Current Psychiatry Reviews - Volume 4, Issue 2, 2008

The illicit drug 3,4-methylenedioxymethamphetamine (MDMA; Ecstasy) has been shown to cause long-term serotonin (5-HT) deficits in rodents and non-human primates, and based on the results of brain imaging studies in frequent Ecstasy users, it appears that MDMA has the potential to affect the human brain in much the same way. Because the 5-HT system is known to take part in the regulation of impulsivity, it has been hypothesized that increased impulsivity may be one of the consequences of MDMA exposure seen in Ecstasy users. The purpose of this review is to evaluate the evidence for a relationship between Ecstasy use and higher levels of impulsivity. Cross-sectional studies that used measures of impulsivity to compare abstinent Ecstasy users to non-users will be summarized, and longitudinal studies that attempted to find changes in impulsivity in Ecstasy users will be examined. In closing, the overall evidence for an association between Ecstasy use and higher levels of impulsivity will be evaluated, and potential explanations for this association will be discussed.

There is growing consensus that it is possible to diagnose probable Alzheimer's disease (AD) in patients prior to the development of mild dementia, which was highlighted by a recent international consensus proposal for new research diagnostic criteria (Dubois B, et al., Lancet Neurology, 2007). Data are accruing from longitudinal studies to support the concept that a specific mild amnesic syndrome, detected through clinical assessment of symptoms and signs, is the most common early manifestation of prodromal AD. Whether or not patients meet typical clinical trial criteria for mild cognitive impairment (MCI), the presence of this syndrome is a very sensitive indicator of AD pathology and elevated likelihood of imminent mild dementia. Diagnostic specificity can be improved in this population through the detection of biomarkers typically associated with AD, including neuroimaging measures of abnormal brain structure and function, as well as cerebrospinal fluid markers. It now appears reasonable, using currently available methods, to diagnose probable AD in individuals who manifest this multidimensional clinicobiologic pattern of abnormalities. Since the likelihood of mild dementia is greatly elevated in these individuals, it is critical to begin to translate this knowledge into standard practice in clinical research with the aim of targeting this population for clinical trials of potential disease-modifying therapies aiming to prevent mild dementia. In this manuscript, evidence for these points is reviewed and a proposal is outlined for translation of this knowledge into a research program.

Alexithymia is characterized by difficulties in recognizing and verbalizing feelings, a paucity of fantasy life, concrete speech, and thought closely tied to external events. The alexithymia construct, formulated from clinical investigations, is multifaceted and includes four distinct characteristics: 1) difficulty identifying and describing feelings; 2) difficulty distinguishing feelings from bodily sensations; 3) diminution of fantasy; and 4) concrete and minimally introspective thinking. An increasing body of studies indicates that alexithymic features exist not only in classic psychosomatic disorders but also in other severe and chronic somatic diseases and psychiatric disorders such as Major Depression, and other Axis I disorders, such as Anxiety Disorders. The aim of the present review was to elucidate the relationships between alexithymia and Anxiety Disorders, in order to investigate the possible psychopathological and therapeutic implications.

Seroprevalence studies indicate that HIV infection rates are elevated among individuals with a severe mental illness (SMI) compared to the general population. The higher prevalence of HIV among individuals with SMI has prompted the development and evaluation of tailored sexual risk reduction programs for these individuals. In this paper, we review the literature on sexual risk-reduction interventions for individuals with SMI, including interventions for both uninfected and infected individuals. We discuss components of successful interventions, identify limitations in the current literature, and highlight directions for future research. Finally, we conclude with implications for clinical practice, including a discussion of the challenges and advantages to implementing sexual risk reduction interventions for individuals with SMI.

Research implicates the emotion of disgust in particular anxiety disorders, but possible processes by which disgust can cause anxiety have not been articulated. We review data from studies of the functional neuroanatomy of disgust in order to elucidate possible processes by which disgust can cause anxiety disorders. First, we examine whether fear and disgust involve different neural substrates. Despite inconsistencies, the data suggest that the amygdala is critical for fear and the anterior insula is critical for disgust. Second, we examine whether the anterior insula fits into current neurobiological models of fear and anxiety. Recent research suggests that the insula projects to neural circuits underlying fear and anxiety and is also involved in activation of the hypothalamic-pituitary-adrenal axis stress response. Additionally, the insula may mediate interoceptive awareness, a critical component underlying anxiety. These functions of the insula provide possible routes by which disgust interacts with and sensitizes the fear and anxiety circuits in order to produce pathological anxiety. The derived temporal routes of disgust's role in anxiety foster testable predictions that may help future research determine if and how disgust functions in anxiety.

Background: Over the past decade, a variety of psychosocial interventions have been reported to be beneficial for bipolar disorder. Acceptance of this literature has been slow in part because most studies have been small and lack rigorous methodology. Furthermore, skepticism about the potential efficacy of psychosocial treatments stems from recognition of the indisputable biological basis of the disorder. Well powered randomized trials are the standard by which pharmacologic strategies demonstrate efficacy. Thus, we review the randomized controlled trials of psychosocial interventions as an adjunct to medication in the treatment of bipolar disorder. Methods: We conducted a literature search to identify randomized controlled studies of Cognitive-Behavioral therapy (CBT), Psychoeducation (PE), Family-Focused Therapy (FFT), and interpersonal social rhythm therapy (IPSRT) for bipolar disorder. Only studies which randomized at least 80 individuals diagnosed with bipolar disorder were selected for review. Results: Nine studies met our inclusion criteria and of these, eight found that adding one of the above psychosocial interventions to pharmacotherapy improved treatment outcomes for individuals with bipolar disorder. None of the psychosocial interventions claims benefit for acute treatment of hypomania or mania; however, CBT, FFT, and IPSRT appear efficacious in treating depressive symptoms and preventing new episodes. PE appears helpful against the recurrence of hypomania or mania, but not depression. Conclusions: These findings support the use of psychosocial interventions in treating individuals with bipolar disorder.