This is the first case report of a patient who received long-term (69-month) adjunctive vagus nerve stimulation (VNS) therapy for treatment-resistant depression (TRD) and reached VNS battery end-of-service (EOS).The patient is a 41-year-old female with depression who entered a study of adjunctive VNS therapy for TRD. Her Hamilton Rating Scale for Depression (HAM-D) scores dropped from a mean of 33.5 (pre-implantation baseline period) to 16 at the end of the 12-week acute-phase treatment period, and then fluctuated from <7 (normal range) to scores in the moderately depressed range (∼20) during long-term follow-up. Three and one-half years after VNS implantation, the patient's HAM-D scores began to increase from a score of 18 to a peak score of 27 ∼ 16 months later (5-years post-implantation). The patient subsequently reported that she could no longer feel stimulation from the device and device interrogation 2 weeks later indicated battery EOS. The patient was hospitalized due to worsened depression, the pulse generator was replaced, and medication adjusted. HAM-D scores through the subsequent 9 months of followup returned to a pattern of fluctuations within the range noted during the long-term follow-up period prior to VNS battery EOS.

This article presents charts from The American Psychiatric Association Practice Guideline for the Assessment and Treatment of Patients with Suicidal Behaviors, part of the Practice Guidelines for the Treatment of Psychiatric Disorders Compendium, and a summary of the assessment information in a format that can be used in routine clinical practice. Four steps in the assessment process are presented: the use of a thorough psychiatric examination to obtain information about the patient's current presentation, history, diagnosis, and to recognize suicide risk factors therein; the necessity of asking very specific questions about suicidal ideation, intent, plans, and attempts; the process of making an estimation of the patient's level of suicide risk is explained; and the use of modifiable risk and protective factors as the basis for treatment planning is demonstrated. Case reports are used to clarify use of each step in this process.

Efforts to identify clinical risk factors for complete suicide through the follow-up of depressed patients have yielded relatively few robust predictors. Those identified by at least three studies are (in order of decreasing frequency) suicidal plans/attempts, male sex, being single or living alone, inpatient status, and hopelessness. Because the best established of these predictors has only modest sensitivity and specificity, the need for other robust tools is clear. A rich body of research has identified two biological risk factors for suicide in depressive disorder: hypothalamicpituitary-adrenal axis hyperactivity and deficits in serotonin function. Moreover, there is now considerable evidence that the dexamethasone suppression test and measures of serum cholesterol concentrations, respectively, may provide a clinically useful reflection of these two mechanisms. Observations that these measures appear to be additive, both with each other and with other clinical risk factors, indicate that a substantial improvement in the clinician's ability to assess suicide risk is possible.