• Journal of the Korean Society of Laryngology, Phoniatrics and Logopedics
• /
• v.30 no.2
• /
• pp.77-81
• /
• 2019

Dysphagia may result from dysfunction of any of the components involved in the complex neuromuscular interaction of swallowing. Hyperfunction of any of the muscles involved in swallowing is a frequent cause of dysphagia. The cricopharyngeus muscle (CPM) is a key component of the upper esophageal sphincter. Cricopharyngeus muscle dysfunction (CPD) refers to the muscle's failure to appropriately and completely relax or expand during deglutition. A variety of disease processes may cause CPD and accurate diagnosis is paramount for appropriate treatment. In appropriately selected patients, intervention at the CPM may yield significant improvement in dysphagia. Interventions include nonsurgical, pharyngoesophageal segment dilatation, botulinum toxin (BoNT) injection, and criccopharyngeal myotomy. Injections of BoNT in patients with CPD have been reported to result in marked relief of dysphagia. Different techniques for instilling BoNT into the CPM have been described. Awake, in-office CPM BoNT injection with electromyography and/or fluoroscopic or ultrasound guidance is performed transcervically or via flexible endoscopy. Operative CPM BoNT injection involves rigid laryngoscopy and esophagoscopy with direct visualization of the CPM. BoNT should be prepared in low-volume, high-concentration dilutions to minimize the potential for undesired diffusion of the toxin. The effects of BoNT occur within weeks of injection and typically last up to 5 or 6 months.

• Journal of The Korean Dental Society of Anesthesiology
• /
• v.10 no.1
• /
• pp.13-19
• /
• 2010

Bruxism is nonfunctional jaw movement that includes clenching, grinding and gnashing of teeth. It usually occurs during sleep, but with functional abnormality of brain, it can be seen during consciousness. Oromandibular dystonia (OMD) can involve the masticatory, lower facial, and tongue muscles and may result in trismus, bruxism, involuntary jaw opening or closure, and involuntary tongue movement. Its prevalence in the general population is 21%, but its incidence after brain injury is unknown, Untreated, bruxism and OMD cause masseter hypertrophy, headache, temporomandibular joint destruction and total dental wear. We report a case of successful treatment of bruxism and OMD after brain injury treated with botulinum toxin A and occlusal appliance. The patient was a 59-year-old man with operation history of frontal craniotomy and removal of malformed vessel secondary to cerebral arteriovenous malfomation. We injected with a total 60 units of botulinum toxin A each masseteric muscle and took impression for occlusal appliance fabrication under general anesthesia. On follow up 2 weeks and 2 months, the patient remained almost free of bruxism. We propose that botulinum toxin A and occlusal appliances be considered as a treatment for bruxism and OMD after brain injury.