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Physical Therapy for Tinnitus

I have had tinnitus for 8 years now_edit

-  I have had tinnitus for 8 years now. I can’t remember the

Last time I went to bed without having to listen to a movie, podcast, audiobook, or anything other than the symphony of ringing in my ears! I have seen countless doctors, physical therapists, and taken personal actions to try and increase my qualify of life, but only Tony has been able to help with that. Tony worked some difficult muscles to get to and WALA! Tinnitus gone. 


Tony is unique in his ability to identify complex issues within the body, while figuring out holistic ways in treating them. I have full confidence in his ability to treat nearly anything given his dedication to research, and his attentiveness to listening to your pains and issues. If you want to see your quality of life improve, start here. I can’t say enough about the treatment I’ve received. THANK YOU, TONY!

Nolan Seiler, Tinnitus Sufferer 

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Tinnitus is a hearing disorder that is present in 8 - 30% of the general population.1,3,4 Its prevalence is higher in men compared to women and higher in whites compared to minorities.2,3 Tinnitus is prevalent in 30.2% of men and 21.7% of women.2,3 Approximately 80% of the population has experienced tinnitus at least one time in their life. Only 5-20% of the population experience tinnitus before the age of 50, indicating most people experiencing it later in life.4 The causes of tinnitus are varied and may include exposure to excessive sounds, otitis, otosclerosis, multiple sclerosis, atherosclerosis, tumors, aneurysms, temporomandibular joint (TMJ) issues, eustachian tube dysfunction, neck disorders, and more.


How Does Hearing Work?

The ear is a very complex structure controlling our hearing and vestibular system. To have a better understanding of how tinnitus can be affected by the neck and jaw, you must first understand how everything in the area works. In addition to that, you will have to understand what can happen in the ear to make it more sensitive to sound and what causes you to hear less sound. I will break it down for you.

Outer Ear

External Ear anatomy
External Ear Anatomy by Research Gate

Sound waves first strike the external ear, consisting of the pinna or auricle, which channels them into the external auditory canal. Within this canal, ear wax is secreted to block unwanted particles from entering. While ear wax can impede hearing, it is less likely to enhance it. Subsequently, the sound waves progress into the middle ear and encounter the tympanic membrane.

Middle ear

Middle ear anatomy
Middle Ear Anatomy. Image by staff (2014). \"Medical gallery of Blausen Medical 2014"

Within the middle ear, sound waves will vibrate the tympanic membrane which connects to the ossicles (malleus, incus, stapes) before reaching the oval window.  Significant modulation of sound happens here in the middle ear. First, the stapedius and tensor tympani muscles connect the malleus with the membrane. When these muscles contract, sound is dampened. If there is laxity of the muscles, there will be sensitization to the sound wave. Second, modulation will occur through the tonus/tightness of the stapedius muscle connecting to the stapes. If the muscle is more contracted, less the sound would be heard and vice versa. Lastly, sound can be modulated through the eustachian tube. At rest, in normal circumstances, the eustachian tube is compressed and recoiled by the distal cartilage.5 Its main role is to equalize pressure between the inner and middle ear. If the pressure is uneven, the ear drum cannot vibrate normally. Increased pressure in the middle ear, usually due to the eustachian tube not opening (Eustachian Tube Dysfunction), will restrict vibrations in the ear drum and thus decrease hearing. If this is prolonged for many years, it can cause hearing loss. If there is not enough pressure in the middle ear and the eustachian tube is too open (Patulous Eustachian Tube), it can cause excessive mobility of ear drum and be more sensitive to noise and cause tinnitus. The eustachian tube automatically opens when you swallow and it is controlled by the tensor veli palatini, levator veli palatini and the salpingopharngeus muscles as they connect to the torus tubiarus. There is also a connection from the eustachian tube and the tensor tympani that serves as a communication between the two in order to better regulate pressures. The connection and dysfunction of the tensor tympani and tensor veli palatini muscles is associated with tinnitus, vertigo, sensation of hearing loss, ear fullness and otalgia.26

If the tympanic membrane at rest is concave or convex in the part of the eustachian called the pars flaccida, it will tell the eustachian tube to open or stay closed to get it to a normal resting state. If the pressure in the area is still low while the eustachian tube is closed, gas may enter by the mastoid cells and tympanic membrane to assist in equalizing the pressure. It has been studied that if the tympanic membrane is put into an abnormal state the other regulatory structures will try to compensate and end up exacerbating the issue.7,8,9

