Term
| what are some causes of non-traumatic intracerebral hemorrhage? |
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Definition
| systemic HTN, vascular malformation, cerebral amyloid angiopathy, neoplasms, disseminated intravascular coagulation (disorder secondary to infection, sepsis, shock, etc), thrombotic thrombocytopenic purpura, and drug related |
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Term
| what characterizes hypertensive cerebral disease's relationship w/systemic HTN? |
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Definition
| this may or may not be associated w/a clinically documented hx of HTN - however other autopsy findings such as L ventricular hypertrophy, cardiomegaly, or nephrosclerosis can indicate a hx of systemic HTN. |
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Term
| what are the different manifestations of hypertensive cerebrovascular disease? |
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Definition
| lacunar infarcts, slit hemorrhages, hypertensive encephalopathy, and massive intracerebral hemorrhage |
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Term
| what are lacunar infarcts? |
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Definition
| multiple or single small cavitary ("lake") infarcts due to development of arteriolar sclerosis and subsequent occlusion. this is seen as an effect of HTN in the deep penetrating arteries/arterioles which supply the *basal ganglia and *hemispheric white matter. microscopically they appear as areas of *tissue loss w/scattered *lipid laden macrophages, *gliosis, and widening of the perivascular spaces w/o tissue infarction. clinically they may be silent or cause neurologic impairment. |
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Term
| where are the most common locations for lacunar infarcts to occur? (*know these*) |
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Definition
| in the lenticular nucleus, thalamus, internal capsule, deep white matter, caudate nucleus and pons |
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Term
| what are slit hemorrhages? |
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Definition
| slit hemorrhages occur when small-caliber penetrating vessels rupture and produce a slit-like cavity surrounded by brownish discoloration (hemosiderin). microscopically there is focal tissue destruction, pigment laden macrophages and gliosis. |
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Term
| what is hypertensive encephalopathy? |
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Definition
| this is seen in malignant HTN - which occurs rapidly over a short period of time. brains affected by this are edematous and may have may have herniation, petechiae, fibrinoid necrosis, and accumulation of these infarcts over time. clinically: diffuse cerebral dysfunction -> focal neurologic deficits, h/a, altered mental status, vomiting, convulsions, gait abnormalities and death may result. |
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Term
| what are 2 disorders associated w/hypertensive encephalopathy? |
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Definition
| *vascular multi-infarct dementia: caused by cerebral atherosclerosis, vessel thrombosis, embolization from the carotids/heart, and cerebral atherosclerosis from chronic HTN. *binswanger disease: when the pattern of injury involves large areas of the subcortical white matter w/myelin and axon loss. |
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Term
| where are hypertensive cerebral hemorrhages likely to occur? why? |
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Definition
| in the putamen, thalamus, lobar white matter, cerebellum, and pons. the blood vessels which supply this area (basal ganglia/thalamus) are small caliber and thus blood pressure increases even more as a result. |
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Term
| what characterizes a hypertensive putamen hemorrhage? |
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Definition
| this usually results in contralateral hemiplegia w/eyes directed toward the affected hemisphere. if small enough, this can resolve - leaving slit-like sub-insular cysts parallel to the claustrum w/cystic replacement of the lateral putamen. the globus pallidus and overlying insular cortex are usually spared, but the hemorrhage may also dissect into the lateral ventricle. surgical resection of basal ganglia hematomas have a poor outcome. |
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Term
| what characterizes a hypertensive thalamic hemorrhage? |
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Definition
| hemiplegia and coma may occur if the midbrain is involved. when large, usually the posterior ventral nuclei and internal capsule are involved - though often the precise point of vascular rupture is never IDed. a *charcot-bouchard microaneurysm may occur in smaller vessels and hemorrhage may occur in tortuous vessels (which mimics aneurysms). |
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Term
| what characterizes a hypertensive cerebellar hemorrhage? |
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Definition
| ipsilateral ataxia, vomiting, forced lateral gaze w/possible brainstem compression and death. when in a hypertensive setting, this is often centered in the central white matter in or near the dentate nucleus - which suggests the origin is either the superior cerebellar artery or anterior inferior cerebellar artery. b/c the posterior fossa is small, expansion of these hemorrhages rapidly leads to tonsillar herniation, medullary compression and cardiorespiratory arrest. surgical evacuation of a cerebellar hemorrhage often has a good outcome. |
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Term
| what characterizes a hypertensive pontine hemorrhage? |
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Definition
| coma, quadriparesis, and dysconjugate gaze. the primary type has a high mortality due to interruption of the autonomic systems regulating cardiorespiratory functions. these hemorrhages are located at the midline basis pons and then expand into the tegmentum and dissects the 4th ventricle. |
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Term
| what characterizes a hypertensive lobar white matter hemorrhage? |
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Definition
| similar to if an infarct occurred in that territory and will present differently depending on the location of the obstructed artery. |
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Term
| what role does the volume of hemorrhage play in outcome? |
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Definition
| the bigger the structure, the more hemorrhage it can accommodate: > 3 cm in a cerebral hemisphere, > 2 cm in the cerebellum, and > 1 cm in the brainstem. |
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Term
