Biological markers in chronic pain syndromes

While acute pain may promote survival and restitution, chronic pain is usually destructive. In acute pain, the clinical symptoms and signs are similar to those seen in anxiety states while the symptoms and signs seen in chronic pain are similar to those seen in depressive syndromes. As there are so many clinical similarities between chronic pain syndromes and depressive syndromes, it has been suggested that the two syndromes share a common pathogenetic mechanism, that the chronic pain syndrome is a masked depression, that the chronic pain syndrome is one syndrome in a spectrum of depressive disorders (depressive spectrum disease) or that the chronic pain syndrome is a variant of depressive disease. In some chronic pain syndromes, there is no organic pathology or pathophysiological mechanism that can account for the pain. These syndromes are called idiopathic pain syndromes and are operationally defined. In idiopathic pain syndromes as well as in depressive disorders, there is an increased frequency of affective disorders in first degree relatives, specific personality traits, shortened REM latencies in sleep EEG, low concentrations of melatonin in serum and urine, low concentrations of 5-HIAA in CSF, sometimes low activity of MAO in platelets, hypersecretion of cortisol, reduced diurnal variation of cortisol in plasma, reduced dexamethasone suppression of cortisol and normal or high concentrations of endorphins, Fraction 1 in CSF. Furthermore, in patients with idiopathic pain syndromes, there are decreased levels of substance P in CSF and low concentrations of dynorphin in CSF. Concerning the main symptoms in the idiopathic pain syndrome, pain, sadness and inner tension, the monoamines, substance P and the activity in dynorphin, beta-endorphin and met-enkephalin systems seem to be of importance.