Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0030552 (paresis)
 5,831 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

N-butyl benzenesulfonamide (NBBS), one of the sulfonamide plasticizers, induced characteristic effects to Wistar rats after acute repeated exposures (300 mg/kg body weight, ip every 6 h). The signs were pica, staggering gait with hindlimb-paresis and splaying, teeth-grinding, self paw-biting and coma. The motor activity parameters showed generalized decreased mobility. The gait and hindlimb abnormalities coexisted with changes of lower motoneuron activity, ie decreased immunoreactivity of choline acetyltransferase in the lumbar spinal cord. The effects became more overt with repeated exposure to NBBS and the severity was increased. These effects were short-lived and the animals soon recovered.
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PMID:Behavioral changes with alterations of choline acetyltransferase immunoreactivities induced by N-butyl benzenesulfonamide. 858 90

We analysed retrospectively our clinical experience with 36 cases of mucormycosis. They were seen during the last 15 years. The diagnosis suspected on clinical grounds, was confirmed in 31 cases by finding the hyphae in hematoxylin-eosin stained material obtained from aspirated or tissue biopsy or by isolation of the fungus in culture. Rhinocerebral mucormycosis was diagnosed in 22 patients. Diabetes was the underlying disorder in 20 cases, kidney failure in one and myelodysplastic syndrome in one. Nine had stable and 11 unstable diabetes (ketoacidosis in 10 and hyperosmolar coma in 1). The earliest sign was facial edema, followed by proptosis, chemosis and extraocular muscle paresis. They were treated by extensive surgical debridement, insulin and antifungal drugs with 69% of survival rate. The disseminated mucormycosis was diagnosed at the autopsy in 5 cases, acute leukemia was the underlying disease in 2 of them. Pulmonary mucormycosis was diagnosed in 2 cases, cutaneous form in 2, sinuorbital form in 4 and brain abscess in one patient. Eight of these 9 cases survived after therapy. We emphasize the importance of an early diagnosis. This can only be made in the presence of a typical clinical setting confirmed by finding the hyphae in tissue or culture. Antifungal drugs along with treatment of the underlying disorder and aggressive surgical debridement must follow.
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PMID:Rhinocerebral and systemic mucormycosis. Clinical experience with 36 cases. 898 Dec 94

Forty-eight post-traumatic brain-injured patients in postcoma-unawareness (PC-U) state, are included in this study. All recovered consciousness at least 1 month after the accident. The muscular tone and movement of all limbs was examined. At least two X-rays of the big joints were taken. Periarticular new bone formation appeared in 26 patients. This heterotopic ossification occurs in severely injured patients, primarily in proximal joints of the upper and lower extremities. Their aetiology in brain injury is unknown. Risk factors include prolonged coma, tone and movements in the involved extremity, and associated fractures. We found that the appearance of periarticular new bone formation had a close correlation with pathological movement (paresis or plegia), a borderline correlation with hypertonus, and no correlation with hypotonus or with associated fractures.
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PMID:Relationship between muscular tone, movement and periarticular new bone formation in postcoma-unaware (PC-U) patients. 904 91

A 16-year-old girl presented with left hemiparesis and right oculomotor nerve paresis due to temporal lobe herniation resulting from a traumatic acute subdural hematoma secondary to a head injury. Computed tomography revealed a subdural hematoma in the right frontotemporal regions and midline structures shifted to the left. She became comatose and underwent an emergency operation. The hemiparesis and newly manifested homonymous hemianopsia on the right side persisted after surgery. Postoperative magnetic resonance imaging showed Kernohan's notch in the cerebral peduncle and infarctions in the occipital lobe and posterolateral part of the thalamus on the left side, contralateral to the supratentorial lesion.
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PMID:Magnetic resonance imaging of sequelae of temporal lobe herniation secondary to traumatic acute subdural hematoma: Kernohan's notch and posterior cerebral artery territory infarctions contralateral to the supratentorial lesion--case report. 904 2

