The rapid cycling variant of bipolar disorder is defined as the occurrence of four periods of either manic or depressive illness within 12 months. Patients suffering from this variant of bipolar disorder have an unmet need for effective treatment. This review examines two major studies in an attempt to update understanding of the current therapies available to treat rapid cycling patients. The first trial compares lamotrigine versus placebo in 182 patients studied for 6 months. The second is a recently completed, 20-month trial comparing divalproate and lithium in 60 patients. Both trials had a double-blind, randomized parallel-group design. The data from the latter study indicate that there are no large differences in efficacy between lithium and divalproate in the long-term treatment of rapid cycling bipolar disorder. In addition, lamotrigine has the potential to complement the spectrum of lithium and divalproate through its greater efficacy for depressive symptoms.

This prospective, longitudinal study compared the frequency and pattern of mood changes between outpatients receiving usual care for bipolar disorder who were either taking or not taking antidepressants. One hundred and eighty-two patients with bipolar disorder self-reported mood and psychiatric medications for 4 months using a computerized system (ChronoRecord) and returned 22,626 days of data. One hundred and four patients took antidepressants, 78 did not. Of the antidepressants taken, 95% were selective serotonin or norepinephrine reuptake inhibitors, or second-generation antidepressants. Of the patients taking an antidepressant, 91.3% were concurrently taking a mood stabilizer. The use of antidepressants did not influence the daily rate of switching from depression to mania or the rate of rapid cycling, independent of diagnosis of bipolar I or II. The primary difference in mood pattern was the time spent normal or depressed. Patients taking antidepressants frequently remained in a subsyndromal depression. In this naturalistic study using self-reported data, patients with bipolar disorder who were taking antidepressants—overwhelmingly not tricyclics and with a concurrent mood stabilizer—did not experience an increase in the rate of switches to mania or rapid cycling compared to those not taking antidepressants. Antidepressants had little impact on the mood patterns of bipolar patients taking mood stabilizers.

The use of antidepressants in bipolar illness remains controversial. This controversy continues to be fuelled by short-term studies that inconsistently report efficacy or no benefit. However, long-term studies have been consistently unfavourable, suggesting that understanding the long-term course of the illness in the setting of antidepressant treatment is important. This is an extraordinary case in which prospectively collected daily mood ratings were available in a type I bipolar individual who had experienced minimal medication changes over a 21-year period was reviewed. Data regarding the number of euthymic days in the setting of antidepressant use and after antidepressant discontinuation were collected.

Induction of cycling and increase in the number of depressed days occurred after five years of continuous serotonergic antidepressant administration. Discontinuation of antidepressants after 11 years of continuous use was associated with only a partial improvement which had a delayed onset. Cycling and increase in depression was noted after years of continuous use of serotonergic antidepressant treatment. Antidepressant-associated destabilisation may occur after long-term exposure and may be associated with prolonged worsening even after antidepressant discontinuation.

Oocytes, in general, are greatly enriched in mitochondria to support higher rates of macromolecular synthesis and critical physiological processes characteristic of early development. An inability of these organelles to amplify and/or to accumulate ATP has been linked to developmental abnormality or arrest. The number of mitochondrial genomes present in mature mouse and human metaphase II oocytes was estimated by fluorescent rapid cycle DNA amplification, which is a highly sensitive technique ideally suited to quantitative mitochondrial DNA (mtDNA) analysis in individual cells. A considerable degree of variability was observed between individual samples. An overall average of 1.59 × 105 and 3.14 × 105 mtDNA molecules were detected per mouse and human oocyte, respectively. Furthermore, the mtDNA copy number was examined in polar bodies and contrasted with the concentration in their corresponding oocytes. In addition, the density of mtDNA in a cytoplasmic sample was estimated in an attempt to determine the approximate number of mitochondria transferred during clinical cytoplasmic donation procedures as well as to develop a clinical tool for the assessment and selection of oocytes during in vitro fertilisation procedures. However, no correlation was identified between the mtDNA concentration in either polar bodies or cytoplasmic samples and their corresponding oocyte.

Objectives: Rapid cycling mood disorder is an important clinical phenomenon. The concept of rapid cycling has evolved since it was first described in 1974. The purpose of this review is to summarise current diagnostic criteria, postulated risk factors and suggested management strategies.

Method: A Medline and Psych-Lit computerised literature search was supplemented by tracing back through the references from existing review work.

Results: Over 80 papers were identified which discussed diagnosis and management of rapid cycling.

Conclusions: DSM-IV provides a useful but narrow definition of rapid cycling. Standard treatment of affective disorder may exacerbate rapid cycling. If a rapid cycling course develops, discontinuation of antidepressants and use of mood stabilisers is recommended.

A case of post traumatic rapid cycling unipolar mania is described in an individual with no apparent genetic predisposition to an affective disorder. A head injury is proposed as being causative. It is suggested that head injury should be included as a cause of rapid cycling affective disorder.