Inner Ear

Inner Ear Pathway
Inner Ear Path.  Case courtesy of OpenStax College,, rID: 44020

The inner ear consists of the vesibulocochlear nerve, vestibular labyrinth, the cochlea, and contains our vestibular system*.   After the sound waves have hit the oval window, it will proceed into the cochlea where the soundwaves are transferred into electrical signals. The cochlea is divided into three compartments: the scala tympani, scala vestibuli, and scala media or endolymphatic duct. The scala media contains endolymphatic fluid and the organ of Corti, which hosts stereocilia(hair cells) situated on the basilar membrane. Above the basilar membrane lies the tectorial membrane, with the Reissner's membrane above that. As sound waves traverse the ducts, they vibrate the fluid, causing movement and vibration of the basilar membrane, the organ of Corti, and Reissner's membrane. This action stimulates the organ of Corti and its hair cells to contact the tectorial membrane, generating electrical signals transmitted to the brain via the cochlear nerve. At the end of the path, the sound wave will hit the round window, which functions as a flexible barrier, allowing the fluid to expand and recoil similarly to a water balloon.

Stereocilia  Case courtesy of OpenStax College,, rID: 44020

In the inner ear, sound modulation occurs by the volume of endolymphatic fluid and its hydraulic pressure it places on the inner ear.25 If the volume is increased it will pressurize the scala media causing rigidity and restrict the vibration of the Reissners and basilar membranes. The opposite happens if the volume is decreased. Fluid volume within the inner ear is regulated through various mechanisms. Production of fluid is facilitated by the stria vascularis and labyrinthine dark cells.26 Regulation occurs via the Basts valve to the endolymphatic sac and through drainage pathways including the inferior cochlear vein, paravestibular canaliculus vein, and vestibular aqueduct.27 Additionally, arterial supply from the labyrinthine and meningeal arteries contributes to maintaining fluid balance.28 In a study by Eckhard in 2015, he was able to show regulation stemming from the parasympathetic nervous system.29 Although he couldn’t figure out which cranial nerve was responsible for this, it is hypothesized that it is likely cranial nerve 7, 9, or 10. Sympathetic neurons in the superior cervical ganglion innervate the endolymphatic sac and could be apart functional reflex unit.30

*I will not go into the vestibular portion of the inner ear here, but just know issues here that cause vertigo can sometimes be cured in one treatment and in other cases multiple sessions to habituate yourself to the movements, except for cases of Menieres Disease.


Evidence for Head, Neck, and Jaw Etiology in Tinnitus Patients

Studies have shown that patients still suffer from tinnitus after cancers, use of ototoxic drugs, exposure to loud sounds, aneurysms, and other known pathologies have been ruled out.31 Also, we have studied many older individuals with hearing degradation who also do not experience tinnitus.32 In research, we have noticed patients who have history of whiplash or other head and neck trauma report tinnitus symptoms.33,34 We also see reports of direct changes of tinnitus severity when a patient changes their head and or neck position.35 In my experience, I have also seen patients acquire tinnitus after a major emotional event in their life. There have been animal studies that show improvements in hypersensitivity to sound, reduction of stereocilia/hair cells damage** and reduced cochlear damage by increasing dopamine levels.36 I have also seen tinnitus in many individuals who experience central nervous system sensitization from chronic pain or traumatic event. Physical therapy interventions such as pain neuroscience education, graded motor imagery, along with other emotional therapeutic interventions have improved symptoms of tinnitus severity and dysfunction in my practice. Let’s go over the first mechanism for tinnitus in relation to the neck and jaw.

** Important to note, exosome ear drops also have been shown to protect steriocilia from damage.


All these structures in the ear that play a factor in sound amplification and dampening are innervated by nerves that travel through the neck and/or jaw. If there is any dysfunction of the neck and jaw, it starts a protective process causing the nervous system to become aware of the danger/threat. Nerves are happiest when they have oxygen, space and movement. A dysfunction can cause muscles to start to guard and tighten up. When they are in this hypertonic state, they can compress the nerve and deprive it of these three things that it needs. A study demonstrated that lateral pterygoid spasm was found to cause injury to auriculotemporal nerve.37 Dysfunction can also start an inflammatory process. Swelling is one of the more potent substances that can sensitize nerves. If there is an excessive quantity of swelling in the area, it can also compress nerves. Since the area is so confined, inflammation of vascular and muscular structures has been found to injure closely situated nerves.38

