Neuroscience

Thanks to the important contributions of the neuroscience work of the last 20 years, we can now refer to it to build a new model in our discipline: integrative psychosomatics. 

Among the scientific contributions of the neurosciences, I have preferred those of Professor Antonio Damasio. I have articulated in the new model of integrative psychosomatics that I have developed, the contributions of Professor Damasio and those of the model of psychosomatic metapsychology. 

Damasio's research initially consisted in answering the question of the existence of consciousness in living beings.
In order to elucidate the biology of consciousness, it was necessary to discover how the brain can construct neuronal configurations that correspond to the relations that the organism establishes with an object. 

The problem of object representation seems less problematic than that of organism representation. Neuroscience has made considerable efforts to understand the neural basis of object representation. Extensive studies of perception, learning, and memory, as well as language, have given us a workable idea of how the brain processes an object, in motor and sensory terms, and an idea of how knowledge about an object can be stored in memory, categorized in conceptual or linguistic terms, and retrieved in the mode of recall or recognition. The object manifests itself, in the form of neural configurations, in the sensory cortices that are appropriate to its nature. For example, in the case of the visual aspects of an object, neural configurations are constructed in a whole series of regions of the visual cortexes, not just one or two, but a whole quantity, which work together to map the various aspects of the object in visual terms. 

On the side of the organism, however, things are different. Although much is known about how the organism is represented in the brain, the idea that such representations might be related to the mind and the notion of Self has received little attention. The question of what might give the brain a natural way to generate the singular and stable reference we call Self has remained unanswered. 

Key words : anorexia nervosa - Fibromyalgia - Intense pain.

I.2.2. Neurobiological models. [4 ;14 ;15 ; 22 ; 36 ; 54]
In recent decades, a large number of neurotransmitters involved in the regulation of eating behavior have been identified, raising the question of a neurobiological vulnerability to eating disorders (ED). The interpretation of the changes observed in patients with binge eating disorder is not based on a single explanation and these abnormalities could be consecutive to dietary restriction, or constitute features preceding the disease and contributing to a possible neurobiological vulnerability.
 

The information from the central nervous system on the energetic balance of the organism comes partly from the secretion of hormones that activate the hypothalamic neuronal pathways (also related to sexuality, memory, integration of emotions, images, perceptions of the body). The different hypothalamic structures involved are the lateral hypothalamus, the arcuate nucleus (which occupies the floor of the hypothalamus; it is located in a region privileged by its proximity to the ventricular cavity and the median eminence traversed by a capillary portal system that directly connects the hypothalamus and the anterior pituitary gland), and the paraventricular nucleus (or periventricular zone of the hypothalamus. Neuronal populations involved in physiological regulation of food intake are found in these hypothalamic nuclei: pro-opio-melanocortin (POMC) neurons are pathways that decrease appetite (anorexigenic) whereas neuropeptide Y and Agouti gene-Related (AgRP) neurons are pathways that stimulate food intake (orexigenic). Schematically, we can distinguish between peripheral and central etiological theories depending on the peptides involved. 

I.2.2.1. Peripheral model. 

In this context, the mediators involved are hormones secreted by peripheral tissues (notably the digestive tract and adipose tissue) which inform the nervous system of the state of gastric replenishment or emptiness as well as the state of the energy balance. There are anorectic hormones (insulin, leptin, cholecystokinin,...) and orectic hormones (ghrelin, cortisol,...). Leptin, a satiety hormone, secreted by adipocytes, inhibits food intake and increases energy expenditure by interacting with specific receptors in the hypothalamus. It activates the synthesis of appetite-inhibiting molecules (POMC and derivatives) and inhibits the synthesis of molecules involved in orexigenic pathways (NPY, AgRP, galanin, orexin A and B). Ghrelin, secreted by the gastric mucosa when the stomach is empty, provokes the sensation of hunger by a mechanism that is the opposite of that of leptin, by stimulating the orexigenic pathways and inhibiting the anorexigenic pathways of the ventral hypothalamus. 

In anorexia nervosa, there is a fall in plasma leptin levels, correlated with the percentage of body fat, and an increase in ghrelin; these variations correspond to a physiological adaptation of the body to fasting. Some authors have suggested a resistance or a mutation of ghrelin receptors to explain the absence of orexigenic effect of ghrelin elevation in anorexia nervosa. 

I.2.2.2. Central model. 

In this context, the eating behaviour would result from a dysfunction of the neuromediators involved in the hypothalamic orexigenic and anorexigenic pathways. 

Serotonin is the neuromediator whose role in weight regulation is best known at present. It decreases food intake by a set of selective phenomena on food intake. Its agonist has an orexigenic action. It acts at the level of the medial hypothalamus by decreasing food intake, particularly of carbohydrates. Anorexic patients have a significant reduction of a serotonin metabolite in the cerebrospinal fluid suggesting a reduction of serotonergic activity. 

The dopaminergic projection from the ventral tegmental area, passing through the lateral hypothalamus, and innervating the forebrain, including essentially the nucleus accumbens, plays a role in the quest for reward and is therefore involved in motivational processes. The desire for reward thus appears to be a motivational stimulus that can be dissociated from the pleasure it is likely to provide. In anorexics, this mesolimbic dopaminergic system could be modified... 

Dysfunction of other neurotransmitter systems involved in the central control of eating has also been suggested. However, the impact of these neurotransmitters in CAT must be articulated with the effect of secreted neuropeptides previously described at the level of the central nervous system. 

Brain imaging techniques reveal morphological abnormalities in the brain. These abnormalities are mainly cortical and mostly reversible. Despite a relative normalization of cortical atrophy after weight regain, a significant proportion of patients continue to present abnormalities of the cerebral ventricles. While white matter volume reductions appear to resolve, gray matter volume reductions persist, even 2 to 3 years after a return to normal weight. These partial results on a small sample suggest that the different structural brain alterations resolve to varying degrees depending on the structures and not in the same way as a function of time. 

Functional neuroimaging studies also reveal abnormalities in cerebral energy metabolism with inferior frontal and temporal hypometabolism in anorexic patients compared to bulimic patients and a more marked decrease in activity in the prefrontal and anterior cingulate regions in restrictive anorexics. Serotonergic activity and frontal lobe function are involved in control attitudes such as obsessive traits and impulsivity, aggressive behaviors. Serotonergic dysfunctions, including the orbitofrontal cortex, may be responsible for a vulnerability to poorly modulated and imprecise control of behavior.