TINNITUS
There are questions that so far have remained unanswered regarding TINNITUS. We know what it is and the many causes and symptoms, but is there a cure, an ultimate solution? I will be navigating through this journey one step at a time, from what it is through to hopefully, a logical and viable hypothesis using existing research by others, studies, practical examples, and my personal experiences. It must be said, not wishing to state the obvious, that the five senses are experienced subjectively. Sight, sound, smell, taste, and touch. Without the subject’s input their experience cannot be ascertained. Can you hear, taste, smell, feel and/or see this? No doubt that is why, with regards to tinnitus the Mayo Clinic states “Tinnitus is the perception of noise or ringing in the ears . . . . . . the phantom noise may vary in pitch . . . . ” Each person’s experience is their own in relation to the pitch (varying frequencies) and volume which can also vary from time to time for each individual. Here it MUST be said for those who suffer from tinnitus that it is neither a perception of noise nor a phantom noise but is real.
The Mayo Clinic outlines may causes of tinnitus in different categories such as:
• Common causes – Age related, loud noise exposure, ear bone changes (they missed ear infections) • Other causes – Meniere’s disease, TMJ (temporomandibular joint) disorders, Head injuries etc. • Blood vessel disorders linked to tinnitus • Medications that can cause tinnitus as wells as the symptoms • Ringing • Buzzing • Hissing etc.
There are also complications that come with having tinnitus. The Mayo Clinic also outlines diagnosis and treatments. Treating underlying health conditions, noise suppression i.e. masking devices and alike as well as medications which they state cannot cure tinnitus. The Mayo Clinic as well as multiple Medical Clinics and Faculties at countless Universities continue with research and conduct studies into treatments but their answers to what the causes are as stated above, do not lend themselves to any solutions. ‘WHAT IS THE PROTAGONIST’ IS THE QUESTION WE SHOULD BE ASKING. Take loud noise as the cause. Many have experienced temporary tinnitus through exposure to loud music, machinery, even gunfire. Why is it temporary? When and why does it become ongoing or become permanent? It is now believed that neuroscience can answer some of these questions. The National Library of Medicine (National Center of Biotechnology Information) under ‘The neuroscience of tinnitus’ has many articles regarding this view. “Neuroscience research has begun to reveal how tinnitus is generated by the brain when hearing loss occurs, and to suggest new avenues for management and prevention of tinnitus following hearing injuries.” - Jos J Eggermont , Larry E Roberts.
‘Maladaptive plasticity in tinnitus--triggers, mechanisms and treatment’ is another article.
“Maladaptive neural plasticity seems to underlie these changes: it results in increased spontaneous firing rates and synchrony among neurons in central auditory structures, possibly generating the phantom percept.” Susan E Shore , Larry E Roberts , Berthold Langguth
Reviewing these two articles.
The first stating “ . . . .how tinnitus is generated by the brain . . .” and “hearing loss occurrence triggers tinnitus following head injuries”, yes but what of the tinnitus experienced when NO such injuries have been sustained? Tinnitus can manifest hearing loss because the frequencies that are already playing in the subject’s ears and masking external incoming frequencies. The second stating . . . . “Maladaptive neural plasticity seems to underlie these changes . . . . . . among neurons in central auditory structures . . . .” We can see a pathway to understanding but even then, they are missing something. NOTE: ‘Generated by the brain, neural plasticity and auditory structures. These are NOT anomalies but are the clue that leads us to the answer we are looking for.
Brain Function - Neurotransmitters.
Molecular Cell Biology. 4th edition “. . . . . . . . . . synapses are the junctions where neurons pass signals to other neurons, muscle cells, or gland cells. Most nerve-to-nerve signalling, and all known nerve-to-muscle and nerve-to-gland signalling rely on chemical synapses at which the presynaptic neuron releases a chemical neurotransmitter that acts on the postsynaptic target cell.” Put simply Neurotransmitters are chemical signals that transmit a message from a nerve cell across the synapse to a target cell.
