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ALS dysphagia pathophysiology: differential botulinum toxin response.

Domenico A Restivo1, Antonino Casabona, Alessia Nicotra

  • 1Neurologic Unit, Nuovo Garibaldi Hospital, Catania, Italy. darestivo@libero.it

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|January 25, 2013
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Summary

Botulinum toxin type A (BoTox-A) improved dysphagia in amyotrophic lateral sclerosis (ALS) patients with upper esophageal sphincter (UES) hyperactivity and no lower motor neuron (LMN) involvement. This suggests BoTox-A may be an alternative to percutaneous endoscopic gastrostomy (PEG).

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Area of Science:

  • Neurology
  • Gastroenterology
  • Pharmacology

Background:

  • Amyotrophic lateral sclerosis (ALS) frequently causes dysphagia, impacting patient quality of life and nutrition.
  • Dysphagia in ALS can stem from upper motor neuron (UMN) or combined UMN/lower motor neuron (LMN) involvement, affecting oral and oropharyngeal muscles.
  • Upper esophageal sphincter (UES) hyperactivity is a specific mechanism contributing to dysphagia in some ALS patients.

Purpose of the Study:

  • To evaluate the efficacy of botulinum toxin type A (BoTox-A) in treating dysphagia in ALS patients with UES hyperactivity.
  • To determine if the presence or absence of LMN involvement influences the response to BoTox-A treatment.
  • To explore BoTox-A as a potential alternative or adjunct to percutaneous endoscopic gastrostomy (PEG).

Main Methods:

  • A study involving 20 ALS patients with dysphagia and UES hyperactivity was conducted.
  • Patients were divided into two groups: those with isolated UMN involvement and those with combined UMN/LMN involvement.
  • All patients received BoTox-A injections into the UES, with dysphagia severity assessed using the Penetration/Aspiration Scale (PAS) at baseline and at 2, 4, and 20 weeks post-injection.

Main Results:

  • A significant reduction in PAS scores was observed at 2 and 4 weeks post-injection.
  • This improvement was primarily driven by patients without LMN involvement (Group 2).
  • No significant PAS reduction was observed in patients with LMN involvement (Group 1).

Conclusions:

  • BoTox-A treatment led to significant dysphagia improvement in ALS patients with isolated UES dysfunction.
  • The findings suggest that different pathophysiological mechanisms in ALS dysphagia result in varied responses to BoTox-A.
  • BoTox-A may offer a viable treatment option for dysphagia in specific ALS patient subgroups, potentially delaying or reducing the need for PEG.