Records describing studies on the pathophysiology and etiology of somatosensory tinnitus were included and are reviewed here. A table compiling the case controlled studies and cross-sectional studies were summarized in Appendix 2 in Supplementary Material (case reports, reviews and book chapters were excluded).

A number of authors suggest the somatosensory stimuli inducing tinnitus are deeply related to abnormal cross-modal plasticity of somatic-auditory interactions (Cacace, 2003; Levine et al., 2007; Herraiz, 2008; Rocha et al., 2008; Koehler and Shore, 2013) whereby somatic modulations of tinnitus results from abnormal auditory neural interactions—distortion of the normal synaptic activity—within the central nervous system, as Sanchez et al. (2007) describes, “The information triggered by muscle contractions is carried by the somatosensory system and, upon reaching the cuneiform nucleus, may influence tinnitus through its projection over the auditory pathway due to an overactivitiy in the cochlear nucleus.” In particular, modulation of hyperactivity of neurons in the dorsal cochlear is triggered by the stimulation of specific ipsilateral cranial nerves, i.e., branch of the trigeminal nerve, explaining how ipsilateral tinnitus may be modulated by head and neck's manipulation (see a review, Kaltenbach, 2006). In guinea pigs, it was demonstrated that DCN bimodal plasticity is stimulus timing-dependant and implicated as an underlying mechanism in tinnitus (Shore et al., 2007; Koehler and Shore, 2013).

Levine et al. (2003) found somatic modulation in patients with tinnitus and deafness patients, identifying neural interactions in the central nervous system as the main protagonists in this process. Levine et al. (2008) also suggest that pulsatile tinnitus is modulated by the somatosensory system of the head or upper lateral neck, presenting two mechanisms; (1) cardiac synchronous somatosensory activation of the central auditory pathway, or (2) distortion of the normal synaptic activity between the somatosensory and auditory central nervous system. Simmons et al. (2008), studying patients who could modulate tinnitus with jaw clench found that an alteration in tinnitus loudness related to a variation in neural activity in the auditory cortex, concluding that tinnitus originates in the central auditory pathway. The same effect has been observed in patients who can modulate their tinnitus with eye movements (Lockwood et al., 2001; Sanchez and Akemi, 2008), and in patients whose tinnitus is modulated by intravenous administration of lidocaine (Reyes et al., 2002). Modulation of tinnitus with oral-facial movements suggest that the classical auditory system is not implicated in tinnitus because limbic structures respond to sound stimulation in patients with tinnitus (through hypoactivity localized in the hippocampus), further indicating the central auditory system and not the cochlea as the origin of tinnitus (Lockwood et al., 1998; Cacace, 2003; Schaette and McAlpine, 2011). In his studies, Levine found that patients could better detect changes in their tinnitus when using isometric maneuvers of the extremities, compared to head/neck maneuvers, suggestive of a major role of the central neural pathway as opposed to the auditory periphery (Cacace, 2003). In fact, a higher prevalence of somatoform disorders in individuals with tinnitus may also relate to certain craniocervical pathological features (e.g., herniated discs or temporomandibular joint syndrome; Chole and Parker, 1992; Rubinstein, 1993; Gelb et al., 1997; Levine, 1999b) and dental and jaw diseases (Han et al., 2009). For example, there is a higher than general incidence of tinnitus in patients and normal hearing who have temporomandibular disorder (TMD) (Levine, 1999b), suggesting that it may be associated with other symptoms of TMD (Chole and Parker, 1992; Bernhardt et al., 2011). The temporomandibular joint (TMJ) is thought to be commonly involved in the ability to modulate tinnitus, particularly its loudness (Ralli et al., 2016). Recently the risk of tinnitus was established as 8.37 times higher for patients with TMD (Bürgers et al., 2013), and unilateral tinnitus is even reported to be on the same side as unilateral TMD (Bürgers et al., 2013). These patients are also reportedly able to regulate their tinnitus through certain jaw or neck movements (Wright and Bifano, 1997a; Vielsmeier et al., 2011, 2012; Bürgers et al., 2013). Since tinnitus is normally related to the opposite risk factors (i.e., older males with hearing loss), such findings postulate that TMJ may be the cause and maintenance of tinnitus (Vielsmeier et al., 2011). It is proposed that TMD can cause tinnitus through the disruption of the trigeminal input (Vielsmeier et al., 2012; Ostermann et al., 2016). Another indication supporting the role of TMD in tinnitus is that the two conditions occur simultaneously. Evidence also shows that worsening of tinnitus coincides with aggravation of TMD (Wright and Bifano, 1997b).