We report a 62-year-old man who developed coma and died in a fulminant course. The patient was well until May 1, 1996 when he noted chillness, tenderness in his shoulders, and he went to bed without having his lunch and dinner. In the early morning of May 2, his families found him unresponsive and snoring; he was brought into the ER of our hospital. He had histories of hypertension, gout, and hyperlipidemia since 42 years of the age. On admission, his blood pressure was 120/70, heart rate 102 and regular, and body temperature 36.3 degrees C. His respiration was regular and he was not cyanotic. Low pitch rhonchi was heard in his right lower lung field. Otherwise general physical examination was unremarkable. Neurologic examination revealed that he was somnolent and he was only able to respond to simple questions such as opening eyes and grasping the examiner's hand, but he was unable to respond verbally. The optic discs were flat; the right pupil was slightly larger than the left, but both reacted to light. He showed ptosis on the left side, conjugate deviation of eyes to the left, and right facial paresis. The oculocephalic response and the corneal reflex were present. His right extremities were paralyzed and did not respond to pain Deep tendon reflexes were exaggerated on the right side and the plantar response was extensor on the right. No meningeal signs were present. Laboratory examination revealed the following abnormalities; WBC 18,400/ml, GOT 131 IU/l GPT 50 IU/l, CK616 IU/l, BUN 30 mg/dl, Cr 2.1 mg/ dl, glucose 339 mg/dl, and CRP 27.4 mg/dl. ECG showed sinus tachycardia and ST elevation in II, III and a VF leads and abnormal q waves in I, V5, and V6 leads. Chest X-ray revealed cardiac enlargement but the lung fields were clear. Cranial CT scan revealed low density areas in the left middle cerebral and left posterior cerebral artery territories. The patient was treated with intravenous glycerol infusion and other supportive measures. At 2: 10 AM on May 3, he developed sudden hypotension and cardiopulmonary arrest. He was pronounced dead at 3:45 AM. The patient was discussed in a neurological CPC, and the chief discussant arrived at the conclusion that the patient had acute myocardial infarction involving the inferior and the true posterior walls and left internal carotid embolism from a mural thrombus. Post mortem examination revealed occlusion of the circumflex branch of the left coronary artery due to atherom plaque rupture and myocardial infarction involving the posterior and the lateral wall with a rupture in the postero-lateral wall. Marked atheromatous changes were seen in the left internal carotid, the middle cerebral and the basilar arteries; the left internal carotid and the middle cerebral arteries were almost occluded by thrombi and blood coagulate. The territories of the left middle cerebral and the occipital arteries were infarcted; but the left thalamic area was spared. The neuropathologist concluded that the infarction was thrombotic origin not an embolic one as the atherosclerotic changes were severe. Cardiac rupture appeared to be the cause of terminal sudden hypotension and cardiopulmonary arrest. It appears likely that a vegetation which had been attached to the aortic valve induced thromboembolic occlusion of the left internal carotid artery which had already been markedly sclerotic by atherosclerosis. It is also possible that the vegetations in the aortic valve came from mural thrombi at the site of acute myocardial infarction, as no bacteria were found in those vegetations.
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PMID:[A 62-year-old man with an acute onset of consciousness disturbances]. 945 48

The removal of a central venous catheter (CVC) can be complicated by rare but potentially life-threatening neurocardiopulmonary distress. The clinical courses of eight patients who had CVC removal complications are reviewed. Seven patients had catheter removal from the right internal jugular vein, and one from the right subclavian vein. The complications occurred after complete removal of the catheter (four patients), after guidewire replacement for catheter change (three patients), and after detachment of the hemostasis side port of the Swan introducer during sheath removal (one patient). Each of them had more than one complication. The major complications were: neurologic paresis or coma (four patients), respiratory failure (four patients), and shock (two patients). One patient died of pulmonary sepsis. The overall mortality rate was 12.5 per cent. Guidelines for safe removal of central venous catheters are proposed. Possible mechanisms of the complications are discussed. We refer to the observed complications as the CVC removal distress syndrome.
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PMID:The CVC removal distress syndrome: an unappreciated complication of central venous catheter removal. 954 47

We present the case of a 13-month old Turkish boy of Kurdish origin with tuberculous meningitis. Fever of unknown origin and neurologic symptoms (loss of ability of walking and free sitting, cerebral seizures, central paresis of the VII. cranial nerve, coma) led to the diagnosis. Cranial CT demonstrated hydrocephalus and enhancement of the basal meninges after contrast injection; the chest x-ray showed an infiltrate in the right upper lobe of the lung and the cerebrospinal fluid (CSF) mild pleocytosis with elevated protein and reduced glucose concentrations. Diagnosis was confirmed by detection of Mycobacterium tuberculosis in the CSF by polymerase chain reaction (PCR). Immediately, surgical and level-controlled tuberculostatic treatment was initiated. The patient recovered completely.
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PMID:[Tuberculous meningitis in a 13-month-old boy: a case report]. 962 48

