Cognitive basis proposed for fatigue after stroke

By Eleanor McDermid, Senior medwireNews Reporter

Research shows that poststroke fatigue (PSF) in patients with nondisabling stroke is tied to a specific type of cognitive dysfunction.

The prospective study, published in Neurology, links impaired attentional and executive impairment, as well as depression and anxiety, to PSF. Rather than being predictive of PSF development, these types of cognitive dysfunction were associated with the presence of PSF at 6 and 12 months after stroke.

In an editorial accompanying the article, Mansur Kutlubaev (Kuvatov's Republican Clinical Hospital, Ufa, Russia) and Gillian Mead (University of Edinburgh, UK) say that it is not clear whether these cognitive deficits cause fatigue or vice versa.

But they note: "The study results are consistent with the hypothesis that a stroke lesion affecting the neural circuits involved in regulation of attention and executive function may contribute to the development of tiredness and aversion to effort, and subsequently to the development of the behavioral phenomenon of fatigue."

Fatigue, as identified on the Fatigue Assessment Inventory, was common in the study, affecting 30.5% of the 99 patients at 6 months after stroke onset and rising to 34.7% at 12 months. But this did not arise from the physical consequences of stroke; the patients had very little or no disability, with a modified Rankin Scale score of 0 or 1 at 6 months after the event.

Nearly two-thirds of the patients who were employed before their strokes had reduced or stopped working at the 6-month follow up, and this was significantly associated with the presence of PSF on multivariate analysis.

In contrast to previous studies, Julien Bogousslavsky (Center for Brain and Nervous System Disorders, Genolier, Switzerland) found that the side and site of the stroke lesion had no bearing on whether patients developed PSF.

But Kutlubaev and Mead point out that the circuitry involved with attention and executive function is spread throughout the brain. Thus "it is not surprising that lesions in different parts of the brain may all contribute to the development of fatigue, by disrupting these neural circuits."

They conclude that the findings represent "an important step toward a better understanding of the mechanisms of PSF," but add that further research is necessary. "This is crucial for clarifying the etiology of PSF, and for the subsequent development of effective treatment strategies for this common and debilitating sequel of stroke."

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