Records describing studies on diagnosis or rate of diagnosis of somatosensory tinnitus were included and are reviewed here. A table compiling the case controlled studies and cross-sectional studies were summarized in Appendixes 3, 4 in Supplementary Material (reviews, thesis, and book chapters were excluded), concerning both epidemiology and diagnosis fields, respectively.

Common attributed risk factors for any subtype of tinnitus are male gender, older in age and hearing problems (i.e., Hazell, 1991; Abel and Levine, 2004; Eggermont and Roberts, 2004; Hoffman and Reed, 2004; Oostendorp et al., 2016), except for TMD-tinnitus patients (Chole and Parker, 1992; Wright and Bifano, 1997b; Vielsmeier et al., 2011; Bürgers et al., 2013). Recent evidence in a British cohort study shows that somatic tinnitus is more common among younger people and it is unrelated to hearing loss or tinnitus severity (Ward et al., 2015). Some of these audiological and demographic traits, may be indeed useful in informing therapy (Won et al., 2013) through the identification of “clinical criteria for useful subtyping of tinnitus patients” (Vielsmeier et al., 2012).

Signs of somatosensory tinnitus include head or neck problems (i.e., temporomandibular joint syndrome, osteophits, arthorosis, spondylosis, myofascial trigger points, etc.), dental or jaw diseases, frequent pain in head, neck, or shoulder girdle, aggravation of events of simultaneous pain and tinnitus, incorrect body postures, and severe bruxism (Sanchez and Rocha, 2011b,c). Such complexity demands a multidisciplinary team (i.e., dentist, physiotherapist) to diagnose.

Somatosensory tinnitus is strongly evidenced when the patient can modulate the loudness or intensity of their tinnitus (Abel and Levine, 2004; Latifpour et al., 2009; Sanchez and Rocha, 2011b,c; Oostendorp et al., 2016). Hence somatic testing may identify patients who could be treated with somatosensory system-related therapies. However, this type of testing receives little attention (Won et al., 2013).

There are various presentations of somatosensory tinnitus to be aware of. Typical cases include gaze-evoked or modulated tinnitus, cutaneous-evoked tinnitus, and tinnitus modulated by movement of corporal elements (i.e., head, fingers, jaw). Gaze-evoked/modulated tinnitus, the modulation of tinnitus by eye movement, provides clues on the potential cortical role in tinnitus (Lockwood et al., 2001). Simmons et al. (2008) found a large sample of patients who were capable of modulating their tinnitus by eye movement, half of whom had developed this ability after undergoing surgery for removal of an acoustic neuroma; these patients were able to change the tinnitus loudness and pitch through eye movement.

Studies of cutaneous-evoked tinnitus (using magnetoencephalographic signals and tactile discrimination tests) have found that cutaneous stimulation of skin on the hand region (specifically palm and fingers) activates the somatosensory system along with the auditory cortical areas in congenitally deaf individuals (Cacace et al., 1999a,b; Cacace, 2003).

