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brahim Aydo
dub
a Department of Clinical Neurophysiology, b Department of Neurology, Ege University Medical School
Hospital, Bornova,
zmir, Turkey
Correspondence to: Professor Cumhur Ertek
n, 1357 SOK, No:1 Da:10 Nilhan
Apt, Alsancak,
zm
r, Turkey. Telephone 0090 232 388 0980; fax 0090 232 4630074.
Received 10 October
1997 and in revised form 2 June 1998;
Accepted 15 June 1998
OBJECTIVE
To evaluate dysphagia at the
oropharyngeal stage of swallowing and to determine the
pathophysiological mechanisms of dysphagia in patients with myasthenia gravis.
METHODS
Fifteen patients with myasthenia gravis
with dysphagia and 10 patients without dysphagia were investigated by a
combined electrophysiological and mechanical method described
previously. Laryngeal movements were detected by a piezoelectric
transducer and the related submental EMG (SM-EMG) and sometimes the EMG
of cricopharyngeal muscle of the upper esophageal sphincter (CP-EMG)
were recorded during dry or wet swallowing. The results of these
electrophysiological variables were compared with those of normal age
matched control subjects.
RESULTS
In patients with myasthenia gravis with
dysphagia, it was found that the time necessary for the larynx to
remain in its superior position during swallowing and swallowing
variability in successive swallows increased significantly compared
with normal subjects and with patients with myasthenia gravis without
dysphagia. The total duration of SM-EMG activity was also prolonged in
both groups but more severely in the dysphagic patients.
Electromyographic activity of the CP sphincter was found to be normal
in the dysphagic patients investigated. All the patients with
myasthenia gravis with dysphagia had pathological dysphagia limits
(<20 ml water) whereas other patients except two, were within normal limits.
CONCLUSIONS
Because the electrophysiological
variables related to oropharyngeal swallowing were prolonged even in
patients with myasthenia gravis without dysphagia, it is concluded that
the submental and laryngeal elevators are involved subclinically in
myasthenia gravis and, because of compensating mechanisms, the patient
may not be dysphagic. As the CP-EMG behaviour was found to be normal, a
coordination disorder between normal CP sphincter muscle and the
affected striated muscles of the laryngeal elevators may be one of the
reasons for dysphagia in myasthenia gravis. This method also made it
possible to investigate the myasthenic involvement in the laryngeal
elevators that cannot be evaluated by other electrophysiological
methods in myasthenia gravis.
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