Current Psychiatry Reviews - Volume 3, Issue 2, 2007

Since the seminal paper by Bremner et al. in 1995 reporting the findings of reduced hippocampal volumes in Vietnam combat veterans, other groups have examined brain morphology in posttraumatic stress disorder (PTSD). However, it is often difficult to compare these studies directly because of differences in types of trauma, length of trauma exposure, age of trauma exposure, and sex. Despite these limitations, many authors have found volume reduction in the hippocampus, suggesting that a structural brain deficit may either predispose to the development of PTSD or be the result of the disorder, or both. In fact, some findings argue that the relatively smaller hippocampal volume in patients with PTSD is a risk factor for the development of PTSD, whereas other findings suggest that hippocampal volume reduction may occur as a result of either stress exposure or PTSD. Regardless of the etiology of the hippocampal volume reduction, early work hints that pharmacological intervention may alter hippocampal volume. This review evaluates and categorizes the existing research of hippocampal volume reduction in patients with PTSD. Other structural brain abnormalities related to PTSD are reviewed. Finally, clinical implications of hippocampal volume reduction in PTSD are considered, particularly the response of the hippocampus to pharmacological intervention.

Social anxiety disorder (social phobia, SAnD) is a chronic, impairing disorder characterised by embarrassment and fear relating to public scrutiny and social performance. In its generalised form it may seem to be a type of extreme shyness or variant of avoidant personality disorder and thus enduring and resistant to change. A discrete subtype has been seen as akin to simple phobia and potentially responsive to behavioural therapies. In this article we critically evaluate the pharmacological regimens that have been used to treat social anxiety disorder. An extensive search was conducted from 1980 through to June 2006. Electronic databases were used including Medline and PsycInfo using search terms including anxiety or phobia with social or treatment or therapeutics, restricted to English language manuscripts. The results of this search are presented by drug category, sorted according to both common clinical practice and strength of evidence. There are effective, well-tolerated, and powerful drug treatments of social anxiety disorder. A significant evidence base supports this assertion. Medication therapy should be considered as a first line treatment of this condition.

Objectives: Depressed patients often have insomnia, daytime sleepiness, and/or changes in sleep architecture. These sleep/wake changes are associated with diminished quality of life, impaired function, diminished treatment response and greater risk of relapse. Antidepressants may cause, exacerbate, or ameliorate these sleep/wake alterations. The sleep/wake effects of bupropion, a norepinephrine/ dopamine reuptake inhibitor (NDRI), are relatively less well established. We carried out this literature review in order to characterize the sleep/wake effects of bupropion, provide an understanding of the antidepressant mechanisms involved and discuss implications for clinical practice. Methods: Manuscripts were identified using PubMed. In addition, reports were selected from references in the original search and reports concerning bupropion extended-release were provided by the manufacturer. Results: Bupropion was not associated with daytime sedation. Sleep disturbance occurs at a low rate, comparable to other modern reuptake inhibitors. Unlike other antidepressants, bupropion does not suppress REM sleep nor increase the risk of periodic leg movement disorder. Conclusion: Bupropion has a unique sleep/wake profile, which may be particularly well-suited for treatment of individuals suffering from depression accompanied by significant fatigue/sleepiness. A lack of REM suppression, which likely reflects bupropion's NDRI mechanism of action, is also distinctive and does not affect antidepressant efficacy.

Compared to the animal literature, the human literature on genetic, hormonal and neural mechanisms underlying the initiation, establishment and maintenance of maternal behaviour is small. While there are obvious parallels in the behaviour itself between human mothers and other mammals, there is little evidence for the primacy of biological mechanisms as opposed to cultural and experiential factors. In particular the concept of a human sensitive period after birth when ‘bonding’ must occur, analogous to the sensitive period in mammals, has lost importance. However there are important similarities between the effects of poor maternal care in other mammals and in human children, specifically inappropriate overactivation of the hypothalamo-pituitary-adrenal axis (HPA) and a subsequent cascade of diverse and adverse consequences. It is likely that such enhanced stress responsiveness and its results does impact on future maternal care, creating the possibility of transgenerational cycles of inadequate maternal behaviour. The implications for antenatal, postnatal and child protection interventions are briefly discussed.

Schizophrenia is characterised by disturbances in language and thought. Semantic priming paradigms have been frequently employed to investigate language function in schizophrenia. The semantic priming effect is the reaction time advantage that is achieved by priming a target to which a participant is responding with a semantically or associatively related word. In schizophrenia, this area of research has produced contradictory results. The current review considers the significance of the specific task parameters employed and the characteristics of the patient sample as possible reasons underlying discrepancies, as well as reviewing the significance of neuroimaging studies. We establish the relatedness proportion effect, where low proportions of related prime-target pairs result in reduced or normal SP in people with schizophrenia, whilst higher proportions lead to increased SP. Additionally, that using indirectly related prime-target pairs results in increased SP in schizophrenia. Further, in terms of patient characteristics, patients with thought disorder produce the most consistently abnormal SP results. We will provide a comprehensive up-to-date review of research on semantic priming effect in schizophrenia, as well as consider the implications of the results.

In the last few years the correlation between personality and genetics has been largely investigated. Harm Avoidance seems to be strongly associated with the serotonin transporter gene. The 5-HT1A and the 5-HT3A serotonin receptors and the D2 and D4 dopamine receptors, seem to be also involved, even if results are less unequivocal. Novelty Seeking seems to be associated with dopamine D4 receptor gene, but also the D2 and D3 dopamine receptors, the 5-HT2A serotonin receptor, the MAO-A and the COMT genes have been hypothesized as involved in this trait. Studies on Reward Dependence, Persistence, Self-Directedness, Cooperativeness and Self- Transcendence dimensions are still conflicting. Though further studies are necessary to replicate and validate those results, genetic factors play an important role for specific susceptibilities of human personality.