Tinnitus, TMJ, Headaches, Neck Pain, Facial Pain, etc. — Possible Treatment

@Mr. Cartman I've been focusing on my scales or muscles in the neck a lot the last few days. I did a google search and found this:

"Some good examples of these relationships are as follows. The temporalis often compensates for inhibited neck flexors and gluteals. The masseters often inhibit those same muscles and the hip flexors. The pterygoids often inhibit the scalenes, the latissimus dorsi, the obliques, the quadratus lumborum, and the hip abductors. If these relationships are left unattended the tension in the jaw muscles increases tremendously resulting in the aforementioned symptoms. Remember that the tension in these muscles is a result of a faulty relationship with other muscles/functions. To simply release these muscles without first figuring out what they are compensating for, could result in destabilizing functional integrity. Treat the cause not the symptoms."
http://neurokinetictherapy.com/temporomandibular-joint-dysfunction

I'm not sure if they are saying the scalene cause the pterygoid problem.

I agree.. It has to be something to it :)

Also, the findings of A Bjorne (Vertigo, Tinnitus and Pain Unit, Ystad Hospital, SE-271 82), which showed that lidocaine injections into the lateral pterygoid reduced tinnitus in a consecutively sampled group of 38 tinnitus patients with 63% according to VAS should not be swept under the rug as well.
 
@Mr. Cartman I think injecting lidocain into the lateral pterygoid is just putting a cap on the end of the chain of the dysfunction so the neuro-noise / pain is not fed into the DCN or whatever nuclues also feeds into the auditory centers of the brain.

The problem is finding what is feeding noise into the lateral pterygoid, assuming that is happening and it is in that direction. The SCM, trapezius, scalenes are likely as well as other neck and upper back muscles. These of course could be set off by yet more muscles in the lower back or throughout the back. These muscles in turn could all be disrupted or perpetuated by yet a systemic neurological or nueromusclar imbalance. It is very complicated obviously since we have been trying to figure this out.

I was working on my scales and SCM a lot more recently. A day or two ago I was having a massive amount of pain on the left side of my neck and wrapping around the back of my head. I don't normally have this except years ago. I've been trying to press on the SCM close to the ear. I was definitely getting a lot of twittching. I'm holding for 30 second increasing the pressure to keep the pain at a 7 out of 10 the whole time.

I'll start pressing and after maybe 10 seconds it will start twitching if it is an active spot. I noticed that only by pressind was I able to get to parts of the cleido mastoid that I could not get to through pincing easily.
 
@Mr. Cartman I think injecting lidocain into the lateral pterygoid is just putting a cap on the end of the chain of the dysfunction so the neuro-noise / pain is not fed into the DCN or whatever nuclues also feeds into the auditory centers of the brain.

The problem is finding what is feeding noise into the lateral pterygoid, assuming that is happening and it is in that direction. The SCM, trapezius, scalenes are likely as well as other neck and upper back muscles. These of course could be set off by yet more muscles in the lower back or throughout the back. These muscles in turn could all be disrupted or perpetuated by yet a systemic neurological or nueromusclar imbalance. It is very complicated obviously since we have been trying to figure this out.

I was working on my scales and SCM a lot more recently. A day or two ago I was having a massive amount of pain on the left side of my neck and wrapping around the back of my head. I don't normally have this except years ago. I've been trying to press on the SCM close to the ear. I was definitely getting a lot of twittching. I'm holding for 30 second increasing the pressure to keep the pain at a 7 out of 10 the whole time.

I'll start pressing and after maybe 10 seconds it will start twitching if it is an active spot. I noticed that only by pressind was I able to get to parts of the cleido mastoid that I could not get to through pincing easily.

Something funny is happening in the neck / jaw area, thats for sure.. My anterior scalenes hurts bad too..
It could be related to elongation of the styloid process though.. Just curious, did you ever have your styloid process and stylohyoid ligament evaluated? It would be very interesting to know if you had something going on in this area as well..
 
@applewine

This is seriously interesting (maxillary constriction, palatal anatomy and the auditory apparatus):

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Article Citation:
Andrea Villano, Barbara Grampi, Roberto Fiorentini, and Paola Gandini (2006) Correlations between Rapid Maxillary Expansion (RME) and the Auditory Apparatus. The Angle Orthodontist: September 2006, Vol. 76, No. 5, pp. 752-758.

Original Article
Correlations between Rapid Maxillary Expansion (RME) and the Auditory Apparatus
Andrea Villanoa, Barbara Grampia, Roberto Fiorentinib, and Paola Gandinic

Abstract

Objective: To evaluate the effects of rapid maxillary expansion (RME) on conductive hearing loss and maxillary constriction.

Materials and Methods: A total of 25 subjects (15 girls and 10 boys, aged between 6 years 8 months to 8 years 2 months) with conductive hearing loss and maxillary constriction were studied. Audiogram, tympanogram, and video-otoscopy were used to investigate the anatomical and physiological modifications of the bony and muscular structure of the maxilla and the auditory apparatus. The records were taken before maxillary expansion (T0), after expansion (7–14 days; T1), and after the retention period (8 months after expansion; T2).

Results: After expansion, the audiometric records indicated an improvement in hearing levels for higher frequencies but not for lower ones. After the retention period, there was a functional improvement in all patients for all frequencies. The recovery of the tympanic membrane's elasticity occurred only after retention, as shown by the standard model tympanogram, which was still flat after expansion.

