Rationale : Prior studies had suggested (a) that a lessened ability to clear ingested forms of the large neutral amino acid (LNAA), phenylalanine (Phe), was associated with having tardive dyskinesia (TD), and (b) that greater availability of a group of LNAA, the branched chain amino acids (BCAA), concomitant with the lower availability of Phe to the brain are associated with a decrease in TD symptoms. The present study was then conducted to test whether increasing the daily intake of the BCAA would decrease the symptoms of TD. Methods : A 2-week trial of a BCAA medical food administered three times a day was conducted in nine men with long neuroleptic treatment histories. Frequency counts of TD movements were collected by videotape throughout the trial and these tapes were analyzed in blind random sequence for both patient and time for TD symptom level changes subsequent to completion of the trial. Plasma levels of the LNAA were also collected throughout the trial. Results : A statistically signiÞcant decrease in the level of TD symptoms was observed for the sample. The symptom changes were also clinically signiÞcant in that six of the nine subjects had symptom decreases of at least 58%, with all subjects having a decrease of at least 38%. BCAA administration increased plasma BCAA concentrations and BCAA / LNAA ratios and decreased plasma Phe concentrations and the Phe / LNAA ratio. Analyses indicated a strong signiÞcant correlation between the percent increase in the plasma BCAA values at the Þrst administration and the percent improvement in TD over the trial in eight of the nine subjects. Conclusions : The BCAA show promise as a treatment for TD. The decrease in TD symptoms seen in the trial may have been modulated by the BCAA treatmentinduced increased availability of the BCAA and decreased availability of Phe to the brain.
One week of light treatment was given to 17 patients with seasonal aflective disorder, close to their times of episode onset in the fall or early winter. They were then withdrawn@om treatment f o r up to 8 weeks while symptom were monitored weekly. The clinical response to light was maintained for variable durations after termination of treatment, but symptoms ultimately returned f o r all srcbjects. Relapses-as dej?ned by criterion scores on the Beck Depression Inventory, Hamilton Rating Scale f o r Depression, supplementary Atypical Symptom Scale, and combined SIGH-SAD scale--occurred across 1-8 weeks of withdrawal. The duration of improvement during withdrawal was correlated with the date of episode onset: initiation of treatment later in the faWwinter season led to longer delays to relapse, and patients with longer episode durations (and earlier episode onset) tended to show accelerated relapse. We were unable to confirm the Fndings of Meesters et al. (7 Aflect Dis 23:75-79, 1991; 3 Aflect Dis 29:4148, 1993b), who concluded that 5 days of light therapy early in the episode succeeded in preventing the development offilly syndromal depression as well as relapse during withdrawal throughout the winter. Depression 2:20-31 (1 994). 0 1994 Wiley-Liss, Inc.
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