A large body of data from a number of different laboratories worldwide has
demonstrated a general tendency for reduced adrenocortical responsiveness i
n Chronic Fatigue Syndrome (CFS). It is still not clear if this is secondar
y to abnormalities leading to decreased activity of corticotropin-releasing
hormone (CRH)- or arginine vasopressin (AVP)-producing hypothalamic neuron
s. primary hypofunction of the CRH neurons has been described on the basis
of genetic and environmental influences. Ether pathways could secondarily i
nfluence hypothalamic-pituitary-adrenal (PIPA) axis activity, however. For
example, serotonergic and noradrenergic input acts to stimulate HPA axis ac
tivity Deficient serotonergic activity in CFS has been suggested by some of
the studies as reviewed here. In addition, hypofunction of sympathetic ner
vous system function has been described and could contribute to abnormaliti
es of central components of the HPA axis.