Circulatory Disorders and Trauma in the CNS Flashcards
Cerebrovascular Accident (CVA) or Stroke
The sudden onset of focal neurologic deficit without regard for etiology.
Most cases are due to embolism of spontaneous, massive hemorrhage.
Third leading cause of death in the US; majority of victims between ages 40-80; men affected more than women.
Three patterns of injury (subtypes):
Infarct (73&); mainly due to hypoxia and ischemia.
Intraparenchymal hemorrhage (19%); most commonly secondary to hypertension.
Subarachnoid hemorrhage (8%); most common cause is rupture of saccular aneurysms.
Symptoms of a CVA: Sudden onset and reaches max intensity within a few minutes or hours; paralysis, sensory loss, speech defects related to site of damage.
Generalized symptoms: vomiting, headache, coma, seizure.
After time, most tissue is gone and there is a cavity with collapse of the tissue; atrophic=forever lose function of that part of the brain (OLD INFARCT); cystic.
Tissue loss and atrophy=widening of the left lateral ventricle.
Infarcts
Represent cell/tissue death and necrosis.
They occur following hypoxia os ischemia, secondary to thromboembolism (MOST COMMON CAUSE OF CEREBRAL INFARCTS), atherosclerosis and/or hypertension.
May be global or regional.
Cause major morbidity and mortality.
Some CVA are transient and reversible and do not result in an infarct.
Non contiguous endothelial lining with atherosclerosis (blood vessel wall injury) leads to a thrombosis.
ACUTE INFARCT: soft, edematous tissue, congested vessels; widened gyri; acutely, it is dead tissue, over time it can be come cystic and lose totally function of that part of tissue.
Secondary to thromboembolism, atherosclerosis, hypotension is death of tissue=death of blood vessels, which then become leaky.
Atherosclerosis and low blood pressure cause local infarct.
Vessels furthest from the blockage feels the biggest effects (border zone).
Children can lose a lot of blood, but because they don’t yet have vascular disease, there is no border zone infarcts (losing blood causes a low blood pressure, and if you have vascular disease can cause infarct to an area because that area is already getting low flow due to disease).
Macrophages come and eat the necrotic tissue.
Major risk factors for atheroscleoris and thus CVA are: diet and hyperlipidemia, hypertension, cigarette smoking, and diabetes.
Transient ischemic attacks (TIA): shown by patients with atherosclerosis of carotid or cerebral vessels; often display transient hemiparesis or loss of speech days or weeks prior to a stroke.
Massive hypertensive hemorrhage: 75% will die usually within first two weeks following the event.
Of 25% who recover, most will have neurologic deficit.
Prognosis in thrombosis or embolism varies with the extent of the damage, age of patient, and degree of debilitation.
Half will have subsequent strokes within a few weeks to months are primary event.
Small percent recover without deficit or recurrence.
Hypoxia
A decreased amount of oxygen in perfused tissue regardless of blood pressure.
Can lead to capillary dilation, vascular stagnation and consequent ischemia.
Ischemia
A decrease in blood supply.
May be local involving narrowed vessels in one area of the brain or generalized due to decreased systemic blood pressure.
Arteriosclerosis
hardening of arteries; can happen in different ways/
Atherosclerosis
hyperlipidemia, affects large and medium arteries mostly; causes large infarcts.
Arteriolosclerosis
Underlying pathology for hypertension; it causes hypertension in small arteries and arterioles that control BP; cause mostly hemorrhages.
Cerebral emboli
Embolus refers to occlusion of a vessel by any material (fragments of clot, vegetations from heart valves, or other fragment material) transported through the circulation from a distant site.
Commonly the result of carotid or cerebral vessel thrombi or rarely atherosclerotic plaque material that breaks off from the vessel wall and lodges distally.
Many emoji arrive in cerebral vessels from systemic circulation and most probably arise from thrombi in carotid arteries.
Embolic occlusions are usually sudden events and are the most common cause of cerebral infarction.
Thrombosis
Occlusion of a vessel in situ. Usually secondary to formation of a blood clot in the intimal of an intra- or extra cranial artery which has already been damaged by atherosclerosis.
Cerebral thrombosis often develops gradually and may be preceded by one or more transient episodes of neurological deficit.
Hemorrhages
Usually associated with hypertension and the consequent damage to small intraparenchymal arterioles.
Most common sites are the basal nuclei, cerebellum and pons.
Blood-brain barrier
In the brain, the endothelial cells have tight junctions between them to restrict free movement of water and small molecules from vascular compartments to the tissue and back.
Endothelial cells possess transport mechanisms that only allow selected types of molecules to cross into the brain and back into vascular system.
This protects the brain from imbibing excess fluids that would result in increased intracranial pressure and brain herniation.
Although, this restricts the passage into the brain of therapeutic agents such as antibiotics and chemo.
Intraparenchymal hemorrhage
19% of CVAs.
Non-traumatic brain hemorrhage, may be massive or multiple and small.
Massive ones are seen in hypertensive people (most common cause); thickening of wall of arterioles (hylanized).
Multiple, small hemorrhages are seen in a variety of conditions: fat embolism, air embolism, thrombocytopenia, arisen poisoning, malaria, leukemia.
Seen in Alzheimer’s patients who have brittle cerebral blood vessel secondary to amyloid deposition.
Micro aneurysms can rupture and produce hypertensive hemorrhage.
A lot of blood introduced into the brain due to disruption of arteriole or small artery.
The gross appearance is that of an intraparenchymal mass of blood; it may dissect into the subarachnoid space or it may rupture into the ventricles (death often results rapidly in this case).
Hypertensive hemorrhage
Most common cause of non traumatic intraparenchymal hemorrhage.
Hemorrhage is often massive, occurring under arterial pressure, and constitutes a rapidly expanding intracranial mass with a direct and immediate threat to life.
Almost always associated with some degree of systolic and/or diastolic pressure elevation.
The hylalinizing process results in a loss of smooth muscle, thinning of the vessel wall, and eventual rupture under pressure.
Subarachnoid hemorrhage
9% of CVA
The most common cause of a SAH is trauma; in CVA however, a nontraumatic subarachnoid hemorrhage is most commonly due to rupture of a saccular aneurysm.
Saccular or Berry aneurysm
A disease of adults
Range in size from 1mm nodules to large masses several cm in diameter; aneurysms larger than 1 cm are more likely to rupture.
Associated with hypertension, but there is no cause-effect relationship known between these.
Also associated with smoking.
More common in some; cause is unknown, but believed that there is a congenital defect in the vessel elastic and/or media.
90% of all aneurysms are found in the anterior portion of the arterial circle.
The most common location is that the juncture of the anterior communicating artery with the ACA.
Clinical presentation:
1. subarachnoid hemorrhage with attendant meningeal signs and vascular spasm (most common).
2. intracranial hemorrhage following rupture into brain parenchyma often associated with rapid death.
3. Expanding intracranial masses which compress the hypothalamus and the optic chiasm, mimicking pituitary tumors.
Leakage of blood from aneurysms into the subarachnoid space sometimes causes severe spasm of other subarachnoid vessels and consequent infarcts due to the release of vasoconstriction chemicals from the necrotic blood.
Prognosis: 30% die from initial hemorrhage, 25% following recurrent bleeding within sex weeks, 25-30% survive with little or no deficits.
ANEURYSMS AND VASCULAR MALFORMATIONS CAN BOTH CAUSE CVA.
