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Valley Psychiatry Article

Risperdal Augmentation of Elderly Treatment Resistant Depression

A study in the January edition of the American Journal of Geriatric Psychiatry suggests that Risperdal could be an effective augmentation strategy for treatment resistant depression in the elderly.

The authors studied the effect of Risperdal augmentation of Celexa on depression relapse prevention in a population aged 55 to 85 years old. They looked at two groups of patients who failed at least one antidepressant trial, including Celexa alone, but responded to augmentation of Celexa with Risperdal for 4-6 weeks. The first group continued with Risperdal augmentation for a further 24 weeks while in the second group placebo replaced Risperdal.

The results were promising. The mean amount of time until depression relapse in the group that continued for 24 weeks with Risperdal augmentation was 142 days while in the group that received placebo it was only 35 days. Further, the relapse rate in the Risperdal plus Celexa group was 53% while in the placebo group it went up to 68%.

The study was limited in some ways though. Although the difference in the time to relapse was seen a clinically significant (142 days versus 35 days) it was not statistically significant, likely because of the relatively small number of subjects. Only one third of the study participants were older than 65 years and patients with dementia were excluded from the study.

Yet the study did include patients with a variety of medical illnesses and on multiple classes of medications. 62 of the 63 patients who entered the maintenance part of the study had a comorbid disease, including musculoskeletal, cardiovascular, neurologic, and gastrointestinal. These patients were on various medications including proton pump inhibitors, ace inhibitors, sulfonamides, statins, corticosteroids, and thyroid hormones.

The authors felt their study suggests that Risperdal augmentation was well tolerated and could be an effective treatment of drug-resistant depression in older patients. They believe this positive effect, which has been seen in other studies of depression augmentation with atypical antipsychotics, was mediated through the monoaminergic neurotransmitter systems associated with depression. It is thought that atypical antipsychotics can increase noradrenergic, serotonergic, and dopaminergic activity.

Risperdal augmentation was not accompanied by tardive dyskinesia, extrapyramidal signs (such as rigidity and tremor), or changes in body weight. However the study duration was too short do derive any conclusion regarding long-term safety.

Valley Psychiatry Article