Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0004134 (ataxia)
 15,886 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In addition to the well-known activities of TRH (stimulation of respiration, antidepressant action, increase of motility, antishock action, therapeutic effects against ataxia, and so forth), some new properties were established. TRH was found (1) to stimulate the contractility of lymph vessels in ultra-low doses and to be useful in the treatment of acute pancreatitis; (2) to normalize cerebral circulation in rats and neonates after asphyxia; (3) to improve the electrophysiological parameters of the retina and pigmented epithelium in rats and man, to exert a long-term positive influence on the health status of patients suffering from senile retinal macular dystrophy; (4) to potentiate the analgesic effect of low doses of morphine in a definite range of doses (analog PR-546). It is of paramount importance that most of the indicated activities of TRH may hold promise for clinical application.
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PMID:[Thyroliberin: new physiological effects and prospects of clinical use]. 138 90

Acute autonomic and sensory neuropathy (AASN), one subtype of acute pandysautonomia, in which dorsal root ganglia and autonomic ganglia are involved is uncommon. Little is so far known on central nervous system involvement in AASN. In the present paper we described a rare case of AASN associated with the central nervous system manifestations such as galactorrhea-amenorrhea syndrome and intractable anorexia. A 30-year-old woman rapidly developed burning pain and numbness in her arms and legs as well as orthostatic syncope. She had severe anorexia and no no menstruation from onset. On physical examination, she was emaciated. There was marked orthostatic hypotension with tachycardia. Skin was dry. Moderate galactorrhea was detected. Neurological examination showed prominent paresthesia and dullness of superficial sensation, predominantly to pinprick and thermal stimuli, segmentally over the neck, occipital scalp, and extremities. Deep sensation was intact. She had no weakness or ataxia. Deep tendon reflexes were almost normal. NCV and SEP were normal, while EEG was abnormal. Sural nerve biopsy demonstrated axonal degeneration with the loss of myelinated, predominantly in small-caliber fibers, and unmyelinated fibers. The levels of HVA and MHPG in CSF were decreased. The autonomic nervous function tests revealed postganglionic dysfunction. alpha-adrenergic system was predominantly impaired, while beta-adrenergic system was relatively preserved. The endocrinological studies demonstrated mild or moderate elevation of PRL basal value and hyper-response of PRL and LH for TRH and LH-RH loading test, which suggested disorder of the hypothalamo-hypophysial system. Cranial MRI showed moderate dilatation of the 3rd ventricle.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Acute autonomic and sensory neuropathy associated with galactorrhea-amenorrhea syndrome and intractable anorexia]. 255 96

The Rolling mouse Nagoya (RMN), Staggerer, Weaver and Reeler, all of which show hereditary ataxia, were intraperitoneally injected with 25 mg/kg of thyrotropin-releasing hormone (TRH-T) or physiological saline, and changes in the motions of these animals were observed by an Animex II and an open field method. All four strains of mice with ataxia showed improvement of ataxia and an increase in the motion volume, but these changes were not necessarily consistent in degree. Improvement of ataxia was most marked in the RMN and the Staggerer, moderate in the Weaver and slight in the Reeler, which showed enhanced tremor. The relationship between the competence of transmitting information in the cerebellum and improvement of ataxia by the injection of TRH-T aroused our interest.
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PMID:The pharmacological effect of thyrotropin-releasing hormone on ataxic mutant mice. 308 1

The distribution of TRH receptors in the membrane fraction of the CNS in ataxic mutant mice (C3Hf/Nem-rol and C57BL/6j-tg) was studied. TRH binding sites in cerebellum and frontal lobe of the ataxic form and the non-ataxic heterozygotes of Rolling Mouse Nagoya were decreased in comparison with the controls, whereas those in the spinal cord of Rolling Mouse Nagoya and cerebellum of Tottering Mouse were increased in the ataxic mice over the controls. Kinetic studies were performed on cerebrum and cerebellum of the different ataxic mutant mice. Such species differences in the distribution of the TRH receptors have to be considered in the action of TRH in individual ataxia cases.
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PMID:Distribution and characterization of the TRH receptors in the CNS of ataxic mutant mouse. 608 74

The effects of thyrotropin releasing hormone tartrate (TRH-T) on the behavior of cytosine arabinoside (Ara-C) induced ataxic mice were studied. The ataxic mice were prepared by injecting 50 mg/kg/day subcutaneously on the 2nd, 3rd and 4th postnatal days. Spontaneous motor activities were measured with a movement spectrum analyzer (ANIMEX-2) and the degree of ataxic gait determined by an open-field study. Cerebella from these animals were subjected to histopathologic examination at 4, 8 and 12 weeks of age. Ataxic gait became improved moderately and spontaneous motor activities increased slightly following administration of TRH-T. The effects of TRH-T on ataxia and spontaneous motility in the Ara-C injected mice varied with the age, and resembled those seen in weaver mice but not those in the Rolling mouse Nagoya. The results also suggest that the effects of TRH-T on the behavior of ataxic mice correlate with the extent of pathologic changes evoked in their cerebella.
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PMID:[Studies on the behavioral pharmacology of TRH-T in cytosine arabinoside-induced ataxic mice: a comparison with genetically ataxic mice]. 640 42

