A family history of psychopathology modifies the decrement in cognitive control among patients with HIV/AIDS

The present study was designed to evaluate the effect of HIV/AIDS on cognitive control and to determine if the effect is modified by familial risk for either alcohol or mood disorders. Sixty HIV-1 seropositive and 75 seronegative volunteers were assigned to four subgroups defined by the crossing of a diagnosis of alcohol dependence in the biological father with diagnoses of either major depressive disorder or bipolar disorder in the biological mother. Cognitive control was evaluated during a task in which subjects were asked, on occasion, to inhibit the impulse to respond in the same physical direction as the stimulus and instead respond in the opposite direction. Event related brain potentials and measures of task performance were recorded. The task evoked a negative shift in a late slow potential (SP) as well as an increment in reaction time when cognitive control was challenged. An important finding was an interaction between trial type, HIV/AIDS, and family history: HIV/AIDS and family history each attenuated the negative shift in the SP to such a degree that no further attenuation could be accomplished by the other. The effects of familial risk for alcohol versus mood disorders were equivalent. In conclusion, the absence of change in a late slow potential following a challenge to cognitive control may represent a marker of familial risk for both externalizing and internalizing disorders. The effects of familial risk on this slow potential are sufficiently robust as to attenuate the effects of HIV/AIDS on the probable generators of the response: the anterior cingulate and prefrontal cortex.     

Sleep and psychopathology

This article examines the relationship between sleep disturbance and psychopathology. Epidemiological, cross-sectional, and longitudinal data suggest a high rate of comorbidity between sleep disturbance and psychopathology, particularly between insomnia, anxiety, and depression. Between 50% and 80% of psychiatric patients complain of sleep disturbances during the acute phase of their illness. Conversely, among treatment-seeking individuals with a primary complaint of insomnia and randomly selected community samples, approximately one third display a concurrent psychopathology, one third exhibit psychological symptoms that do not necessarily exceed the threshold for a psychiatric disorder, and another third present insomnia as a functionally autonomous disorder. There is a positive relationship between severity of sleep disturbances and concurrent psychopathology, but unequivocal evidence of a cause-and-effect relationship is still lacking. However, longitudinal data suggest that anxiety and stressful life events often precede acute sleep difficulties, whereas persistent insomnia may be a risk factor for subsequent development of depression. Implications for the prevention and treatment of coexisting sleep disturbance and psychopathology are discussed.     

Temporality and psychopathology

The paper first introduces the concept of implicit and explicit temporality, referring to time as pre-reflectively lived vs. consciously experienced. Implicit time is based on the constitutive synthesis of inner time consciousness on the one hand, and on the conative–affective dynamics of life on the other hand. Explicit time results from an interruption or negation of implicit time and unfolds itself in the dimensions of present, past and future. It is further shown that temporality, embodiment and intersubjectivity are closely connected: While implicit temporality is characterised by tacit bodily functioning and by synchronisation with others, explicit temporality arises with states of desynchronisation, that is, of a retardation or acceleration of inner time in relation to external or social processes. These states often bring the body to awareness as an obstacle as well. On this basis, schizophrenia and melancholic depression are investigated as paradigm cases for a psychopathology of temporality. Major symptoms of schizophrenia such as thought disorder, thought insertion, hallucinations or passivity experiences may be regarded as manifesting a disturbance of the constitutive synthesis of time consciousness, closely connected with a weakening of the underlying pre-reflective self-awareness or ipseity. This results in a fragmentation of the intentional arc, a loss of self-coherence and the appearance of major self-disturbances. Depression, on the other hand, is mostly triggered by a desynchronisation from the social environment and further develops into an inhibition of the conative–affective dynamics of life. As will be shown, both mental illnesses bear witness of the close connection of temporality, embodiment and intersubjectivity.     

Shame and psychopathology

The origins of the word "shame" recall the concept of the infraction of integrity both as scandal and as individualization. The human experience of shame stretches along a continuum from modesty to disabling interpersonal terror. Unlike other basic affects, its emergence is a fundamental moment in the process of self-awareness and self-object differentiation. Neglected by psychiatry because it was regarded as a moral concept, today it is possible to hypothesize that it has a biologic basis that one can attempt to describe in terms of corticothalamic pathways. In this respect, like other affects, it could be considered as a cognitive shortcut to activate specific and evolutionally useful behavioral patterns, such as concealment or a request for affiliation. It is fairly ubiquitous in psychopathology, but is clinically much more structured in its abnormal expressions in anxiety disorders, particularly social phobia, obsessive-compulsive disorder, eating disorders, body dysmorphic disorder, and even in bipolar mood disorder. In schizophrenia it has been described as being one stage in the construction of delusion. Its presence is connected to interpersonal relationship (altruism) though it seems absent in autism. The assessment of shame experiences in psychiatric patients could be useful for both pharmacological and psychotherapeutic strategies, and could provide a categorization of a new psychopathology based on abnormal affects.     

Externalizing psychopathology and the error-related negativity

Prior research has demonstrated that antisocial behavior, substance-use disorders, and personality dimensions of aggression and impulsivity are indicators of a highly heritable underlying dimension of risk, labeled externalizing. Other work has shown that individual trait constructs within this psychopathology spectrum are associated with reduced self-monitoring, as reflected by amplitude of the error-related negativity (ERN) brain response. In this study of undergraduate subjects, reduced ERN amplitude was associated with higher scores on a self-report measure of the broad externalizing construct that links these various indicators. In addition, the ERN was associated with a response-locked increase in anterior theta (4-7 Hz) oscillation; like the ERN, this theta response to errors was reduced among high-externalizing individuals. These findings suggest that neurobiologically based deficits in endogenous action monitoring may underlie generalized risk for an array of impulse-control problems.     

Toward DSM-V and the classification of psychopathology

The Diagnostic and Statistical Manual of Mental Disorders (DSM-IV) developed by the American Psychiatric Association (1994) is a compelling effort at a best approximation to date of a scientifically based nomenclature, but even its authors have acknowledged that its diagnoses and criterion sets are highly debatable. Well-meaning clinicians, theorists, and researchers could find some basis for fault in virtually every sentence, due in part to the absence of adequate research to guide its construction. Some points of disagreement, however, are more fundamental than others. The authors discuss issues that cut across individual diagnostic categories and that should receive particular attention in DSM-V: (a) the process by which the diagnostic manual is developed, (b) the differentiation from normal psychological functioning, (c) the differentiation among diagnostic categories, (d) cross-sectional vs. longitudinal diagnoses, and (e) the role of laboratory instruments.