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Suicide is a serious public health problem in the US, yet its neurobiological underpinnings are poorly understood. Suicide is highly correlated with depressive symptoms, and considerable evidence suggests that depression is associated with a relative deficiency in serotonergic neurotransmission. Serotonergic circuits also mediate impulsivity, a trait obviously relevant to suicide. These findings, taken together, suggest that alterations in the serotonergic system might contribute to suicidal behavior, serving as an impetus for researchers to scrutinize the serotonin transporter (SERT) as a potential substrate for the pathophysiology of suicide. Using post-mortem brain tissue, platelets, and DNA from suicide completers and attempters have not provided unequivocal evidence for a pre-eminent role for the SERT in the pathophysiology of suicide. This paper provides a review of several studies that have evaluated the role of the SERT in the pathophysiology of suicide.

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The authors developed a comprehensive plan focusing on the early identification and management of problematic behaviors in an effort to reduce seclusion and restraint in a psychiatric emergency service and to increase adherence to hospital standards for its use. Hospital data for nine months before and nine months after the implementation of the plan were retrospectively reviewed. Two key factors that were believed to increase the likelihood of episodes of seclusion and restraint were ineffectual management of problematic behavior and inadequate monitoring. The plan, when instituted, was associated with a 39 percent reduction of instances of seclusion and restraint. Compliance with hospital standards increased to 100 percent.