Comments on selected recent dysphagia literature

Abstract

Hamdy et al. note, ‘‘Oropharyngeal dysphagia occurs in up to a third of patients presenting with a unilateral hemiplegic stroke, yet its neurophysiological basis remains unknown.’’ They continue, ‘‘Animal data indicate that stimulation of either cortical hemisphere can initiate swallowing, which suggests that dysphagia after a stroke is due to damage either to both hemispheres or to the brainstem swallowing centre. However, neuropathological examination of dysphagic stroke patients either at necropsy or with magnetic resonance imaging has shown that, in many cases, the lesion is discrete and unilateral.’’ The authors previously reported on the use of transcranial magneto-electric stimulation (TCMS) to identify the corticofugal projections to the muscles of swallowing [1]. They found ‘‘that oral muscles, such as the mylohyoids are represented symmetrically between the two hemispheres, whereas muscles of the pharynx and oesophagus are represented very asymmetrically, with most individuals having a dominant swallowing hemisphere, independent of handedness.’’ Based on these earlier findings, Hamdy et al. generated ‘‘two hypotheses to explain why a unilateral hemispheric stroke might cause oropharyngeal dysphagia.’’ They state, ‘‘First, innervation of the brainstem by both hemispheric centres might be required to initiate swallowing, so destruction of either would leave inadequate cortical function to evoke normal swallowing. . . . Alternatively, since there is functional asymmetry between the two hemispheres for pharyngeal function, oropharyngeal dysphagia would result from damage to the hemisphere where the dominant pharyngeal centre was located. This second hypothesis would also predict that swallowing should remain normal if the dominant centre for pharyngeal function was present on the unaffected hemisphere.’’ The authors recruited 20 patients with unilateral hemiplegic stroke within the previous 6 weeks. Patients underwent the following evaluations: (1) clinical examination by a speech and language therapist using a standardized bedside assessment, (2) standardized neurological assessment, (3) submental electromyography (EMG) of mylohyoid muscles, (4) pharyngeal EMG via an intraluminal catheter positioned with manometric guidance, (5) EMG of muscles of the thenar eminence (muscles that have contralateral but symmetrical hemispheric representation), and (6) an experimental protocol using TCMS to determine excitability thresholds and motor-evoked response amplitudes and latencies. Eight of the 20 patients had oropharyngeal dysphagia, and the other 12 patients swallowed normally. Computed tomography of the brain revealed that 4 of the dysphagic patients had right hemisphere infarcts and 4 had left hemisphere infarcts. Six of the nondysphagic patients had right hemisphere infarcts, and 6 had left hemisphere infarcts. Hamdy et al. report, ‘‘Our study has shown that patients dysphagic after unilateral hemisphere stroke have smaller pharyngeal responses from the unaffected hemisphere than do non-dysphagic patients, irrespective of the side and level (cortical or subcortical) of the lesion. . . . One possible explanation for this difference is that the smaller responses are a reflection of the asymmetrical motor representation of pharyngeal function on the cerebral cortex. In other words, with damage to the hemisphere containing the predominant pharyngeal centre, swallowing cannot be maintained by the smaller pharyngeal centre in the unaffected hemisphere.’’ The authors continue, ‘‘The similarity in mylohyoid responses between dysphagic and non-dysphagic stroke patients is consistent both with our observation that the dysphagic patients had predominantly pharyngeal swallowing problems, and the fact that the pharyngeal phase of swallowing is the most important clinical determinant of aspiration in stroke populations. Furthermore, . . . our findings suggest that the cortical control of Dysphagia 13:116–120 (1998)