Neurological messages and responses are continuous AND constantly changing, neurotransmissions in flux, the auto neurosensory function (ANF) which is in play even when there’s no apparent external stimuli. Not enough importance has been placed on this process. In certain circumstances when the external stimuli are abnormal and continuous, neurotransmissions increase and/or alter and because of the brain’s neuroplasticity these new signals become the new norm, becoming the default action and reaction, therefore creating abnormal neurotransmissions. It is the brain that has adjusted its messages to the body and its neuroplasticity has created a new default. Applying these processes to the central auditory structures, we must break down its elements and determine what changes occur to them when there are abnormal and/or normal continuous external stimuli and how maladaptive neuroplasticity affects the brain function relating to the auditory cortex.
For this paper, we will restrict ourselves to only SOME of the cochlear structures.
• Stereocilia. • Cochlear fluid containing two types of fluid: perilymph and endolymph. • Vestibulocochlear nerve (auditory nerve) also known as the cranial nerve which consists of the vestibular and cochlear nerves (auditory cortex both left and right).
Neurotransmissions are sent to the auditory structure and back, even when no external sound stimulus is present. This is its ‘normal’ function and that which keeps the auditory structure active. [ANF]. External stimuli enter through the tympanic membrane causing vibrations. These vibrations move the tiny bones of the middle ear and are transferred through the cochlear fluids creating movement in the stereocilia. This in turn causes neurotransmitter release at the basal end of the hair cells. “The mechanical movement of this hair bundle generates an alternating hair cell receptor potential. This occurs in the following manner. When the stereocilia are bent in the direction of increasing stereocilia length, ion channels in the membrane open, allowing potassium ions to move into the cell. The influx of potassium ions excites, or depolarizes, the hair cell.” -
This in turn progresses through the cochlear nerve which translates the frequencies and forwarding them to the auditory cortex which is the part of the temporal lobe that processes auditory information, and thus the process continues. When all is functioning well, even with fluctuations in sound types and volumes the auditory structure makes the needed adjustments. In the event of abnormal and/or continuous external stimuli such as exposure to loud music, machinery, even gunfire the stereocilia are deflected in the opposite direction, the ion channels are shut and the hair cell is inhibited, or hyperpolarized, restricting the release of neurotransmitters from the base of the hair cell. Now if we read the introduction of ‘Audiology and Neurology – A Prospective Study of the Effect of Cochlear Implantation in Tinnitus’ “Many hypotheses have in common that central neural mechanisms play a key role in its development. Most of these hypotheses state that tinnitus is caused by maladaptive plastic changes in the central auditory pathways as a reaction to peripheral hearing loss [Cacace et al., 2016].” we can see confirmation by some researchers that neuroplasticity plays a role in its influence on tinnitus and hearing loss. How do these changes caused by maladaptive neural plasticity make tinnitus continuous? These changes increase neurotransmitter release causing auditory nerve overactivity, the worst-case scenario being that in some cases the intractable tinnitus is caused by compression on auditory nerves by the artery at the brainstem root entry zone of the nerve. ANF is in play and external stimuli is converted to electrical impulses, it stands to reason that the auditory nerve overactivity increases electrical impulses directly back to the auditory structures deflecting the stereocilia to the opposite direction, the ion channels are shut, and the hair cells are inhibited without external stimuli. The newly created internal electrical impulses from the overactive auditory nerve then becomes a continuous cycle. What has happened is neurotransmitter switching “. . . . . . . . . brain plasticity in which an environmental stimulus causes neurons to replace one neurotransmitter with another” - Hui-quan Li, Marta Pratelli, Swetha Godavarthi, Stefania Zambetti and Nicholas C. Spitzer, i.e. maladaptive neuroplasticity, hence we have continuous tinnitus.
Why does the volume fluctuate, becoming acute then moderate, changing apparently at random?
