Temporomandibular joint hyperlaxity can be divided into subluxation and dislocation. TMJ subluxation is the anterior displacement of the condylar head beyond the articular eminence in which the patient is able to reduce themselves with relative ease back into a normal positioning of the condylar head in the glenoid fossa. TMJ dislocation, similarly, is the anterior displacement of the condylar head beyond the articular eminence, but the patient is unable to reduce this malpositioning by their own efforts and requires professional assistance. For persistent chronic dislocation, treatment options include intraarticular injection of sclerosing agents or autologous blood, plication of capsular TMJ ligaments1, endoscopic anchoring procedures2, surgically induced mechanical impediments to translation (i.e. LeClerc procedure3), lateral pterygoid myotomy,4 and articular eminectomy (Myrhaug technique)5.


The Indiana University’s Oral and Maxillofacial Surgery Department protocol for patients with recurrent TMJ dislocation is based on the severity, frequency, and persistence of their episodes as well as the patient’s systemic health. Sequencing of treatment may initially include conscious self-limitation on maximal incisal opening and a soft diet. If the dislocations persist limited mobility may be achieved by applying guiding elastic or MMF for variable time periods. While various surgical interventions have been described we most commonly perform an eminectomy for a patient who was refractory to initial nonsurgical interventions and had persistent dislocation. This procedure involves placement of a preauricular incision with a superior release in the hairline. The dissection is then performed in a layered fashion to the zygomatic arch, and a subperiosteal dissection is performed to expose the glenoid fossa and articular eminence. The articular eminence is then reduced to eliminate any interference to the posterior seating of an anteriorly displaced condylar head. However there are times in which a patient is not a surgical candidate as in patient #1 or a patient with persistent dislocation despite surgical intervention.


Botulinum toxin is a zinc-dependent endoprotease neurotoxin that induces flaccid muscular paralysis and is produced by the gram-positive, anaerobic, spore forming bacteria Clostridium botulinum. This potent neurotoxin exerts its inhibition of muscular contraction by causing proteolysis of SNARE proteins in the presynaptic terminal at the neuromuscular junction. These proteins normally allow for “docking” of acetylcholine vesicles at the terminal membrane of the junction, and are required for vesicular fusion and acetylcholine release. Without acetylcholine available to bind on the post-synaptic terminal of the neuromuscular junction, muscular contraction is not possible. Clostridium botulinum produces seven strains of toxin, which are classified as types A, B, C1, D, E, and F, and all have the same mechanism of action. Of these types, botulinum toxin type A (BTX-A) is the most potent on humans and is commercially available as Botox (USA) and Dysport (UK). Because the amount of Botox necessary to exert clinical effects is so miniscule, dosage is measure in units of biologic activity rather than weight (mg). This measurement was established utilizing a standardized mouse model, in which 1 unit was the amount necessary to kill 50% (LD50) of 18-20g female Swiss-Webster mice when injected intraperitoneally. Botox is used to address many maxillofacial functional and cosmetic conditions, including strabismus, blepharospasm, facial and cervical dystonia, torticollis, myofascial pain disorder, facial rhytids, Frey’s syndrome, facial hyperhidrosis, and sialorrhea.


The primary masticatory muscles include the temporalis, masseter, medial pterygoid, and lateral pterygoid (see Table 1). The lateral pterygoid muscle is the only of the primary muscles that contribute to the opening action of the jaws. It is this muscle that presumably contributes to open lock by hyperactivity or spasm that contributes either to hypermobility anterior to the articular eminence or the difficulty with reduction of the condyle posteriorly into the glenoid fossa. This muscular structure is the target of Botox therapy in this method of treatment.


Table 1. Muscles of mastication.

Table 1. Muscles of mastication.


There are a few case reports in the literature that have described the technique of LPM Botox injections for TMJ open lock. Fu and Chen provided a case series of 5 patients treated for either unilateral or bilateral recurrent TMJ dislocation. Each patient was treated with a single course of bilateral LPM injections of 25-50 units Botox injections and a 4-5 day period of maxillomandibular fixation was applied post-injection. Only one patient experienced a recurrent dislocation within 2 days of initial treatment, which is presumed to have occurred prior to the maximum onset of the therapeutic action of the Botox. No other recurrences were noted during the subsequent 3-24 month follow-up period and no complications were encountered with treatment.


Though no complications were noted in Fu and Chen’s case series, there are some potential complications of the procedure. Martinez-Perez and Ruiz-Espiga7 reported 3 cases in 2004 of the successful use of LPM Botox injections of 50 MU for TMJ dislocation. One of their 3 patients experienced a brief unpleasant phase of velopharyngeal incompetence with nasal fluid reflux for several weeks after her initial treatment, which eventually resolved. Similarly, Bouso and Gonalez9 reviewed their experience of 4 cases of LPM Botox injections for recurrent TMJ dislocation, each of which was treated with bilateral 20-40 MU Botox injections under EMG guidance. One patient in their case report of 4 patients experienced a brief course of dysphagia that required a mechanical soft diet. Pharyngeal paralysis (partial or complete) does seem to be the most pertinent risk, which typically results in VPI or dysphagia. Although the use of EMG guidance should theoretically help prevent this complication, the study by Bouso and Gonzalez shows that it does not completely eliminate the risk.


The largest case series describing the use of Botox for TMJ open lock found in our literature search was that of Ziegler and Muhling6. They wrote a case series of 21 patients that were treated for recurrent TMJ dislocation of various causes (habitual dislocation, organic psychosis). The treatment consisted of 50-100 units Botox administered at bilateral LPM via EMG guidance via transcutaneous approach through the sigmoid notch. The treatments were performed regularly at 3-month intervals from 6-18 months. During the three month treatment intervals in which patients were receiving botox, only two patients experienced recurrence. Four additional patients did experience recurrence at 11, 14, and 17 months after their final treatment was administered. Botox generally begins to exert its initial effects 2-4 days after administration, with maximal flaccid paralysis noted at 7-10 days. The duration of action is typically 2-5 months, which is dose dependent. In the case of early recurrences (3-6 months), the likely etiologic factor is the loss of therapeutic effect of the Botox on the muscle, with resumed spastic muscular hyperactivity. In the case of late recurrences, it may be possible that the Botox provides some level of scarring and reduced laxity of the surrounding soft tissue anatomy, but eventually this tissue slowly becomes lax again over time with increased function after of the Botox loses its efficacy. In either instance, retreatment with a similar dose is typically effective.


The most commonly described method of administration of the LPM Botox is on an awake patient without sedation or local anesthesia. This is preferable mainly because the need for activation of the LPM by the patient in order to register and confirm intramuscular placement of the needle utilizing EMG. However, Bouso and Gonalez described a technique to elicit muscular EMG response from the LPM on patient’s undergoing the procedure under general anesthesia, which they described on a patient in their case series that was unable to tolerate the procedure under local. They described the use of striking the chin with a reflex hammer (originally described by Moore and Wood) to elicit an EMG response to confirm needle placement. The strict avoidance of non-depolarizing paralytics is a key point to success with this technique.


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