Fatigue has been defined as the self-recognized state in which an individual experiences an overwhelming sustained sense of exhaustion and decreased capacity for physical and mental work. Key features of fatigue include constant tiredness, lack of energy, lack of motivation, and difficulty concentrating on and executing tasks. Fatigue is a significant health care issue; it affects 20–40% of the general population, and can have an impact on quality of life.

Unfortunately, it is difficult to treat something that is not understood; understanding is limited because fatigue is so complex, with components to be found in the realms of biology, sociology and psychology.

But most of us can agree that symptoms of fatigue, including difficulty concentrating on and executing tasks, would suggest a component of attention deficit. The so-called “attention system” consists of these networks:

• The alerting network.

• The orienting network.

• The executive control network.

An article in the February edition of the journal “Arthritis and Rheumatology” explored the hypothesis that fatigue in the inflammatory arthritic disease ankylosing spondylitis (AS) is associated with structural abnormalities in brain networks related to features of attention: the sensory salience network, the orienting network, and the executive control network.

The researchers accomplished this by having subjects with AS complete the Fatigue Severity Scale, the Affect Intensity Measure, and the McGill Pain Questionnaire, in addition to undergoing assessments of brain gray matter and white matter connectivity utilizing magnetic resonance imaging (MRI). And they found a relationship between fatigue in AS and brain cortex (gray matter) thinning in nodes of the orienting network (itself consisting of two types of attention networks), and brain cortex thickening in the executive control network. In addition, those subjects with high fatigue scores had white matter changes in these networks, consistent with diminished white matter tract integrity.

Of particular interest is the finding that greater fatigue was associated with thinning in the somatosensory cortices, areas primarily involved in sensory discrimination, but which have also been found to be abnormal in a variety of chronic pain conditions. And while it might be the case that these abnormalities are due to factors such as pain or central processes related to fatigue, it is also possible that the thinning of cortex in somatosensory areas leads to fatigue via sensory-attention integration.

Of course, the fatigue-associated structural changes could also be due to coexisting symptoms, such as pain, depression, or loss of mobility—particularly as the Fatigue Severity Scale scores were associated with pain and other clinical manifestations of chronic illness.

Remember the complexity of fatigue.

Still, at least as a starting point for future research, the data presented in this article do suggest that fatigue in AS is associated with abnormalities of the attention network and sensory salience.

Perhaps some day these brain networks will be the targets of therapies directed at alleviating the burden of fatigue in patients for whom fatigue only worsens other symptoms.

Symptoms such as chronic pain.

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