| other than hemorrhage volume, what are some of the other determinants of outcome? |
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Definition
| the most severe types of hemorrhage can give rise to *cerebral edema, which has a high potential for herniation and death - but can be controlled through medications or craniotomy. asymmetric brain edema and mass effect w/*midline shift can lead to uncal-parahippocampal and cingulated herniations. if there is caudal displacement of the rostral brainstem, this can result in *brainstem compression and *duret's hemorrhage (secondary pontine hemorrhages - vessels feeding the pons are being stretched and can rupture). |
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Term
| what are secondary changes of cerebral infarction? |
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Definition
| thrombosis, embolization, cerebral edema, ischemic-hypoxic injury (loop where hemorrhage leads to ischemia which leads to hemorrhage, etc), spread of 2ndary infarction around primary lesion and at remote sites, various herniations, secondary vascular compromise w/possible hemorrhagic infarction, and duret's hemorrhage (secondary pontine hemorrhage = very poor prognosis) |
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Term
| what happens when dural sinus thrombosis occurs in the superior sagittal sinus? |
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Definition
| this is the most common form of dural sinus thrombosis and is seen in women on OCPs, or pts suffering from malnutrition, dehydration, malignancy, and hypercoagulable states. pts with this will present w/headaches, hemiplegia, seizures, and increased ICP. grossly, if the dura is removed, parasagittal hemorrhagic cortical infarction and distended thrombosed superficial cortical veins are seen draining the sagittal sinus. |
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Term
| what happens when dural sinus thrombosis occurs in the cavernous sinus? |
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Definition
| thrombosis of the cavernous sinus often is related to an infection such as a dental abscess, sinusitis, or facial skin infection. this may involve the 3,4,6 cranial nerves and the opthalmic division of the trigeminal nerve = sensory symptoms of the face. extension into the opthalmic veins can cause proptosis of the eye. |
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Term
| what types of cerebral vascular malformations can result in intracerebral hemorrhage? |
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Definition
| arteriovenous malformations (AVMs), cavernous hemangiomas, venous angiomas, mixed angiomas, and capillary telangiectasia |
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Term
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Definition
| these are the largest and most dangerous vascular malformation - often clinically symptomatic w/seizures, h/a, and focal neurological deficits. most are supratentorial (few involve the spinal cord). grossly AVMs appear as enlarged veins/arteries (hematoma-like). microscopically, they are composed of large blood vessels of highly variable size+thickness - the walls may have extreme fibromuscular thickening to thinned areas of fibrous connective tissue which is vulnerable to rupture. the elastic lamina is often interrupted and frayed and focal calcifications are often found. the brain parenchyma between the vascular channels is often atrophic and gliotic w/hemosiderin deposits as evidence of prior hemorrhage. |
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Term
| what is a cavernous hemangioma? |
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Definition
| these benign tumors are most common in the cerebral subcortical white matter of the frontal lobe (possible personality changes). grossly, they are a few cm in diameter. microscopically, they have many closely approximated small-large vascular channels w/thin fibrous walls w/o a muscularis. brain parenchyma between vessels is atrophic w/hemosiderin deposits. this may be difficult to distinguish from an AVM, however AVMs tend to be found more around the temporal lobe. |
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Term
| what characterizes venous malformations as sources of intracerebral hemorrhage? |
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Definition
| venous malformations are found in the white matter of the cerebellum, cerebrum, meninges, and spinal cord and can cause sudden unexpected death in the young. microscopically, these appear as a group of mildly thickened veins w/walls of uniform thickness separated by normal appearing white matter. *sturge-weber syndrome is when angiomatous masses in the cortical leptomeninges cause mental retardation, seizures, hemiplegia, and skull radio-opacities. |
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Term
| what characterizes ruptured cerebral aneurysms? |
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Definition
| this presents most commonly w/*subarachnoid hemorrhage and sudden death in young/middle-aged adults (exercise, cocaine). complications include vasospasms which can result in ischemia, edema, infarction, and herniation - which can block CSF flow and contribute to mortality via ICP. |
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Term
| what else can present as non-traumatic sub-arachnoid hemorrhage besides ruptured cerebral aneurysms? |
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Definition
| blood dyscrasias, anticoagulant/thrombolytic therapies, and leukemia. |
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Term
| what is a berry aneurysm? |
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Definition
| most are found near major arterial branch points in *anterior circulation - such as the circle of willis and may occur in multiple. there is increased incidence among pts w/adult polycystic kidney disease, ehlers-danlos syndrome, and marfan syndrome. predisposing factors: smoking, HTN, and drugs like cocaine which increase BP. many are asymptomatic, but if large enough - they can cause painful h/a and the pt can seek medical attention before it ruptures. these are not congenital but develop over time due to a defect in the media of the vessel. |
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Term
| what is cerebral amyloid angiopathy (CAA)? |
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Definition
| in this disorder usually affecting pts in their 60s, amyloidogenic peptides deposit in the walls of medium-small caliber meningeal and cortical vessels, leading to hemorrhage superficially located in the *intracranial or *subarachnoid blood vessels of any lobe. the hemorrhage is due to weakened walls and may extend into the subarachnoid space and even produce a subdural hematoma - resembling trauma. blood vessels affected by this stain congo red (but appear green). |
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