Conclusions: The auditory function in patients with conductive hearing loss may be corrected through correction of the palatal anatomy, which influences the muscular function of the tubal ostia and allows a normal activity of the tympanic membrane and the auditory apparatus. Positive effects on conductive hearing loss are possible additional benefits of RME treatment, but this does not indicate that patients with conductive hearing loss without an accompanying maxillary constriction should consider this as a treatment approach.

Keywords: Rapid maxillary expansion, Hearing loss

Accepted: October 2005; Final version received: May 2005

aResearch Fellow, Department of Orthodontics, University of Pisa, Italy
bDepartment Head, Hospital of Massa Carrara, Otolaryngology, Massa Carrara, Italy
cProfessor, Department of Orthodontics, University of Pisa, Italy

Corresponding author: Dr. Barbara Grampi, Department of Orthodontics, University of Pisa, via Confienza 14, Vercelli 13100 Italy (barbaragrampi@tin.it)

INTRODUCTION

The dental literature discussing correlations and connections between the stomatognathic system and other apparatuses is constantly increasing. One of the most interesting topics is the correction of skeletal and/ or dental transverse problems of the maxilla.

Orthopedic and orthodontic results are often associated with unexpected therapeutic effects on other apparatuses, such as the auditory one. The limited data in the literature on this specific topic suggests the possibility of improving hearing levels by correcting the palatal anatomy.

In this literature, there are studies that attest to the positive effect of palatal expansion in improving hearing. Braun1 observed a correlation between hearing loss and maxillary constriction. Rudolph2 stated that tubal malfunction was more frequently seen in children who had extremely high palatal arches, as well as malformations of the palate and nasopharynx, that may predispose them to otitis media. According to Laptook,3 the orthopedic effect of rapid maxillary expansion (RME) helps to improve hearing levels in patients with maxillary deficiency. The effect of the expansion on the palatal and nasopharyngeal tissues improves the functioning of the pharyngeal ostia of the eustachian tubes. Laptook3 reported that patients' hearing improved within the first 10 days and also noted that this improvement continued during the active phase of treatment.

Gray4 found that recurrent serous otitis media decreased remarkably in subjects treated with RME.

According to Timms5–7 hearing levels improved after expansion. Hazar et al8 reported a significant improvement in hearing within 4 weeks of RME treatment. According to Fingeroth,9 maxillary expansion may improve hearing loss related to middle ear and eustachian tube problems. Ceylan et al10 performed RME on 14 patients (11 girls and 3 boys) aged between 10 years 4 months and 16 years 9 months (average age 12 years 11 months ± 1 year 9 months) with conductive hearing loss and maxillary deficiency. They found that hearing levels had significantly improved during the active expansion period; and although they observed some relapse in the hearing level after the retention period (about 4.5 months), it did not significantly affect the overall results obtained.

Pirelli et al11 selected 15 patients (9 girls and 6 boys, average age 11.5 ±1 year) who showed malocclusion characterized by maxillary crowding and transverse constriction. These patients had some breathing difficulties and hearing loss. They all underwent RME to correct the transverse discrepancy and to evaluate a potential improvement in hearing. After expansion, 9 subjects presented normal hearing while 6 of them showed a slight improvement. After expansion, 13 subjects showed normal levels of hearing and 2 subjects showed a slight hearing loss.

All of these studies reported on the short-term effects of rapid palatal expansion on hearing loss, but there is a lack of information on the long-term results. A report by Taspinar et al12 evaluated these effects over a 2-year period on 35 subjects and reported that RME had a positive effect on hearing levels. At the end of the retention period, the improvement tended to reverse, but the reversal was of a clinically small magnitude. On the other hand, in 26% of the patients, improvements in hearing levels were not statistically significant.

Our study originated from an analysis that showed certain patients, those with clinical symptoms of recurrent serous otitis resistant to antibiotic therapy and with conductive hearing loss, have a small maxilla with a high palatal vault and transverse discrepancy. The fact that a transverse deficiency may be a preexisting or a predisposing cause to this kind of alteration was investigated. A change in the palatal anatomy causes alterations in the relationship between the internal peristafilini muscles or palatal levators,13 the external peristafilini muscles or tensors of the soft palate, and the bones where they insert into the palate itself.

Physiologically, the peristafilini (levators and tensors) are muscles that open and close the pharyngeal ostia of the eustachian tube13 and clear its internal parts of the mucus secreted to humidify and lubricate the inner tube. If the palatal arches are high and the transverse dimension is deficient, these muscles insert in a stretched, hypofunctional, and cramped state, obstructing the mucus deflection. The mass of mucus and the virulent exudates lead to recurrent serous otitis. To restore the correct palatal anatomy, increasing the transverse dimension, brings the muscular ends near the tubal ostia. This may cause an improvement in tonicity and in the physiological opening and closure of the tubal ostia, facilitating the mucus outlet.

To test this theory, the possibility of modifying the anatomy of the palatal vault through orthopedic-orthodontic therapy was investigated. The effects on muscular activity were studied, as well as the reduction of otitis and the improvement of hearing levels. Therefore, RME was performed to improve auditory function through anatomic and muscular change of the tube and improvement of air perfusion at its entrance.

MATERIALS AND METHODS

Among the patients needing rapid palatal expansion for orthodontic reasons, 25 subjects (15 girls and 10 boys) between 6 years 8 months and 8 years 2 months of age were selected. All selected subjects reported recurrent serous otitis with conductive hearing loss (Table 1).

