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)

We report a 47-year-old woman with progressive multifocal leukoencephalopathy (PML). She was a carrier of HTLV-I virus, and developed subacute right hemiparesis and marked motor aphasia. She had a malignant lymphoma in the left neck and basal cell carcinoma in the right inguinal region. Three months after the onset, she became unable to walk because of the right leg weakness or to speak because of motor aphasia. Magnetic resonance imaging (MRI) revealed multifocal T2-high lesions in the white matter of the left frontal lobe, and a brain biopsy revealed demyelinating pathology. A biopsy of the left parotid gland revealed a diffuse pleomorphic type large B cell lymphoma. Although anti-HTLV-I antibody was positive in the serum and cerebrospinal fluid (CSF), no adult T-cell leukemia (ATL) cells were found in the blood or CSF. The patient was then admitted to our hospital. Neurological examinations revealed severe motor aphasia, mild sensory aphasia/cognitive impairment, right hemiplegia, mild right hemihypesthesia, limb-kinetic apraxia in the left hand, idiomotor apraxia, agraphia, perseveration, marked spasticity and brisk tendon reflex in four extremities, and positive bilateral pathological reflexes. MRI showed multifocal T2-high lesions mainly in the cerebral white matter, predominantly in the left hemisphere, and partly in the cerebral cortex. No gadolinium enhancement was found. In addition, 99mTcECD-SPECT showed a broad decrease in cerebral blood flow (CBF) in the cortex. Anti-HTLV-I antibody was positive but anti-HIV antibody was negative in serum. ATL cells were found in 1-3% of the peripheral white blood cells after admission. CSF examination revealed that the cell count (1/microl), protein level (24 mg/dl), and IgG index (0.4) were all normal. However, the myelin basic protein level (321 pg/ml; normal < 102) was increased, JC virus DNA was detected by PCR, and anti-HTLV-I antibody (x 8) was detected in CSF. The regulatory region of the JC virus DNA in the CSF was partly deleted; immunostaining with anti-JC virus protein antibodies revealed the existence of JC virus in biopsied brain specimens, and these findings were consistent with PML. Her symptoms such as motor aphasia, cognitive dysfunction and left hemiparesis were subacutely progressive, and she developed akinetic mutism two weeks after admission. Since the efficacy of cytosine arabinoside for PML has been reported, she was administered 80 mg/day of the drug for five days. After treatment, her communication function was mildly improved but the efficacy was transient. Since it has been reported that HTLV-I, as well as HIV, activates the JC virus promoter and its proliferation, the latent infection of HTLV-I in the central nervous system (CNS) in this case might have stimulated the JC virus proliferation, promoting lesion extension over the cerebral cortex. There have been only a few reports of broad decreases in CBF by SPECT in PML patients. Further MRI and SPECT studies on PML patients are therefore necessary to evaluate the significance of HTLV-I in promoting the JC virus infiltration into the CNS.
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PMID:[A case of progressive multifocal leukoencephalopathy presenting white matter MRI lesions extending over the cerebral cortex and a marked decrease in cerebral blood flow on SPECT, and associated with HTLV-I infection]. 1602 67

Both carotid endarterectomy and carotid artery stent placement with filter embolic protection present a higher risk for patients with internal carotid artery (ICA) lesions containing intraluminal thrombus. Despite the risk associated with intervention, patients with symptomatic intraluminal thrombus who were enrolled in the North American Symptomatic Endarterectomy Trial did better with surgical than medical treatment. We describe the novel use of an endovascular "internal cross-clamping" technique in two patients with symptomatic intraluminal thrombus in the ICA. A 57-year-old woman presented with a history of multiple episodes of left upper-extremity numbness, mild dysarthria, and agraphia occurring over the previous 24 hours. Cranial magnetic resonance imaging revealed a scattered watershed infarction of the right hemisphere and a critical stenosis of the right ICA. An 81-year-old man awoke with hemiplegia and inability to follow commands after undergoing a complicated carotid endarterectomy. Computed tomographic perfusion imaging demonstrated an increased time to peak in the left middle cerebral territory, and emergent angiography demonstrated both intimal flaps and thrombus in the endarterectomy bed. The lesions in both patients were treated with endovascular stent placement using both proximal and distal flow occlusion--a functional "internal cross-clamping"--for embolic protection. To our knowledge, this is the first report of internal trapping and stent placement for symptomatic carotid stenosis containing intraluminal thrombus. This treatment strategy should be added to the armamentarium of endovascular surgeons in selected patients with symptomatic carotid intraluminal thrombus.
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PMID:"Internal cross-clamping" for symptomatic internal carotid artery thrombus. Report of two cases. 1807 62

After a cerebral infarction, some patients acutely demonstrate contralateral hemiplegia, or aphasia. Those are the obvious symptoms of a cerebral infarction. However, less visible but burdensome consequences may go unnoticed without closer investigation. The importance of a thorough clinical examination is exemplified by a single case study of a 72-year-old, right-handed male. Two years before he had suffered from an ischemic stroke in the territory of the left posterior cerebral artery, with right homonymous hemianopia and global alexia (i.e., impairment in letter recognition and profound impairment of reading) without agraphia. Naming was impaired on visual presentation (20%-39% correct), but improved significantly after tactile presentation (87% correct) or verbal definition (89%). Pre-semantic visual processing was normal (correct matching of different views of the same object), as was his access to structural knowledge from vision (he reliably distinguished real objects from non-objects). On a colour decision task he reliably indicated which of two items was coloured correctly. Though he was unable to mime how visually presented objects were used, he more reliably matched pictures of objects with pictures of a mime artist gesturing the use of the object. He obtained normal scores on word definition (WAIS-III), synonym judgment and word-picture matching tasks with perceptual and semantic distractors. He however failed when he had to match physically dissimilar specimens of the same object or when he had to decide which two of five objects were related associatively (Pyramids and Palm Trees Test). The patient thus showed a striking contrast in his intact ability to access knowledge of object shape or colour from vision and impaired functional and associative knowledge. As a result, he could not access a complete semantic representation, required for activating phonological representations to name visually presented objects. The pattern of impairments and preserved abilities is considered to be a specific difficulty to access a full semantic representation from an intact structural representation of visually presented objects, i.e., a form of visual object agnosia.
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PMID:[Associative visual agnosia. The less visible consequences of a cerebral infarction]. 2140 Sep 59

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


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