Chronic Fatigue Syndrome

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Chronic Fatigue Syndrome Defined

The chronic fatigue syndrome (CFS) has been defined as a distinct clinical entity characterized by chronic, often relapsing, but always debilitating fatigue lasting for at least 6 months and causing impaired overall physical and mental functioning. Recent CDC criteria (1994) have been broadly formulated in order to standardize research in the field resulting in an operating framework which includes cognitive difficulties, pharyngitis, tender lymphadenopathy, muscle pain, joint pain, headache, sleep disturbance or poor sleep, and post-exercise malaise as central features of the illness. Since a precise etiology for the syndrome remains elusive, the diagnosis is largely made by exclusion once specific medical and psychiatric disorders are ruled out. A central imperative, is to determine to as great an extent as possible, whether there are any single or relatively small set of pathophysiologic entities causing the syndrome.

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Varied Pathophysiology Proposed for CFS

Investigations into the pathophysiology of CFS have remained inconclusive although several possibilities exist. For example, it might be expected that CFS patients could demonstrate striated muscle deficiencies. However, skeletal muscle energetics, structure and histopathology, physiology, and glycolytic activity have been normal and electromyographic results have been inconclusive in these patients. In vivo analyses of muscle energetics are similarly suggestive but not definitive. Cardiac studies have not consistently demonstrated defects in day-to-day cardiac fitness among CFS patients compared to other deconditioned people. Infectious and immune pathology have often been suspected but not conclusively demonstrated as major etiologic factors although studies hint at impaired inflammatory cytokines and cellular immunity.

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Altered Regulatory Systems in CFS

Studies of the integrative and regulatory systems have been provocative; there seems compelling information concerning abnormalities in the cardiovascular regulatory areas of the brainstem and in other vasoregulatory CNS which areas may be associated with impaired vagal tone in response to synchronized breathing malfunction of central and peripheral nervous system, an inability to completely activate skeletal muscle , and abbreviated exercise capacity due to inappropriately low heart rate and early fatigue during treadmill testing. Associated neuroendocrine dysfunction, impaired hypothalamic-pituitary-adrenal interactions, and associated neurohumoral findings which can produce impairment in cardiovascular regulation of the blood pressure and cardiac output have been described. There is thus evidence for a deficit in neuroendocrine regulatory mechanisms which may limit organ and tissue function directly, or indirectly through decreased blood pressure and impaired tissue level perfusion. The peripheral circulatory beds and central nervous system are particularly vulnerable to cardiovascular inadequacy. Whether dysfunctional cardiovascular homeostasis is a primary abnormality in CFS or whether it is a secondary effect may not be critical in this regard: maladaptive changes in blood pressure and blood flow could easily produce many of the signs and symptoms associated with CFS such as light-headedness, impaired cognition, inappropriate sweating and temperature instability. The possibility that CFS findings result from low blood pressure or decreased tissue perfusion stemming from impaired circulatory regulation is attractive and merits further investigation.

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Orthostatic Intolerance in Adolescent CFS is consistent with the Postural Tachycardia Syndrome

Upright posture is, along with exercise, one of two fundamental human stressors requiring rapid and effective circulatory and neurologic compensations in order to maintain blood pressure, cerebral blood flow, and consciousness. The physiology of upright posture is unique to hominids and cannot be easily studied in animals. Recent investigations lend credence to the hypothesis that CFS results at least in part from low upright blood pressure by strongly implicating neurally mediated hypotension (NMH), a form of orthostatic intolerance, in the symptomatology of chronic fatigue syndrome in adults. In their landmark observations, Rowe and coworkers produced NMH in twenty-one of twenty-two patients with CFS using head-up tilt (HUT), a standard orthostatic maneuver which rapidly produces enhanced sympathetic tone while decreasing parasympathetic tone in normal subjects. An earlier work, however, reported somewhat different findings in adolescents with CFS who had tachycardia often associated with hypotension during orthostasis. This is the orthostatic tachycardia syndrome described at least since 1940 under many aliases. Recently the syndrome has undergone a renaissance as the "postural orthostatic tachycardia syndrome", acronymically "POTS", reported in adults by workers at the Mayo clinic and also as the syndrome of chronic orthostatic intolerance reported by the Vanderbilt group. We reported the first pediatric cases of POTS. Our data has shown that the pattern of orthostatic intolerance during HUT in the adolescents with CFS is predominantly POTS.

 

 

 


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POTS and Chronic Orthostatic Intolerance
Chronic Fatigue Syndrome