After their visit to the otolaryngologist, all subjects underwent a thorough clinical-anamnestic investigation and a series of instrument examinations. Apart from the usual orthodontic diagnostic records necessary for the orthodontic treatment, some otolaryngologic examinations were obtained to better investigate the auditory problem:

An audiogram to examine the auditory function;
A tympanogram to analyze the variations in elasticity of the tympanic membrane related to the pressure changes in the external auditory tube; and
A video-otoscopy, which allows the instrumental observation of the external auditory tube and the tympanic membrane.

All the subjects' parents were well informed and knowledgeable about the risks and benefits of the examinations, and they gave their consent for the additional procedures their children had to undergo.

The 25 selected subjects underwent RME. The appliance had two or four bands, and the screw was adjusted three times a day for 7 to 14 days until the necessary expansion for each subject was accomplished.

The tympanogram and the audiogram were performed before the palatal expansion (T0) and after the expansion (7–14 days; T1) to evaluate all changes in the anatomy and physiology of the bony and muscular structure of the maxilla and the auditory apparatus. The video-otoscopy, because of its complexity and high costs, was performed only at the beginning (T0) and at the end of the retention period (T2).

During treatment, no anti-inflammatory, antibiotics, or serous fluidifying medicine were given. The 25 subjects showed a conductive hearing loss before expansion (T0) as confirmed by instrument analysis.

(a) The audiogram highlighted a conductive and not a sensorineural hearing loss (Table 2).

This allowed the exclusion of any ear anatomical malformation and suggested the presence of serous fluid, which partially reduced the elasticity of the tympanic membrane causing the perception of a muffled or almost an absence of sound at lower frequencies at T0.

The hearing loss was greater for frequencies between 250–1000 Hz, quite normal between 1000–2000 Hz, and less between 2000–4000 Hz. All subjects started to perceive sounds starting at 30 dB and above. Normal hearing was recorded between 0 dB and 20 dB. Hearing loss was defined as mild from 20–30 dB, moderate at 30–40 dB, and maximum at 60 dB,14 more precisely between 250 Hz and 1500 Hz.

At T0, 11 subjects could hear in both ears at 40 dB, while 8 subjects could hear at 40 dB in the right ear and 30 dB in the left ear; 2 subjects had a threshold of 50 dB in the right ear and 30 dB in the left one; 3 subjects could hear at 30 dB in the right ear and at 40 dB in the left one; and 1 subject could hear frequencies of 50 dB in both ears.

(b) At T0, the tympanogram was flat in all subjects in both ears, confirming the short elasticity of the tympanic membrane and suggesting that hearing loss was due to serous secretions that could not flow away from the inner part of the membrane (Table 3).

At T0, the video-otoscopy revealed the presence of a thick mucous exudate in variable quantities at the pharyngeal entrance of the tube (Figure 1.

The statistical evaluation was made through the variance analysis, which allows highlighting of the test differences at different frequencies over time. The six different cases drawn from the measurement at the three frequencies for both ears were analyzed. For each case, a comparison test of measurements over time (T0, T1, and T2) was then calculated.

RESULTS

After palatal expansion (T1), the same instrument analysis used for the diagnosis revealed the following results (Table 2):

(a) The audiogram at 250–1000 Hz did not register any improvement, apart from four subjects where a slight improvement was recorded as follows: one subject had an improvement in both ears, and three subjects in one ear only. For frequencies between 1000–2000 Hz, mild improvements were recorded in all subjects who were normal at 2000– 4000 Hz. This data might suggest that the 2 weeks during which the appliance was activated were not sufficient to allow the complete elimination of serous secretions from the internal part of the ear.
(b) The tympanogram was flat in almost all subjects apart from four subjects: one subject revealed a slight improvement in the right ear, another subject in the left ear, and two subjects in both ears (Table 3).

After the retention period (T2), both the tympanogram and the audiogram were carried out for the third time to evaluate the long-term effect of the maxillary orthopedic therapy.

(a) The audiogram revealed total recovery of the auditory function and that the decibel and hertz values were similar to the normal values in all subjects in both ears (Table 2).
(b) After retention (T2), the tympanogram showed a standard model, highlighting the total recovery of the tympanic membrane's elasticity. For this reason, its function was perfectly normal (Table 3). After retention (T2), the entrance of the tube was free of serous secretions, as shown by the video-otoscopy (Figure 2).

The results of the variance analysis demonstrated that in the six different situations the comparisons were significantly different than those at T0 and T1 at 250–1000 Hz. The same results were present when considering only three frequencies. If P > F < .0001, the estimated parameter has a statistically significant value. The contrast and P > F show the differences between the test's results two by two and, even in this case, the differences were always significant (Table 4).

