Fibromyalgia and Chronic Pain

Biography

Biography: Neil R McGregor

Abstract

Pain usually starts in a localized region and in the majority of chronic pain syndromes over time it can spread to encompass multiple body regions. The current hypothesis is that this wide spread pain is related to the development of central sensitization. In a series of reproduced studies the author has found that a different mechanism may be involved. An increased excretion of amino acids (a diuresis event) correlated with the exacerbation of pain (VAS scores) but the excretion declined with duration of the pain syndrome suggesting a whole body amino acid depletion event. These events were associated with changes in serum sodium, osmolality and the presence of widespread pain. The fall in serum amino acids correlated with a fall in urea in both serum and urine which appeared to be associated with the change in the renal function. Assessment of eGFR revealed that few patients had evidence of kidney disease. These changes seem to mimick, at a lower level, those seen with Diabetes Insipidus or a Syndrome of Inapproriate Antidiuretic Hormone excretion (SIADH). No patients could be classified as SIADH as the osmolality and sodium levels were not outside the normal two standard deviation limits. It appears that an inflammatory mediated change in protein synthesis occur via the EIF2 and mTORC1 gene pathways. An hypothesis based upon epigenetic influences on EIF2 associate protein synthesis inhibition will be presented including the potential roles of posture, malabsorption, exercise, viral dsRNA and bacterial toxins in the development of pain syndromes.