In respect to modulation of tinnitus through of head and neck, Levine (1999a) reported that 68% of 70 patients could modulate tinnitus through maneuvers of the head, neck, or less intensely, maneuvers of limb. Similarly, Sanchez et al. (2002) found both patients with tinnitus (65.3% of 121 persons) and healthy subjects (14% of 100) could modulate or develop, respectively, tinnitus through 16 different maneuvers, and later found 57.9% of a study population could modulate tinnitus using nine different maneuvers (Sanchez et al., 2007). Simmons et al. (2008) found that, in 93 subjects able to modulate tinnitus by jaw clench, 90% could increase the loudness of their tinnitus, and 50% could alter the pitch. In a different assessment, the same authors found that 78% of their sample of 45 subjects could modulate their tinnitus with movement of the head or neck, mainly using the cranial and cervical nerves and using forceful maneuvers. In another study, Won et al. (2013) found that in 57% of tested ears in a population sample of 163 patients, tinnitus (especially unilateral tinnitus) was modulated through neck maneuvers or jaw maneuvers, decreasing and increasing tinnitus loudness respectively. The authors also reported that in their sample bilateral and low-pitch tonal tinnitus was rarely modulated by movement and may even be aggravated by somatic therapy. More distal movement is also observed to modulate tinnitus. Cullington (2001) reported the case of a 78-year-old man with severe hearing loss implanted with a cochlear implant in his right ear was able to modulate his tinnitus by moving his finger. Fascinatingly, this patient reported that the quicker the movement, the more intense was tinnitus loudness; passive or isometric movement did not modulate the tinnitus (Sanchez and Akemi, 2008). See Table 1 for a summary of somatic maneuvers.

Even when the patient cannot self-modulate tinnitus, it may be altered by other kinds of stimuli, using maneuvers to increase activity of the trigeminal nerve such as passive muscular palpation to find myofascial trigger points (MFT), relaxation, and massage (Simmons et al., 2008; Sanchez and Rocha, 2011b; Shore, 2011; Won et al., 2013).

Records describing studies on the treatment of somatosensory tinnitus were included and are reviewed here by treatment category. Case controlled studies and cross-sectional studies were summarized in Appendix 5 in Supplementary Material.

Studies have accounted the benefits for tinnitus of treating (temporomandibular disorder) TMD. Wright and Bifano (1997a) studied tinnitus in TMD patients and reported that 56% had been cured and 30% had a significant improvement with cognitive therapy and modulation through maneuvers. However, it has also been found that that severe tinnitus is less likely to improve with TMD therapy (Wright and Bifano, 1997a). Another similar study has shown that younger patients with moderate tinnitus were more likely to experience relief of their tinnitus through TMD therapy (Wright and Bifano, 1997b). Tinnitus severity as a predictor of the effectiveness of TMD therapy has already been proposed by others including Erlandsson et al. (1991) and Bush (1987).

The presence of fluctuating tinnitus is another factor that may associate with TMD treatment effectiveness (e.g., Tullberg and Ernberg, 2006).

One form of TMD treatment is occlusal splint therapy (Attanasio et al., 2015). In their study involving this treatment in patients presenting with chronic subjective tinnitus Attanasio et al. (2015) divided patients into three groups according to whether TMD was absent, present, or the patient was considered predisposed to TMD. Patients were subjected to treatment with a neuromuscular occlusal splint for 6 months (using the splint at night time) and rated for the severity of tinnitus using 10-point visual analog scale and Tinnitus Handicap Inventory (THI; Newman et al., 2004) questionnaire. Post-treatment THI scores were reduced in all groups but was most pronounced in the TMD (experience or predisposed) groups. The authors concluded that, once otologic disorders and neurological diseases are excluded, that clinicians should refer patients for an evaluation of the temporomandibular joint and subsequently to treat patients with TMD or a predisposition to it.

