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Previous studies have shown a link between mental health functioning and involvement in HIV risk practices. The present research examines how well one specific group of men who have sex with other men (MSM) fare in terms of their mental health functioning, and then focuses on how mental health functioning relates to HIV risk practices in this population. The study was based on a national random sample of 332 MSM who use the Internet to seek men with whom they can engage in unprotected sex. Data collection was conducted via telephone interviews between January 2008 and May 2009. Depression is more common among men in this population than in the adult male population-at-large. All other measures of mental health functioning that were examined (self-esteem, impulsivity, current life satisfaction, optimism about the future) indicated low rates of mental health problem. Contrary to expectations, in nearly all instances, mental health functioning was not related to HIV risk practices.

More work needs to be done to understand the causes of depression among these men, and to assess how, if at all, depression relates to risk practices in this population. These findings suggest that factors other than mental health problems must be considered if one wishes to understand HIV risk taking in this population.

Impairment of intelligence in Duchenne muscular dystrophy (DMD) patients was described by Duchenne de Boulogne himself in 1868. Further studies report intelligence disorders with mayor impairment of memory. The aim of the present study was to assess the presence of affective and personality disorders in a group of children affected by DMD. Twenty six male DMD patients, mean age eleven and four months years old, were assessed for their affective and personality disorder. Only eight subjects had a total IQ below average with major difficulties in verbal and visual-spatial memory, comprehension, arithmetic and vocabulary. All the subjects presented some disorders: tendency to marginalization and isolation, self-depreciation, sense of insecurity, hypochondriac thoughts and marked state of anxiety. These disorders are often a dynamic prolongation of a psychological process which starts when the diagnosis is made and continues, in a slow and latent fashion, throughout the evolution of the disease.

Although first rank symptoms focus on positive symptoms of psychosis they are shared by a number of psychiatric conditions. The difficulty in differentiating bipolar disorder from schizophrenia with affective features has led to a third category of patients often loosely labeled as schizoaffective. Research in schizophrenia has attempted to render the presence or absence of negative symptoms and their relation to etiology and prognosis more explicit. A dichotomous population is a recurring theme in experimental paradigms. Thus, schizophrenia is defined as process or reactive, deficit or non-deficit and by the presence or absence of affective symptoms. Laboratory tests confirm the clinical impression showing conflicting responses to dexamethasone suppression and clearly defined differences in autonomic responsiveness, but their patho-physiological significance eludes mainstream theory. Added to this is the difficulty in agreeing to what exactly constitutes useful clinical features differentiating, for example, negative symptoms of a true deficit syndrome from features of depression. Two recent papers proposed that the general and specific cognitive features of schizophrenia and major depression result from a monoamine-cholinergic imbalance, the former due to a relative muscarinic receptor hypofunction and the latter, in contrast, to a muscarinic hypersensitivity exacerbated by monoamine depletion. Further development of these ideas will provide pharmacological principles for what is currently an incomplete and largely, descriptive nosology of psychosis. It will propose a dimensional view of affective and negative symptoms based on relative muscarinic integrity and is supported by several exciting intracellular signaling and gene expression studies. Bipolar disorder manifests both muscarinic and dopaminergic hypersensitivity. The greater the imbalance between these two receptor signaling systems, the more the clinical picture will resemble schizophrenia with bizarre, incongruent delusions and increasingly disorganized thought. The capacity for affective expression, by definition a non-deficit syndrome, will remain contingent on the degree of preservation of muscarinic signaling, which itself may be unstable and vary between trait and state examinations. At the extreme end of muscarinic impairment, a deficit schizophrenia subpopulation is proposed with a primary and fixed muscarinic receptor hypofunction.

The genomic profile of bipolar disorder and schizophrenia overlap and both have a common dopaminergic intracellular signaling which is hypersensitive to various stressors. It is proposed that the concomitant muscarinic receptor upregulation differentiates the syndromes, being marked in bipolar disorder and rather less so in schizophrenia. From a behavioral point of view non-deficit syndromes and bipolar disorder appear most proximate and could be reclassified as a spectrum of affective psychosis or schizoaffective disorders. Because of a profound malfunction of the muscarinic receptor, the deficit subgroup cannot express a comparable stress response. None -theless, a convergent principle of psychotic features across psychiatric disorders is a relative monoaminergic-muscarinic imbalance in signal transduction.

Genetic risk for depressive disorders is poorly understood despite consistent suggestions of a high heritable component. Most genetic studies have focused on risk associated with single variants, a strategy which has so far only yielded small (often non-replicable) risks for depressive disorders. In this paper we argue that more substantial risks are likely to emerge from genetic variants acting in synergy within and across larger neurobiological systems (polygenic risk factors). We show how knowledge of major integrated neurobiological systems provides a robust basis for defining and testing theoretically defensible polygenic risk factors. We do this by describing the architecture of the overall stress response. Maladaptation via impaired stress responsiveness is central to the aetiology of depression and anxiety and provides a framework for a systems biology approach to candidate gene selection. We propose principles for identifying genes and gene networks within the neurosystems involved in the stress response and for defining polygenic risk factors based on the neurobiology of stress-related behaviour. We conclude that knowledge of the neurobiology of the stress response system is likely to play a central role in future efforts to improve genetic prediction of depression and related disorders.

Somatoform disorders are often the main cause for seeking professional advice and performing a number of specialist checks. The aim of the study was to determine the frequency of somatoform disorders in the form of headaches in children and adolescents neurologically diagnosed and the risk factors thereof. Analysis of the biological and situational risk factors were established. Somatoform disorders were diagnosed in 27 out of 276 children with headaches. We concluded that in the differential diagnosis of headaches, somato-form headaches should not be omitted as every 10th patient in the developmental age diag nosed on the neurological ward because of headache shows signs of somatoform heada -ches. In diagnostically difficult cases it is recommended that analysis of biological and situational risk factors be performed with special attention paid to chronic disease of the patient and/or in his immediate family, the patient's psychological disorders and dysfunctional or low social status families. The creation of separate criteria for somatoform disorders of the developmental age should be considered.

Exposure therapy is a widely used treatment for patients with post-traumatic stress dis -order. It involves reduction of fear through progressive exposure to frightening stimuli in a therapeutic environment. Here we propose a new method designed to improve the effectiveness of exposure therapy. We hypothesized that device-guided breathing during exposure therapy can increase the capability of the patient to undergo effective exposure. The successful application of the method is described for a single patient. Using a device to slow and regularize breathing, the patient was calmed and experienced a greater sense of control and a profound effect of the exposure. The use of the breathing-guiding device is believed to reduce arousal level and excitability of sympathetic “fight-flight” behaviors. The present study suggests that device-guided breathing integrated with exposure therapy may provide a practically feasible and potentially promising non-pharmacological treatment after trauma.