DISCUSSION

RME is used to correct maxillary constriction with posterior crossbites. It also improves respiration by increasing the width of the nasal passages.15–17

Brown1 suggested that maxillary constriction, which is one of the causes of nasal stenosis, can affect the eustachian tubes and the middle ear, and result in hearing loss. In animals, rapid palatal expansion results in cranioskeletal displacements18, and skeletal changes that occur in the mouth, oropharynx, nasal cavity, and nasopharynx tend to modify the soft tissue architecture overlying these bony structures.19

Some patients affected with hearing loss also have a history of recurrent upper respiratory tract infections.1,2 The general improvement in nasal physiology after RME minimizes the drying of the pharyngeal mucosa and decreases the upper respiratory tract infections and otitis media, which is a common cause of conductive hearing loss.2,5,7,20

Progressive deafness occurs through an increase in the tympanic membrane concavity as a result of pressure loss. Chronic otitis media is an example of conduction deafness because in this disorder air conduction is impaired.2 With RME, palatal and pharyngeal soft tissues can be modified and tubal ostia may function more normally.3,7 As a result, air passes through the tube, and pressures on both sides of the tympanic membrane are balanced. Thus, the tympanic cavity and the ossicular chain can vibrate freely and function normally.2,7

Anatomical correlations between the middle ear and nasopharynx may explain the action of RME in hearing improvements. The middle ear is connected to the nasopharynx by the eustachian tube, which in turn communicates with the nasal cavities and the oropharynx. As RME has certain effects on the nasal cavity and palate, it may also affect the eustachian tube functions. In addition, the tensor veli palatini muscle may affect hearing improvements. Furthermore, the fact that this muscle lays at or near the eustachian tube orifices and enters into the soft palate plays an important role in the opening of the eustachian tube orifices.9

The eustachian tube connects the tympanic cavity to the nasal part of the pharynx, and its orifice lies on its respective lateral nasal pharyngeal wall. Physiologic obstruction of the eustachian tube comes from the tensor veli palatini muscles at their origins. It keeps the tube from opening in response to negative pressure in the middle ear. Negative pressure in the middle ear, by itself, may be another cause of tubal malfunction. If the tube is blocked, air in the tympanic cavity is absorbed into the mucosal cells (and may at times be replaced with serous or mucous secretions) with loss of pressure, increasing concavity of the tympanic membrane, and progressive deafness.1,21

The peristafilini muscles open and close the pharyngeal ostia of the eustachian tube13 and clear its internal parts of the mucus secreted to humidify and lubricate the inner tube. If they are hypofunctional, the mucus deflection is impaired and the mass of mucus and the virulent exudates lead to recurrent serous otitis.

The results of this study highlight that all subjects selected for palatal expansion and with conductive hearing loss showed incomplete improvement at instrument examination. At T1, the membrane was able to recover its elasticity, and the improvement caused by the decongestion of the tube was considerable at the audiometric test for frequencies between 1000 Hz and 4000 Hz, but not for the lower ones (250–1000 Hz). After 8 months, a complete recovery of the auditory function from the lowest (250 Hz) to the highest values (4000 Hz) occurred.

This improvement, which is more significant in the long term, attests to the necessity of a certain period of time to eliminate the serous fluid after the anatomical improvement in the tubal entrance. The tympanogram data, which certify the tympanic membrane's elasticity, support this assumption. After RME, the tympanogram is still flat in almost all subjects despite the normal functioning of the tubal ostia. After retention (T2), the tympanogram shows its standard model because the tympanic membrane is no longer prevented from vibrating by serous fluid and the edema.

The present study demonstrates that improvements in hearing after RME occur after the expansion period for higher frequencies but not for lower ones, and after the retention period (8 months) for both higher and lower ones.

These data do not agree with those of Ceylan et al.10 These authors report a statistically significant improvement after the active treatment, but a decrease after the retention period. This relapse is not considered relevant by the authors and may be caused by soft tissue relapse.

Timms6 criticized this study because the subject selection was made more on the malocclusion than on hearing loss, and it registered only ranges and means instead of individual levels of hearing loss. The study by Taspinar et al12 allows a longer evaluation, too. The first audiometric recording was taken before expansion and the second after satisfactory expansion of the maxillary arch was obtained (approximately 18 days after). After that, the RME was fixed in the mouth and used as a retention device for 6 months, and the third recording was taken at the end of this period. At the end of this 6-month period, a rigid transpalatal arch with an extension throughout anterior teeth was inserted and used for 2 years. At the end of this period, the fourth registration was taken. In this study, the long-term stability may be assumed to be due to the rigid retention after expansion, which was not used in the other studies. This study was different from Taspinar's study because it did not show long-term results, which will be the subject of further research.

From the analysis of the limited literature on this topic, it can be assumed that in patients with conductive hearing loss with maxillary constriction, palatal expansion may improve the auditory function leading to more physiological activity of the pharyngeal ostia of the eustachian tube.11

CONCLUSIONS

The results of this study confirm and highlight the possibility of improving the auditory function of patients with conductive hearing loss through the correction of palatal anatomy.
Positive effects on conductive hearing levels are considered as a possible additional benefits of RME treatment but does not indicate that patients with conductive hearing loss should consider RME as a treatment approach without an accompanying maxillary constriction.

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Source: http://pinnacle.allenpress.com/doi/full/10.1043/0003-3219(2006)076[0752:CBRMER]2.0.CO;2
 
@applewine

You got to see this case report.

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"The Institute for Nerve Medicine is excited to bring this case study to you this month since we have recently had patient cases where our exclusive Interventional MRI procedures have been able to correct Tinnitus symptoms. While we are currently writing a medical peer review paper that will soon publish our findings, we wanted to bring this wonderful breakthrough to our patient and physician community since this is something that we can provide immediate treatment planning for that is measurably more accurate and clinically efficient.

