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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.

Human performance, particularly that of the warfighter, has been the subject of a large amount of research during the past few decades. For example, in the Medline database of medical and psychological research, 1,061 papers had been published on the topic of “military performance” as of October 2003. Because warfighters are often pushed to physiological and mental extremes, a study of their performance provides a unique glimpse of the interplay of a wide variety of intrinsic and extrinsic factors on the functioning of the human brain and body. Unfortunately, it has proven very difficult to build performance models that can adequately incorporate the myriad of physiological, medical, social, and cognitive factors that influence behavior in extreme conditions. The chief purpose of this chapter is to provide a neurobiological (neurochemical) framework for building and integrating warfighter performance models in the physiological, medical, social, and cognitive areas. This framework should be relevant to all other professionals who routinely operate in extreme environments. The secondary purpose of this chapter is to recommend various performance metrics that can be linked to specific neurochemical states and can accordingly strengthen and extend the scope of the neurochemical model.

This article concludes that dietary choline and tryptophan could influence motivational state. Investigates the link between diet and motivational state. In particular, examines how the neurotransmitter precursors choline and tryptophan are derived from the diet, how an increase in these precursors can enhance the production of the neurotransmitters acetylcholine (ACh) and serotonin (5‐HT) in the brain, and finally how the increase in these neurotransmitters can increase neuronal function and, as a result, brain activity. Increased synaptic release of both ACh and 5‐HT was found to be associated with increased brain activity. A new “neurotransmitter binding theory” is hypothesised, which is then used to associate increased brain activity with elevations in mood and an increased ability to concentrate, think and make rational decisions.

The purpose of this paper is to investigate the body-mind problem from a mathematical invariance principle in relation to personality dynamics in the psychological and the biological levels of description.

The relationship between the two mentioned levels of description is provided by two mathematical models as follows: the response model and the bridge model. The response model (an integro-differential equation) is capable to reproduce the personality dynamics as a consequence of a determined stimulus. The invariance principle asserts that the response model can reproduce personality dynamics at the two levels of description. The bridge model (a second-order partial differential equation) can be deduced as a consequence of this principle: it provides the co-evolution of the general factor of personality (GFP) (mind), the it is an immediate early gene (c-fos) and D3 dopamine receptor gene (DRD3) gens and the glutamate neurotransmitter (body).

An application case is presented by setting up two experimental designs: a previous pilot AB pseudo-experimental design (AB) pseudo-experimental design with one subject and a subsequent ABC experimental design (ABC) experimental design with another subject. The stimulus used is the stimulant drug methylphenidate. The response and bridge models are validated with the outcomes of these experiments.

The mathematical approach here presented is based on a holistic personality model developed in the past few years: the unique trait personality theory, which claims for a single personality trait to understand the overall human personality: the GFP.