Catálogo de publicaciones - libros

Multiple sclerosis (MS) is a demyelinating disease of the central nervous system (CNS) and a leading cause of disability among young adults ( Anderson et al., 1992 ; Jacobson et al., 1997 ; Noonan et al., 2002 ; Sorpedra and Martin, 2005 ). Common symptoms include loss of motor control or sensation in the limbs, loss of bowel or bladder control, neuropathic pain, optic neuritis, sexual dysfunction, and cognitive dysfunction. The etiology of MS remains uncertain; however, considerable evidence suggests that environmental factors interact with genetic factors to cause disease ( Kurtzke and Hyllested, 1987 ; Noseworthy et al., 2000 ; Sospedra and Martin, 2005 ). Suspected environmental factors include viral infection and stress.

The genesis of individuality serves as an adaptive mechanism and includes the nongenetic modification of several developmental dimensions such as growth, maturation, and learning.As a consequence, modified stress responsiveness, coping strategies, and susceptibility for diseases develop interdependently. Until today, knowledge on the neurobiology of individuality has only marginally been integrated into the understanding of the pathophysiology, prevention, and therapy of diseases.

Multiple sclerosis (MS) is a chronic, often disabling disease of the central nervous system (CNS) affecting up to 350,000 people in the United States ( Anderson et al., 1992 ; Jacobson et al., 1997 ; Noonan et al., 2002 ). As with many autoimmune diseases, it affects women at roughly twice the rate of men, and the prevalence appears to be increasing ( Cooper and Stroehla, 2003 ; Jacobson et al., 1997 ). Common symptoms include, but are not limited to, loss of function or feeling in limbs, loss of bowel or bladder control, sexual dysfunction, debilitating fatigue, blindness due to optic neuritis, loss of balance, pain, cognitive dysfunction, and emotional changes ( Mohr and Cox, 2001 ). There is a growing literature suggesting that stress may affect risk of exacerbation in patients with MS ( Mohr et al., 2004 ). This chapter will briefly review pathology and pathogenesis of MS, examine the literature on stress in MS, describe the laboratory studies on response to stress, and propose three hypothesized mechanisms by which stress might affect risk of MS exacerbation.We will also briefly review the literature on psychosocial mediators of the relationship between stressful life events and MS inflammation and discuss future directions for research in humans.