Stroke Flashcards
Hypoxia
Oxygen deficiency which causes cell injury by reducing aerobic oxidative respiration
Ischaemia
Reduced tissue blood flow
Infarct (ion)
A localized area of ischemic tissue necrosis (death), usually coagulative necrosis
Liquefactive necrosis
Hypoxic ischaemic necrosis that occurs in the CNS
Digestion of dead tissue into a liquid mass - tissue outline not preserved
What is stroke?
Cerebrovascular disease encompassing:
Ischaemic Stroke - those that cause hypoxic ischaemic infarction of the brain
Intracerebral (intraparenchymal) and subarachnoid haemorrhages - hemorrhagic stroke
List the most common types of ischaemic stroke.
Global cerebral ischaemia (hypoxic ischemic encephalopathy)
Focal cerebral ischaemic (ischemic infarction) caused by thrombosis or embolism
List the common causes of haemorrhagic stroke.
Hypertensive intraparenchymal haemorrhage Ruptured aneurysm (subarachnoid haemorrhage)
Which is most common - an ischaemic or hemorrhagic stroke?
Ischaemic
List the subtypes of the focal ischaemic stroke.
Embolic (from thrombosis elsewhere) - infarct can be reperfused = hemorrhagic infarct
Thrombotic - due to cerebral atherosclerosis = infarct usually pale
What causes global cerebral ischaemia?
Decrease in cerebral perfusion e.g. cardiac arrest, shock, severe hypotension
Same effect as severe respiratory depression (generalized hypoxia)
What is the clinical outcome of a generalized hypoxia ischaemic stroke?
Depends on the severity of the insult
Which parts of the brain are more vulnerable to ischaemic injury?
Hippocampus
Purkinje cells of the cerebellum
Watershed areas
What are the watershed areas of the brain?
Border Zone or Watershed areas lie between arterial perfusion territories (i.e. at the most distal reaches of arterial blood supply)
What causes focal ischaemic strokes?
Obstruction of blood supply to a localized area of the brain
Vascular occlusion may be the result of embolism to the brain (usually from a thrombus = thromboembolism) or thrombosis of cerebral vessels due to atherosclerosis
What are the most common blood vessels occluded in a local ischaemic stroke?
Large vessels - most commonly the Middle Cerebral Artery
Small penetrating vessels (those supplying the basal ganglia, thalamus and internal capsule)
Where do sources of emboli come from?
Heart:
- Mural thrombus complicating MI
- Thrombosis complicating AF
- Thrombosis complicating valvular diseases
Aorta and Carotid Arteries
- Thrombosis developing over atheromatous plaques
Paradoxical emboli
- Thromboemboli from the venous circulation may pass through a cardiac septal defect into the arterial circulation and embolize to the brain
Name the two types of infarcts, based on the haemorrhage within the infarct.
Haemorrhagic (red) infarct
Non-hemorrhagic (bland) infarct
What is a hemorrhagic (red) infarct?
Typically associated with embolic events
Multiple, sometimes confluent petechial haemorrhages
Due to reperfusion of damaged tissue through collateral circulation or following fibrinolysis of thromboembolic material in the occluded vessel and leakage of blood through necrotic vessels
What is a non-haemorrhagic infarct associated with?
Thrombosis
Name the different management techniques for infarcts.
Thrombolytic therapy is used in thrombotic cases
This is contraindicated in Haemorrhagic infarcts
What is the penumbra?
This is the area which lies around the ischaemic area and is potentially reversible if circulation is restored
Which artery supplies the internal capsule?
Upper halves of anterior and posterior limbs are supplied by the MCA.
Describe the gross appearance of an infarct that has occurred 0-6 hours before a patients death.
Undetectable macroscopically (except if haemorrhagic)
What happens to the gross appearance by 48 hours?
Blurring of gray/white matter interface
Infarct is pale, soft, swollen, ill-defined
Extensive vasogenic edema due to disruption of BBB and passage of fluid into extracellular space
What happens to the gross appearance from 2-10 days.
Area of brain infarct becomes gelatinous and friable
Infarct has well defined border
What happens to the gross appearance from 10 days to 3 weeks?
Tissue breaks down and liquefies leaving cystic spaces (fluid-filled cavities) lined by dark grey tissue (gliosis)
Describe why a brain edema follows an infarct.
Tissue necrosis triggers inflammation
Inflammation & loss of structural integrity of blood vessels = disruption of BBB
Increase in vascular permeability and extravasation of fluid = Vasogenic Edema
Edema may be severe enough to increase ICP and brain herniation
Describe the histological appearance in the early stage (12-24 hours).
Cytoplasmic eosinophilia and nuclear pyknosis = red, dead, neurons
Neutrophilic infiltrates are evident early on, subside after about 48 hours
Describe the microscopic appearance of the subacute stage (24 hours to 2 weeks)
Tissue necrosis, macrophage infiltrates, vascular proliferation and starting gliosis
Describe the microscopic appearance of the repair stage (2 weeks onwards)
Removal of necrotic tissue by macrophages, leaving a cystic space surrounded by gliosis
What additional features does the haemorrhagic infarct show microscopically?
Blood extravasation and resorption
What is gliosis the indicator for?
CNS injury
What characterizes gliosis?
Hypertrophy and hyperplasia of mainly astrocytes - main glial cells = astrogliosis
Form a dense web that surrounds lesions in the CNS
Which blood vessels does hypertension affect?
Deep penetrating arteries and arterioles that supply the basal ganglia and hemispheric white matter and brainstem
What does hypertension lead to in cerebral arterioles?
Hyaline atherosclerosis - thickening of their walls and narrowing of their lumens = predisposition to vascular occlusion and rupture
Also potentiates cerebral atherosclerosis = predisposition to thrombosis
What causes hyaline atherosclerosis?
Plasma protein leakage across injured endothelial cells and extracellular matrix deposition by vascular smooth muscle cells
= response to HTN
What does rupture of larger calibre penetrating vessels lead to?
Large intracerebral (intraparenchymal) haemorrhages
What does rupture of small-caliber penetrating vessels leads to?
Small, slit haemorrhages
What are lacunar infarcts?
Small infarcts due to vascular occlusion
What are minute aneurysms?
Charcot-Bouchard micro-aneurysms = may be the site of rupture and bleeding in the basal ganglia - due to HTN
What is the most common cause of non-traumatic deep brain parenchymal haemorrhages?
HTN
What do hypertensive intraparenchymal haemorrhages commonly involve?
Basal ganglia (50-60% of cases)
Thalamus
Pons
Cerebellum
What are Duret Haemorrhages and what causes them?
Linear haemorrhages seen in the midline of midbrain and pons in cases of uncal herniation
Tearing of the penetrating veins and arteries supplying the upper brainstem during progression of transtentorial herniation
What is the most common cause of a SAH?
Non-traumatic (spontaneous) rupture of a saccular berry aneurysm in a cerebral artery
What is the most common symptom of a SAH?
Severe thunderclap headache of sudden onset
Usually signs of meningeal irritation too - photophobia, positive Kernigs, neck stiffness, headache
Also signs and symptoms of raised ICP
What may also cause a SAH?
Extension of traumatic haematoma Rupture of HTN intracerebral haemorrhage into the ventricular system Vascular malformations Hematologic disturbances Brain tumours
What causes saccular “berry” aneurysms?
Congenital defect in arterial wall
Not present at birth, but develop at young age
Occur at arterial branching points
HTN also a risk factor for developing berry aneurysms and increases risk of rupture
