Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0018991 (hemiplegia)
 3,997 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A case associated with multiple cerebral vascular anomalies, which consisted of fenestration of the middle cerebral artery, arteriovenous malformation and aneurysm of the anterior communicating artery, was reported. A 48 year-old male has been suffering from the left paralysis and mental disorder after the initial attack of subarachnoid hemorrhage, and the second attack resulted in the deterioration of the symptoms. He was admitted to our clinic on October 28, 1974. On neurological examination, mental disorders, such as disorientation, emotional incontinence, amnesia and acalculia, hemiplegia on the left and meningeal irritation signs were observed in admission period. Physical examination was negative. Cerebral angiographic findings were as follows: 1) Moderate vasospasm of the right internal carotid artery at the terminal segment, mild bowing of the anterior cerebral artery and stretching of the frontparietal opercular branches of the middle cerebral artery were observed. 2) Right frontpolar arteriovenous malformation fed by the frontobasal artery and the frontopolar artery, and drained via the aberrant cortical vein into the superior sagittal sinus. 3) Aneurysm of the anterior communicating artery was opacified by left carotid angiography. 4) An abnormal vessel derived from the terminal segment of the right internal carotid artery and terminated at the portion of the sphenoidal segment of the middle cerebral artery. Complete loop was formed between genuine middle cerebral artery and this abnormal artery. He was operated with dissecting microscope on November 11, 1974. The arteriovenous malformation at right frontopolar region was totally removed and aneurysm of the anterior communicating artery was clipped. According to the operative findings, the arachnoid membrane over the right frontopolar region was turbid and adhered to the adjacent tissues. On the contrary, no abnormal findings suggestive of previous subarachnoid hemorrhage were observed around the region of the anterior communicating artery aneurysm. These findings showed that subarachnoidal bleeding was caused by rupture of the arteriovenous malformation of right frontopolar region, but not by the aneurysm on the anterior communicating artery. The postoperative course was uneventful and during the hospitalization the patient starts on rehabilitation therapy. The authors discussed the genesis of fenestration of the middle cerebral artery and relation among these combined vascular anomalies. We inferred that fenestration of the middle cerebral artery arose from the in complete fusion of procursor vascular network in embryonic stage. Additionally, we emphasized that it was necessary to make a distinction between these two terms "fenestration" and "duplication".
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PMID:[A case of multiple anomalies of cerebral vessels--fenestration of the middle cerebral artery aneurysm of the anterior communicating artery and arteriovenous malformation on the frontopolar region (author's transl)]. 55 79

A 74-year-old right-handed man with multiple cerebral infarction who presented with dementia simulating dementia of Alzheimer type (DAT) is reported. He had been well until April 20, 1987 when he developed transient right hand palsy lasting overnight. Eleven days later, he became confused, disorientated, and amnestic. He was admitted to this hospital on June 8. Physical examination revealed hypertension (170/90mmHg). On neurological examination, his consciousness was clear but he was demented. He showed disorientation, amnesia, and urinary incontinence. His most prominent symptom was disturbance of speech, including fluent aphasia and alexia with agraphia. Additionally, he showed ideomotor apraxia, construction apraxia, right-left agnosia, finger agnosia, and acalculia. On July 9, he had a transient attack of right hemiplegia with confusion. The brain CT scan performed on admission was unremarkable except for cavum septi pellucidum and a small low density area in the right basal ganglia. However, single photon emission computed tomography (SPECT) by 123I-labeled N-isopropyl-p-iodoamphetamine disclosed hypoperfusion of the cerebral blood flow in the border zones of the temporoparietal and frontal lobes on the left. A follow-up brain CT scan taken one month later demonstrated low density in the new areas corresponding to hypoperfusion shown by SPECT. Although the clinical features of the present case resembled those of DAT, dementia in this case was regarded as the result of multiple cerebral infarction since it occurred acutely with mild motor deficits, and brain CT scans and SPECT showed lesions indicating focal cerebral ischemia.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Multi-infarct dementia clinically simulating dementia of Alzheimer type. A comparison with angular gyrus syndrome]. 278 20

We report the case of a patient with myelin oligodendrocyte glycoprotein (MOG)- antibody-associated disease presenting with tumefactive demyelinating lesion. Neurological examination showed aphasia, acalculia, agraphia, alexia, left-right disorientation, and right hemiplegia. Brain magnetic resonance imaging revealed a large monofocal lesion with mild brain edema and ring enhancement. Stereotactic brain biopsy was performed, and neuropathological findings showed inflammatory demyelination and preserved axons without tumor cells. A cell-based assay detected anti-MOG antibody in the cerebrospinal fluid. Neurological symptoms gradually improved after steroid pulse therapy. MOG-antibody-associated diseases should be considered in the differential diagnosis of tumefactive demyelinating lesion.
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PMID:A case of myelin oligodendrocyte glycoprotein-antibody-associated disease presenting with tumefactive demyelinating lesion. 3247 83