Lastly, improper joint mechanics can sensitize or restrict nerve conductivity. If a joint isn’t moving correctly or stuck in an improper place, then it has a chance to crowd areas and tighten structures that aren’t supposed to be taught. Nerves can be caught in these areas of impingement. The amount of pressure and/or how long it has been compressed will play a factor if individuals will experience transient symptoms or permanent nerve damage.  Pressure on nerves can cause one or more symptoms of pain, numbness, tingling, increased or decreased tone of a muscle, and/or decrease function of a structure. More related to the inner ear, it can cause dysautonomia, dysregulation of cochlear fluids, abnormal sensation in the tympanic membrane and improper function of the stapedius and tensor tympani muscles. The tympanic membrane receives sensory innervation from the auriculotemporal branch of the trigeminal nerve, auricular branch of vagus nerve, auricular branch of the facial nerve on the outer side of the membrane. The glossopharyngeal nerve innervates the membrane on the inner side.39 Compression to this nerve may cause variable symptoms of pain and/or dysautonomia to spread through the nervous network in the area.40 The tensor tympani muscles are innervated by the tympanic plexus (glossopharyngeal nerve, facial nerve, and connecting branches to internal carotid plexus). It will also communicate with trigeminal nerve via otic and pterygopalatine ganglia. In addition to that, it communicates with the vagus nerve via the glossopharyngeal nerve which supplies the mucosa of middle ear, mastoid cells, auditory tube and parotid gland.41 The stapedius muscle is innervated by the facial nerve. The muscles that control the opening of the eustachian tube are innervated by the trigeminal nerve(tensor veli palatini muscle) and the vagus nerve(levator veli palatini and salpingopharyngeus). The medial and lateral pterygoid muscles also can aid in eustachian tube function and is controlled by mandibular branch of the trigeminal nerve. The eustachian tube’s mucosa is innervated by the pterygopalatine ganglion, which also connects directly with the trigeminal nerve and to the tympanic plexus, which controls the middle ear. The eustachian tube itself gets its innervation by the otic ganglion and sphenopalatine nerve and sensory innervation from pharyngeal and tympanic plexus.***

Tympanic Plexus
Tympanic Plexus

  In summary, impaired electrical activity through these nervous pathways may alter the position of the ossicles via the tensor tympani and stapedius muscles. It can alter endolymphatic regulation via the endolymphatic sac and produce improper regulation of the tympanic cavity causing impaired tension/mobility of the tympanic membrane. Repeated stimulation of the auriculotemporal nerve may stimulate cranial nerve five’s other branches, cranial nerve seven, cranial nerve nine and ten by way of crossover interneurons (ephases) and other elements in the reticular formation. In a study by Sims & Stack in 2007, repeated auriculotemporal nerve stimulation causes reflex reactions with CN 5,7,9 and 10 to produce movement disorders, breathing impairment and involuntary movements that ceased when noxious stimuli ceased. Also important to note, a few cases of tinnitus have been relieved temporarily and permanently by a Novocain block to some of these nerves.

  • Novocain block to Auriculotemporal nerve: 2 cases abolished tinnitus permanently. Garnett Passe, 1951

  • Novocain Block of Sympathectomy Partial relief: 8, Complete relief: 5 Unaltered: 3 Franz et al., 1998

  • After local anesthetic was applied to C1-2 facet joints, patients reported within 10 minutes that their tinnitus had diminished significantly. Franz et al., 1998

  • 20 yr Chronic subjective tinnitus completely disappeared within 4 weeks with intermittent short time application of cervical collar. Thereafter, tinnitus was deliberately again induced by head inclination, set on with anterior tilt of 14°, reaching maximum strength by 23°. Tinnitus stopped with return to neutral head position. Bechter et al., 2016


*** The glossopharyngeal nerve probably plays the predominant role in tubal innervation. Sympathetic innervation of the tube depends on the sphenopalatine ganglion, the otic ganglion, paired glossopharyngeal nerves, the petrosal nerves, and the caroticotympanic nerve (Proctor, 1967). Mitchell (1954) suggested that the parasympathetic nerve supply is derived from the tympanic branch of the glossopharyngeal nerve. Nathanson and Jackson (1976) provided experimental evidence for secondary parasympathetic innervation via the Vidian nerve from the sphenopalatine ganglion. – Swarts & Rood, 2005


The Temporomandibular Joint (TMJ) Itself

Temporomandibular Joint TMJ
FIGURE A, The temporomandibular joint. B, Close up of temporomandibular joint. (B, Redrawn from Neumann DA: Kinesiology of the musculoskeletal system—foundations for physical rehabilitation, St Louis, 2002, CV Mosby, p. 357.)

