Chronic Fatigue Syndrome Introduction Chronic fatigue synd

CFS prevalence rates in the United States are estimated at a minimum of 4 to 10 cases per 100,000 adults 18 years of age or older (Fukuda & Gantz, 1995). In one U.S. study (Evengard et al., 1999), the prevalence among medical patients was found to be about 1%. A several-fold higher prevalence rate of self-reported CFS-like illness exists according to preliminary, unpublished results from a 17,000-person survey coordinated by Centers for Disease Control in an unreferred San Francisco population (Fukuda & Gantz). The typical patient seeking medical care for CFS is usually a Caucasian woman between the ages of mid-20s and late-40s (Evengard et al.; Fukuda & Gantz).

Characteristics of CFS include unexplained, persistent or relapsing chronic fatigue of new or definite onset that is not a result of exertion or alleviated by rest, and it results in reduced levels of functioning. Four or more specific symptoms, persisting or recurring for six or more consecutive months, not predating the fatigue, are present. These symptoms include impairments in short-t

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Depression is possibly the most serious of the psychological problems faced by subjects diagnosed with CFS. Kurlowicz (1993) confirmed high prevalence rates of major depression and appreciable symptoms in medically ill persons. The study found that depression related to medical illness raised the potential for suicide. Reasons for high suicide rates for persons suffering from clinical depression included, isolation, loneliness, despair, boredom, depression, uselessness, loss of loved ones, economic hardships, unhappiness with life, psychological afflictions, and catastrophic life events resulting in loss of purpose and meaningfulness. Kurlowicz (1993) reported that a variety of social factors were implicated in the development of depression. Depression was often accompanied by anxiety borne of repressed resentment and rage. Through the neurochemical abnormalities that underlie the pathophysiology of depression were not fully understood, the most likely hypotheses pointed to disturbances of monoamine neurotransmission. This factor accounted for the known antidepressant effect of medications that blocked re-uptake of neurotransmitters at nerve endings in the brain. The exact anatomic location of the neurochemical alterati
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