Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0036690 (sepsis)
 59,461 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A case of multiple spontaneous intracerebral hematomas is presented. A 67-year-old man with 7 years history of hypertension had sudden clumsiness in his right hand and an hour later dysarthria appeared. A CT scan taken 3 hours after the onset revealed two well demarcated high density areas in the left putamen and in the parietal subcortex. A diagnosis of multiple intracerebral hematomas was made. On neurological examination he was midly stuporous (13 points of Glasgow Coma Scale). Dysarthria, right hemiparesis and right extensor plantar response were seen. CT scan of 6 hours later disclosed the same findings as the previous study. He recovered well and neurologically free in a few days. On the following CT scans both hematomas were isodense 2 weeks later, and ring-like enhancement effect was noted. CT scan showed normal appearance 7 weeks later. On MRI using 0.5 T unit t-1 and t-2 weighted spin echo images of these hematomas also showed the similar chronological changes. The history, these CT and MRI studies suggest that two hematomas of this case occurred almost simultaneously in one cerebral hemisphere. No causative factors such as blood dyscrasias, AVM, angioma, septicemia, malignancies or sinus thrombosis was identified. We consider that a hypertensive intracerebral hematoma of the putamen was followed by the parietal intracerebral hematoma within a few hours, although amyloid angiopathy was not completely excluded because no cerebral biopsy of the lesion was performed.
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PMID:[A case report of simultaneous multiple intracerebral hematomas]. 338 86

A 62-year-old man developed clumsiness, vertical ophthalmoplegia, right-side dominant parkinsonism, pyramidal signs, limb-kinetic apraxia and dementia. His brain MRI and SPECT revealed mild fronto-parietal atrophy and hypoperfusion predominately on the right side. At the age of 65, the patient died of sepsis. The duration of his illness was approximately 3 years. Clinical diagnosis was corticobasal degeneration (CBD). On neuropathological examination, there was no neuronal loss and many neurofibrillary tangles (NFTs) in the cerebral cortices. Basal ganglia and substantia nigra showed moderate to severe neuronal loss. And there were many NFTs and argyrophillic threads (threads) in the subthalamic nucleus and nuclei of the brainstem. These findings were almost compatible to those of PSP. However, the following findings were atypical for PSP, 1) mild atrophy and absence of gliosis in the tegmentum of the brain stem, 2) Mild neuronal loss in the subthalamic nucleus and the dentate nucleus without grumose degeneration. Furthermore, characteristic findings were noted on modified Gallyas-Braak stain. Numerous threads and many astrocytic plaques (AP) were shown in cerebral cortices, which were particular to CBD cases. So this case demonstrated neuropathological findings of both PSP and CBD. Therefore, it was difficult to classify this case as either PSP or CBD, and we diagnosed this case as a neuropathological overlapping case of both PSP and CBD.
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PMID:[A case manifested overlapping neuropathologic features of both progressive supranuclear palsy (PSP) and corticobasal degeneration (CBD)]. 956 3