Treatment of cerebellar ataxia with buspirone: a double-blind study

@article{Trouillas1996TreatmentOC,
  title={Treatment of cerebellar ataxia with buspirone: a double-blind study},
  author={Paul Trouillas and Jing Xie and Patrice Adeleine},
  journal={The Lancet},
  year={1996},
  volume={348}
}

Topics from this paper

Idiopathic Late-Onset Cerebellar Ataxia with Phenytoin: A Case Report
TLDR
A case of a 30-year-old male patient who had chief complaints of ataxia, giddiness and vomiting and had past medical history of epilepsy for which he was adherent to phenytoin from past four years is reported.
Comprehensive systematic review summary: Treatment of cerebellar motor dysfunction and ataxia
TLDR
Evidence regarding ataxia treatment is reviewed according to American Academy of Neurology methodology and data are insufficient to support or refute the use of numerous agents.
Treatment Options in Degenerative Cerebellar Ataxia: A Systematic Review
The etiology of cerebellar ataxia (CA) is heterogeneous and includes easily identified and often reversible causes (i.e., drug toxicity and vitamin B12 deficiency) as well as irreversible
5-HT2A receptor-mediated excitation on cerebellar fastigial nucleus neurons and promotion of motor behaviors in rats
TLDR
It is shown that only 5-HT2A receptors among the 5- HT2 receptor subfamily are expressed and localized in the rat cerebellar fastigial nucleus (FN), one of the ultimate outputs of the spinocerebellum precisely regulating trunk and limb movements.
Neurochemistry and Neuropharmacology of the Cerebellar Ataxias
The predominant (though not exclusive) reference to degenerative ataxias is due to the fact that the specificity of the affected cell populations should allow anticipation of more or less specific
Buspirone and serotonin in spinocerebellar ataxia
Use of fluoxetine for treatment of Machado‐Joseph disease: an open‐label study
Context – Machado‐Joseph Disease (MJD/SCA3) is an autosomal dominant spinocerebellar degeneration that evolves to disability and death. Experimental data have shown that serotonin is an important
...
1
2
...

References

SHOWING 1-6 OF 6 REFERENCES
Autoantibodies to glutamate decarboxylase in a patient with cerebellar cortical atrophy, peripheral neuropathy, and slow eye movements.
TLDR
Serum and cerebrospinal fluid samples taken from one patient with sporadic cortical cerebellar atrophy associated with peripheral neuropathy and slow eye movements contained anti-glutamate decarboxylase autoantibodies, which suggest a participation of autoimmunity in the pathogenesis of some cases of sporadic Cerebellar cortical atrophy.
Use of buspirone for treatment of cerebellar ataxia. An open-label study.
TLDR
Nine patients with mild or moderate cerebellar dysfunction who completed the study showed significant improvement in clinical and self-assessment ratings, but not in a motor performance test, posturography, State-Trait Anxiety Inventory, and Beck Depression Inventory, suggesting buspirone may be effective in treating mild to moderate Cerebellar ataxia.
[Effect of buspirone, a serotonergic 5-HT-1A agonist in cerebellar ataxia: a pilot study. Preliminary communication].
TLDR
Preliminary data might confirm a link between cerebellar ataxia and the metabolism of serotonin, as suggested by the proposed serotonergic hypothesis.
Serotonin, the cerebellum, and ataxia
Raphe organization of cerebellar monaminergic systems morphogenesis of serotonergic neurons serotonergic receptors in cerebellum and inferior olive neurophysiology of cerebellar serotonergic
Improvement of cerebellar ataxia with levorotatory form of 5-hydroxytryptophan. A double-blind study with quantified data processing.
TLDR
The levorotatory form of 5-hydroxytryptophan significantly improved the ataxia score and significantly modified the time of standing upright, the spread of feet, the speed of walking, speaking, and writing.
Indoleamine neurons and their processes in the normal rat brain and in chronic diet‐induced thiamine deficiency demonstrated by uptake of 3H‐Serotonin
TLDR
Whether changes in the brains of normal, pair‐fed control, and thiamine deficient rats are disturbances in the ability of certain indoleamine neurons to take up and retain 3H‐5HT or true neuronal degeneration is unresolved.