Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0007758 (cerebellar ataxia)
 3,609 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A quantitative evaluation of cerebellar ataxia, with an ataxia score (total, static, kinetic) and the measurement of objective values relating to the major symptoms, was used in 21 patients with hereditary ataxias treated for 12 months with high doses (16 mg/kg/day) of d-l-5-HTP, l-5-HTP or the combination d-l-5-HTP (16 mg/kg/day)--benserazide (6 mg/kg/day). The data obtained from regular examination were processed by computer. The ataxia showed a significant regression at the 12th month, mainly in the static forms and speed of speech. l-5-HTP appeared to be more effective than d-l-5-HTP. Regression of the cerebellar ataxia was also observed in non-degenerative conditions such as multiple sclerosis and surgical lesion of the anterior lobe vermis, showing that 5-HTP was active on the cerebellar syndrome in general. The regression of the cerebellar ataxia was very slow in inherited diseases and continued for 2 or 4 months after the treatment stopped. A serotoninergic cerebellar control of movement is discussed.
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PMID:Regression of cerebellar syndrome with long-term administration of 5-HTP or the combination 5-HTP-benserazide. 633 64

18 patients with degenerative cerebellar ataxia were given for 12 months, high doses of D-L-5 Hydroxytryptophan (16 mg/kg/day) with a peripheral inhibitor of 5-HTP Decarboxylase. The ataxia was regularly evaluated with a semi-quantitative score and quantitative measurements, allowing a computerized processing of the data. A highly significant improvement of the static ataxia was observed at the 12th month, while adiadocokinesia, hypermetria and dysarthria were also influenced. These results could correspond to the presence of serotoninergic nerve terminals in the cerebellar cortex, the cerebellar deep nuclei and the inferior olivary complex. Moreover, the improvement of the ataxia continued for 3 months after treatment stopped, suggesting an effect distinct from the classical neuromediation phenomenon.
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PMID:[Regression of human cerebellar ataxia under long term administration of 5-hydroxytryptophan]. 678 64

A quantitative evaluation of cerebellar ataxia, with an ataxia score (total, static, kinetic) and the measurement of objective values related to the major symptoms, is proposed. 21 patients with heredo-ataxias were treated for 12 months with high doses (16 mg/kg/day) of D-L-5-HTP, L-5-HTP or the association D-L-5-HTP (16 mg/kg/day)-Benserazide(6 mg/kg/day). A computerized processing of the data obtained by regular examination was performed. The ataxia showed a significant regression at the 12th month, mainly in the static performances and in the speed of speech. L-5-HTP appeared to be more active than D-L-5-HTP. The regression of the cerebellar ataxia was also observed in non degenerative conditions such as multiple sclerosis and surgical injury of the anterior lobe vermis, showing that 5-HTP was active on the cerebellar syndrome in general. The regression of the cerebellar ataxia was very slow in inherited diseases and continued for 2 or 4 months after the treatment stopped. A serotoninergic cerebellar control of motricity is discussed.
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PMID:[Regression of the cerebellar syndrome under long-term administration of 5-HTP or the combination of 5-HTP and benserazide. 26 cases quantified and treated using computer methods]. 698 1

A review concerning the characteristics of the cerebellar serotoninergic system is presented. In rat, cat and oppossum, the perikarya of origin are located in the brain stem raphe nuclei and in other brainstem structures. The projections to the cerebellar layers and deep nuclei include synaptic connections, but also non synaptic terminals, especially in a diffuse cortical plexus. Serotoninergic receptors have been described: 5-HT1B in the molecular layer and 5-HT2 in the inferior olive. Serotonin exerts neurophysiological effects on several target cells, directly or indirectly, presynaptically or postsynaptically. A modulatory effect on Purkinje cells is well documented. In thiamine deprived animals, a specific serotoninergic cerebellar syndrome includes a selective degeneration of the serotoninergic cerebellar system, an increase of the 5-HIAA cerebellar values and an exaggerated serotoninergic turnover. In human heredoataxias (Friedreich's ataxia and cerebellar cortical atrophy), serotoninergic disturbances have been observed in the CSF, including low 5-HIAA values and an increased serotoninergic turnover. Therapeutic results have been obtained with L-5-HTP, a precursor of serotonin, in several conditions presenting cerebellar ataxia. L-5-HTP resistance of olivopontocerebellar atrophies may be explained by the destruction of serotonin-sensitive target cells, especially Purkinje cells.
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PMID:The cerebellar serotoninergic system and its possible involvement in cerebellar ataxia. 833 97