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)

Homolateral ataxia and crural paresis is a recognized vascular syndrome. However, confirmation of the causative lesion rests principally on one earlier case with multiple other infarcts. We studied a patient with the clinical syndrome; computerized tomography revealed a lucency that appeared within 1 week of the infarct. Localization of the lesion to the superior portion of the posterior limb of the internal capsule and thalamus is in accord with the original conclusions of Fisher and Cole.
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PMID:Homolateral ataxia and crural paresis: case report. 719 30

Twenty-three 2- to 5-month-old Beagle dogs were fed a purified thiamine-deficient ration (2 to 3 micrograms of thiamine/100 g of ration) at a rate of 40 to 70 g/kg of body weight/day depending on age. Eleven dogs were used as principles, 6 as pair-fed controls, and 6 as ad libitum-fed controls. Controls were treated once a week with an IM dose of 300 micrograms of thiamine hydrochloride/kg of body weight. Three stages of clinical disease occurred in the principals: (i) an initial short (18.0 +/- 7.9 days) stage of induction, during which the dogs usually grew suboptimally, but were otherwise healthy, (ii) an intermediate stage of preliminary clinical signs of deficiency, characterized by a variable period (58.5 +/- 37.0 days) of progressive inappetance, failure to grow, loss of body weight, and coprophagia, and (iii) a terminal stage, which, in most dogs, was abrupt in onset and short (7.6 +/- 6.0 days) and consisted of either a neurologic syndrome or sudden unexpected death syndrome. Eight of the principals developed the neurologic syndrome characterized by anorexia, emesis, CNS depression, paraparesis, sensory ataxia, torticollis, circling, exophthalmos, tonic-clonic convulsions, profound muscular weakness, recumbency, and then died. Common reflex abnormalities included exaggerated patella reflex, proprioceptive and supporting reflex deficits, induced torticollis and ventroflexion of head, and absent eye menace (blink) reflex. Three other principals developed the sudden unexpected death syndrome. Common signs of deficiency were inappetance and paresis. Two were found dead and 1, with severe ECG abnormalities (including elevation of ST segment and tall or deeply inverted T waves), was killed.
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PMID:Experimentally induced thiamine deficiency in beagle dogs: clinical observations. 719 32

Hexosaminidase deficiency diseases or GM2-gangliosidoses were originally described as infantile encephalopathies. Recently, hexosaminidase deficiencies have been found with different phenotypes, including juvenile and adult encephalopathies, cerebellar ataxias, and motor neuron diseases. Individual cases have resembled Ramsey-Hunt syndrome, olivopontocerebellar ataxia, Friedreich ataxia, amyotrophic lateral sclerosis, Kugelberg-Welander disease, Fazio-Londe disease, and Charcot-Marie-Tooth disease. Tremor, dystonia, spastic paresis, and psychosis have been seen. Since few diagnosable causes for these system atrophies are known, these patients should be tested for hexosaminidase deficiency. These recessive disorders fit a multiple loci/multiple alleles genetic scheme, and a clinical genetic classification is presented.
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PMID:The clinical spectrum of hexosaminidase deficiency diseases. 719 92

A partial deficiency of pyruvate decarboxylase (PDC) was demonstrated in a child with hyperlactatemia and progressive ataxia, bulbar paresis, ophthalmoplegia, and polyneuropathy. Subacute necrotizing encephalomyelopathy (SNE) was found at necropsy. The association of SNE and PDC deficiency has been reported rarely, but a review of the diverse metabolic defects associated with SNE suggests that decreased PDC activity may be the common feature of SNE.
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PMID:Pyruvate decarboxylase deficiency in subacute necrotizing encephalomyelopathy. 724 88

Lasalocid was given to horses in a series of sequentially increasing single oral doses ranging between 5 and 30 mg/kg of body weight, with an appropriate washout period between treatments. One of the 5 horses died after a dosage of 15 mg/kg, 1 of 3 horses died after 21 mg/kg, 1 of 3 horses died after 22 mg/kg, and 1 of 2 horses died after 26 mg/kg. The LD50 of lasalocid for horses was estimated to be 21.5 mg/kg. Monensin was given to horses in a similar manner at dosages of 1, 2, and 3 mg/kg of body weight. One of the 2 horses died after a dosage of 2 mg/kg and 1 horse died after a dosage of 3 mg/kg. The clinical signs of toxicosis observed in horses given either drug were progressive and included depression, ataxia, paresis, and paralysis with partial anorexia. Intermittent profuse sweating was observed before death in horses given monensin.
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PMID:Toxic effects of lasalocid in horses. 727 Oct 10

