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Author: admin | 15.10.2015 | Category: Homeopathic Treatment For Tinnitus

A final common pathway for tinnitus is hypothesized to exist for all patients with tinnitus. Its function is the transition of the sensory to the affect component of the symptom of tinnitus. Single Photo Emission Computerized Tomography (SPECT) with the radio isotope TC99-HMPAO has identifie side to side perfusion asymmetries highlighted by that of the amygdala - hippocampal complex. It is hypothesized that a fundamental function of the amygdala - hippocampal structures is the establishment of a paradoxical auditory memory for tinnitus.
A Final Common Pathway (FCP) is hypothesized to exist for all patients with tinnitus, particularly of the severe disabling type (SIT). Historically, this search for understanding how the transition from sensory to affect occurs in the brain is not new. The concept of William James, the Father of American Psychology is suggested to find application to a FCP for tinnitus. Single Photon Emission Computerized Tomography (SPECT) with the radioi sotope Tc-99 HMPAO is a detection method which provides information of cerebral perfusion in brain.
Based on clinical experience with tinnitus particularly of the severe disabling type and supported by SPECT imaging of the brain, the medial temporal lobe system is speculated to be a key site of action of processing of an aberrant auditory signal resulting in a paradoxical auditory memory; and an accompanying parallel transition in processing of the sensory to the affect component of the symptom of tinnitus. In other words, the eterogeneity of the symptom of tinnitus is reflected in FCP for tinnitus. The FCP is presented as a hypothesis focusing on a process within the MTLS of a paradoxical auditory memory with speculations as to its clinical applications for both diagnosis and treatment. It is hypothesized that for all sensory systems the sensory and affect components are linked by memory.2 The experience of the sensation is a perceptual image of the stimulus. Psychology and neuroscience evidence have differentiated between long term and short term memory. The modulator of the sensory component is considered to be the efferent system and the process of masking.3 The modulator of the afferent component is considered to be stress. In the patient with tinnitus, particularly of the severe disabling type it is hypothesized that both the hippocampus and amygdala of the MTLS are significant for the transition of the sensory to the affect component. In summary, the FCP model for tinnitus involving the medial temporal lobe system is initiated in the MTLS by the process of establishment of a paradoxical memory. Our approach is clinical and attempts to identify not all components of the FCP but rather to focus on one aspect, specifically memory which is considered at present to be clinically most significant; and is explainable by what has been reported for understanding brain function specifically memory. The activity in the brain that corresponds to memory can be found in the medial temporal lobe system. Crick's comments on the problem of visual awareness I believe can be applied to that of tinnitus - an auditory perceptual phenomenon.6,31 Specifically, investigations for tinnitus are necessary from a psychological and a neuro-science perspective for the issues of attention and very short term memory.
The MTLS can be considered an information processing pathway for the integration of sensory and affect components of all sensory inputs. The perception of a auditory image, considered to be "normal", is hypothesized to be determined by a normal masking function. It has become apparent to us from our clinical experience with SPECT since 1989, that the manner in which the brain processes auditory sensory information is radically different with or without the presence of tinnitus. The consequences of the identification of a FCP for tinnitus and the role of the MTLS are considered significant.
The following SPECT images of the brain demonstrate multiple perfusion asymmetries, highlighted by the MTLS (Fig. The FCP for tinnitus provides a rationale and model for understanding the integration, interaction, translation, and transformation of the sensory auditory signal to the affect behavioral response. An initial process, in the MTLS, is hypothesized to be the establishment of a paradoxical auditory memory for tinnitus. SPECT imaging of brain provides an ability to identify regions of interest in the brain which demonstrate perfusion asymmetries frequently found in patients with tinnitus of the severe disabling type.
The processes involved in the establishment of the symptom of tinnitus particularly of the severe disabling type and the problems encountered, relate to the overall problem and question over centuries of what is the relationship of mind and brain and what are the processes involved in such identification. Sound Therapy International - Tinnitus treatment, relieve stress and get emotional relief. Sound Therapy International – Tinnitus treatment, relieve stress and get emotional relief.
Sound Therapy is an environmental health method Environmental health is a new field of treatment which brings together mainstream and alternative health practices. From time to time our listeners come back to me and say that they have not received the full level of recovery from Sound Therapy they may have been hoping for with tinnitus or other hearing issues.
How to Get Bigger Results from Sound Therapy   From time to time our listeners come back to me and say that they have not received the full level of recovery from Sound Therapy they may have been hoping for with tinnitus or other hearing issues. Research on sounds that stimulate the brain Jim Millburn embarked on a course of Sound Therapy after reading how it could bring about a number of improvements to brain function generally.
Training your brain is a hot concept currently with Todd Sampson on the ABC demonstrating the power of brain training exercises and all the buzz about brain plasticity. Dr Donna Segal has been a long term colleague and collaborator with me and is one of our Sound Therapy Consultants in Indianapolis. When most people are faced with the fact that they may be losing their hearing, they will  often opt for denial.
