Several different neurotransmitters, such as serotonin, g-aminobutyric acid (GABA), and glycine, have been implicated in myoclonus; however, myoclonus and other neurologic features of OMS are unlikely to be due to single neurotransmitters. Steroids (adrenocorticotrophic hormone and pred-nisone appear to be most effective in restoring neurological function but have multiple trophic effects on brain (Pranzatelli 1994). Antiepileptic drugs and an array of neuroceptor-active drugs are not effective in treating myoclonus or opsoclonus (Pranzatelli 1992). A subgroup of children with OMS has low CSF concentrations of the serotonin metabolite 5-hydrox-yindoleacetic acid (5-HIAA) and the dopamine metabolite homovanillic acid (HVA), but treatment with ACTH may further lower 5-HIAA (Pranzatelli et al. 1998a). It has been speculated that serotonin receptors which are found in neuroblastoma (Pranza-telli 1992), may be one target of immunologic injury. Mood problems and obsessive-compulsive disorders in OMS could relate to serotonin also; however, neu-roblastoma is replete with other neurotransmitter receptors as well. The level of free choline in the CSF has not been found to be different in OMS patients than in controls (Pranzatelli et al. 1998b).

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