Eleven cases presenting a syndrome of the medulla oblongata are discussed with reference to the findings of clinical and angiographic investigation. The diagnosis of Wallenberg's syndrome is justified when the classic symptoms are apparent (Horner's syndrome, nystagmus, dysphonia and dysphagia, ataxia, ipsilateral sensory impairment of the face and contralateral elsewhere, and accompanying vegetative disturbances). If additional symptoms such as a facial or extra-ocular muscle paresis, especially hemiparesis, exist, another, more lateral or medial, syndrome of the oblongata should be considered. Angiographic findings vary considerably, ranging from a normal vertebral artery or posterior inferior cerebellar artery (PICA) to an occlusion of these arteries (in three and two of the 11 cases respectively). Modification are often seen in the anterior inferior cerebellar artery (AICA). A kind of complementary supply in the PICA-AICA region must occasionally exist. Localised processes affecting these vessels rather than diffuse multifocal vascular processes would lead to Wallenberg's syndrome. It is difficult to conclude from the clinical picture where a possible responsible vascular narrowing or obliteration may lie, even if pareses of the limb were present.
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PMID:[Clinical and angiographic findings in vascular medullary syndromes (author's transl)]. 731 26

We presented a rare care who had right frontal lobe infarction, with left side pseudoataxia, and the mechanism, causing pseudoataxia, was considered. The patient, a 51 year-old, righ-handed male, was admitted on August 9, 1980, complaining of left-side pseudoataxia. About p.m. 7:00, July 29, 1980, he suddenly noticed numbness of the left foot, and he found himself difficulty in standing in the next morning. He had a mild paresis and tactile-tactile of the left side including the face, which was rapidly improved. However, there was pseudoataxia of the left extremities, which had not been improved. On physical examination, dysarthria, aphasia, finger agnosia, difficulty in right left orientation or muscle weakness was not recognized, and there was no sensory disturbance except for slight impairment of stereognosis, two point discrimination and vibratory sense. Demonstrable impairment of tactiletactile from was observed in the left hand. Notable dysmetria, terminal tremor and dysdiadochokinesia were seen in the left limbs, which were remarkably worsened with eyes closed. However, tapping and line-drawing tests were normal. Babinski-Weil's test disclosed typical compass gait. There was marked swaying in Romberg position. Tandem gait was impossible with a tendency to decline the left. Deep reflexies were normal except for mildly hyperactive radial reflex in the left. Carotid and vertebral angiographies revealed neither evidence of vascular occlusion nor displacement of vessels CT scan demonstrated a low density area, which included the right inferior and middle frontal gyri, the head of the right caudate nucleus and a part of anterior crus of right internal capsule. There was enlargement of anterior horn of the right lateral ventricle. Caloric test, electronystagmography, eye tracking test or optokinetic nystagmus test disclosed no abnormalities. Vibration induced falling, which is the postural reaction to muscle vibration during standing (Ekuland, G., 1972), was not recognized when the left Achiles' tendon was stimulated. Pseudoataxia of this patient differed from the typical cerebellar or vestibular ataxia. From a review of the literatures concerning frontal pseudoataxia, almost all cases had no distinct cerebellar signs, and showed positive Romberg's sign. The impairment of tactile-tactile form and postural reaction to vibratory stimulation to the left leg, appeared in this case, could be hardly explained by the lesion of parietal lobe or deconnection syndrome. Sensory perception of parietal lobe and pyramidal motor system were thought to be almost normal in this case. Therefore, these findings should be due to impairment of integration center between sensory and motor systems. The pseudoataxia in frontal lesion seems to occur as the results of involvement of this center, in which caudate nucleus maybe has important role, but not as the results of disturbances in the front-ponto-cerebellar or front vestibular pathway.
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PMID:[Frontal pseudoataxia, discussion on its mechanism (author's transl)]. 732 87

