Open Access Highly Accessed Research article

Cortical swallowing processing in early subacute stroke

Inga K Teismann1,2*†, Sonja Suntrup1,2†, Tobias Warnecke1, Olaf Steinsträter2, Maren Fischer1,2, Agnes Flöel3, E Bernd Ringelstein1, Christo Pantev2 and Rainer Dziewas1

Author Affiliations

1 Department of Neurology, University of Muenster, Albert-Schweitzer-Str.33, 48149 Muenster, Germany

2 Institute for Biomagnetism and Biosignalanalysis, University of Muenster, Malmedyweg 15, 48149 Muenster, Germany

3 Department of Neurology, Charite Universitätsmedizin Berlin, Charitéplatz 1, 10117 Berlin, Germany

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BMC Neurology 2011, 11:34 doi:10.1186/1471-2377-11-34

Published: 11 March 2011

Abstract

Background

Dysphagia is a major complication in hemispheric as well as brainstem stroke patients causing aspiration pneumonia and increased mortality. Little is known about the recovery from dysphagia after stroke. The aim of the present study was to determine the different patterns of cortical swallowing processing in patients with hemispheric and brainstem stroke with and without dysphagia in the early subacute phase.

Methods

We measured brain activity by mean of whole-head MEG in 37 patients with different stroke localisation 8.2 +/- 4.8 days after stroke to study changes in cortical activation during self-paced swallowing. An age matched group of healthy subjects served as controls. Data were analyzed by means of synthetic aperture magnetometry and group analyses were performed using a permutation test.

Results

Our results demonstrate strong bilateral reduction of cortical swallowing activation in dysphagic patients with hemispheric stroke. In hemispheric stroke without dysphagia, bilateral activation was found. In the small group of patients with brainstem stroke we observed a reduction of cortical activation and a right hemispheric lateralization.

Conclusion

Bulbar central pattern generators coordinate the pharyngeal swallowing phase. The observed right hemispheric lateralization in brainstem stroke can therefore be interpreted as acute cortical compensation of subcortically caused dysphagia. The reduction of activation in brainstem stroke patients and dysphagic patients with cortical stroke could be explained in terms of diaschisis.