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Discomfort as the Outcome of Parafunctional Clenching

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Abstract

Parafunctional clenching is a deleterious mood for trigeminal and postural muscular tissues. Moreover, this misunderstood oral habit generates an overstimulation and nociception from the trigeminal territory. If considering various connections between trigeminal and non-trigeminal nervous centers, these are high-potential disruptive factors for physiological pathways through a supposed “neuronal overflowing” mechanism. Stressing conditions do emphasize these disturbances by a central influence (sensitization). Clinical dysfunctional outcome can be highly invalidating for patients and often disconcerting for clinicians. We clearly admit that to spontaneously make a link between the oral sphere and these signs or symptoms seems often illogical. That can happen with uncommon forms of fibromyalgia, migraine, or chronic fatigue, especially with stressed and/or introverted patients. But this kind of persistent events must incitate any clinician to unearth and eliminate the severe parafunctional clenching.

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Notes

  1. 1.

    In fact they are closely interrelated according to phylogenetic, ontogenetic, and embryological data. In order to open the Eustachian tube, the TVP makes a lateral movement with the medial pterygoid muscle and interposed fascia. Modifications in the intratympanic pressure result from a Eustachian tube dysfunction: this can explain some hypoacousis and tinnitus observed in TMD [9].

  2. 2.

    The ocular motor system is connected to postural muscles by the medial longitudinal fasciculus (MLF); it is a pathway between the motor and sensory nuclei of the cranial nerves and the anterior horn of the spinal cord, connecting the cranial nerves which intervene in head and eye motility [67] and in equilibration based on its important nervous origin in the vestibular nuclei [10, 55]. It has additional connections with the RF, the CC, the cerebellum, and the CGN. Through its ophthalmic branch (V1), V already plays a part in oculomotility, in the development of orientation selectivity, and more largely in the regulation of the oculo-cephalogyrus system. The oculomotor afferents could reach either the trigeminal MeN [23] or the trigeminal SP [74]. Some studies [14, 105] identified the trigeminal afferents pathways (V1) as the external ocular muscles (EOM), trigeminal ganglion, trigeminal SnC, and cervical medulla (C1,C2). Furthermore, fibers from the trigeminal MeN project to the medial vestibular nucleus. A recent study revealed that a monosynaptic pathway exists between vestibular nuclei and masseter motor neurons [24]. Some trigeminal proprioceptive afferents [21, 25, 30, 50, 59, 93, 104, 107] go across the SnI [49, 120] or NP [120] and project to the cerebellum. Some of these trigemino-cerebellar physiological projections come from PR [31]. Trigeminal afferents (for instance periodontal afferents) have proven that they supplement nicely visual messages to postural stabilization [39]. These are treated by the ­cerebellum with the purpose of refining the balance of the cranio-cervico-facial sphere in posture and motor coordination. These scientific data confirm previous data about possible trigeminal disturbances in the oculo-cephalogyrus system [79]. The evidence of a relationship between functional neck and trigeminal muscle afferent systems was found in the upper cervical chord and lower medulla where trigeminal afferents activate the m. splenius, m. biventer cervicis, and m. complexus [1]. Studies explain this type of close functional coupling between the trigeminal and cervical systems [12, 13, 33, 47, 126]. Jaw-muscle spindle afferents could reach the spinal cord through relays in the SnO and parvocellular RF [26]. Trigeminal inputs project from the NS to all levels of the cord [76, 94, 119]. Neonative polysynaptic pathways could transmit trigeminal stimulations all the way to the lumbar spinal cord. Electromyographic studies in humans [6, 20, 29, 80, 86, 124, 127] have attempted to prove that the trigeminal afferents could contribute to the regulation and stabilization of head posture during physiological functions such as mastication and swallowing. Let’s note that simple changes in the mandibular position have immediate repercussions on the EMG activity of head posture muscles, especially the trapezius [17]. Other EMG studies have also revealed the functional repercussions between the nuchal tonic reflex and the tone of the stomatognathic muscles [36, 38, 63, 71, 96]; trigeminal afferents can modify this reflex [79]. More evidence came from a 7-week-old embryo who responded to a stimulation of trigeminal receptors with a nuchal muscle reflex contraction called the trigemino-neck reflex [108]; this reflex is a sign of early nervous connections between the trigeminal system and head posture system. A new variant of trigemino-cervical reflex was observed in swine [62], but it is not yet been demonstrated in humans. A mouth-opening reflex was reported in a 14-week-old human fetus reacting to palmar stimulation [46]; these data confirm the previously noted connections between the V and the superior spinal roots. The activity of the obliquus capitis inferior muscle is EMG recorded during bruxism [124] which could explain some painful cervical symptoms when such stomatognathic parafunctions persist. In the same way the SCM under EMG responds to different masticatory movements and to intense durable voluntary clenching episodes [129]; this is confirmed for the SCM [20] as well as for the m. trapezius [127]. There is a reflex interaction between nociceptive trigeminal afferents and both upper and lower cervical spinal cord motor neurons [98].

  3. 3.

    These data could help to understand why rifle marksman’s results improve after an occlusal ­equilibration [78].

  4. 4.

    An asymmetrical sensory information originating from that area (e.g., unbalanced occlusion) would affect the head position or its perception and consequently produce a postural asymmetry of other body segments from top to bottom. It has been shown that the loss of occlusal supporting zone has a unilateral and bilateral influence on the weight distribution at the feet during clenching [128]. More recently a potential-evoked-signal investigation revealed that disturbance of the cortical functions regulating visual-motor integration could increase the risk of TMD [99]. Therefore, disorders in head posture regulation – even in body equilibrium – can occur via a trigemino-ocular dysfunction; for example, inputs from MOE, via the V1, could be disturbed by excessive V3 afferents elicited by exacerbated clenching. As we know today it is difficult to identify the CNS levels possibly caused by such disturbances: low pathways with the TBNC and high pathways with the colliculus superior [92], the cerebellum, etc. Regardless, the overstimulated and nociceptive afferent process intensifies reticular influence on motor neurons of stomatognathic [110, 112] and other muscles by creating as much spasticity as the limbic system (emotional factors).

  5. 5.

    During awakening, the serotonin activates some synthesis which is responsible to deferred ­setting of low sleep and paradoxal sleep (REM) by regulating the biosynthesis of hypnogenic substances. The sleeping would occur by diminution of the 5-HT bulbar neuronal activity and by liberation of these substances. The locus coeruleus is well known to be an important nervous structure in physiology of sleeping. It is rather curious to note that ancient French anatomists have originally given to this locus the name of trigeminal vegetative nucleus. Otherwise it has been shown that some hypothalamic 5-HT neurones are activated during awakening particularly during stressful events [54].

  6. 6.

    With the exception of spinal and brainstem detectors, the thermostatic center is primarily represented by the anterior hypothalamus and the preoptic area [10]; more precisely the hypothalamus ventralis posterior fights against cold and the anteromedial supraoptic area fights against heat. The thermosensitive neurons of the region react to blood temperature and to inputs brought by the fibers connected to the cutaneous and muscular thermoreceptors (Ruffini’s corpuscles and Krause’s corpuscles). In vertebrates fever is a major defensive process; prostaglandins, particularly PGE2, help raise the hypothalamic thermostat. However we know that an experimental destruction of the posterior hypothalamus leads to akinesia and the anterior hypothalamus to hyperkinesia.

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    Francis Hartmann & Gérard Cucchi

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Hartmann, F., Cucchi, G. (2014). Discomfort as the Outcome of Parafunctional Clenching. In: Stress and Orality. Springer, Paris. https://doi.org/10.1007/978-2-8178-0271-8_12

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