Temporomandibular dysfunction (TMD) is associated with 40% of people experiencing tinnitus, 42% experiencing ear pain, 18% reporting diminished hearing and 23% reporting dizziness.42 From a musculoskeletal component, the jaw is attached to inner ear by means of the superior lateral pterygoid muscle. In some of the population, it directly attaches to the ossicles by way of the retrodiscal tissue and discomalleolar ligament.43,44,45,46,47,48,49,50,51 Before delving into the impact of jaw dysfunction on the ear, it's crucial to recognize that various dysfunctions can affect the jaw, like any other joint in the body. Just as shoulder can have numerous dysfunctions causing pain, the jaw will exhibit similar complexity. Also, pain can be referred from other parts of the body to the jaw just as the neck can send pain to shoulder. For further insight into temporomandibular disorders (TMD), refer to my previous post on Understanding Jaw Dysfunction. For purposes of this review, be aware that the mandible can commonly assume a more retracted position than its intended. Many believe the reason for this can be a structural issue caused by lack of posterior support or weakness in the muscles of mastication. I believe it is multifactorial. These factors play a role, but also there could be other factors the push it over the edge. Bruxism (grinding of teeth typically at night) due to stress or emotional trauma can cause excessive retraction.  The lateral pterygoid muscle attaches to disc and when these muscles are stressed too much from grinding, they can tighten up similarly to how individuals experience delayed onset muscle soreness and tightness after weightlifting. When it remains in a tightened hypertonic state, it can cause a common issue where the disc displaces anteriorly. When this happens, the mandible will retract posteriorly placing extra pressure on to sensitive tissues. This will cause more pain and swelling, which in turn causes the muscles to guard more and they will continue to feed off each other and worsen. The longer they are in this guarded position, the more of a chance the muscles will become atrophied and less able to perform their function. This is where it can turn into a chronic issue. Many are unaware, but temporomandibular disorder (TMD) ranks as the second most prevalent musculoskeletal disorder, following chronic low back pain.10 This underscores the considerable lack of support for individuals grappling with this condition. Personally, I feel a God given purpose to enact positive changes within this underserved community and strive to help in any way possible.

Another cause of excessive mandibular retraction is from prolonged positioning, typically at night or from the hand supporting chin in sitting. If prolonged posterior pressure is placed on the mandible, it can also displace the disc. This is similar to how a disc in the spine can be herniated by prolonged sitting.

Lastly, trauma with a sharp quick force backward can also herniate that disc forward.  When the mandible is in a hyper-retracted state it pinches the sensitive retrodiscal tissue, can cause erosion of glenoid fossa (lack of normal 3mm joint space), will inhibit the lateral pterygoids causing atrophy, will compress the  eustachian tubes and tympanic plates and impinge on auriculotemporal nerve which is situated postero-medial to TMJ capsule and chorda tympani nerve.14, 52 The auriculotemporal nerve lies next to the TMJ and is a branch of the trigeminal nerve. If there is any dysfunction in the TMJ, it will affect this nerve in some way.53 When compression or sensitization occurs, some of the sound modulation that is controlled by the trigeminal nerve can be affected. If the lateral pterygoids are atrophied, it will worsen the mechanics even more since this muscle helps with preventing excessive posterior translation (retraction) and joint shearing. It will also affect the malleus function since it directly attaches to the malleus in some of the population. The sub-branches of the trigeminal nerve (buccal and lingual nerves) pass through the lateral pterygoids and can become impinged if the muscle is in an abnormal state. This is most likely why individuals with tinnitus can change their tinnitus with mandibular movements.


When individuals experience pulsatile tinnitus, clinicians will start looking to arteries for the cause. After serious medical conditions are ruled out, a more likely cause can be from impingement of the maxillary artery as it runs through the two heads of the lateral pterygoids. This will add arterial pressure in the tympanic artery which supplies blood to the cochlea.

