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)

The mutant strain of Wistar rats carrying an autosomal recessive gene defect is characterized by a sequence of progressively developing behavioural alterations including hyperexcitability, tremor, olfactory and gustatory automatisms, bradykinesia, ataxia, rigidity, paresis and cachexia. The stereotypy and locomotor responses to increasing doses of apomorphine hydrochloride and D-amphetamine sulphate, and the catalepsy response to increasing doses of haloperidol were studied in mutant rats at the age of 6-7 weeks. In the mutants, both the stereotypy and locomotor responses to amphetamine were enhanced, while stereotypy and locomotor effects induced by apomorphine were unaltered. The cataleptic response to haloperidol was significantly diminished compared to controls. These findings indicate a derangement in the function of basal ganglia in the mutants.
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PMID:Stereotypy, locomotor and cataleptic effects produced by drugs influencing dopaminergic systems in a mutant strain of Wistar rats: a genuine model of basal ganglia dysfunction? 653 16

An acute episode of encephalopathy after the infusion of 16 g methotrexate is reported in a 12-year-old girl with osteogenic sarcoma. The complication occurred during the 11th treatment course, when severe vomiting and diarrhea were followed by a low urine output with consecutive toxic concentrations of methotrexate in serum and cerebrospinal fluid leading to severe systemic and central nervous system toxicity. The onset of the central nervous system toxicity was acute with slurred speech, paresis of the external rectus eye muscles, ataxia, and hemiparesis, and symptoms resolved completely after 30 hours by treatment with calcium leucovorin and forced diuresis. After management of the cerebral and systemic toxicity, high-dose methotrexate treatment could be reinstituted, and was followed by no further complications. In contrast to the transient cerebral dysfunctions, probably caused by embolization of tumor tissue in the early course of high-dose methotrexate treatment, the acute neurologic syndrome observed in the current case after the prolonged use of methotrexate seemed to be related to direct central nervous system toxicity of the drug.
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PMID:Transient encephalopathy during the late course of treatment with high-dose methotrexate. 658 97

Copper deficiency was diagnosed in piglets from a farm in the Transvaal. The mortality rate among 5 to 8-week-old piglets had been sporadic but considerably high over a 12 month period. Affected animals showed signs of ataxia, posterior paresis, horizontal nystagmus, inability to stand and front and hind limb paddling movements. Death ensued from 3-5 days after the onset of clinical signs. A paucity of myelin in the spinal cord and degenerative lesions involving elastic fibres of the aorta and pulmonary artery were detected. Tissue copper levels were low in both clinically affected and unaffected piglets on the farm, and the copper content of the diet fed to sows and growing piglets was considered inadequate. The lesions related to copper deficiency are described with emphasis on those in the spinal cord and great blood vessels, and the pathologic processes resulting in hypocupraemic lesions are considered.
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PMID:Copper deficiency in piglets characterized by spongy myelopathy and degenerative lesions in the great blood vessels. 663 90

The neurotoxic effects of tri-o-cresyl phosphate (TOCP) were studied in the cat to define the elements of neurologic testing and to correlate dysfunction with the results of histopathologic studies. Neurologic examination of treated cats categorized clinical signs of TOCP-induced delayed neurotoxicity in the cat into four stages: leg weakness, mild ataxia, severe ataxia, and paresis. These deficits correlated well with histopathological lesions found in the central and peripheral systems. The improvement seen, is attributed to regeneration and/or collateral sprouting of remaining axons of peripheral nerves that would not be expected in tracts of the central nervous system.
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PMID:Neurologic manifestations of tri-O-cresyl phosphate delayed neurotoxicity in cats. 664 17

In a patient with the syndrome of crural paresis and homolateral ataxia, administration of trihexyphenidyl resulted in improvement of disabling unilateral ataxia and gross intention tremor. Symptoms returned when drug therapy was interrupted. CT showed a radiolucent lesion deep in the parietal white matter close to the internal capsule.
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PMID:Improvement of ataxic hemiparesis with trihexyphenidyl. 668 36

Two adult rottweiler dogs were evaluated for slowly progressive ataxia and paresis of all four limbs of over seven months duration. On neurologic examination, signs referable to a lesion in the cervical spinal cord affecting motor and sensory white matter tracts were found. Both dogs were necropsied and were found to have demyelinating lesions in the spinal cord, brain stem, and deep cerebellar white matter. Primary morphologic alterations were intact naked axons and thinly myelinated axons accompanied by reactive astrogliosis. The spinal cord lesions tended to have bilateral symmetry and were found in the lateral funiculi and occasionally in the dorsal funiculi. The cause and pathogenesis of the lesion were not determined.
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PMID:A leukoencephalomyelopathy of rottweiler dogs. 673 Feb 16