Wright (2000) suggested oro-myofunctional therapy as an effective alternative to occlusal splints therapy. Their study involved patients from the US air force seeking treatment for tinnitus, dizziness, and/or nonotologic otalgia without an identifiable cause and presenting with TMD symptoms in the temple, jaw, or preauricular area. Patients were provided a dental orthotic and TMD self-care instructions. After 3 months of orthotic wear, the percentages of patients reporting at least moderate symptom improvement of their tinnitus, dizziness, otalgia, and/or TMD were 64, 91, 87, and 92%, respectively. Follow-up telephone calls 6 months after completion of TMD therapy revealed that all patients maintained their symptom improvements. These findings imply that TMD was affecting the patients' otologic symptoms.

Usually it includes splints therapy, therapeutic exercises for the lower jaw and occlusal adjustment in combination with counseling.

For a long time, scientists have investigated the effects of dental and stomatognathic therapies in tinnitus (Junemann, 1941; Gelb and Arnold, 1959; Dolowitz et al., 1964; Kelly and Goodfriend, 1964; Gelb et al., 1967; Koskinen et al., 1980; Ioannides and Hoogland, 1983; Cooper et al., 1986; Bush, 1987; Rubinstein and Erlandsson, 1991). According to the findings of Rubinstein (1993), almost one-third of patients report improvement in their tinnitus after mandibula movements and/or pressure on their TMJs. More recently, Bürgers et al. (2013) found that stomatognathic therapy had a positive effect on tinnitus symptoms in 44% of their TMD-tinnitus patients (n = 25), up to 3–5 months after the first intervention; while promising it is noted that there was no control group in this study. Using dental functional therapy, the authors found an improvement on acute or subacute tinnitus in 100% of the patients but little improvement in patients with chronic tinnitus. It is important to note that the authors discussed an individual therapeutic strategy with each patient before the start of treatment. The authors suggested long term studies are conducted to assess the outcome and advised caution when interpreting current epidemiological data.

Chiropractic therapy is a correction therapeutic treatment of an abnormal movement pattern through the manipulation of the vertebral column and extremities. Only three studies related to chiropractic treatment of tinnitus were identified and all three were case studies. Alcantara et al. (2002) described the chiropractic therapy in a 41-year-old woman with history of ear pain, tinnitus, vertigo, altered hearing, ear infections, and headaches, and who was diagnosed TMD and cervical subluxation. The authors reported a complete relief from the TMD symptoms, including tinnitus, after only 9 treatments (2 months). The treatment involved the application of high-velocity low amplitude adjustments. Kessinger and Boneva (2000) also reported progress in a 75-year-old patient who received upper cervical specific chiropractic care which resulted in improvements in vertigo, tinnitus, and hearing loss. These authors concluded that the success of chiropractic therapy was due to improvement in cervical spine function.

DeVocht et al. (2003) also describes the chiropractic management of a 30-year-old woman with TMJ pain. The patient suffered daily from unremitting jaw pain for 7 years accompanied by headache, tinnitus, decreased hearing, and a feeling of congestion in her right ear. Twenty months of chiropractic treatment resulted in total resolution of all symptoms except fullness of the right cheek.

Combined with chiropractic care, muscular relaxation (through massage and stretching exercises) is used in clinical practice. For instance, evidence suggests that palpation of masseter, pterygoid, and sternocleidomastoid muscles or myofascial trigger points can modulate tinnitus (Rocha et al., 2008; Teachey et al., 2012). Björne (2007) reported on the effectiveness of stretching exercises targeting the suboccipital muscles, along with rotation movements in the atlanto-occipital joint and relaxing exercises, on a TMD patient population (no control group). Bjorne notes that patients with Ménière's were more likely to present with TMJ and cervical spine disorder's symptoms (including tinnitus), than people who do not have Ménière and using a coordinated therapy of TMJ and cervical spine disorder (relaxation and posture) found improvements in self-reported tinnitus severity that were retained up to 3 year follow up.

Latifpour et al. (2009) evaluated 24 subjects from an original pool of 41 subjects (non-randomized), divided into two groups: treatment and control group. The authors compared self-training of stretching, posture training, and acupuncture, targeting muscle symmetry and balance in the jaw and neck, and later reported an improvement of tinnitus in the treatment group. In this blinded study they observed immediate and long term (3 months) improvements in the treatment group.

