Depression in patients with schizophrenia during an acute psychotic episode.

There is disagreement about whether depressive symptoms in schizophrenia are part of the basic disease process, or whether they represent adverse effects of treatment with antipsychotic medications. In a sample of initially antipsychotic drug-free acutely hospitalized patients with schizophrenia (N = 104), we measured change in depressive symptoms after 4 weeks of treatment. We also examined the relationship of changes in depressive symptoms to changes in positive and negative schizophrenic symptoms. Depressive symptoms improved after 4 weeks of antipsychotic medication treatment, and their improvement corresponded with improvement in both positive and negative schizophrenic symptoms. These results suggest that depressive symptoms in schizophrenia are related to the disease process itself, at least during acute exacerbations of schizophrenia. Depressive symptoms may be responsive to antipsychotic medications directly or as a secondary response to improvement in positive and negative symptoms.

Rapid-cycling bipolar disorder. An overview of research and clinical experience.

Although many studies of RCBD have been reported over the last 2 decades, knowledge remains limited. Higher incidence in women is the sole clearly replicated finding in most studies. This finding might be mediated by cyclothymia, a temperament that is of higher prevalence in women and that might be considered as a normal variant of RC. Many questions remain unanswered. Review of putative risk factors, such as hypothyroidism and treatment with antidepressants, provides no conclusive answers. There is clinical evidence to implicate both factors. In principle, the thyroid connection can be approached rationally, yet there seems to be no relationship between thyroid status and response to thyroid augmentation. For this reason and given the potential risks of long-term thyroid use, this strategy should not be the first one to be tried in RC. Cumulatively, naturalistic studies over the past 30 years have strongly implicated antidepressants in switching and cycle acceleration, yet the double-blind, controlled, prospective studies that are needed to provide definitive answers are unlikely to be conducted for ethical reasons discussed in this article. Bipolar family history of RC probands appears indistinguishable from non-RC probands, indicating that most likely RCBD does not breed true. Although RC seems to be more lithium resistant with less likelihood of being symptom-free after 2 to 5 years of follow-up, many of these patients nonetheless have resolution of the RC course. There is no marked difference in suicide rates. An association of RC with bipolar type II, D-M-I pattern and those who switch into mania or hypomania on antidepressants is a provocative possibility: Antidepressants might introduce RC by first inducing a switch during a depressive episode, creating a D-M-I pattern, a pattern that is poorly responsive to lithium, which eventually degenerates into RC. Again, this sequence might be mediated by the high prevalence of cyclothymia in bipolar II patients. Thus, data from phenomenology, family history, and long-term outcome do not support RC as a separate entity. RC appears to be a temporary complicated phase in the illness, not a stable feature. This was noted by Kraepelin: I think I am convinced that that kind of classification must of necessity wreck on the irregularity of the disease. The kind and duration of the attacks and the intervals by no means remain the same in the individual case but may frequently change, so that the case must be reckoned always to new forms. Data by Gottschalk et al testify to the chaotic mood swings of contemporary bipolar disorder. Moreover RC is seen in other medical diseases, such as epilepsy, in which patients have phases of increase in frequency of episodes (seizures) that become refractory to treatment. Further longitudinal prospective studies are required to understand the complexity of this intriguing phenomenon and to provide better treatments. Algorithms deriving from tertiary research or university-based clinical experience may not generalize to RC or otherwise treatment-resistant bipolar patients seen in more routine practice. Illness severity in RCBD generally precludes double-blind controlled investigations. Meanwhile, clinicians may rely on discontinuing antidepressants, maintaining patients on combined mood stabilizers--of which valproate is probably the most useful--and making judicious use of atypical neuroleptics. Benzodiazepines and alcohol (which produce withdrawal), caffeine, stimulants, exposure to bright light, and sleep deprivation during excited phases should be avoided. Thyroid and nimodipine augmentation can be considered in those with the most malignant course. These are patients who need the maximal support that their psychiatrist can provide them. Office visits must be arranged as the last appointment of the day.

Severe imipramine-induced myoclonus in a patient with psychotic bipolar depression, catatonia, and schizencephaly.

Mild myoclonus is reasonably common with various cyclic antidepressants. However, antidepressants rarely cause severe myoclonus, and no risk or predisposing factors have been reported in the literature. We report a case of exceptionally severe myoclonus developing at therapeutic doses and modest serum levels of imipramine. The patient went on to experience dystonia and catatonia. Both of these were in typical settings (after haloperidol and with psychotic bipolar depression, respectively) and responded to typical treatment. On further investigation, the patient was found to have left-sided schizencephaly and a corresponding history of very mild developmental delay. We suggest that the onset of one movement disorder after drug therapy (eg, myoclonus) may predict the development of other movement disorders (e.g., catatonia). We further propose that severe tricyclic-induced myoclonus should prompt the physician to rule out a coexisting structural lesion of the central nervous system.

Lorazepam treatment of psychogenic catatonia: an update.

Six papers have reported the efficacy of lorazepam in alleviating catatonic symptoms that have psychogenic causes. The authors report five new cases of catatonia; three patients responded favorably and two failed to respond to lorazepam. Investigation of the nonresponders revealed the presence of pernicious anemia in one and postpartum psychosis in the other. These findings demonstrate that lorazepam has an important role in the treatment of catatonic symptoms. Its effects appear to be specific for psychogenic catatonic states and for conditions in which biogenic amines, specifically dopamine and gamma-aminobutyric acid, play a part. The authors stress intramuscular administration of lorazepam for patients in catatonic states because this route provides the psychiatrist with immediate results that assist with early diagnosis and treatment.