Somatic marker hypothesis - Wikipedia

Somatic marker hypothesis - Revolvy

22/05/2014 · So what is the Somatic Marker Hypothesis

The goal of the Demand/Control model has been to integrate understanding of the social situation with evidence of emotional response, psychosomatic illness symptoms and active behaviour development in major spheres of adult life activity, particularly in the highly socially structured work situation. However, when the model was being developed, one likely platform for this work, sociological research exploring illness in large population studies, often omitted the detailed level of social or personal response data of stress research, and thus much integrating work was needed to develop the model.

(1994) relates it, think of the somatic marker ..

and thus enhance the somatic marker trigger

This theory holds that such decisions are aided by emotions, in the form of bodily states, that are elicited during the deliberation of future consequences and that mark different options for behavior as being advantageous or disadvantageous.

For the somatic marker hypothesis ..

There is a great deal of evidence that job loss and unemployment produce significant deterioration in mental health (Fryer and Payne 1986). The most common outcomes of job loss and unemployment are increases in anxiety, somatic symptoms and depression symptomatology (Dooley, Catalano and Wilson 1994; Hamilton et al. 1990; Kessler, House and Turner 1987; Warr, Jackson and Banks 1988). Furthermore, there is some evidence that unemployment increases by over twofold the risk of onset of clinical depression (Dooley, Catalano and Wilson 1994). In addition to the well-documented adverse effects of unemployment on mental health, there is research that implicates unemployment as a contributing factor to other outcomes (see Catalano 1991 for a review). These outcomes include suicide (Brenner 1976), separation and divorce (Stack 1981; Liem and Liem 1988), child neglect and abuse (Steinberg, Catalano and Dooley 1981), alcohol abuse (Dooley, Catalano and Hough 1992; Catalano et al. 1993a), violence in the workplace (Catalano et al. 1993b), criminal behaviour (Allan and Steffensmeier 1989), and highway fatalities (Leigh and Waldon 1991). Finally, there is also some evidence, based primarily on self-report, that unemployment contributes to physical illness (Kessler, House and Turner 1987).

Search results for `Somatic marker hypothesis` - …

Application of the somatic marker hypothesis to …

Eslinger (1996) in particular would later take up this call for the importance of EF (the PFC) in managing the social conduct of the individual. He argued that EF contains "social executors" that each serve certain social functions: (1) social self-regulation: processes needed to manage the initiation, rate, intensity, and duration of social interactions; (2) social self-awareness: knowledge and insight about oneself and the impact of one's behavior on others in social settings; (3) social sensitivity: the ability to understand another's perspective, point of view, or emotional state [similar to empathy]; and (4) social salience: regulate somatic and emotional states that impart a sense of meaningfulness to social situations and to specific individuals within that situation. (p. 390). The latter is clearly related to Damasio's (1994) idea of a somatic marker system that imparts the motivational/emotional salience and valence to information being held in mind that concerns plans and goals. Eslinger (1996) views the social disability arising from EF impairment as frequently being the most distinctive feature beyond just the cold cognitive impairments. He states "Yet there is no comprehensive model of executive function that addresses the interrelationship of cognitive and social aspects of behavior, including the various impairments that can occur." (p. 389). He lists the following as some of the social deficits arising from PFC (hence EF) damage – demanding and self-centered behavior, lack of social tact and restraint, impulsive speech and actions, disinhibition (of immediate self-interests), apathy and indifference, and lack of empathy, among others.

The somatic marker hypothesis: still many questions …

A further problem with most definitions of EF is the relative dearth of attention given to emotional and motivational aspects of self-regulation. While this is certainly discussed by Luria (1966) and others who described the consequences of frontal lobe injuries in humans and primates (Damasio, 1994; Dimond, 1980; Fuster, 1997; Stuss & Benson, 1986) it has been largely ignored in most other conceptualizations of EF in the past 20 years. This is particularly so in accounts of EF using cognitive psychology and information processing models. Exceptions have been Fuster's theory of cross-temporal synthesis (1997), Damasio's (1994) somatic marker theory, Stuss and Benson's (1986) hierarchical model, and my own hybrid model of EF (Barkley, 1997a, 1997b). None are based on the computer metaphor of brain functioning that underlies information processing models of EF. Perhaps this is because computers do not have emotions that need self-regulating and do not have to self-motivate.

The Somatic Marker Hypothesis: A Neural Theory of …

Dimond (1980) and later Lezak (1995) were correct, I believe, in noting several additional problems that have continued to be ignored by many in the subsequent history of EF to the present time. One of these is the relative sparse recognition in the history of EF of its importance for social functioning and effectiveness, or what Dimond called our . Ciairano et al. (2007) at least acknowledged the importance of EF in cooperative social behavior. Eslinger (1996) especially noted the importance of EF in social functioning. Specifically, Dimond referred to ". . . the capacity to respond to appropriate social patterns, to regulate social life and to integrate adequately and successfully with others" that was so important about PFC functioning (p. 510; Dimond, 1980). There is a striking social pathology associated with PFC damage, Dimond (1980) argued, that goes largely unappreciated in efforts to describe the major functions of the PFC. Perhaps this is owing in large part to the fact that clinicians and neuroscientists nearly always study such patients in isolation (individually) and in relatively short periods of time (a few hours at most at a time) in unnatural settings (clinics and labs) and with EF measures that are largely "cold" cognitive in nature that would miss this aspect of functioning or detect only the smallest instances of its degradation. Dimond (1980) makes a special point of noting the hundreds of cases of PFC-injury that did not manifest many of the changes in cold cognition or mental functioning attributed to this region by others except for marked changes in planning and social functioning (pp. 505-508).