Another therapy worth noting here; in a pilot study with 11 patients, Kaute (1998) reported improvement in vestibular disturbances through the method of Arlen's Atlas Therapy, normally applied to whiplash-injured patients, concluding it to be indicated where tinnitus may be caused by neck muscle tension. This study suggest that muscular relaxation may play a significant role in the treatment of tinnitus but high quality explanatory studies (i.e., comparison with a control, blinded, randomized allocation), are needed.

Somatic modulation therapy (treatment aiming to modulate the intensity of a given symptom, by movement) has rarely been studied beyond case studies. Sanchez et al. (2007) were the first to investigate the effect of repetitive training maneuvers with head and neck muscle contractions, focusing on its value as a tinnitus retraining therapy. The authors found it to have a significant effect on the modulation patterns but not in the daily perception of tinnitus.

In the case of a 39-year-old woman who developed gaze-evoked tinnitus after surgery to remove a left vestibular Schwannoma, therapy consisted of a repetitive gaze training and tinnitus was resolved after 14 weeks (Sanchez and Akemi, 2008). Interestingly, there was both a “horizontal” and “vertical” gaze effect on tinnitus and the vertical component responded more quickly to treatment suggesting more than one neural network or process was involved in this case.

In another case, a 54-year-old man with severe tinnitus noticed an improvement through tactile stimuli to the ipsilateral postauricular area, head rotation, opening of the mouth, and clenching teeth and mandible lateralization (Sanchez and Akemi, 2008). In another case of tinnitus improvement through tactile stimulation was reported in a single patient by Emmert et al. (2014); the patient reported a decrease in tinnitus intensity in the left ear when a tactile stimulus was applied (block-design using EPI sequence—the patients touched on the right cheek on seven blocks of 25 s, intercalating with 25 vs rest).

Recent evidence reported a significant improvement in tinnitus using transcutaneous electrical nerve stimulation (Herraiz et al., 2007; Vanneste et al., 2010). Trans-electrical nerve stimulation (TENS) of areas of skin close to the ear increases the activation of the dorsal cochlear nucleus through the somatosensory pathway and may augment the inhibitory role of this nucleus on the CNS and thereby ameliorate tinnitus (Herraiz et al., 2007).

Vanneste et al. (2010) applied transcutaneous nerve stimulation in the upper cervical nerve in 240 patients with the ability to modulate tinnitus and found a significant suppression of tinnitus. Although only 18% of the patients responded to the treatment, 43% declared an improvement and six patients reported a total suppression of tinnitus (Vanneste et al., 2010). Herraiz et al. (2007) showed that trans-electrical nerve stimulation led to improvements in 46% of somatic tinnitus patients (reduced VAS tinnitus severity scores) after 2 weeks of treatment. Intermittent “typewriter”—sound like tinnitus was the most responsiveness. Herraiz et al. (2007) also noted that tinnitus caused by a somatosensory injury had a better response than somatic tinnitus with an otologic disease.

Standardizing the indications and method could increase the efficacy of electrical stimulation in somatic tinnitus according to most authors. These results are promising so further controlled trials are warranted.

Only one relevant record describing a pharmaceutical treatment was included. In this case study McCormick and Walega (2015) reported the successful treatment of refractory somatic tinnitus with cervical epidural injection of 80 mg triamcinolone acetonide. The patient was 61-year-old male with previous history of bacterial otitis media.

No surgical treatment studies specific to somatosensory tinnitus were identified. One case study worth mentioning however was that of a 65 years old patient with left sided tinnitus and with left sided cervical neck pain who experienced a complete resolution of somatic tinnitus for over 1 year through radiofrequency ablation of the left C2–C3 medial branches of the dorsal ramus ipsilateral to tinnitus symptoms (Gritsenko et al., 2014).

The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.