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)

In clinical evaluation of 13 kid goats with viral leukoencephalomyelitis, diseases goats were found to be usually 2 to 4 months old, afebrile, and with unaltered mental status. The most frequent neurologic signs were posterior paresis and ataxia. Pleocytosis and lymphopenia were consistent antemortem laboratory findings. Absence of other abnormal laboratory and radiographic changes were also typical of the disease. Confirmation of the diagnosis can be obtained only be thorough histologic examination of the brain and spinal cord.
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PMID:Differential diagnosis of viral leukoencephalomyelitis of goats. 100 95

When 2 horses were dosed with cultures of a Fusarium moniliforme isolate that had previously caused only hepatosis, 1 developed brain oedema and hepatosis, and the other only leukoencephalomalacia. A 3rd horse developed both leukoencephalomalacia and hepatosis after being dosed with another isolate obtained from maize which was associated with a natural outbreak of the nervous form of the disease. Since leukoencephalomalacia and hepatosis could be induced by the same culture material, it was concluded that both syndromes were manifestations of the same toxicosis. There was also some evidence that leukoencephalomalacia might be specifically induced by the administration of smaller doses of the culture material to horses over a longer period. The clinical signs of nervous disorder included ataxia, paresis, apathy, hypersensitivity, frenzy, and other locomotory and psychic disturbances. Autopsy showed that the brains were oedematous, and focal areas of liquefactive necrosis were present in the cerebral white matter. In 1 case the malacic areas were not confined to the subcortical white matter but were microscopically visible in the cerebral cortex as well. An histopathological examination of the areas bordering on the malacic areas revealed rarefication of the white matter, perivascular haemorrhages, oedema and cellular infiltration composed mainly of plasma cells and eosinophiles. Many of the macrophages in these areas contained lipfuscin-like granules, but these granules also occurred extracellularly in the neuropil. In the layers of the cortex nearest the malacic areas, satellitosis and neurophagia were commonly seen.
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PMID:Leukoencephalomalacia: a mycotoxicosis of Equidae caused by Fusarium moniliforme Sheldon. 101 50

A patent, who suffered from nonprogressive athetotic-myoclonic hyperkinesia of the left arm and spastic paresis of the underdeveloped left leg since early childhood, experienced a febrile episode at the age of 23, after which a weakness and ataxia of the right limbs with frequent falling persisted; at the age of 28, he developed a right-sided rigidity, tremor at rest and mask-like face as sequelae of encephalitis disseminata exacerbations. The violent intention myoclonus of the left side of the body could be abolished by stereotactic coagulation in the V.o.p and V.o.a and zona incerta until death 11 days later. The athetotic myoclonic hyperkinesia is the consequence of a left-sided severe status marmoratus of the right putamen with extensive loss of nerve cells and shrinkage. The additional nerve cell loss in the right substantia nigra due to demyelinating encephalitic foci did not produce Parkinson symptoms, because these require a normal striatum. This loss did, however, exaggerate the original hyperkinesia to a violent intention myoclonus, which was abolished by interruption of denatatothalamic afferents to the V.o.p nucleus and of pallidothalamic afferents to the V.o.a nucleus. The Parkinson syndrome of the right side is due to demyelinating foci of different ages. The Parkinson symptoms were manifest on the right side, because the left status marmoratus did not severely reduce the striatal nerve cells. In this case, there is no indication that the introduction of the stereotactic electrode has precipitated new demyelinating foci.
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PMID:Stereotactic treatment of action myoclonus in a case of combined status marmoratus and multiple sclerosis. A contribution to the pathophysiology of basal ganglia with multiple lesions in both the striatum and the substantia nigra. 109 75

Clinical signs of toxicosis, neurologic lesions, and elevated tissue residues of methylmercury (MM) were produced in 12 pigs by oral administration of 1.29, 0.86, 0.64, and 0.43 mg mercury/kg of body weight daily as methylmercuric hydroxide (MMH). Clinical signs which began on day 17 were ataxia, dysmetria, blindness, convulsions, paresis, and death. Time of onset of signs was inversely related to size of daily dose. Microscopic lesions were found in the cerebrum brain stem, and spinal cord, and correlated well with clinical signs. The cerebrum in which severity of lesions was directly related to length of exposure was the most severely affected region of the central nervous system (CNS). Lesions were neuronal necrosis, neuronophagia, cortical vacuolation, axon swelling, gliosis, leptomeningitis, and vascular fibrinoid necrosis. Neuronal necrosis was most extensive within mid and deep cerebrocortical laminae. Brain residues of MM were directly proportional to the size of daily dose, and statistically significant. Distribution of MM among different tissues was rather uniform with highest concentrations found in liver, followed by kidney, muscle, spleen, and brain.
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PMID:The pathology of subacute methylmerculialism in swine. 125 8

A 38-year-old man developing slowly progressive left facial paresis was admitted to our hospital. The clinical diagnosis of "adhesive arachnoiditis was made. The first operation was performed in December 1987, and his symptom disappeared postoperatively. Three years later, left facial paresis recurred together with trunkal ataxia. A computed tomography and magnetic resonance image revealed two tumors located at the left cerebellopontine angle region and in the left middle cerebral fossa. These two tumors were thought to arise in the different cranial nerve. Under the clinical diagnosis of acoustic neurinoma associated with facial nerve neurinoma, the two step-operation was designed for total removal of the tumor in December 1990 and January 1991. Intraoperative finding confirmed that these two tumors had the different origin. Pathologic diagnosis was compatible with neurinoma. This patient had no family history of "Neurofibromatosis".
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PMID:[Acoustic neurinoma associated with facial neurinoma--a case report]. 128 93

