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According to the "pain adaptation model", temporomandibular disorder (TMD) pain induces a paradoxical activity of masticatory muscles: an agonistic hypoactivity during jaw closing and a weak antagonistic activity during jaw opening (agonist/antagonist co-activation); the pain-induced motor regulation implies the segmental trigeminal (V) motor system and/or CPG. This model has been extended to other types of musculoskeletal disorders (MSD). However, despite its power, this model does not fit with all types of neck muscle activities in neck pain. This discrepancy may be due: to the complexity of the cervical spine (with its numerous agonist, antagonist and synergist muscles), and to the specificities of the cervical neuromuscular system in interrelationships with the control of body and head posture, the patency of the upper airway depending on head/ cervical posture, the neck and arm/shoulder muscles' activity, and finally, the neck and masticatory muscles' activity. Besides pain, psychological stress may induce motor dysfunction in MSD (e.g. kinesiophobia, difficulty switching off). Finally, it is hypothesised that tongue dysfunction could be connected to TMD (due to intersegmental coordination between V, VII and XII motor nuclei): the weakness of the agonistic activity of masticatory muscles would favour immature deglutition, where facial muscle (VII) activity predominates over masticatory muscle (V) activity. [ABSTRACT FROM AUTHOR]

L'articulation temporo-mandibulaire (ATM) est une articulation complexe, les surfaces articulaires non concordantes s'adaptant grâce au tendon du muscle ptérygoïdien latéral qui coulisse entre elles lors de tous les mouvements mandibulaires. Il n'existe pas de parallélisme anatomoclinique entre l'importance de l'atteinte articulaire et la gravité des symptômes ressentis par le patient. L'anatomie descriptive de l'ATM est bien connue, malgré une certaine variabilité, mais son aspect dynamique l'est moins en l'absence d'un système d'imagerie adapté au suivi tridimensionnel d'un sujet en temps réel. L'abord pluridisciplinaire de la pathologie des dysfonctions de l'ATM a fait progresser la connaissance de l'anatomie fonctionnelle de cette articulation. Le nerf mandibulaire en assure l'innervation motrice et sensitive pouvant initier un cercle vicieux entre spasmes et douleurs. L'imputabilité des symptômes otologiques, présents lors de certains cas de dysfonctions de l'ATM, ne peut être retenue de façon systématique. The temporomandibular joint (TMJ) is a complex joint, with the mismatched articular surfaces adapting to one another via the tendon of the lateral pterygoid muscle which slides between them during all jaw movements. There are no anatomical or clinical correlations between the significance of a joint condition and the severity of symptoms experienced by the patient. The descriptive anatomy of the TMJ is well-known despite some variability, but its dynamic aspects are less so due to the lack of an imaging system adapted to three-dimensional follow-up of an individual in real time. A multidisciplinary approach to TMJ dysfunctions has prompted a more in-depth knowledge on the functional anatomy of this joint to be developed. Motor and sensory innervation is derived from the mandibular nerve, which may lead to a vicious circle between spasms and pain. A causal relationship with otological symptoms present in some cases of TMJ dysfunctions cannot be considered as standard. [ABSTRACT FROM AUTHOR]

Summary: Introduction: Hypertrophy of the masticatory muscles most commonly affects the masseter. Less common cases of isolated or associated temporalis hypertrophy are also reported. Parafunctional habits, and more precisely bruxism, can favor the onset of the hypertrophy. This condition is generally idiopathic and can require both medical and/or surgical management. Observation: A 29-year-old patient was referred to our department for an asymmetric swelling of the masticatory muscles. Physical examination revealed a bilateral hypertrophy of the masticatory muscles, predominantly affecting the right temporalis and the left masseter. Major bruxism was assessed by premature dental wearing. The additional examinations confirmed the isolated muscle hypertrophy. Benign asymmetric hypertrophy of the masticatory muscles promoted by bruxism was diagnosed. Treatment with injections of type A botulinum toxin was conducted in association with a splint and relaxation. Its effectiveness has been observed at six months. Discussion: Few cases of unilateral or bilateral temporalis hypertrophy have been reported, added to the more common isolated masseter muscles hypertrophy. The diagnosis requires to rule out secondary hypertrophies and tumors using Magnetic Resonance Imaging. The condition is thought to be favoured by parafunctional habits such as bruxism. The conservative treatment consists in reducing the volume of the masticatory muscles using intramuscular injections of type A botulinum toxin. Other potential conservative treatments are wearing splints and muscle relaxant drugs. Surgical procedures aiming to reduce the muscle volume and/or the bone volume (mandibular gonioplasty) can be proposed. [ABSTRACT FROM AUTHOR]