These are 5-HT2C, linked to weight gain, 5-HT2A, linked to its antipsychotic action and relief of some of the extrapyramidal side effects experienced with the typical neuroleptics.It has been found that D-amino acid oxidase, the enzyme that catalyses the breakdown of D-amino acids (e.g. D-alanine and D-serine — the neurotransmitters) is inhibited by risperidone.Risperidone acts on the following receptors:
Dopamine receptors: This drug is an antagonist of the D1 (D1, and D5) as well as the D2 family (D2, D3 and D4) receptors, with 70-fold selectivity for the D2 family. It has "tight binding" properties, which means it has a long half-life. Like other antipsychotics, risperidone blocks the mesolimbic pathway, the prefrontal cortex limbic pathway, and the tuberoinfundibular pathway in the central nervous system. Risperidone may induce extrapyramidal side effects, akathisia and tremors, associated with diminished dopaminergic activity in the striatum. It can also cause sexual side effects, galactorrhoea, infertility, gynecomastia and, with chronic use reduced bone mineral density leading to breaks, all of which are associated with increased prolactin secretion.Serotonin receptors: Its action at these receptors results in a relatively lesser tendency to cause extrapyramidal side effects, like the reference substance clozapine.Alpha α1 adrenergic receptors: This action accounts for the orthostatic hypotensive effects and perhaps some of the sedating effects of risperidone.Alpha α2 adrenergic receptors: Risperidones action at these receptors may cause greater positive, negative, affective, and cognitive symptom control.Histamine H1 receptors: effects on these receptors account for its sedation and reduction in vigilance.
Other features that may be seen on muscle biopsy include variability in fibre size, increase in internal and centralized nuclei, type 1 fibre hypotrophy with normally sized type 2 fibres, increased glycogen storage and variable vacuoles on light microscopy
The diagnosis is confirmed by sequencing of the EPG5. Differential diagnosis
This includes ataxia–telangiectasia, Chédiak–Higashi syndrome, DiGeorge syndrome, Griscelli syndrome and Marinesco–Sjögren syndrome. Treatment
There is no known curative treatment presently. Hearing aids and cataract surgery may be of use. Control of seizures, heart failure, and treatment of infection is essential. Tube feeding may be needed. Eponym
Vici syndrome was first described by Carlo Dionisi-Vici et al. (Rome, Italy) in an article from 1988 about two brothers with a previously unreported disorder. Since then, a few articles have reported the same disorder, which subsequently obtained the name Vici syndrome.About 10 years later, del Campo et al.