In this case study we have a patient that developed significant hyperacusis and tinnitus possibly due to multiple medications with tinnitus listed as a side effect. The patient had no relieving factors with persistent tinnitus that affected her ability to sleep on a daily basis. MR-Neurography imaging noted that there was facial nerve irritation as it exits the stylomastoid formen and passes inferior to the external auditory canal which would be consistent with a focal entrapment or irritative syndrome.

Based on these findings the patient proceeded with an Interventional Open MRI guided facial nerve block below the external auditory canal. Medications utilized for this procedure included Marcaine, Celestone and Hyaluronidase. Immediately post procedure the patient noted a significant improvement in her tinnitus. The patient indicated that on a pain scale with 10 being the worst and 1 being no symptoms her tinnitus had gone from a 10 out of 10 pre-procedure to a 1 out of 10 immediately post-procedure. She had a recurrence of her symptoms however at approximately two weeks post-procedure she began to note an overall improvement most likely attributed to the hyaluronidase injected around the facial nerve.

At an additional follow up at four weeks post procedure the patient was still reporting significant improvements in her neck and shoulder pain. She was also maintaining a 50% reduction in her tinnitus with some hyperacusis. Due to the persistent and progressive improvements the possibility of an additional repeat procedure with hyaluronidase was discussed in the event the patient reached a plateau in her progress or began to experience any recurrence.

This was a patient that was experiencing significant symptoms that affected her daily life following a procedure. For over 6 years the patient suffered from these debilitating symptoms with no improvements. The patient has and continues to maintain marked improvement from the Interventional MRI guided procedure targeting the facial nerve for her auditory symptoms. There are numerous tinnitus patients that had been unresponsive to a large variety of treatments including medications. This has been a groundbreaking find in the treatment of tinnitus patients. Hopefully further research will lead to effective treatment for patients suffering from debilitating tinnitus."

Source: http://www.nervemed.com/news/january-2011-case-study-landmark-tinnitus-treatment-by-inm
 
@Mr. Cartman

No, I have not have mine evaluated. I also read that those abnormalities can be quite common in the population without any problems, probably much like the bulging discs.

I read the first paper, but that sort of treatment is definitely not for me. It is not related to my probable cause and my tinnitus is not bad enough to want to mess with that.

The second paper seems to be related to opening the bite for improving hearing and was very long so I didn't read all of it.
 
@Mr. Cartman

Do you eat dairy? Do you eat food like baked goods that contain dairy? You might want to try to go 100% dairy free.

I have had three symptoms which can be linked to dairy. Acne on my back (dairy hormones). Eczema (reported to be caused by dairy).

And, last but not least, muscle pain. I just read that dairy could be causing muscle pain.

Apparently it is related to the proteins whey and casin. This is interesting because back when my muscle pain started it was when I started taking whey protein supplement for my weight training.

Apparently the acne is caused by the fats (hormones) in dairy, highest in things like butter and milk.

Here is a link talking about dairy being one of the primary causes of pain:
http://bodytechnician.com/foodallergies.html

If the dairy is causing any additional irritation in any way that could have caused the problem or prevented the problem from getting better. I have never tried going %100 dairy free in all these years. Dairy can be in things like cold cuts / lunch meats even I found out. Did you know that? The proteins. Some high quality brands may not have it though like Boars Head. Going 100% dairy free may not be easy.

I've reduced my dairy significantly by cutting out butter and my acne on my back has reduced significantly. My eczema was going away, but during Christmas I had lots of baked goods and notice the eczema blisters came back. I don't know if that was the cause.

I've only been off dairy completely for maybe a month and even then it can sneak in. Eczema, muscle pain and back acne. All linked to dairy. I can believe it, though there can be multiple causes. None of those is lactose related though. It is either hormone/fats for the acne or protein related for the muscle pain and I'm not sure what causes the eczema. I did have adult onset eczema around the time I started eating tons of butter every day. The only other thing I ate that was unusual was this chops masala spice blend.
 
@Mr. Cartman

Do you eat dairy? Do you eat food like baked goods that contain dairy? You might want to try to go 100% dairy free.

I have had three symptoms which can be linked to dairy. Acne on my back (dairy hormones). Eczema (reported to be caused by dairy).

And, last but not least, muscle pain. I just read that dairy could be causing muscle pain.

Apparently it is related to the proteins whey and casin. This is interesting because back when my muscle pain started it was when I started taking whey protein supplement for my weight training.

Apparently the acne is caused by the fats (hormones) in dairy, highest in things like butter and milk.

Here is a link talking about dairy being one of the primary causes of pain:
http://bodytechnician.com/foodallergies.html

If the dairy is causing any additional irritation in any way that could have caused the problem or prevented the problem from getting better. I have never tried going %100 dairy free in all these years. Dairy can be in things like cold cuts / lunch meats even I found out. Did you know that? The proteins. Some high quality brands may not have it though like Boars Head. Going 100% dairy free may not be easy.

I've reduced my dairy significantly by cutting out butter and my acne on my back has reduced significantly. My eczema was going away, but during Christmas I had lots of baked goods and notice the eczema blisters came back. I don't know if that was the cause.

I've only been off dairy completely for maybe a month and even then it can sneak in. Eczema, muscle pain and back acne. All linked to dairy. I can believe it, though there can be multiple causes. None of those is lactose related though. It is either hormone/fats for the acne or protein related for the muscle pain and I'm not sure what causes the eczema. I did have adult onset eczema around the time I started eating tons of butter every day. The only other thing I ate that was unusual was this chops masala spice blend.

