Botulinum Toxin Type A in the Management of Oromandibular Dystonia and Bruxism

Oromandibular dystonia (OMD) refers to involuntary spasms of masticatory, lingual, and pharyngeal muscles. Phenomenologically, there are seven types of OMD: jaw-closing dystonia (JCD); jaw-opening dystonia (JOD); jaw-deviation dystonia (JDD); lip and perioral dystonia; lingual dystonia; pharyngeal dystonia; and combination OMD (1). OMD may be seen in isolation (focal dystonia), as part of a more widespread segmental cranial dystonia, or as part of a multisegmental or generalized dystonia. In 1910, the French neurologist Henry Meige described a syndrome, sometimes still referred to as Meige’s syndrome, that occurred predominantly in middle-aged women and consisted of spasms of the eyelids as well as contractions of the pharyngeal, jaw, and tongue muscles (2). Because Meige was not the first to describe the disorder (Horatio Wood, a Philadelphia neurologist, described facial and oromandibular dystonia in 1887) (3), the syndrome is nowmore accurately referred to as cranial dystonia. The etiologies of OMD are diverse (Table 33.1). The leading cause is primary (idiopathic) dystonia, which is often associated with other dystonias, particularly cervical and cranial. Some cases of OMD may be manifestations of inherited disorders; however, DYT1 dystonia, caused by a mutation of the torsinA gene on chromosome 9q34, the most common form of inherited dystonia, rarely involves the cranial structures (4). A patient with adult-onset OMD and no obvious family history of dystonia has