A less common area of impingement is at the mandibular condyle on to the anterior tympanic artery. Also important to note, the maxillary artery supplies the eustachian tube. This makes it possible that fixing the state of the lateral pterygoids can also improve eustachian tube function. Other known reasons of pulsatile tinnitus can be from venous sinus stenosis, sigmoid sinus diverticulae (focal outpouching of the normal semicircular sigmoid sinus groove expanding in to the mastoid air cells and/or temporal bone cortex), or an arteriovenous fistula.11 Another study found the occipital artery to be a cause for pulsatile tinnitus secondary to stenosis of the carotid artery.12 Posteriorly displaced mandible has been known to put pressure on the tympanic vein and vessels that restrict flow to the auditory tube. When this happens, it can cause burning sensations of the tongue, impaired taste, impaired salivation, ear and visual complaints.13

As previously explained, the temporomandibular joint (TMJ) is a compact structure with intricate vascular and neurological components susceptible to injury in TMJ disorders. Ash & Pinto proposed that otic symptoms may arise from damage to parasympathetic nerve fibers of the auriculotemporal nerve, originating from the otic ganglion and tympanic plexus (glossopharyngeal nerve), leading to reflex vascular spasms in the labyrinthine system due to abnormal stimulation of these fibers.54 Irritation of the auriculotemporal nerve can result in otalgia due to its extensive innervation of the articulation, tympanic membrane, anterosuperior zone of the external ear, tragus, and other structures, explaining the auricular pain experienced.55 Johansson stressed that when considering nerve entrapment etiology, such as with the auriculotemporal nerve, factors extend beyond anatomical mobility and bone deformities.56 They include inflammation of vascular and muscular structures, which can alter and constrict anatomical passages, potentially damaging closely situated nerves.57 Loughner et al. corroborated this, affirming that lateral pterygoid spasm and hypertrophy can indeed lead to injury of the auriculotemporal nerve.57 When lateral pterygoids spasm, the maxillary artery can become compressed and increase blood flow into the anterior tympanic artery which also can produce pulsing sensations or tinnitus.58

            A rare condition associated with pulsatile tinnitus is Tensor Tympani Syndrome (TTTS). Symptoms indicative of TTTS may include: sharp stabbing ear pain, dull earache, tinnitus often accompanied by clicking, rhythmic, or buzzing sensations, a feeling of pressure or blockage in the ear, tympanic flutter, pain, numbness, or burning sensations around the ear, cheek, and neck, mild vertigo, nausea, distorted or muffled hearing, and headaches.15,16,17,18 Chronic trigeminal neuralgic pain induced by TTTS can lead to central pain sensitization. Tensor tympani spasm has been linked to various conditions such as Meniere’s Disease, where sectioning of the tensor tympani muscle has been proposed as a treatment and secondary otologic symptoms including tinnitus, ear pain, and related symptoms in myofascial pain syndrome, temporomandibular disorder (TMD), and TMJ dysfunction.19,20,21,22,23,59

            Another vascular issue that is closely linked to tinnitus is from poor venous return. When endolymphatic volume becomes high (endolymphatic hydrops) it is associated with tinnitus, hearing disorders, and vestibular issues. One reason for this is compression of the internal jugular vein. This can happen from upper crossed syndrome and poor posture which I will talk about in the cervical section. Excessive endolymphatic fluid in the scala media can place pressure on the stria vascularis causing cell death and hearing loss. If it progresses the Reissners membrane can rupture and form a fistula between the canals. This has been found to heal on its own at times, but before it does it can cause hearing or vestibular issues. It can also rupture the sacculus and utricle in the vestibular labyrinth. This leads to stereocilia damage. In addition to that, It can also rupture the oval window. More often the oval window will rupture from head trauma or barotrauma from diving. These diagnoses can be ruled out by an ENT.

The Cervical Complex

Thoracic outlet syndrome
Thoracic Outlet Syndrome Image by

Many are familiar with the condition of thoracic outlet syndrome where entrapment of the brachial plexus can occur in the interscalene space. However, less discussed is the connection of the sympathetic chain to these nerve roots via the ramus communicans, which are communicating branches linking spinal nerves and autonomic nerves. Studies have indicated that severe thoracic outlet syndrome (TOS) patients can even develop autonomic disorders like pseudoangina, atrial fibrillation, and chest discomfort. The rami communicans nerves link spinal nerves to the sympathetic plexus, while the sympathetic plexus is also located between the alar fascia of the neck and the longus colli and longus capitis muscles. These muscles are often injured in whiplash incidents and commonly atrophy due to poor posture. In some cases, the sympathetic plexus may be entrapped between the alar fascia and the weakened longus colli and capitis muscles, leading to a double crush syndrome, both indirectly via TOS and directly in the ventral cervical spine.