Yeah, I do eat dairy.. Do you? Maybe we should stay away from dairy for a while just to see what happens? :)

Im reading through some reports, and Ive decided to try out a lot of things, but Ill start out with the non-invasive stuff, and to stay away from dairy for a while would be pretty non-invasive :)
 
@Mr. Cartman This guy had his family start taking whey protein daily and they all started experiencing pain in their shoulder and neck:

http://forums.menshealth.com/topic/63643898175055191

I know my pain started in the shoulder and neck and it was around the time I started taking whey protein back in 2005/2006. It only spread from there.

Did you ever take whey protein isolate products?
 
Hi there, Everyone,

My Tinnitus started up in November - a constant high-pitched sound in both of my ears - that oscillates ("throbs") louder and softer with my heartbeat from time to time, which I have generally learned isn't so much a circulatory issue as it is an inflammatory issue. After exhausting eustachian tube inflammation possibilities, I've had a confirmed diagnosis that TMJ / neuromuscular conflict is principally to blame. I've been seeing a chiropractor for general physical health and have been noticing a gradual improvement of my symptoms over time.

Last night, I had a bit of a breakthrough. The chiropractor trained me in proper pillow use (I'm a side sleeper most of the time, and sometimes sleep on my stomach - evidently a no-no for neck/back issues, BTW), and indicated that my pillow needs to curl up under my chin, in between my shoulder and neck, to provide proper nighttime support. I tried this, and this morning found the volume of my tinnitus in my left ear (the side of the ear where I slept) much improved.

Does anyone have experience with neck/head/back alignment being the cause of their tinnitus? How closely is this phenomenon related to TMJ directly?

I'll be meeting with a world leading maxillofacial surgeon in Boston in a couple of weeks, and I'm hoping to get more answers at that time about my options for treating me. I'd be curious if anyone else here has seen connections between back/spine/neck health and their overall TMJ-related Tinnitus.
 
@Mr. Cartman This guy had his family start taking whey protein daily and they all started experiencing pain in their shoulder and neck:

http://forums.menshealth.com/topic/63643898175055191

I know my pain started in the shoulder and neck and it was around the time I started taking whey protein back in 2005/2006. It only spread from there.

Did you ever take whey protein isolate products?

I dont really suspect whey proteins to be the cause though, but Ive eaten a ton of them in the past.. And it wont hurt to go dairy free for a little while.. Are you going to skip dairy products for a while to see if it helps?
 
Hi there, Everyone,

My Tinnitus started up in November - a constant high-pitched sound in both of my ears - that oscillates ("throbs") louder and softer with my heartbeat from time to time, which I have generally learned isn't so much a circulatory issue as it is an inflammatory issue. After exhausting eustachian tube inflammation possibilities, I've had a confirmed diagnosis that TMJ / neuromuscular conflict is principally to blame. I've been seeing a chiropractor for general physical health and have been noticing a gradual improvement of my symptoms over time.

Last night, I had a bit of a breakthrough. The chiropractor trained me in proper pillow use (I'm a side sleeper most of the time, and sometimes sleep on my stomach - evidently a no-no for neck/back issues, BTW), and indicated that my pillow needs to curl up under my chin, in between my shoulder and neck, to provide proper nighttime support. I tried this, and this morning found the volume of my tinnitus in my left ear (the side of the ear where I slept) much improved.

Does anyone have experience with neck/head/back alignment being the cause of their tinnitus? How closely is this phenomenon related to TMJ directly?

I'll be meeting with a world leading maxillofacial surgeon in Boston in a couple of weeks, and I'm hoping to get more answers at that time about my options for treating me. I'd be curious if anyone else here has seen connections between back/spine/neck health and their overall TMJ-related Tinnitus.

Hi! Thanks for chiming in! :)

The pillow tip might not be a bad idea, and to be honest, I think neuromuscular conflict could be spot on.. At least in my case.. :)

Not sure about the back alignment, but it seems like the C2 ganglion might play a role in some cases of tinnitus, and so does the lateral pterygoideus which is located in the jaw, just to name a few possible causes.

Please let us know what the maxillofacial surgeon has to say :)
 
I too have TMJ issues and cervical spine issues. My oral surgeon did a TMJ mri this week and found the right side to have an anterior dislocation but I haven't spoken to him about this.
My neurologist (who I went to see about the problem) got the results and read them to me. The opposite side of my head has the dislocation on the right. My left ear is symptomatic.
I wear a bite guard but doesn't help. I also always have slept on my back and never put pressure on my sides of my jaw.
Kaelon: who is the dr in town?
Neurologist is going to do MRA for pulsatile tinnitus this week as I do have some components of it, and also some components of the tympanic membrane being stiff, and that can possibly be due to neck tightness and in turn making the eardrum spasm.
So, my sound is low and rumbling, not a hiss, squeal or ring. When I am laying down, the sound is just slightly quieter than when upright, and bending head forward turns the mulitiple oscillating tones into one tone for a minute or so, then goes back to multi tones.
IS THERE HABITUATION for this type? Still not sleeping at night.
 
Hi there, Everyone,

My Tinnitus started up in November - a constant high-pitched sound in both of my ears - that oscillates ("throbs") louder and softer with my heartbeat from time to time, which I have generally learned isn't so much a circulatory issue as it is an inflammatory issue. After exhausting eustachian tube inflammation possibilities, I've had a confirmed diagnosis that TMJ / neuromuscular conflict is principally to blame. I've been seeing a chiropractor for general physical health and have been noticing a gradual improvement of my symptoms over time.

