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165 Cards in this Set

  • Front
  • Back
how high do strokes rank as far as causes of death in the US?
third - they cause 160,000 deaths per year
what is the stroke belt?
a group of 12 contiguous states that have stroke death rates more than 10% higher than the rest of the country - Kentucky is a part of it
what are the non-modifiable risk factors for stroke (4)?
1) age; 2) sex (men); 3) race (black); 4) family history
what are the major modifiable risk factors for stroke (6)?
1) hypertension; 2) cardiac diseases; 3) previous stroke and TIA; 4) carotid bruit/stenosis; 5) tobacco; 6) diabetes
what are other weaker factors (list)?
hyperlipidemia, alcohol, oral contraceptives, sickle cell, polycythemia, hyperhomocysteinemia, drug abuse
what is a TIA?
a brief episode in which neurological deficits occur and then disappear completely
how long do most last, and by definition how long can one last?
only a few minutes to an hour, but by strict defniition it can persist for up to 24 hours
what is TIA an important predictor of stroke in?
20% of patients with a new stroke or in patients who have had one or more prior TIA
what are the four classes of strokes?
1) cerebral infarction; 2) cerebral infarction secondary to central embolization; 3) intracerebral hemorrhage; 4) subarachnoid hemorrhage
why might it be misleading to be too specific about the incidence of the different forms of stroke?
the frequency depends in part on age, gender, geographic location, and whether the data were collected from clinical, radiographic, or autopsy studies
what is cerebral infarction defined as?
ischemic necrosis of brain tissue
how common is it compared to other cerebrovascular disease?
most common
what are the majority due to?
what is the mortality in the first 30 days?
where do atherosclerotic changes first appear in, on the way to the brain (3)?
at the base of the carotid (at origin, bifurcation, and distal segment), vertebral (at origin and distal segment), and basilar arteries
as far as main brain arteries, what is the order of these atherosclerotic changes?
middle, then posterior, then anterior cerebral arteries, in that order
in what patients does arteriolosclerosis (small vessel disease) most commonly cause cerebral infarction (2)?
1) diabetics; 2) those with hypertensive cardiovascular disease
what inflammatory diseases of arteries can result in cerebral infarction (4)?
1) meningovascular syphilis; 2) arteritis secondary to infection; 3) collagen vascular disease; 4) granulomatous arteritis (by obstruction or stenosis)
what else can cause cerebral infarction (list)?
compression of cerebral vessels by mass such as tumor, vascular spasm, systemic hypotension, prolonged hypoxia or hypoglycemia, fibromuscular hypoplasia of carotid arteries, polycythemia, many others
what are the most important factors in determining the character of infarction (4)?
1) site of occlusion; 2) size of occluded vessel; 3) duration of occlusion; 4) collateral circulation
what does collateral circulation occur through (6)?
1) carotid and vertebral arteries; 2) external carotid arteries; 3) ophthalmic arteries; 4) circle of Willis; 5) leptomeningeal anastomosis; 6) penetrating arteries
what type of regulation is abolished once infarction occurs, and what is the result?
once infarction occurs, atuoregulation of bloodflow is abolished, and there is vasoparalysis
what are the vessels like, and what does blood flow vary with?
vessels are maximally dilated - blood flow varies with perfusion pressure
how does the infarcted area respond to CO2 or vasoactive drugs?
it does not
how long does it take for these metabolic changes to occur after infarction?
they occur almost immediately
what happens to acid/base balance in tissues, and what shift in metabolism occurs?
tissue acidosis occurs early in ischemia, and there is a shift to glycolytic metabolism
what accumulates due to this metabolism?
what happens to cellular membrane potentials, and what does this lead to?
cellular depolarization that leads to increases in extracelulular potassium ions and subsequent failure of the Na/K ATPase pump
what move into the cell (3) and what is the result?
sodium, chloride, and water move into cells, resulting in cytotoxic edema
what neurotransmitter was mentioned to be released and cause a problem, and what is this problem?
several neurotransmitters are released into the extracellular space, but especially glutamate, which leads to excitotoxicity
what happens to calcium balance ni the ischemic area, and why?
loss of the transmembrane gradient leads to increased intracellular calcium influx
what does this lead to?
activation of second messenger systems
what are produced that can damage lipids, proteins, and nucleic acids?
free radicals
what immune cells are activated, and what do they cause?
neutrophils are activated, and consequently produce cytokines
what gene expression was said to be altered (3)?
1) heat shock proteins; 2) c-fos; 3) c-jun
what is the ischemia penumbra?
the ischemic zone surrounding the irreversibly injured core, in which blood flow Is somewhat greater than the core and has the potential of not being irreversibly damaged
what are the gross features of cerebral infarction one to two days after the infarction?
loss of definition between grey and white matter, softening, congestion, edema, and often slight darkened discoloration
what are the gross features of cerebral infarction two to ten days after the infarction?
softening, clear-cut demarcation of infarcted tissue, increasing edema
what happens from ten days to several months after?
liquefaction and cyst formation
how long does it take a 1cm cyst to form?
one month
what structures in the head are most susceptible to hypoxia?
what are the next most susceptible (4 things, in order from least to most susceptible, after neurons)?
oligodendroglia, astrocytes, microglia, blood vessels
what does cerebral infarction look like microscopically after six to twelve hours (2 features)?