There is a natural neurotransmitter synchronicity that exists within the motor circuits in the brain. Neuromolecular Imaging Shows Temporal Synchrony Patterns between Serotonin and Movement within Neuronal Motor Circuits in the Brain - Patricia A. Broderick. Neurotransmitter activity fluctuates depending on an individual’s own activity and generally within the individual’s natural temporal synchrony patterns. For example, if an injury occurs, a lower back muscular strain for instance, neurotransmitters increase, originating from the cerebellum a natural part of the ANF, blood flow increases etc and the area tightens, and a large part of the tightening is because the electrical impulses become trapped within the muscle tissue, neurotransmissions from the cerebellum demanding a normal response, increase to achieve the response. Various therapies can be applied to heal the area, one being acupuncture, or a more advanced targeted acupuncture (dry needling) applied to the muscle to assist with decreasing pain and improving function through the release of myofascial trigger points (knots in the muscle). If the injury has been ongoing, a mild electrical discharge occurs, usually flowing down through the legs, releasing any trapped electrical impulses, and relaxing the surrounding muscles. Neurotransmitter synchronicity therefore heightens neural activity and the already overstimulated auditory cortex increases along with it, causing the tinnitus to increase. The significance of this can be found in the ‘Addendum’ CASE STUDY - SUBJECT K101 item #8 where the subject’s tinnitus all but disappeared albeit for a period of ten days after the subject’s first experience with dry needling in the target area. The addendum also explains the subject’s minor right auditory cortex increase due to some damage to stereocilia cluster in right ear.
NOTE: Dry needling IS a known therapy for multiple sclerosis an autoimmune disease. This will be discussed in another paper with a view to understanding ANF, maladaptive neuroplasticity and its relationship with autoimmune disease. [It should be noted here and now that TINNITUS is in fact as autoimmune disease].
Regarding tinnitus, the ANF® has been amplified in the temporal lope due to maladaptive neuroplasticity thus overstimulating the auditory cortex, first the right auditory cortex then to the left. Regarding tinnitus, the ANF has been amplified in the temporal lobe due to maladaptive neuroplasticity thus overstimulating the auditory cortex, first the right auditory cortex then to the left. This amplification, as stated previously increases electrical impulses directly back to the auditory structures deflecting the stereocilia to the opposite direction, the ion channels are shut, and the hair cells are inhibited without external stimuli. Over time this may damage said stereocilia, so this must be constantly evaluated. Three ways to tackle these phenomena. One, by lowing the hyperactive impulses coming from the auditory cortex by targeted transcranial magnetic stimulation [TMS] . Two, by examining other maladies that may increase movement within neuronal motor circuits and treat them, to minimize neurotransmitter activity thus reducing the possibility of the overactive auditory cortex being affected by neurotransmitter synchronicity. FINALLY, CREATING A RESPONSE WITHIN THE AUDITORY CORTEX I.E. SOUND TECHNOLOGY BORDERING ON A SUBSONIC APPLICATION USING THE MULTIPLE FREQUENCIES SPECIFICALLY RELATED TO THE INDIVIDUAL’S TINNITUS AS WELL AS BLOCKING FREQUENCIES NOT AFFECTED, BY USING SOUND CANCELLING TECHNOLOGY, THEREBY SPECIFICALLY TARGETING THE TINNITUS WITHOUT AFFECTING THE UNAFFECTED STEREOCILIA. BY CREATING THIS UNIQUE THERAPEUTIC REGIMEN, WHICH NEEDS TO BE CONTINUOUS THEREBY ALTERING THE FUNCTIONAL PLASTICITY AND/OR STRUCTURAL PLASTICITY, STABILIZING NEURAL ACTIVITY RELATED TO TINNITUS AFFECTED AUDITORY STRUCTURE. IT IS CRUCIAL NOT ONLY TO ADJUST NEURAL ACTIVITY BUT TO ALSO ALLOW THE STEREOCILIA TO RETURN TO THEIR NORMAL RESTING POTENTIAL. THIS IS AT THE HEART OF THE N-OF 1 CLINICAL TRIAL THAT WILL BEGIN SHORTLY TO GATHER DATA, TO CONFIRM THIS HYPOTHESIS. IF SUCCESSFUL SECOND STAGE TRIALS WILL TAKE PLACE USING A CROSS SECTION OF SUBJECTS TO ENABLE THE DEVELOPMENT OF A PRACTICAL THERAPY TO REDUCE TINNITUS AND/OR ELIMINATE IT ALTOGETHER. THIS THEAPY AND IT'S PROCESSES ARE SUBJECT TO A PATENT PENDING.
