Fig. 2.

Schematic drawing of our model. (1) Somatic processes. (2) Behavioral and conscious representation. s. = setpoint. Somatic processes (left side): The existence of casual triggers leads to the activation of autoimmune responses. Previous exposure to these triggers might have led to a changed of the “prior,” the set-point for starting and regulating the autoimmune response. The production of pro-inflammatory cytokines leads to the activation of the neuro-inflammatory reflex and, consequently, to increased activity of the afferent vagal nerve. This activation might interfere with afferents of other compartments of the vagus nerve, originating from the mechanoreceptors of the heart. Chronic summation or interference of the combined activation might have changed the “prior” for starting and regulating the activation of the solitary nucleus and may therefore lead to reduced coupling with dorsal nucleus of the nervus vagus. Consequently, parasympathetic modulation of the heart rate decreases. Information about autoimmune activation is relayed to midbrain centres and initiates sickness behavior. Behavior and conscious representation (right side): Sickness behavior reduces locomotor activity, increases sleepiness and at the same time sleep disorder. Previous activations of sickness behavior might have changed the prior for triggering sickness behavior, and it becomes learned as being a chronic state. This leads to secondary deconditioning of the patients, loss of muscle strength and chronic changes in heart rate variability. Further processing of the signal induces the feeling of fatigue, loss of drive and anhedonia. The conscious processes start to interfere with focused attention, leading to enduring concentration deficits, which is fostered by deconditioning and chronic changes of heart rate variability