A novel immunosuppressant, succinyl acetone (4,6-dioxoheptanoic acid), was studied in dogs. Results with bolus intravenous injections at doses ranging from 50 to 1600 mg/kg showed dose-dependent alpha and beta half-lives, ranging from 30 to 80 min and 7 to 27 hr, respectively. Results suggested that continuous i.v. infusion was necessary to maintain constant plasma levels. Four dogs were given 9.2 Gy total-body irradiation and autologous marrow transplants along with continuous i.v. infusion of succinyl acetone at 50, 100, 200, or 400 mg/kg/day for 21 days, and all four had rapid, sustained hematopoietic engraftment. However, two of the four dogs receiving 200 and 400 mg succinyl acetone/kg/day, respectively, developed bilateral hind-limb ataxia, with histologically confirmed cerebellar lesions in the dog given the higher dose, thus establishing a potential dose-limiting neurotoxicity. Prevention of graft-versus-host disease was studied in recipients of allogeneic marrow. Dogs were given 9.2 Gy TBI, followed by hematopoietic grafts from unrelated DLA-nonidentical or DLA-haploidentical littermate dogs. Succinyl acetone was given as continuous infusion for 21 days after transplant at doses of 100-300 mg/kg/day. Starting succinyl acetone on the day of marrow infusion in four dogs failed to prevent rapid onset of acute GVHD, and dogs survived no longer than controls. Starting succinyl acetone 3 days before transplant delayed the onset of acute GVHD and prolonged survival significantly compared with that of dogs not given postgrafting immunosuppression (P = 0.008); survival was comparable to that in previously reported dogs given either methotrexate or cyclosporine as postgrafting immunosuppression (P = 0.88 and 0.99, respectively). Seven of the sixteen allogeneic recipients developed evidence of neurotoxicity during succinyl-acetone infusion. Neurological dysfunctions were manifested by hind-limb ataxia and posterior paresis. In conclusion, succinyl acetone significantly delayed the onset of GVHD and prolonged survival of DLA-nonidentical marrow graft recipients but did not induce graft-host tolerance and was associated with dose-limiting neurotoxicity.
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PMID:Pharmacologic, toxicologic, and marrow transplantation studies in dogs given succinyl acetone. 144 Aug 68

We investigated motor function and pain sensation in the gracile axonal dystrophy (GAD) mutant mouse, using the tail-flick test and the rotarod test. GAD (gad/gad) and normal sib mice (gad/+ or +/+) were used between 5 and 11 weeks of age, during which time the behavioral signs of GAD mice shifted from sensory ataxia (about 4 to 8 weeks of age) to paresis (after about 9 weeks of age). In the tail-flick test, significant shortening of latency was observed at 6 and 8 weeks of age in female GAD mice, in comparison with normal female mice. This may be related to dysfunction or degeneration of axons in the fasiculus gracilis, whose collaterals are thought to control the transmission of nociceptive information. In the rotarod test, a cumulative chi 2 test showed significant reduction in the performance times of GAD mice beginning at 5 and 6 weeks of age in males and females, respectively, indicating that the rotarod test can detect the development of motor incoordination as early as these ages. The performance times of GAD mice dropped sharply from 9 weeks of age onwards, and this is believed to reflect the progression of paresis. The rotarod test therefore appears to be a good method of quantifying behavioral changes in GAD mice and to be applicable both to objective selection of GAD mice before 8 weeks of age and to evaluation of drugs to treat ataxia or paresis.
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PMID:Behavioral study on the gracile axonal dystrophy (GAD) mutant mouse. 145 62

This review focuses on the features of pseudotumor cerebri in the pediatric age group. There is no sex predilection in children, and obesity does not appear to be an important factor. Infants and young children may present with irritability, apathy, or somnolence, rather than headache. Dizziness and ataxia may also occur. Papilledema is infrequently noted in pediatric patients if the fontanelles are open or the sutures are split. Pre-adolescents appear more likely than adults or adolescents to have manifestations of their pseudotumor cerebri other than headache and papilledema, including lateral rectus pareses, vertical strabismus, facial paresis, back and neck pain. Among the etiologies that are particularly pertinent to children are tetracycline therapy, malnutrition or renutrition, and the correction of hypothyroidism. Children with pseudotumor cerebri are at risk for visual loss and their visual function must be closely monitored. Surgical intervention is imperative when vision is threatened.
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PMID:Pediatric pseudotumor cerebri (idiopathic intracranial hypertension). 147 50

Five patients with superficial anterior cerebral artery territory infarcts in the paracentral area are reported, who developed a hemiparesis which was predominant in the leg, and with homolateral ataxia in the arm. A similar neurological picture was not observed in 1736 patients who were admitted over an eight year period to a primary care stroke centre with their first stroke. Involvement of corticopontine fibres at their origin, together with damage to the lower limb motor strip or underlying white matter, appears to have been the cause of a clinical syndrome (homolateral ataxia and crural paresis) which has been ascribed to lacunar infarction.
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PMID:Homolateral ataxia and crural paresis: a syndrome of anterior cerebral artery territory infarction. 147 93

Twelve years following the diagnosis of a histologically proved Sarcoidosis, a patient developed a central paresis of one lower limb. Two years later, tetraparesis, bladder dysfunction, ataxia and an internuclear bilateral ophthalmoplegia occurred. In CSF oligoclonal IgG without dysfunction of the blood brain barrier was found. On the basis of these data multiple sclerosis was diagnosed.
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PMID:[Simultaneous occurrence of sarcoidosis and MS or sarcoidosis within the clinical picture of multiple sclerosis?]. 152 36


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