The sympathetic cervical plexus envelops the internal carotid artery and extends into the tympanic cavity, where it and other nerves forms the tympanic plexus. Additionally, the vagus nerve lies between the anterior scalene muscle and the clavicular portion of the sternocleidomastoid muscle, potentially becoming entrapped there. As these nerves innervate the organs, various seemingly unrelated symptoms may arise.

The sympathetic and parasympathetic nerves partly innervate the muscosal transport mechanism of the tympanic cavity and eustachian tube, the tympanic membrane, cochlear fluid regulation via the stria vascularis, the endolymphatic sac, and vestibular arteries. The vagus nerve also innervates muscles such as the salpingopharyngeus and levator veli palatini, aiding in eustachian tube opening. Studies suggest that stimulation of these nerves may alter blood flow to the cochlea and other regulatory mechanisms.

On the dorsal side, the cervical plexus, also known as Cruveilhier's plexus, consists of nerve bundles originating from the C1 to C3 nerve roots. Main branches include the greater and lesser occipital nerves, suboccipital nerves, third occipital nerve, and anterior and posterior auricular nerves. The cervical plexus anastomoses with various nerves, potentially influencing the aural complex.

            Individuals today are predisposed to these dysfunctions through the prolonged postures we assume at work or through repetitive upper extremity use in front of us. We tend to not use our postural muscles and hang out on the passive structures until muscles start to atrophy. When they become weak, they are susceptible to spasming.  When we do start to activate them, they get overworked, tighten up, and put pressure on your nerves and vessels. Then you are back down the same circular slope where you are irritating these sensitive structures and causing dysfunction which cause your muscles to tighten up more and more. Anterior structures in the chest tend to be tight and posterior structures in upper back tend to be weak. Tightness becomes present in the back of the upper neck and weak in the anterior neck. We call this upper crossed syndrome. It can be difficult to correct because you can over stretch and irritate things more or give up on strengthening because you don’t see improvements in symptoms till at least 4-5 weeks depending on many other factors. The posterior upper neck is another area of issue, since tightness is present here. Many of the same nerves in certain individuals will transfix through the suboccipitals, semispinalis capitis, sternocleidomastoid, and trapezius musculature.

Endolymphatic Hydrops and Cervicogenic Headaches

As we have seen already, there is little doubt that impairment of the respective nerves that innervate the inner ear may cause fluid imbalances such as increased endolymphatic production, however for the endolymphatic pressure to become so great that the Reissner’s membrane ruptures, it is reasonable to expect that additional neurogenic factors play a part in the dysfunction. Especially considering the vast amount of hydrops sufferers who also suffer from headaches. The vestibulocochlear venous system drains into the sigmoid sinus, which proximally becomes the internal jugular vein. It has been shown that the internal jugular vein has reduced outflow in headache patients. It has even been demonstrated by means of CT venography that the internal jugular vein may be compressed by the transverse process of the C1 vertebrae. Restricted venous outflow will cause craniovascular hypertension and headaches. It may also restrict outflow via the vestibular and cochlear veins, quite possibly being responsible for the extreme buildup of endolymphatic fluids. Research shows there is high correlation between jaw pain and headaches. In my experience, most of the time we can abolish the headaches by treating the upper cervical spine. Look for follow up posts to be made about cervicogenic headaches.

Don’t let providers tell you there is no hope for a cure to tinnitus and that you must learn to deal with it. If you are able to change your symptoms with neck and or jaw movements, it usually means at least some to all of your symptoms can be improved. A study in 1997 by Wright and Bifano, found that TMD patients with coexisting tinnitus report 46 to 96 percent tinnitus improvement or resolution from TMD therapy. A survey taken two years after TMD therapy suggests the tinnitus improvement is sustained over time. The dysfunctions can be many and one specific treatment cannot be provided and must be individualized. Finding a physical therapist that is familiar with neck and jaw dysfunction, nervous system desensitization, and the inner workings of the auditory system can come up a detailed treatment plan and achieve optimal outcomes for you.



Works Cited

1.    Møller, A.R. (2011). Epidemiology of Tinnitus in Adults. In: Møller, A.R., Langguth, B., De Ridder, D., Kleinjung, T. (eds) Textbook of Tinnitus. Springer, New York, NY.