Three life-threatening respiratory complications are regularly encountered in patients who survive the initial insult from a diffuse brain stem lesion--central alveolar hypoventilation, upper airway obstruction, and aspiration pneumonitis. From treating 13 patients who did survive, a surgical plan for managing the respiratory sequelae of such injuries has evolved and consists of: 1)Diaphragm pacing to correct hypoventilation; 2) tracheostomy for bypass of the upper airway obstruction; 3) gastrostomy for bypass of the impaired structures of swallowing; 4) surgical closure of the larynx to prevent aspiration. All 13 patients manifested central apnea, which was controlled in five by bilateral phrenic nerve stimulation and in eight by unilateral stimulation. All patients required tracheostomy to provide an airway for artificial ventilation and for secretion removal. In ten patients aspiration necessitated gastrostomy. The spontaneous recovery of the ability to swallow allowed closure of the gastrostoma in three but in others aspiration remained a serious complication. One patient died of massive aspiration after discharge from the hospital. Three patients had surgical closure of the larynx to prevent aspiration. Seven patients are alive; six of them are leading productive lives, though several have severe disability due to paresis or ataxia. Six died after discharge from the hospital. Three deaths were not related to the basic problem but the three others may have been.
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PMID:Characteristics and surgical management of respiratory complications accompanying pathologic lesions of the brain stem. 738 27

The acute and subchronic toxicity of monenzine (preparation Elancoban -- 100 of Elanco Co., USA) to male lambs for fattening aged 3-4 months and weighing 16-28.5 kg was studied. It was established that the single per oral dose of 5 mg/kg weight of the natrium monoenzine salt causes a temporary lack of appetitie but no changes in the behavior and the general state of the animals. The use of a 10 and 30 mg/kg weight dose of the preparation led to death of the lambs on the 72nd-120th hour. The toxicity was clinically manifested by anurexia, arumination, ataxia, paresis, and paralysis of the limbs, tachicardia, taxipnea, hypothermia and showed down and weakened rumen movements. Erosive rumitis and abomasis, catharrhalhemorrhagis duodenitis, hemorrhages on the epicardis, hyperremia and parenchymal organ oedema, 3-4 times increased gall-bladder with numerous nodes having a sunken center on its walls were observed pathologo-anatomically, while microscopically blood vessel disturbances (hyperremia, hemorrhages and oedema) of the lungs, heart, spleen, endocrinal glands (thyroid, adrenal and hypophysis), the brain, and the leptomeninges, liver distrophy, distrophic nephrosis and necrotic holecystitis were obvious. Following a long term (30 days) application to the fodder in 10 and 50 g/t doses, monenzine-natrium does not have a negative effect on the behaviour, general condition, clinical and biochemical blood composition and the structural build up of the inner organs, but in the first 5-10 days of the treatment it causes loss of appetite. Additional specific investigations are needed to elucidate the effect of the preparation on body gain.
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PMID:[Acute and subchronic monensin toxicity for lambs]. 741 27

Cytokines are now recognized to play important roles in the physiology of the central nervous system (CNS) during health and disease. Tumor necrosis factor alpha (TNF-alpha) has been implicated in the pathogenesis of several human CNS disorders including multiple sclerosis, AIDS dementia, and cerebral malaria. We have generated transgenic mice that constitutively express a murine TNF-alpha transgene, under the control of its own promoter, specifically in their CNS and that spontaneously develop a chronic inflammatory demyelinating disease with 100% penetrance from around 3-8 weeks of age. High-level expression of the transgene was seen in neurons distributed throughout the brain. Disease is manifested by ataxia, seizures, and paresis and leads to early death. Histopathological analysis revealed infiltration of the meninges and CNS parenchyma by CD4+ and CD8+ T lymphocytes, widespread reactive astrocytosis and microgliosis, and focal demyelination. The direct action of TNF-alpha in the pathogenesis of this disease was confirmed by peripheral administration of a neutralizing anti-murine TNF-alpha antibody. This treatment completely prevented the development of neurological symptoms, T-cell infiltration into the CNS parenchyma, astrocytosis, and demyelination, and greatly reduced the severity of reactive microgliosis. These results demonstrate that overexpression of TNF-alpha in the CNS can cause abnormalities in nervous system structure and function. The disease induced in TNF-alpha transgenic mice shows clinical and histopathological features characteristic of inflammatory demyelinating CNS disorders in humans, and these mice represent a relevant in vivo model for their further study.
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PMID:Spontaneous inflammatory demyelinating disease in transgenic mice showing central nervous system-specific expression of tumor necrosis factor alpha. 747 82


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