Botulinum Toxin Treatment for Oropharyngeal Dysphagia Associated With Diabetic Neuropathy treatment.

Botulinum Toxin Treatment for Oropharyngeal Dysphagia Associated With Diabetic Neuropathy treatment.

Chemical myotomy of the cricopharyngeus (CP) muscle by botulinum neurotoxin type A (BoNT/A) has been effective in reducing or abolishing dysphagia associated with upper esophageal sphincter (UES) hyperactivity of different etiologies. In the present study, we evaluated the efficacy of BoNT/A injections into the CP muscle in diabetic patients with severe oropharyngeal dysphagia associated with diabetic autonomic and/or somatic peripheral neuropathy. Our findings suggest a potential benefit from BoNT/A treatment in dysphagia associated with diabetic neuropathy. Randomized controlled trials are needed to confirm this observation.

Swallowing permits the ingestion of fluids and food without aspiration. A number of processes are required for normal swallowing, including voluntary and reflexive motor control, as well as integrity of several cranial nerves and muscles. Disruption of normal swallowing, dysphagia, is a frequent sequela of many neurological and neuromuscular disorders.

Autonomic and/or peripheral neuropathy is a common complication of diabetes and is due to chronic hyperglycemia and diabetic microvascular disease involving vasa nervorum. Dysphagia has been observed in diabetic patients, but its prevalence has never been assessed. Moreover, whether dysphagia in diabetic patients is caused by diabetic neuropathy and whether the pathophysiological features of nerve involvement are the same in all diabetic patients with dysphagia is not known . Although all phases of swallowing can be involved, oropharyngeal dysphagia due to hyperactivity of the cricopharyngeus (CP) muscle of the upper esophageal sphincter (UES) is the prevalent abnormality . A prospective study in 33 diabetic patients evaluated by esophageal manometry showed isolated or combined involvement of the upper and lower esophageal sphincter in ∼60% of patients.

In diabetic patients, oropharyngeal dysphagia associated with autonomic and/or somatic peripheral neuropathy is likely more frequent than previously presumed, and its pathophysiology has not been completely elucidated (3,4,6). Although all phases of swallowing can be involved, the oropharyngeal phase is the most frequently impaired phase in diabetic patients (1,3,4,6). Control of oropharyngeal swallowing is mediated by voluntary and involuntary (reflexive) mechanisms. Although voluntary swallowing is not an autonomic function, it is allowed by the coordination of two muscles: the IC muscle, which controls the voluntary component, and the CP muscle of the UES, which controls the involuntary (reflexive) component. During voluntary swallowing, the activation of the IC muscle is synchronous with the relaxation of CP muscle, thus allowing the bolus to transit into the upper esophageal tract. In patients with dysphagia due to diabetic neuropathy, the coordination between the two muscular components (CP and IC) is impaired. This can be assessed by dynamic EMG analysis. In all our diabetic patients, the IC muscle showed neuropathic changes and reduced activity during swallowing. The denervation of the IC muscle induces the reduction of its voluntary activation with consequent impairment to the physiological balance between these two components. In fact, the reduction of the voluntary activation (contraction) may lead to a tonic hyperactivation of the CP muscle that cannot be inhibited and causes a defective control of voluntary and reflexive mechanisms during voluntary swallowing. A long-lasting block of the parasympathetic fibers innervating the CP muscle might be useful for treating UES hyperactivity.

Percutaneous injection of BoNT/A has been already used to successfully treat CP muscle hyperactivity associated with various neurological diseases (10–14). Our study demonstrated that BoNT/A is a safe and very effective treatment also for dysphagia associated with diabetic neuropathy.

The advantage of BoNT/A treatment is that it can be performed in an outpatient clinic, needing neither hospitalization nor anesthesia. It can be repeated when the symptoms reappear, retains the same efficacy, and requires no specific follow-up. However, this treatment may have potential risks. The diffusion of BoNT/A into the nearby laryngeal muscles might lead to laryngeal spasm or to worsening of the preexisting dysphagia. For this reason, the treatment must be carried out under electromyographic guidance by an expert operator in order to identify the target muscle and to rule out the possible diffusion of the botulinum toxin into the nearby laryngeal muscles.