Rolling mouse Nagoya (RMN), an ataxia mutant mouse, is adequate to checking up the efficacy of drugs on the ataxic movement disorders. The effects of some drugs on the ataxia of RMN were investigated by open field study. The drugs administered to RMN were as follows: TRH, FLA-63, DL-threo-DOPS, phenoxybenzamine and propranolol. Ataxic gait of RMN were remarkably improved by TRH, but remained unchanged by other drugs. The pretreatments with FLA-63, DOPS and phenoxybenzamine were not influenced to the antiataxic effects of TRH, while the pretreatment with propranolol increased the antiataxic effect of TRH in RMN. These results suggest that mechanism of the improvement of ataxic gait by TRH may not be sufficiently explained through only changing norepinephrine metabolism.
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PMID:[Ataxia in rolling mouse Nagoya and the norepinephrine system--a psychopharmacological study]. 682 Dec 92

The effects of TA-0910 (1-methyl-(S)-4,5-dihydroorotyl-L-histidyl-L- prolinamide), a new thyrotropin-releasing hormone (TRH: L-pyroglutamyl-L-histidyl-L-prolinamide) analog, on ataxia were compared with those of TRH given by oral administration. The ataxic models used were the Rolling mouse Nagoya (RMN) showing genetic dysfunction of the cerebellum and striatum, rats with chemical degeneration of the inferior olive induced by 3-acetylpyridine (3-AP, 40 mg/kg, i.p.) and rats with a lesion of the thoracic spinal cord induced by mechanical compression. TA-0910 (1, 3, 10 mg/kg per day) clearly showed ameliorating effects on all these ataxic models. The dose-dependent effect of TA-0910 (10 mg/kg per day) on the gait of RMN was sustained until 2 weeks after the end of its 2-week administration. TRH (100, 300 mg/kg per day) also showed ameliorating effects on ataxia in RMN and 3-AP-treated rats. The ameliorating action of TA-0910 on ataxia was 100-300 times more potent than that of TRH.
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PMID:Effects of TA-0910, a novel orally active thyrotropin-releasing hormone analog, on the gait of ataxic animals. 776 82

A two-dimensional analysis of cerebellar ataxia was performed by using video-computer motion measurement system, PEAK, which has been developed and produced by U.S.-Japan-Chatanuuga Co., Ltd. The analyses of gait, heel-knee tapping test, finger-nose test and heel-knee test were made on 23 cases of spinocerebellar degeneration (SCD) as compared with the 9 healthy. The cases of SCD included olivopontocerebellar atrophy (OPCA), hereditary OPCA, late cortical cerebellar atrophy (LCCA), hereditary LCCA, Joseph disease and dentatorubropallidoluysian atrophy. The results of analyses by the computer demonstrated slow movement of gait, decrease of flexion angle at knee joint at the swing phase of the gait. Heel-knee test revealed irregular, dysrhythmic movements of heel. The interval of the tapping showed great variance and its standard deviation of the average was found to be increased. And the average values were so increased as to implement slow movements of the heel. These above-mentioned findings were also observed in the tests of finger-nose and heel-knee as well. Oral intake of TA0910, TRH derivative, which was synthesized and produced by Tanabe pharmaceutical Co. Ltd. in Japan improved slow movements of the tests. Disorders of range, direction, and rate of the movements, as usually observed in the patient of ataxia, could be well recognized to be alleviated following the administration and the effects were statistically significant. Application of the computerized instrument to analysis of ataxia would be very beneficial in the neurological bed-side clinical examination.
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PMID:[A refined evaluation of cerebellar ataxia and its application to treatment of spinocerebellar degeneration]. 817 29

Degenerative spinocerebellar ataxia has a rare association with hypogonadotropic hypogonadism. In this report we present the results of the detailed endocrine evaluation and magnetic resonance imaging in one such patient. A 20-year-old male with progressive cerebellar ataxia, hypogonadism, and short stature was investigated. Basal testing revealed hypogonadotropic hypogonadism (LH < 5 mU/L, FSH < 5 mU/L, testosterone 2.5 nM/L). There was no rise in LH after stimulation with LHRH, peak LH level being < 5 mU/L. Insulin hypoglycemia testing was consistent with GH deficiency, with peak GH being 3.2 mU/L. On TRH stimulation, there was no significant rise in prolactin, though the TSH response was normal. Magnetic resonance imaging revealed cerebellar atrophy. The anterior pituitary was atrophic, with a height of 1.4 mm. The posterior pituitary and the pituitary stalk were normal in size and position. This patient with degenerative spinocerebellar ataxia had multiple pituitary hormone deficiencies. The results of our endocrine evaluation and MR imaging lead us to believe that these deficits may result from a lesion at the level of the pituitary gland.
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PMID:Multiple pituitary hormone deficiencies in a patient with spinocerebellar ataxia: magnetic resonance imaging and hormonal studies. 825 53

It is often difficult to estimate slight alterations in the severity of ataxia by bed-side neurological examinations. We analyzed the heel-knee tapping test, which has often been used as a standard bed-side examination to check incoordination in lower limbs, using a new motion measurement system "video/computer motion measurement system". We studied 9 normal controls and 21 patients with spinocerebellar degenerations (SCD). In patients with SCD, the up-and-down motion range of the heel was variable and the heel moved in the anterior-and-posterior direction, because of knee sways during the test. Following oral administration of TRH analogue, TA-0910, above-mentioned findings were clearly improved. Analysis of spatial and time elements of the knee joint demonstrated quantitative improvement. Therefore, an effect of TA-0910 on incoordination of the lower limbs could be proved objectively by a computer motion measurement system.
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PMID:[A study of heel-knee tapping test in cerebellar ataxia by a motion measurement system]. 877 95


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