Abstract
Reduced basal ganglia function has been associated with fatigue in neurologic disorders, as well as in patients exposed to chronic immune stimulation. Patients with chronic fatigue syndrome (CFS) have been shown to exhibit symptoms suggestive of decreased basal ganglia function including psychomotor slowing, which in turn was correlated with fatigue. In addition, CFS patients have been found to exhibit increased markers of immune activation. In order to directly test the hypothesis of decreased basal ganglia function in CFS, we used functional magnetic resonance imaging to examine neural activation in the basal ganglia to a reward-processing (monetary gambling) task in a community sample of 59 male and female subjects, including 18 patients diagnosed with CFS according to 1994 CDC criteria and 41 non-fatigued healthy controls. For each subject, the average effect of winning vs. losing during the gambling task in regions of interest (ROI) corresponding to the caudate nucleus, putamen, and globus pallidus was extracted for group comparisons and correlational analyses. Compared to non-fatigued controls, patients with CFS exhibited significantly decreased activation in the right caudate (p = 0.01) and right globus pallidus (p = 0.02). Decreased activation in the right globus pallidus was significantly correlated with increased mental fatigue (r2 = 0.49, p = 0.001), general fatigue (r2 = 0.34, p = 0.01) and reduced activity (r2 = 0.29, p = 0.02) as measured by the Multidimensional Fatigue Inventory. No such relationships were found in control subjects. These data suggest that symptoms of fatigue in CFS subjects were associated with reduced responsivity of the basal ganglia, possibly involving the disruption of projections from the globus pallidus to thalamic and cortical networks.
Highlights
There has been increasing interest in the neural correlates of fatigue and other symptoms that afflict individuals with chronic fatigue syndrome (CFS)
Using functional magnetic resonance imaging, chronic administration of the anti-viral and inflammatory cytokine interferon alpha was shown to reduce the neural response of the basal ganglia to a hedonic reward task [19], and changes in neural activity were in turn highly correlated with symptoms of fatigue [19]
The data suggest that the neurocircuitry of fatigue in CFS patients may share a similar basis in the basal ganglia as is observed in other neurologic disorders and cases of basal ganglia lesions, as well as in the context of immune activation
Summary
There has been increasing interest in the neural correlates of fatigue and other symptoms that afflict individuals with chronic fatigue syndrome (CFS). Administration of inflammatory stimuli has been shown to alter basal ganglia function in association with fatigue [19]. Using functional magnetic resonance imaging (fMRI), chronic administration of the anti-viral and inflammatory cytokine interferon alpha was shown to reduce the neural response of the basal ganglia (ventral striatum) to a hedonic reward task [19], and changes in neural activity were in turn highly correlated with symptoms of fatigue [19]. Similar results have been found after acute administration of endotoxin to healthy volunteers where the basal ganglia response to hedonic reward was found to be reduced [20] Taken together, these data suggest that inflammatory stimuli including viruses, cytokines and cytokine inducers can cause fatigue through alterations in basal ganglia function
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