A 30-year-old female became comatose due to embolic occlusion of the basilar artery, caused by surgical injury to the origin of the vertebral artery during removal of a neurinoma in the upper thoracic paravertebral region. The basilar artery occlusion was treated by local fibrinolysis through a microcatheter. Two weeks later she recovered her consciousness but suffered mutism. Her speech disturbance was characterized by severe ataxic dysarthria known as "cerebellar mutism" but without cranial nerve paresis. The mutism gradually improved during the following 3 months. This is case of cerebellar mutism was apparently due to ischemic stroke. Disturbance by hypoperfusion of the cerebellum and brain stem may have been involved in the pathogenesis of cerebellar mutism.
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PMID:Cerebellar mutism after basilar artery occlusion--case report. 980 3

We report a 96-year-old Japanese man who developed a sudden onset of left hemiplegia and coma. He was found to have diabetes mellitus, hypertension, and atrial fibrillation since 1996 with occasional episodes of congestive heart failure. He was otherwise apparently well until July 5 of 1997 when he developed a sudden onset of unresponsiveness and convulsion involving his right hand and was admitted to our hospital. On admission, his BP was 210/120 mmHg, heart rate 76/min and irregular, BT 36.5 degrees C, and Cheyne-Stokes respiration. General medical examination was otherwise unremarkable. Neurologic examination revealed semicoma, conjugated deviation to the right, loss of oculocephalic response, left facial paresis of central type, flaccid left hemiplegia, and bilateral Babinski sign. Pertinent laboratory findings are as follows: BUN 47 mg/dl, creatinine 1.46 mg/dl, GPT 69 IU/l, LDH 1,142 IU/l, and CK 385 IU/l. A chest x-ray film revealed cardiac enlargement and EKG showed left ventricular hypertrophy and atrial fibrillation. Cranial CT scan revealed low density areas involving the right anterior cerebral and the right posterior cerebral artery territories. He was treated with an intravenous osmotic agent and short course of intramuscular steroid. He remained unconscious despite these treatment and developed sudden cardiopulmonary arrest three weeks after the admission. The patient was discussed in a neurological CPC and the chief discussant arrived at the conclusion that the patient had suffered from cerebral embolism of cardiac origin. The cause of the death was ascribed to acute subendocardial myocardial infarction. Most of the participants agreed with this conclusion. Postmortem examination revealed an old subendocardial myocardial infarction involving the posterior septal region and posterolateral wall of the left ventricle. Neuropathologic examination revealed hemorrhagic infarctions involving the territories of the right anterior cerebral, right middle cerebral, right posterior cerebral, and left anterior cerebral arteries. The left A1 portion of the anterior cerebral artery was hypoplastic, and the left pericallosal artery appeared to have been receiving blood supply from the right anterior cerebral artery through the anterior communicating artery. The large arteries in the base showed marked arteriosclerosis; particularly, the initial portion of the right posterior artery showed near complete arteriosclerotic occlusions. These characteristic arterial changes appeared to be the reason why this patient suffered from an extensive infarction from what appeared to have been a single episode of cerebral embolism probably initially involving the right internal carotid artery.
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PMID:[A 96-year-old man with consciousness disturbance, convulsion, and left hemiplegia of acute onset]. 1006 67

Major neurologic complications secondary to cyclosporine are well documented and are known to include confusion, cortical blindness, seizure, spasticity, paresis, ataxia and coma. Most previous reports attribute these to white matter central nervous system (CNS) lesions or white/grey matter border lesions. Many predisposing factors have been identified, including: elevated levels of cyclosporine, hypomagnesemia, hypocholesterolemia, aluminium toxicity, high dose steroids, hypertension and infection. However CNS events attributed to cyclosporine have been reported without any of these risk factors. We report a case of a child developing multiple white and grey matter thalamic and cortical lesions along with acute neurologic deterioration, and then review cyclosporine mediated CNS injury, including the roles of P-glycoprotein and cyclophilin.
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PMID:Cyclosporine-induced white and grey matter central nervous system lesions in a pediatric renal transplant patient. 1008 60


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