Last night, I had a bit of a breakthrough. The chiropractor trained me in proper pillow use (I'm a side sleeper most of the time, and sometimes sleep on my stomach - evidently a no-no for neck/back issues, BTW), and indicated that my pillow needs to curl up under my chin, in between my shoulder and neck, to provide proper nighttime support. I tried this, and this morning found the volume of my tinnitus in my left ear (the side of the ear where I slept) much improved.

Does anyone have experience with neck/head/back alignment being the cause of their tinnitus? How closely is this phenomenon related to TMJ directly?

I'll be meeting with a world leading maxillofacial surgeon in Boston in a couple of weeks, and I'm hoping to get more answers at that time about my options for treating me. I'd be curious if anyone else here has seen connections between back/spine/neck health and their overall TMJ-related Tinnitus.

I don't think a maxiofacial surgeon is going to be of help unless you have some obvious physical trauma to the area. If it is functional problem of the tissue then you are most likely going to need manual pressure therapy to the muscle sinvolved. I suggest looking into Julie Donnelly (Julstro). She has multiple resources.

I would tend to think that if the tinnitus is caused by trigger points in these muscles though that you would obviously be feel pain already in these muscles. Maybe that is the case.
 
I dont really suspect whey proteins to be the cause though, but Ive eaten a ton of them in the past.. And it wont hurt to go dairy free for a little while.. Are you going to skip dairy products for a while to see if it helps?

The whey protein may have increase the irritability. Having a high dose at the time in the form of a supplement isolate may have given a greater reaction. Even after stopping of course the muscle will not return without manual pressure therapy. I haven't taken that whey protein in 10 years. I don't know if that was a contributing factor, but it was around the same time.

Yes, I'm gong to stay 100% dairy free for all three reasons: eczema, acne and muscle pain.
 
I don't think a maxiofacial surgeon is going to be of help unless you have some obvious physical trauma to the area. If it is functional problem of the tissue then you are most likely going to need manual pressure therapy to the muscle sinvolved. I suggest looking into Julie Donnelly (Julstro). She has multiple resources.

I would tend to think that if the tinnitus is caused by trigger points in these muscles though that you would obviously be feel pain already in these muscles. Maybe that is the case.

This is really helpful, thanks, @applewine. I have more questions and observations, and can use your help.

I have sore jaw joints, and the tissue under my jaw is very sore -- I suspect from nighttime teeth grinding -- and my meeting with my first maxillofacial surgeon was able to confirm that, while I don't have any skeletal problem, I did have fairly swollen tissues around my joints and that they were "likely causing some of the distress." That said, I do not feel in excruciating pain or anything like that. Other things:
  • I can reduce the volume of my tinnitus by moving my lower jaw in the direction of the ear that I want to silence. I understand that what is basically happening here is that I am moving the tightened muscles away from the neuromuscular paths that stimulate the auditory nerve.

  • I can intensify volume and/or create secondary (equally high-pitched) tones by clenching my teeth.

  • If I tilt my head (as to strain my neck), I can increase the volume of the T in the same way as clenching my teeth in the ear corresponding to the neck muscle being strained.

  • Steam, hot showers, and hot compresses reduce Tinnitus volumes, but this relief is short-lived and the Tinnitus comes back to full volume usually within minutes of the exercise.

  • Otherwise, at rest, I have a persistent high-pitched sound in both of my ears that persists perpetually.
What sort of treatment options should I be looking at?
 
yes, I too would love to know what kind of treatments would be helpful for this sort of T, surrounding the jaw and neck muscles.
I had steroid injections in both areas and had silence for just the day after.
Trigger point therapy? Massage? Chiro? and what if you have extreme pain when someone physically touches the area......
 
yes, I too would love to know what kind of treatments would be helpful for this sort of T, surrounding the jaw and neck muscles.
I had steroid injections in both areas and had silence for just the day after.
Trigger point therapy? Massage? Chiro? and what if you have extreme pain when someone physically touches the area......

That's fascinating, @SleeplessSoul. I've had the same exact experience, except by taking Prednisone (50mg) as a steroid, rather than a steroid injection. My T was completely silenced the following day and remained pretty quiet while I was on the steroids. But volume spiked within a few days of the 50 mg high (I was on a 10-day taper, so by day 3/4, it had started spiking again). Who have you met and what treatment options have you pursued so far?
 
Met with oral surgeon, he did injections and MRI .....then with my neurologist of 25 years who is doing an MRA just to rule out any blood vessel problems or brain issues. He said that neck tightness can cause the muscles inside the eardrum to spasm, or that a blood vessel could be hardening that runs near the auditory nerve.

Had my spine pain management Dr. give me injections into the trap muscle a couple of months ago, but no effect on T. He said he could do a cervical epidural but that there is no neural pathway from the C spine to the brain, but he has seen stranger things happen.

My back is against the wall as I have terrible myofascial pain in my neck and jaw and it's very hard to have any sort of manual Physical Therapy in that area because of sensitivity and the pursuant headaches that I get after someone touches me near C5, 6, 7 or the mandible area.

The steroids were did help with the noise, sadly just for a day. Sleep is very difficult. I thought you were having success with some NSAIDS and some other things. I know you tried the steroids and amoxicillin too. If the steroids worked, could you stay on them for a longer course instead of the 10 day taper?