ADDENDUM CASE STUDY - SUBJECT K101 MEDICAL HISTORY AND RELATED PERSONAL HISTORY
1. Medication taken from 1986 (Marevan – warfarin sodium 3mg – 4mg) due to replacement of aortic valve at age 30. This will become relevant later.
2. Multi-instrumentalist and vocalist. First experienced continuous tinnitus in the right ear during the mid-1990’s caused by excessive external sound volume. Very mild condition and not causing discomfort in any way. This remains static for a decade and a half. (Historical diagnosis would be that some damage to stereocilia in right ear would exist, possibly only within one cluster).
3. NOTE: SUBJECT IS PHYSCIALLY FIT DUE TO YEARS OF WORKING AS A CARPENTER, REGULAR GYM WORKOUTS INCLUDING WEIGHTS AND 26 YEARS OF MARTIAL ARTS TRAINING.
4. During late 2010 tinnitus begins to increase, first in the right ear followed by some increase in the left ear but not as pronounced. The subject, at the time was unaware that he/she was experiencing complex partial seizures. Once the subject became aware of this, medical advice was sought, and a Neurologist (associate professor) was engaged. After several CT scans which showed a small shadow in the temporal region (as the subject had open-heart surgery and the sternum was wired together at the time of the surgery an MRI was out of the question), the subject was advised to undergo exploratory surgery, however a low-voltage MRI was located, and a scan was taken. The discovery of a birthmark (‘port wine’ stain) on the temporal lobe or the remanence of one. No other evidence of hemangioma appeared. No such hemangioma appears on the subject’s skin nor is there any history of epilepsy with either the subject or any member of his family. ‘Remanence’ is the operative word here. The subject’s warfarin sodium intake stabilized at 3mg per day over the years with an INR (International normalised ratio) in the lower range, the subject’s dosage was raised to the upper range thus causing the ‘port wine’ stain to bleed which in turn triggered the complex partial seizures increasing neurotransmissions causing auditory nerve overstimulation/hyperactivity.
5. Warfrin dose adjusted, and the subject is now taking 500mg levetiracetam as directed and continues to do so.
6. A single seizure did occur when the levetiracetam dosage was lowered however it was later determined that antibiotics (amoxicillin) taken due to a throat infection affected the ability of the levetiracetam to control the onset of seizures.
7. Since the continuous tinnitus began, as with many sufferers it tends to fluctuate.
8. Due to the subject’s physical labour (carpentry), and gym training some lower back issues had begun to occur. One of the subject’s training partners recommended dry needling (trigger-point acupuncture). Described by the subject as an electrifying experience, the subject first had the procedure around the shoulder area then on the lower back when returning for a second treatment. After the latter treatment, tinnitus disappeared apart from the mild condition the subject experienced some 20 years before. This new outcome lasted for 10 days then gradually increased over a period of 3 weeks, back to the levels prior to dry needling treatment. This phenomenon usually only occurs once to such a degree and subsequent dry needling to the lower back area only slightly lowers the level of tinnitus. Occasional acupuncture and deep muscle massage since, reduces tinnitus volume slightly but the subject now has acute tinnitus.