Introduction Falvo (2005) writes on the medical and psychosocial aspect of chronic disease including fibromyalgia. Fibromyalgia is defined as a rheumatologic disease in which the patient experience widespread pain, coupled with aching and stiffness of muscles and/or joints, plus fatigue, sleep disturbances, and broadly distributed sites of tenderness (tender joints) (Millea & Hollaway, 2000, cited in Flavio, 2005, p. 421). The pain and uneasiness linked to fibromyalgia are spread, occurring in the hips, lower back, shoulders, and neck and other sites. The author refutes fibromyalgia as a degenerative disease because it does not cause damage to joints or bones; therefore, there is no definitive diagnostic test or objective findings that can validate the condition. Because of the lack of exceptional laboratory tests applied for diagnosis of the condition, diagnosis is centered on individuals’ testimony of history and symptoms, regarding the identifiable tender points as the major diagnostic indicator. Falvo (2005) notes that fibromyalgia can manifest other symptoms besides musculoskeletal pain, such as irritable bowel syndrome or headaches. Falvo (2005) argues that this condition can occur parallel with other sevre rheumatic disorders including rheumatoid arthritis and lupus. Moreover, psychological signs of depression and anxiety often accompany fibromyalgia. This chronic illness can impact an individual’s quality of life and can lead to interpersonal challenges due to its symptoms. The author underscores the significance of validating the individual’s symptomatic complaint in that it helps restores self-esteem and self-control, assisting them to adjust to their symptoms. Cause of Fibromyalgia According to the findings of Liu, Mantyh, & Basbaum, (1997), enduring physical or emotional abuse subjected to a person may produce some physiological alterations in that individual. It has been proven that a substantial group of people diagnosed with this illness that were subject to chronic stress from physical and emotional abuse, shared a common physiological outcomes. These outcomes include increased levels of N-methyl-D-aspertatesubstance P (NMDA-SP) and a rise in the expression of c-fos , which is a protein released under stress and found in neurons corresponding with pain. These outcomes considerably point to chronic stress as an impetus for hyperalgesia in FMS. The resultant hyperalgesic state is a product of chronic muscular hypersensitivity to fatigue and pain, denoted as a stress-induced, diathetic, neuromuscular hyperalgesic condition (Ellis, n.d). Benett (1999) concluded that an ultimate understanding of pathogenesis of non-nociceptive pain is prerequisite for disqualifying FMS as a somatoform disturbance. Moreover he proposes that there may be needed a review of the concept of somatoform abnormalities, to classify them under clinical conditions by virtue of the knowledge physiology. The author defined the neurological pain course as gush of nerve impulses that emanates from nociceptors in visceral or somatic tissues (p. 386). In the course, nerve “impulses travel in peripheral nerves, with a first synapse in the dorsal horn and a second synapse in the thalamus, and end up in the cerebral cortex and other supraspinal structures. This results in a p