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BACKGROUND: At low doses, risperidone acts as a 5-HT2 antagonist. Preclinical data suggest 5-HT2 antagonists may enhance the action of serotonin. This report examines the clinical use of risperidone to augment selective serotonin reuptake inhibitor (SSRI) anti-depressants in patients who have not responded to SSRI therapy. METHOD: In 8 patients with major depressive disorder without psychotic features (DSM-IV) who had not responded to an SSRI, risperidone was added to the ongoing SSRI treatment. Hamilton Rating Scale for Depression scores were obtained before and after the addition of risperidone. RESULTS: These 8 patients remitted within 1 week of the addition of risperidone. Risperidone also appeared to have beneficial effects on sleep disturbance and sexual dysfunction. CONCLUSION: Risperidone may be a useful adjunct to SSRIs in the treatment of depression.

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BACKGROUND: Repetitive self-injurious behavior (SIB) is a dangerous and often treatment-refractory syndrome encountered frequently in clinical practice. The authors sought to determine if oral naltrexone could decrease SIB in a sample of adult psychiatric patients. METHOD: Seven female patients with SIB accompanied by analgesia and dysphoria reduction were administered oral naltrexone (50 mg/day) in an open-label trial. All patients demonstrated persistent and clinically significant SIB prior to receiving the drug. Mean follow-up period was 10.7 weeks. RESULTS: SIB in six of seven patients ceased entirely during naltrexone treatment. Two patients who discontinued naltrexone briefly experienced the rapid resumption of SIB, which again ceased after resumption of naltrexone therapy. One patient exhibited superficial cutting on two occasions while receiving naltrexone, a rate that reflected a significant reduction of SIB. CONCLUSION: These preliminary observations are consistent with the hypothesis that the endogenous opioid system is involved in cases of SIB that are accompanied by analgesia and dysphoria reduction. Additional placebo-controlled studies that explore the effectiveness of naltrexone in treating patients with this syndrome are warranted.

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To assess biologic risk factors in suicidal behavior accurately, it is necessary to distinguish prospective from retrospective design. The former studies are more likely to elicit information concerning possible risk factors in suicide, whereas the latter may be better indicators of biologic traits. In both types of investigations, measures taken close to the suicide attempt are more likely to reflect the biologic state of the individual at the time of the behavior. Although the abnormalities present in suicidal individuals are not entirely clear, most evidence to date suggests an overactivity of the hypothalamic-pituitary-adrenal axis and a dysregulation of both serotonin and adrenergic metabolism. These systems are interrelated. Both animal and human studies have established that a multivariate biologic approach is necessary to the understanding of the pathophysiology of suicide.

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To assess biologic risk factors in suicidal behavior accurately, it is necessary to distinguish prospective from retrospective designs. The former studies are more likely to elicit information concerning possible risk factors in suicide, whereas the latter may be better indicators of biologic traits. In both types of investigations, measures taken close to the suicide attempt are more likely to reflect the biologic state of the individual at the time of the behavior. Although the abnormalities present in suicidal individuals are not entirely clear, most evidence to date suggests an overactivity of the hypothalamic-pituitary-adrenal axis and a dysregulation of both serotonin and adrenergic metabolism. These systems are interrelated. Both animal and human studies have established that a multivariate biologic approach is necessary to the understanding of the pathophysiology of suicide.

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Urinary norepinephrine and epinephrine levels (microgram/day) were measured at two-week intervals during the course of hospitalization in the following patient groups: post-traumatic stress disorder (PTSD); major depressive disorder (MDD); bipolar I, manic (BP); paranoid schizophrenia (PS); and undifferentiated schizophrenia (US). The mean norepinephrine level during hospitalization was significantly higher in PTSD (76 +/- 10.4 micrograms/day) than in BP (60.6 +/- 8.4 micrograms/day), MDD (41.2 +/- 4.7 micrograms/day), PS (33.4 +/- 4.9 micrograms/day) and US (34.3 +/- 5.9 micrograms/day) groups, according to Duncan's multiple range test, (F(4,39) = 6.94, p less than 0.0003). The norepinephrine elevations in the PTSD group were sustained throughout hospitalization. The only other group to show mean levels in this range was the BP group in the first sample after hospital admission. This finding supports prior psychophysiological studies indicating increased sympathetic nervous system activity in PTSD patients. The mean epinephrine level during hospitalization was also significantly higher in PTSD (22.7 +/- 2.4 micrograms/day) than in MDD (13.6 +/- 1.7 micrograms/day), PS (14.7 +/- 2.4 micrograms/day), and US (18.9 +/- 1.8 micrograms/day), but not higher than in BP (21.5 +/- 2.7 micrograms/day). The relationship of epinephrine levels among diagnostic groups was sustained throughout hospitalization. It appears likely that the main underlying mechanisms for elevations of both hormones are psychological, but further work will be required to establish the exact nature of these mechanisms.

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Urinary free-cortisol levels (micrograms per day) were measured by radioimmunoassay at 2-week intervals during the course of hospitalization in the following patient groups: posttraumatic stress disorder (PTSD); major depressive disorder; bipolar I, manic; paranoid schizophrenia; and undifferentiated schizophrenia. The mean cortisol level during hospitalization was significantly lower in PTSD (33.3 +/- 3.2) than in major depressive disorder (49.6 +/- 5.9), bipolar I, manic (62.7 +/- 6.7), and undifferentiated schizophrenia (50.1 +/- 8.9), but was similar to that in paranoid schizophrenia (37.5 +/- 3.9). The same differences across groups are evident in the first sample following hospital admission. This finding of low, stable cortisol levels in PTSD patients is especially noteworthy, first because of the overt signs of anxiety and depression, which would usually be expected to accompany cortisol elevations, and second because of the concomitant chronic increase in sympathetic nervous system activity shown in prior psychophysiological studies of PTSD and reflected in marked and sustained urinary catecholamine elevations previously reported in our own PTSD sample. The findings suggest a possible role of defensive organization as a basis for the low, constricted cortisol levels in PTSD and paranoid schizophrenic patients. The data also suggest the possible usefulness of hormonal criteria as an adjunct to the clinical diagnosis of PTSD.

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Norepinephrine and epinephrine were measured serially in 24-hour urine collections from 99 male psychiatric inpatients with mixed diagnoses. The group was blindly divided into those with a previous history of at least one suicide attempt (N = 38) and those without such a history (N = 61). The ratio of norepinephrine-to-epinephrine levels was significantly lower in the group with a history of suicide attempts. The authors discuss the possibility that a low norepinephrine-to-epinephrine ratio is a risk factor for suicidal behavior.

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