Involvement of the Amygdala in Two Different Forms of the Inhibitory Avoidance Task

Abstract

Severe persistent or relapsing fatigue is the most disabling symptom in patients with chronic fatigue syndrome (CFS). Clinical and brain imaging studies with proton magnetic resonance spectroscopy support the view that fatigue in CFS is central, i.e., brain-derived. It seems likely that an interruption of the basal ganglia pathways integrating voluntary motor output to the afferent sensory input and cognitive processing is the neural basis of fatigue in CFS. A genome-wide microarray study in patients with CFS suggests significant changes in gene expression of pathways responsible for immune modulation, oxidative stress, and apoptosis. Altered neural cell membrane signalling in regional brain areas induced by downstream effects of these changes may explain the paroxysmal and fluctuating nature of symptom severity in many CFS patients. It is possible, but not yet proven, that CFS is due to a neurological channelopathy.