hyaline arteriosclerosis)


What are the causes of non-traumatic subarachnoid hemorrhage?

-Rupture of sacculur aneuryms (Berry Aneurysm)**most common

-Rupture of mycotic/atherosclerotic aneurysm
-extension of intracerebral hemorrhage (going into ventricular system and out into subdural space)


what are the risk factors for developing a saccular/berry aneurysm

-being female
-polycystic kidney disease
-Type III collagen deficiency
-coarctatation of aorta


where are saccular aneurysms most likely to occur?

-sites of congenital weakness at arterial bifurcations
-more likely anterior than posterior circulation

especially at:
-bifurcation of middle cerebral artery
-junction of ICA and posterior communicating artery
-anterior communicating artery


complications of ruptured aneurysm?

-subarachnoid haemorrhage (+/- intraparanchymal)
-cerebral oedema and raised ICP
-vasospasm and infarction (vessels in circle of willis)
-ventricular obstruction