1) ischemic neuronal damage; 2) decrease in oligodendroglial cells
what change occurs between one and three days?
PMNs are present around vessels
what change occurs after three to five days?
macrophages start to appear
what begins between three and seven days (2)?
1) capillary proliferation; 2) activation of astrocytes
what happens between seven days to months after infarction?
macrophages clear out degenerated tissue, leaving a cyst
what is the cyst surrounded by?
numerous astrocytes and astrocytic processes
what is the onset of cerebral thrombosis like?
stuttering onset
when does cerebral thrombosis often occur (2)?
1) upon arising; 2) at night
what are risk factors for cerebral thrombosis (2)?
1) older patients; 2) atherosclerosis
how common are seizures and headaches with cerebral thrombosis?
what fraction of patients with cerebral thrombosis become comatose?
one third
do TIAs commonly occur with cerebral thrombosis?
what are the most common sources of cerebral emboli (3)?
1) heart; 2) atherosclerotic plaque of aorta; 3) atherosclerotic plaque of carotid arteries
what are the major cardiac sources (4)?
1) arrhythmia (atrial fibrillation or other); 2) MI with mural thrombus; 3) endocarditis; 4) complication of surgery
what classifications of endocarditis were said to cause cerebral embolus (3)?
1) rheumatic; 2) bacterial (acute and subacute); 3) non-bacterial (marantic) endocarditis
what are other sources of emboli (4)?
1) fat; 2) tumor; 3) surgical complication; 4) carotid artery trauma
what problem can develop if there is reperfusion of the previous anemic infarction due to lysis of embolic material?
hemorrhagic infarction - a "no flow, reflow" phenomenon
where do cerebral emboli most commonly occur (distribution of what artery)?
most common in distribution of middle cerebral artery (although they can occur in almost any vessel and can be multiple)
where are the lesions of cerebral emboli, and especially hemorrhagic infarctions usually located (2)?
1) cortex; 2) cortico-medullary junction
what else might be seen in other parts of the body when there is cerebral embolus?
emboli to other organs
do TIAs commonly occur with cerebral embolus?
what fraction become comatose with cerebral embolus?
one quarter
is more than one brain region often involved?
how common are seizures and headache with cerebral embolus?
what good outcome can occur in some?
rapid improvement
what additional complications may emboli from vegetations in bacterial endocarditis cause (4)?
1) septic encephalitis; 2) brain abscesses; 3) microabscess; 4) mycotic aneurysms
what are mycotic aneurysms, and where are they typically located?
outpouching of arteries, usually distal to the bifurcation of the major arteries of the circle of Willis
what may mycotic aneurysms be due to?
embolic occlusion of the vasa vasorum of vessels
what do these aneurysms give rise to when they rupture?
they give rise to subarachnoid and intracerebral hemorrhage
what was said to be an uncommon source of emboli to the brain?
fat emboli
what do fatty emboli follow (2 events)?
1) trauma to long bones; 2) trauma to fatty tissue
what does fat pass through before it reaches some small cerebral arteries and capillaries?
pulmonary capillaries
what do fat emboli give rise to, and where are they usually found?
gives rise to petechial hemorrhages and are usually found in central white matter of cerebral hemispheres
what is the most common cause of intracerebral hemorrhage?
where does hypertension particularly cause acceleration of atherosclerosis?
in blood vessels of central grey matter and brainstem
what are microaneurysms on vessel walls called, that are caused by hypertension?
Charcot-Bouchard aneurysms
where are these small aneurysms found?
on the small penetrating intraparenchymal cerebral arteries
are these in grey or white matter, and in what locations in the brain do they exist (3)?
in the central grey matter of the: 1) cerebral hemisphers; 2) brainstem; 3) cerebellum
what may these Charcot-Bouchard aneurysms be the underlying cause of?
large hypertensive intracerebral hemorrhages
what other damage does hypertension cause in vessel walls?
fibrinoid necrosis
what is the most common place for a hypertensive intracerebral hemorrhage, and what % of them occur there?
putamen - 40%
what other specific locations were mentioned to have hypertensive intracerebral hemorrhages (incomplete list - 3)?
1) thalamus; 2) pons; 3) cerebellum
what do these large hypertensive hemorrhages do to the parenchyma, and what do they frequently rupture into (2)?
they dissect the parenchyma, and frequently rupturie into the ventricles and subarachnoid space
what is the tissue around the hematomas covered by?
petechial hemorrhages
what % of patients with hypertensive intracerebral hemorrhages die within the first 30 days?
what location of hemorrhage often leads to rapid death within a few hours?
pontine hemorrhage
what happens to the hemorrhages that occur in the basal ganglia?
they rupture into the lateral ventricle
how long do these take to lead to death?
several days
what happens to the clot if the patient survivese?
the clot shrinks, becomes "chocolate covered", and the edema subsides
what forms in the area destroyed by hemorrhage?
a cavity begins to form
what happens to its walls, and how long does this take?
its walls become rust-colored, irregular, and firm within six weeks
what substance is found in large amounts in this type of hemorrhage?
what are three things said to be associated with lacunar infarction?
