Tarsal tunnel syndrome

of HPA-axis function. Other psychiatric illnesses, particularly depression, often coexist with PTSD and can themselves cause HPA-axis abnormalities. Additional confounding factors which may affect the interpretation and comparison of the studies cited include psychotropic drug therapy, I current or previous substance abu se and differing control groups." It is extremely difficult to eliminate these variables, even in very carefully designed clinical studies. We have recently reported increased ACTH responses to intravenously administered naloxone in six of 13 patients with severe PTSD;7this finding could not be satisfactorily explained on statistical analysis by either medication effects or associated psychiatric illness, nor was it related to previous . alcoholism. Naloxone, a pure opioid antagonist, causes ACTH and cortisol release by blocking the inhibitory effect of endogenous opioids on CRH-secreting neurones of the hypothalamus.10 It therefore tests the entire HPA axis, in contrast to synthetic CRH, which assesses only the pituitary-adrenal component. We also found that the ACTH and cortisol responses to stimulation by vasopressin (which acts directly at the pituitary level) were normal in all seven PTSD patients tested (our unpublished data). This combination of results suggests an abnormality of HPA-axis function above the level of the pituitary gland in at least some patients with PTSD. Certain suprahypothalamic structures such as the hippocampus modulate HPA-axis function, contain glucocorticoid receptors, and are affected by chronic stress. It is therefore possible that dysfunction of the HPA axis in PTSD patients may be due to alterations in such higher brain centres. Large-scale studies which test the HPA axis at and above the hypothalamus, as well as at the pituitary and adrenal levels, are necessary to clearly define the site and magnitude of any HPA-axis abnormalities in PTSD.