5.1 Introduction

Oromandibular dystonia or OMD is a neurologic disorder affecting both males and females with onset primarily in the fifth and sixth decades of life. It is characterized by repetitive, involuntary, patterned contractions or spasms of the masticatory, lingual, and perioral musculature. Typically, the dystonic movements are action induced and can impair speech, mastication, and swallowing, and cause significant social embarrassment. OMD is a subset of cranial-cervical dystonias, and when the symptoms of OMD are coupled with blepharospasm, the condition is known as Meige syndrome. Like other focal dystonias, it is usually a primary condition related to an underlying disorder at the levels of the basal ganglia and cerebellum. However, it may also occur secondary to other causes such as drug exposure (especially neuroleptics), Wilson disease, and peripheral injury such as dental procedures. ^{1 ,​ 2 ,​ 3 ,​ 4}

Oromandibular dystonia may be classified as jaw opening, jaw closing, jaw deviation, and tongue protrusion subtypes, with most cases representing a combination of these subtypes. Perioral movements (depressor anguli oris [DAO], platysma) and head turning (sternocleidomastoid muscle [SCM]) may also be associated, but it is not clear whether they are compensatory to the OMD or part of a more complex multifocal dystonia such as Meige syndrome.

5.2 Workup

Patients should be evaluated for a family history of dystonia or the presence of other dystonias. A detailed drug and psychiatric history is also very important to exclude the possibility of tardive dystonia secondary to dopaminergic antagonists or neuroleptic drugs. ¹ Some OMDs may be alleviated by a sensory trick, ⁵ or geste antagoniste, such as singing, chewing on a toothpick, placing an olive pit into the gingivobuccal sulcus, or scratching the chin. These sensory tricks afford temporary symptomatic relief. However, custom oral appliances may significantly benefit patients with jaw-opening OMD and can eliminate the need for botulinum toxin injections in some patients. ^{6 ,​ 7}

Oral agents may be used as first-line treatment for OMD; these show benefit in approximately one-third of these patients. ⁸ Evaluation by a neurologist for consideration of such treatment is a prudent initial step. Botulinum neurotoxin (BoNT) injections can also be used to reduce or eliminate involuntary movements and are well established as a treatment since their first description by Brin et al and Blitzer et al ^{9 ,​ 10} in 1987. Patients with jaw-closing OMD tend to respond better than patients with the other types of dystonic movements. Imaging may reveal evidence of prior head trauma or abnormality of the basal ganglia or cerebellum. Blood tests are not routinely performed prior to initiation of BoNT therapy, although low serum ceruloplasmin and certain genetic markers may be consistent with the diagnosis of dystonia.

5.3 Selection of Treatment Areas and Injection Anatomy

5.3.1 Jaw Deviation/Protrusion

Involuntary spasms of the external (lateral) pterygoid muscles are responsible for jaw-deviation and jaw-protrusion movements. Treatment of these OMD movements begins with injecting the external pterygoids. This muscle consists of two heads; the superior head originates on the greater wing of the sphenoid bone, and the inferior head originates on the lateral surface of the lateral pterygoid plate and runs posterolateral. The superior and inferior heads converge to insert into the medial aspect of the condylar process of the mandible (Fig. 5‑1).

Unilateral action of these muscles causes lateral jaw excursion to the contralateral side. Bilateral action of these muscles causes jaw protrusion or jaw opening. The internal (medial) pterygoids are primarily jaw closers but can work with the external pterygoids in jaw deviation (Fig. 5‑2). The anterior aspect of the temporalis muscles may also be targeted to treat jaw-deviation–related dystonia. ⁸

5.3.2 Jaw Closing

Involuntary actions of the masseter, temporalis, and internal or medial pterygoid muscles are responsible for jaw-closing OMD movements (Fig. 5‑3). Initial treatment involves injecting the masseter and temporalis muscles first and adding treatment of the internal pterygoid for nonresponsive cases or suboptimal results.

The masseter originates from the anterior two-thirds of the zygomatic arch and the zygomatic process of the maxilla. It inserts on the inferior and lateral surface of the angle and lower ramus of the mandible (Fig. 5‑4). The internal (or medial) pterygoid originates from the medial surface of the lateral pterygoid plate, pyramidal process of palatine bone, and maxillary tuberosity. It inserts on the medial angle of the mandible, forming a U-shaped sling around the inferior mandible border with the masseter. These two muscles elevate the mandible, enabling forced closure of the mouth.

The temporalis muscle is a broad fan-shaped muscle originating from the temporal lines on the parietal bone of the skull and inserting into the coronoid process of the mandible after passing medial to the zygomatic arch. It is covered by a strong thick fascia that can be felt as resistance when administering injections. It elevates and retracts the mandible (Fig. 5‑5).

The jaw-closing muscles are characterized by larger masses of contractile tissue ¹¹ compared with the jaw-opening muscles and accordingly require larger doses of BoNT. They respond better to BoNT treatment compared with the jaw-opening OMDs. ¹²

Related posts:

1 Pharmacology of Botulinum Neurotoxins 3 Botulinum Neurotoxin for Facial Dystonia 11 Botulinum Neurotoxin for Palatal Myoclonus 9 Botulinum Neurotoxin for Hyperfunctional Facial Lines 14 Botulinum Neurotoxin for Migraine 17 Botulinum Neurotoxin for Frey Syndrome

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