1) fibrinoid necrosis; 2) hyalinization of the media; 3) narrowing of the lumen of small vessels in hypertension
what are lacunar infarctions like in size and composition?
small, usually less than 1cm areas of cystic encephalomalacia
is there usually a prodrome in intracerebral hemorrhage?
often no prodrome
what is a major risk factor for intracerebral hemorrhage?
during what hours do intracerebral hemorrhages often occur?
during waking hours
what is the presenting symptom in most patients with intracerebral hemorrhage?
severe headache
what else do patients sometimes experience (2)?
1) stiff neck; 2) seizures
what % go into coma?
what is the mortality rate?
what is the most common cause of blood in the SAS?
head trauma
is this a subarachnoid hemorrhage, and why?
no, because "subarrachnoid hemorrhage" connotates a nontraumatic cause of bleeding into the SAS
what are common causes of SAH (3)?
1) AV malformation; 2) extension of bleeding from primary intracerebral hemorrhage; 3) ruptured aneurysms
what are other causes mentioned (2)?
1) blood dyscrasias (imbalance of blood constituents); 2) cerebral neoplasms
what specific type of aneurysm is the most common cause of nontraumatic hemorrhage into the SAS?
saccular aneurysm (berry aneurysm)
what % of autopsies are these aneurysms present in?
1 to 3%
in what portion of brain vessels do 95% of these aneurysms occur in?
anterior cerebral circulation (5% in posterior circulation)
what arteries are the most common sites (4)?
1) internal carotid; 2) middle cerebral; 3) anterior cerebral; 4) anterior communicating
what are these small areas of ballooning of arteriees thought to be due to?
a congenital defect of the media at the bifurcation of arteries, and superimposed degeneration of the internal elastic membrane
what else is thought to play a role in their development?
besides rupturing into the SAS or brain parenchyma, how can these aneurysms cause symptoms?
by enlarging and acting as masses, compressing cranial nerves or other structures
where else can hemorrhage from these formations spread, in some instances?
to the subdural space
what other problem can hemorrhage into the SAS cause in arteries, and what is the result?
spasms, which lead to cerebral infarction
what is occasionally found in association with bleeding into the SAS?
hydrocephalus, caused by interference with flow of CSF
in what % of patients are saccular aneurysms multiple?
15 to 20%
what symptoms always occur in patients with subarachnoid hemorrhage?
1) severe headache; 2) stiff neck
when do they occur (time of day or other situation - 2)?
1) during day; 2) during exertion
what fraction have coma?
one third
what fraction have seizures?
one third
how does the age group affected compare to that of other hemorrhages?
are there usually many focal signs of subarachnoid hemorrhage?
no, few
in what locations do large atherosclerotic or fusiform aneurysms occasionally occur (3)?
basilar, vertebral, or internal carotid arteries
in what cases do these rupture?
they generally do not rupture
what problems may they cause?
compression of adjacent and underlying neural structures
besides saccular aneurysms, what else causes SAH?
vascular malformations
where are vascular malformations (congenitally malformed veins, arteries or capillaries) most commonly encountered (2)?
1) cerebral leptomeninges; 2) brain parenchyma
what shape are they often in, and what orientation?
often wedge-shaped and directed toward the ventricle
what problems do vascular malformations cause (2)?
1) repeated SAH; 2) focal seizures
what finding were vascular malformations said to often be the source of in the brain?
intracranial bruits
what are the types of vascular malformations (4)?
1) capillary telangiectasis; 2) cavernous malformations; 3) arteriovenous malformation; 4) venous malformation
what is capillary telangiectasis?
small dilated capillaries separated by normal neurla tissue
where are they most commonly found (2)?
1) pons; 2) cerebral white matter
what are cavernous malformations, and what was said not to be present?
dilated sinusoidal vessels without intervening neural tissue
where are arteriovenous malformations most commonly located in the distribution of?
the middle cerebral ratery
where are venous malformations most commonly found?
in the SAS over the spinal cord
what is thrombosis of the cerebral venous sinuses or veins seen in association with (list)?
infections, heart disease, post-operative trauma, carcinoma, fever, blood dyscrasias, dehydration, cachexia, hypotension, and also in the puerperium (the four week period following childbirth)
where is thrombosis most commonly found (2)?
1) superior sagittal sinus; 2) superior cerebral veins
where can thrombosis of the sinus spread to, that has disastrous neurologic consequences?
into the bridging superficial venous system
what does thrombosis of the venous system cause (3)?
1) hemorrhage into leptomeninges; 2) hemorrhagic infarction; 3) massive hemorrhage in underlying cortex/white matter