Brain tumors are, after leukemias, the most frequent fatal neoplasms of infancy. The clinical features and symptoms are often markedly different from those observed in the adult forms, according to the peculiar anatomy and behaviour of the child. Persistent headache, vomiting, astenia , behavioral alterations may be the precocious findings. Later, some more specific and suggestive signs such as strabismus, dyplopia , fast head size increase, funduscopic alterations, ataxia, paresis and nystagmus may be observed. On their appearance a prompt diagnostic work-up should be performed. The tumors of the posterior fossa (cerebellar astrocytoma and medulloblastoma, brainstem glyoma , hependimoma in decreasing order of frequency) generally cause precocious symptoms because of the small dimension of the subtentorial space; the presence in this region of several fundamental nuclei and pathways may explain how also small tumors may cause severe deficits. Supratentorial tumors (astrocytoma, malignant glyoma , hependimoma , craniofaringioma ) often show a more prolonged latency and may begin with signs of endocranial hypertension, seizures, or sometimes with hormonal troubles according to the involved anatomic structures. Hypothalamic astrocytoma is responsible of an extreme weight loss as far as to a cachetic status, due to the hyperincretion of GH. Finally, plexus papilloma, dermoid, optic nerve glyoma , oligodendroglyoma , germinoma, teratoma are responsible of a small number of child brain tumors, with different localization and symptomatology.
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PMID:[Clinical course of brain tumors in childhood]. 673 95

10 young patients from 7 to 16 years of age with moyamoya disease were treated by temporal muscle graft (encephalo-myo-synangiosis: EMS) for the purpose of increasing extracranial and intracranial collateral circulation. Ischemic cerebrovascular symptoms and signs were encountered in all of them without intracranial hemorrhage. The patients were observed for 6-26 months after the first operation. Transient ischemic attacks disappeared in 4 out of 7 patients, and improved in frequency and duration in the remaining 3. Paresis of the limbs disappeared in 1 patient and improved in 2. In 2 patients, facial palsy disappeared and dysarthria improved as well. Ataxia disappeared in 2 patients, and involuntary movement of the extremities disappeared in 2. There were no ineffective cases clinically. In postoperative carotid angiography, the middle cerebral arteries were visualized clearly to the peripheral portion mainly via the thickened deep temporal arteries, and the abnormal vascular networks in the region of the basal ganglia reduced in size in most of patients. Improvements in intelligence quotient, electroencephalogram and cerebral blood flow were also obtained in several patients, respectively. EMS seemed to be an effective surgical treatment in young patients with moyamoya disease who suffered from cerebral ischemic symptoms.
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PMID:Treatment of moyamoya disease by temporal muscle graft 'encephalo-myo-synangiosis'. 682 12

Hearing loss in an uncommon symptom in multiple sclerosis (MS). In nine patients with MS, seven with unilateral hearing loss and two with bilateral impairment, accompanying symptoms and signs included facial numbness, hemifacial paresis or spasms, ipsilateral limb ataxia, nystagmus, vertigo, tinnitus, and spastic-ataxic gait. Central auditory dysfunction was suggested by audiometric findings and/or by brainstem auditory evoked potentials in all nine patients. Clinical improvement in two was accompanied by return toward normal in the results of audiometric or electrophysiologic studies. Hearing impairment should be sought in patients with MS and appropriate studies pursued.
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PMID:Hearing loss in multiple sclerosis. 684 85

A chronic, progressive form of experimental allergic encephalomyelitis was produced by immunization of rabbits with bovine brain white matter proteolipid apoprotein. Clinical signs appeared 4 to 13 months after sensitization, and were characterized by ataxia and limb paresis which progressed to flaccid paralysis and incontinence. Light and electron microscopic observations showed both acute and chronic nonsuppurative myelitis or encephalomyelitis accompanied by primary demyelination. Myelin damage was most evident in the spinal cord but was also present in the optic nerve and brain. The neuropathology was consistent with lesions of chronic experimental allergic encephalomyelitis produced by central nervous system tissue, and resembled lesions of multiple sclerosis as well. These observations suggest that protein may be involved in the pathophysiology of demyelinating diseases. A mechanism for the chronic course of the disease is discussed.
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PMID:Chronic experimental allergic encephalomyelitis induced in rabbits with bovine white matter proteolipid apoprotein. 710 65


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