Abstract
Chronic Fatigue Syndrome (CFS) patients have reported that alterations in attention, concentration and memory contribute significantly to social and occupational dysfunction. However, little empirical work has substantiated these claims. This dissertation documents the neuropsychological deficits of CFS patients and then explores the relationship of those deficits to affective and immunological functioning. Thirty-three patients (25 female, eight male) who met Centers for Disease Control criteria for CFS were matched on gender, age, and education with two appropriate reference groups: (1) 33 normal, healthy control subjects, and (2) 33 renal pre-transplant patients (medical controls). Subjects were administered a neuropsychological battery which was heavily loaded with measures of attention and concentration (Continuous Performance Test, WAIS-R Digit Span, WAIS-R Digit Symbol, Enhanced Cued Recall, Rey-Osterrieth Complex Figure, Stroop Color Word Test, and Trail Making Test). A MANOVA revealed that the performance of both the CFS subjects and medical controls was below that of the healthy controls on a gross measure of attention, concentration and psychomotor speed. However, only the performance of the CFS patients was below that of the healthy controls on specific measures of sustained attention, concentration and speed of cognitive processing. Repeated measures ANOVAs then revealed that the CFS group demonstrated no deficits in memory storage or retrieval; any memory difficulties noted in the literature were likely due to an attentional deficit which resulted in difficulties encoding information. The data of a larger group of CFS subjects (N = 71) was then explored using hierarchical multiple regression analyses. First, the role of affect proved to be negligible in explaining variance in the neuropsychological measures. However, affect did help to explain subjects' self-report of cognitive difficulties. Second, cognitive processing was partially explained by immune markers indicative of lymphocyte activation (HLA-DR, CD26), and ability to encode information was partially explained by impaired immune function (natural killer cell cytotoxicity and lymphoproliferative response to PHA). Self-report of cognitive difficulties was independently explained by affect and two indicators of lymphocyte dysregulation (CD4/CD8 and response to PHA). Possible explanations for these immune and neuropsychological relationships are considered, and the clinical implications of our findings are discussed.