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21 Cards in this Set
- Front
- Back
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Rosenthal fibers found in
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low grade, pilocytic astrocytoma
Alexander's disease (leukodystrophy) Old scars |
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Uncal herniation
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Midbrain level
1. CN III - pupil dilates (ipsilateral to herniation, and eventually to ipsilateral oculomotor palsy) 2. PCA/SCA - visual cortex (the ipsilateral posterior cerebral artery may be compressed) 3. Cerebral peduncles - ipsi- or contralateral hemiparesis (Ipsilateral peduncular compression leads to hemiparesis or hemiplegia on the side opposite the lesion, while contralateral peduncular compression leads to hemiparesis or hemiplegia, ipsilateral to the original lesion) 4. AP compression - aqueductal compression hydrocephalus |
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Duret hemorrhage
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Compresses midline midbrain and pons caudally
Blood vessel are arterial, and hemorrhages result from stretching of perforating vessels of the stem. |
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Causes of Infarction
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Atherosclerosis
Arteriolarsclerosis (HTN, diabetes) - causes lacunar infarcts Embolism |
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Causes of cerebral hemorrhage
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Hypertension
Aneurysm Arteriovenous formation |
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transient ischemic attack
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pidly developing clinical signs of focal (at times
global) disturbance of cerebral function, lasting less than 24 hours |
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Sequence of microscopic changes in brain infarcts
> 1 hour |
Microvacuoles within neurons (swollen mitochondria)
Perineuronal vacuolation (swollen astrocytic processes) |
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Sequence of microscopic changes in brain infarcts
4-12 hours |
Neuronal cytoplasmic eosinophilia
Disappearance of Nissl bodies Pyknotic nuclei Leakage of blood-brain barrier |
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Sequence of microscopic changes in brain infarcts
15-24 hours |
Neutrophil infiltration begins
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Sequence of microscopic changes in brain infarcts
2-3 days |
Macrophages (foam cell) appear
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Sequence of microscopic changes in brain infarcts
5 days |
Neutrophilic infiltration stops
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Sequence of microscopic changes in brain infarcts
~1 week |
Proliferation of astrocytes around core infarct
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Non-neoplastic ring enhancing lesion
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Toxoplasmosis
Abscesses |
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Neoplastic Ring enhancing lesions
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GBM
Metastatic Carcinoma Lymphoma |
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New form CJD
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Amyloid plaque surrounded by vacuoles, "florid plaques"
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Prion disease
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Intracytoplasmic plaque, astrocytosis, neuronal loss
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CJD
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Late adult onset of dementia, focal neurological deficits, evidence of cerebellar, pyramidal, extrapyramidal and gray matter involvement.
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Progressive multifocal leukoencephalopathy
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Opportunistic infection of AIDS. Infection of JC virus.
3 cardinal features of soft white matter: -abnormal oligodendrocytes with glassy, jelly bean like purple intranuclear inclusions found predominately at the periphery of lesion - Bizarre astrocytes with large hyperchromatic, irregular nuclei -Demyelination |
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HIV encephalitis
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Pathognomonic: Multinucleated cells with numerous small dark nuclei and granular eosinophilic cytoplasm
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Cowdry Type A bodies
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Eosinophilic oval in nucleus with clear border
Seen in: Herpes encephalitis (intranuclear) CMV (intranuclear and intracytoplasmic) Subacute sclerosing panencephalitis (intranuclear and intracytoplasmic) |
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Difference between Wernicke's disease and Leigh's disease
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Both are due to energy deficiency so infarct occurs in areas of brain. Both hit pontine tegmentum and have sponginess of gray and white matter.
Wernicke's disease: deficiency in B1 Affects mammillary body Leigh's disease (subacute necrotizing encephalopathy): affects the substantia nigra |