While I was on the amoxicillin after the injections for 5 days, the sound was a little quieter but since there is no known infection, I just can't be staying on that either.

What is your next step?
 
The whey protein may have increase the irritability. Having a high dose at the time in the form of a supplement isolate may have given a greater reaction. Even after stopping of course the muscle will not return without manual pressure therapy. I haven't taken that whey protein in 10 years. I don't know if that was a contributing factor, but it was around the same time.

Yes, I'm gong to stay 100% dairy free for all three reasons: eczema, acne and muscle pain.

Please let me know how it goes :)
 
@Mr. Cartman I haven't had any dairy, but...

I just had some raw nightshades (roma tomatoes) and had a big eczema flare up. I mention this because nightshades are the one other thing in addition to dairy some people say cause muscle pain. The nightshades are more linked to eczema though I think and dairy to acne, but they may both cause muscle pain.
 
@Mr. Cartman Interesting article on TMJ and breathing. I'm reading this now. It talks about the diaphram muscle as well as mouth breathing. I knew mouth breathing could cause overuse of the scalene muscles, but I think this article goes into more. Of a side note the physical therapist that my orofacial pain specialist refereed me to was talking about breathing a lot.

http://www.bioline.org.br/request?os04023

Also very weird is I was messing around with holding my breath. If I hold my breath and push it to my upper chest and tip back my neck, shoulders, upper back I start to brown out after only a few seconds. This is not related to holding the breath because I can hold my breath for a couple minutes without that happening. I was messing around with my breathing and posture.
 
youreproof-610x310.jpg

Could bad posture be contributing to are tinnitus?:D
 
I found this interesting in talking about one possible cause of fibromyalgia. It talks about the hippocampus:

The Pain Brain: Hippocampal Atrophy Found in Fibromyalgia
http://www.prohealth.com/library/showarticle.cfm?libid=19595

It mentions several neurotransmitters like GABA, NAA. Not sure, but I didn't find anything on them except maybe if you have too much it causes burn-out.

I did some searching on the hippocampus and REM sleep after that and found this:

"During REM sleep, high levels of acetylcholine in the hippocampus suppress feedback from hippocampus to the neocortex, and lower levels of acetylcholine and norepinephrine in the neocortex encourage the spread of associational activity within neocortical areas without control from the hippocampus"

Acetycholine is mentioned again, which is supposed to be invovled in trigger points, though in the peripheral nervous system. I don't know however how the CNS and PNS interact with ACh at the motor end plate though.

I then looked up the neocortex and it is involved in sensory perception. Temperature, pain etc. Not sure if that is why I'll feel cold or burning sensations all over my body randomly. Lots of nervous system components are involved in those sensations from peripheral fiber (c, a-delta etc), to dorsal root ganglia outside the spine to the CNS. In my case the small fiber biopsy was negative (c, a-delta fibers) and the DRG didn't seem likely according to my neurologist. There is some gluten autoimmune disease which has been reported to effect the DRG and for some time I thought I might have that. I didn't pursue super advanced testing however and the regular tests were negative and I had relapses while gluten free.

It would be interesting of course if reducing the release of acetacholine through behavior could cause a build up of acetylcholine in the hippocampus to greater levels which would then lower levels of acetacholine in the hippocampus better. One may be able to determine if this was happening by looking for frequent vivid dreams as evidence of stronger REM sleep. Vivid dreams should be present perhaps if there is good sleep quality and if you aren't having vivid dreams then that may be an indicator of a problem when sensory problems are present.

A few google searches may also show people talking about precursers to ACh in the diet as well as something called Galantamine which prevents the breakdown of ACh temporarily. It is supposed to cause vivid dreams. http://dreamstudies.org/galantamine-review-lucid-dreaming-pill/

I wouldn't go for the pill directly, but it could possibly be added to a behavioral modification regimen that conserves ACh release.

All of this is highly speculative and a long shot of course.

Edit: As for what behavioral modification I'm referring to you will have to find my earlier post which discuses that. I had experimented with that some and definitely started experiencing vivid dreams and waking up frequently. My mood also increased because I wasn't releasing dopamine and other neuro-transmitters so much. I only went for 30 days, so it may take a longer experiment.
 
I meant to say build up of ACh in the hippocampus would then lower ACh in the neocortex better. That is consistant with what the quote says, not lower ACh in the hippocampus. I'll have to find that link to the study of what happened when they injected ACh into the brain and where it was. Also, I'm not clear on the difference between a "buid up" and a "large release" as far as activity and activation.

Am I the only person who took amphetamine medications? That would cause a lot of norepinephrine release I believe. I also quit them abruptly which caused a very bad year or two of reactions.
 
Am I the only person who took amphetamine medications?
Hardly! I was a dexadrine/ritalin kid, and then I used adderall on and off in college. Of course, I also took a ton of other stuff, and I was a premature baby, so who knows which did what....

One may be able to determine if this was happening by looking for frequent vivid dreams as evidence of stronger REM sleep. Vivid dreams should be present perhaps if there is good sleep quality and if you aren't having vivid dreams then that may be an indicator of a problem when sensory problems are present.

This is sort of interesting because last time I was in crisis mode with my T was during last summer, and I know from looking over my journals from that period, that the point where things started to improve coincided with some incredibly visual, powerful, almost spiritual dreams. Then I got back into smoking weed on a regular basis, my dreaming got a lot less interesting, and lo and behold here I am going bonkers with tinnitus all over again.
 

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