<unk>  disorder appears to be a genetically inherited neurochemical dysfunction that may involve autonomic imbalance; decreased GABA-ergic tone; allelic polymorphism of the catechol-O-methyltransferase (COMT) gene; increased adenosine receptor function; increased cortisol. In the central nervous system (CNS), the major mediators of the symptoms of<unk>  disorders appear to be norepinephrine, serotonin, dopamine, and gamma-aminobutyric acid (GABA). Other neurotransmitters and peptides, such as corticotropin-releasing factor, may be involved. Peripherally, the autonomic nervous system, especially the sympathetic nervous system, mediates many of the symptoms. Increased flow in the right parahippocampal region and reduced serotonin type 1A receptor binding in the anterior and posterior cingulate and raphe of patients are the diagnostic factors for prevalence of<unk>  disorder. The amygdala is central to the processing of fear and<unk> , and its function may be disrupted in<unk>  disorders.<unk>  processing in the basolateral amygdala has been implicated with expansion of dendritic arborization of the amygdaloid neurons. SK2 potassium channels mediate inhibitory influence on action potentials and reduce arborization.
Anxiety
Akathisia
Phobia
Malaise
Sickness behavior
High-functioning autism
Body image disturbance
Antidepressant discontinuation syndrome  Antidepressant discontinuation syndrome  1