Pharmacogenomics in Psychiatric Practice.

Pharmacogenomic testing in psychiatry is becoming an established clinical procedure. Several vendors provide clinical interpretation of combinatorial pharmacogenomic testing of gene variants that have documented predictive implications regarding either pharmacologic response or adverse effects in depression and other psychiatric conditions. Such gene profiles have demonstrated improvements in outcome in depression, and reduction of cost of care of patients with inadequate clinical response. Additionally, several new gene variants are being studied to predict specific response in individuals. Many of these genes have demonstrated a role in the pathophysiology of depression or specific depressive symptoms. This article reviews the current state-of-the-art application of psychiatric pharmacogenomics.

Cranial electrotherapy stimulation for the treatment of chronically symptomatic bipolar patients.

OBJECTIVE: The aim of this study was to determine if cranial electrotherapy stimulation (CES) is beneficial in chronically symptomatic bipolar (CSBP) subjects. METHODS: A retrospective chart review of all consecutive CSBP subjects who were prescribed CES collected demographic and clinical information. RESULTS: The Clinical Global Impression improved significantly [mean (SD), 2.7 (0.6) at baseline vs 2.0 (0.0), t = 0, P < 0.001], but mood symptoms change minimally. There were very few adverse effects of CES. CONCLUSIONS: Patients with CSBP continue to experience symptoms with CES but also are modestly improved.

Sleep disturbances in euthymic bipolar patients.

BACKGROUND: Sleep disturbance has been implicated in both prodromal and syndromal phases of bipolar illness. METHODS: Charts of bipolar disorder (BD) patients who had been euthymic for at least 2 months were reviewed for mood symptoms, Clinical Global Impression scores, Global Assessment of Functioning scores, and sleep. RESULTS: Among 116 patients, 10 never achieved a euthymic interval of 2 months' duration. Among the remaining 106 euthymic patients, 59 (55.6%) had BD I, 23 (21.7%) had BD II, and 24 (22.8%) had BD not otherwise specified (NOS). The mean age was 43.3±SD 14.6, and 35% were male. A total of 25 patients (23.6%) had a clinically significant ongoing sleep disturbance (27.1% of those with BD I, 21.7% of those with BD II, and 16.6% of those with BD NOS). Of 16 patients for whom a sleep description was available, 25% had difficulty falling asleep, 81.25% had middle insomnia (2 patients experienced both), and none had early morning awakening. Eleven patients (10.4%) received sleep aids, and 33 (31.1%) received sedating antipsychotics (3 patients received both). CONCLUSIONS: Sleeping aids and sedating antipsychotics can potentially disguise an underlying sleep disturbance. Thus, it is possible that study patients taking these medications (n = 58; 54.7%) suffer from a sleep disturbance that is being adequately or inadequately treated.

Current and emerging therapies for the management of bipolar disorders.

Bipolar disorder is a complex condition to treat because agents that may be effective for a specific phase may not be effective for other phases, or may even worsen the overall course of the illness. Over the last decade there has been an increase in research activity in the treatment of bipolar illness. There are now several agents that are well established for the treatment of acute mania (lithium, divalproex, carbamazepine, nearly all antipsychotics), acute bipolar depression (lamotrigine, quetiapine, olanzapine/fluoxetine combination), and relapse prevention (lithium, lamotrigine, divalproex, most second generation antipsychotics). There are also novel treatments that are being studied for all three phases. These include eslicarbazepine, cariprazine, MEM-1003, memantine, tamoxifen and pentazocine for acute mania; pramipexole, modafinil, armodafinil, divalproex, lurasidone, agomelatine, cariprazine, lisedexamfetamine, riluzole, RG-2417, bifeprunox, ropinirole, GSK1014802, and magnetic stimulation for bipolar depression; and asenapine, lurasidone, and cariprazine for relapse prevention. Additionally, there are accumulating data that antidepressants, particularly serotoninergic ones, are not particularly effective in acute bipolar depression and may worsen the course of the illness.

Tardive dysphoria: antidepressant-induced chronic depression.

OBJECTIVES: A significant number of depressed individuals experience inadequate benefit from long-term antidepressant use. This paper investigates the hypothesis that in some individuals persistent use of antidepressants may be prodepressant. METHODS: Literature regarding the effect of long-term use of antidepressants was reviewed by searching PubMed and Ovid data bases with terms: antidepressant tachyphylaxis, treatment-resistant depression, chronic depression and antidepressant tolerance. RESULTS: Antidepressant treatment-resistant patients frequently had a positive initial response to antidepressants. When resistance appeared, initial increases in dose or medication changes usually resulted in transient improvement. Eventually, the episodic course of the original depressive illness was replaced with a continuous, unresponsive depressive syndrome. We propose the term tardive dysphoria to describe this phenomenon. CONCLUSIONS: The phenomenon of antidepressantinduced depression, or tardive dysphoria, needs to be experimentally examined in blinded, randomised antidepressant discontinuation studies.