2.    Hackenberg B, O'Brien K, Döge J, Lackner KJ, Beutel ME, Münzel T, Pfeiffer N, Schulz A, Schmidtmann I, Wild PS, Matthias C, Bahr-Hamm K. Tinnitus Prevalence in the Adult Population-Results from the Gutenberg Health Study. Medicina (Kaunas). 2023 Mar 20;59(3):620. doi: 10.3390/medicina59030620. PMID: 36984621; PMCID: PMC10052845.

3.    Batts, Shelley et al. Tinnitus prevalence, associated characteristics, and related healthcare use in the United States: a population-level analysis The Lancet Regional Health – Americas, Volume 29, 100659

4.    Bhatt JM, Lin HW, Bhattacharyya N. Prevalence, Severity, Exposures, and Treatment Patterns of Tinnitus in the United States. JAMA Otolaryngol Head Neck Surg. 2016 Oct 1;142(10):959-965. doi: 10.1001/jamaoto.2016.1700. PMID: 27441392; PMCID: PMC5812683.

5.    Bluestone & Klein, Otitis media in infants and children, 2001

6.    Ramirez Aristeguieta et al., 2010

7.    Csakanyi Z., Katona G., Josvai E., Mohos F., Sziklai I. Volume and surface of the mastoid cell system in otitis media with effusion in children: a case-control study by three-dimensional reconstruction of computed tomographic images. Otol Neurotol. 2011;32(1):64–70A

8.    Lima P. A., Sampaio L. P., Damasceno N. R. (2014). Neurobiochemical mechanisms of a ketogenic diet in refractory epilepsy. Clinics 69 699–705. 10.6061/clinics/2014(10)09 Schiffman E., Ohrbach R., Truelove E., et al. Diagnostic criteria for temporomandibular disorders (DC/TMD) for clinical and research applications: recommendations of the International RDC/TMD Consortium Network and Orofacial Pain Special Interest Group. Journal of Oral & Facial Pain and Headache. 2014;28(1):6–27. doi: 10.11607/jop.1151.

9.    Stenfors, L. E., B. Salen, and B. Winblad. "The role of the pars flaccida in the mechanics of the middle ear." Acta Oto-Laryngologica 88.1-6 (1979): 395-400.

10. Lansley JA, Tucker W, Eriksen MR, Riordan-Eva P, Connor SEJ. Sigmoid Sinus Diverticulum, Dehiscence, and Venous Sinus Stenosis: Potential Causes of Pulsatile Tinnitus in Patients with Idiopathic Intracranial Hypertension? AJNR Am J Neuroradiol. 2017 Sep;38(9):1783-1788. doi: 10.3174/ajnr.A5277. Epub 2017 Jul 13. PMID: 28705815; PMCID: PMC7963710.

11. Cowley et al., 2009

12. Chwatowa & Kurljandsky, 1977

13. Clarke, 1962

23. Westcott M (2010) Hyperacusis a clinical perspective on management. Tinnitus Discovery - Asia and Pacific Tinnitus Symposium, Auckland 123: 1311.

24. Böhmer R, Angell CA. Elastic and viscoelastic properties of amorphous selenium and identification of the phase transition between ring and chain structures. Phys Rev B Condens Matter. 1993 Sep 1;48(9):5857-5864. doi: 10.1103/physrevb.48.5857. PMID: 10009119.

25. Moller, Textbook of tinnitus, 2010

26. Lo, W. W., et al. "The endolymphatic duct and sac." AJNR: American Journal of Neuroradiology 18.5 (1997): 881.

27. B. Kellerhals (1979) Perilymph Production and Cochlear Blood Flow, Acta Oto-Laryngologica, 87:3-6, 370-374, DOI: 10.3109/00016487909126435

28. Scaramella, John G. "Hyperhomocysteinemia and left internal jugular vein thrombosis with Ménière's symptom complex." Ear, nose & throat journal 82.11 (2003): 856-865.

29. Eckhard, A., et al. "Regulation of the perilymphatic–endolymphatic water shunt in the cochlea by membrane translocation of aquaporin-5." Pflügers Archiv-European Journal of Physiology 467 (2015): 2571-2588.

30. Brechtelsbauer PB, Baxter ARG, Prazma J, Xie DH, Pillsbury HC. Innervation of the Endolymphatic Sac. Arch Otolaryngol Head Neck Surg. 1992;118(3):260–264. doi:10.1001/archotol.1992.01880030042010

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