I recently saw a segment on the ABC about Dystonia being treated with magnetic brain stimulation. Patricia Joudry dedicated her life to helping others with their personal and spiritual development through her work. The greatest journey of my life has been being able to help many thousands of people to have better ear and brain health for life, through Sound Therapy. Toxins from the environment can enter and build up in our bodies, making us sick without knowing why. In a continuing study at the medical school in Hanover, Germany, the researchers discovered the degree to which the patient's general well-being plays a role in connection with tinnitus. While some people examined in the study hardly noticed their tinnitus others suffered a lot from the continuous ringing or buzzing in their ears. Unfortunately you cannot use our pictures, as we do not have the copyright, but only have the right to use them on our website. To play the media you will need to either update your browser to a recent version or update your Flash plugin.
Subjective tinnitus is a clinical disorder, defined traditionally as a perception of sound (a tone, a hum or a hiss) that is experienced in the absence of an externally evoking auditory stimulus.
The relationship between stressfully loud sounds (acoustic over-stimulation) and subjective, neural-generated tinnitus is well known and is well documented. The auditory trauma that follows acoustic over-exposure is indeed well documented, and frequently consists of an acute or chronic inflammation of the primary (Type-I) auditory neurons within the cochlea. In the mammalian nervous system, naturally occurring (endogenous) neuroactive opioid (peptide) substances called dynorphins (DYNs) are profoundly involved in the regulation of biological responses to all forms of stress, and correspondingly play a significant negative role in neural inflammatory disorders, edema, cytotoxicity, hyperalgesia and neural pathology.
Aside from the possibility that endogenous cochlear DYNs are likely to contribute to the excitotoxic, Type-I auditory neural dendritic swelling and inflammation that typically follows acoustic over-stimulation, how else might the receptor properties of DYNs be connected to the symptomology of tinnitus?
In summary, following acoustic over-stimulation, an endogenous cochlear mechanism is likely to exist whereby a DYN-mediated increase in receptor sensitivity to GLU could selectively enhance Type-I auditory neural activity, and thereby contribute significantly to the production of an acute (reversible) tinnitus, and temporary inflammation, in a manner that is reminiscent of the reported mechanism of action of sodium salicylate.
The LOC dendrites and cell bodies (LOC nuclei) of the DYN-bearing axon terminals that directly innervate cochlear Type-I auditory dendrites, are located in the brainstem.
Adjacent perfusion asymmetries involving the frontal, temporal and parietal lobes suggest a interneuronal network resulting in the transition of the sensory to the affect components of the symptom of tinnitus.
Descartes regarded the mind as something immaterial, separate from brain but interacting with it in some manner.
Fear and stress in tinnitus patients particularly of the severe disabling type are a result of a paradoxical auditory memory of an aberrant dysynchronous auditory signal.
The establishment of a paradoxical auditory memory for tinnitus is hypothesized to be the initial process localized in the medial temporal lobe.
Demonstrations of SPECT imaging of rain in patients are presented to support this hypothesis. The heterogeneity of response both for sensory and affect has been reported by professionals of all disciplines who are involved in tinnitus diagnosis and attempts for its control. The Papez circuit proposed the anatomical basis of emotion to consist of the cingulate gyrus which connects with the parahippocampal gyrus and peripheral area of the temporal lobe. The anatomical components are best seen by a saggital section of the medial surface of the brain; and ventral views of the base of brain. Non-declarative memory, also called implicit memory, includes all abilities which are unconscious and expressed through performance.16 Such abilities provide for cumulative changes in perceptual and response systems of new skills and habits, priming, simple classical conditioning, and non-associative learning. Its chieffunction is the transition of a aberrant dysynchronous auditory sensory signal to a affective behavioral response (Fig.
This conceptualization is a basic tenet of the FCP for tinnitus of the cochleovestibular system.

The sensory and affect components are considered to be in a constant state of reciprocal interaction. For memory, alterations occur in the hippocampal formation with the establishment of a paradoxical memory for an aberrant dysynchronous signal. I consider the experimental and theoretical work of consciousness as reflected in memory, to be a starting point to explain our SPECT findings to date. Neurobiological theories of tinnitus awareness need to be developed and tested using a combination of molecular, neurobiological and clinical imaging studies. It is possible that there is a localization in the MTLS for all sensory inputs similar to that which exists in the motor cortex. Specifically, the anatomic substrate where integration of sensory and affect components occurs for the auditory system, is suggested at this time to be in the MTLS.
Interference in masking within brain, initially at brain stem is hypothesized to set in motion a cascade of events wherein the sensory component is overwhelmed by that of the affect due to the establishment of a paradoxical auditory memory. Hinton et al.35 have described such neuronal networking in investigations simulating brain damage. For the first time, here is a model which may differentiate tinnitus between its sensory and affect components both from its clinical and basic science perspectives. Jacobson L, Sapolsky R: The role of the hippocampus in feedback regulation of the hippothalamic - pituitary - adrenal cortex axis. LeDoux JE: Information flow from sensation to emotion plasticity in the neural computation of stimulus value. It arose in response to a series of environmental diseases or illnesses that could not be addressed with conventional methods. It’s certainly heartening to know that the brain can change and be re-built at any age and we can improve instead of just degenerating.
As a Doctor of Audiology who teaches audiology students about tinnitus, she has a wealth of experience in this field. Living in Australia, we are now at the dead of winter, about to witness the turning of the year in about a week’s time.
This is partly because hearing loss is usually very gradual, so you adapt to it and don’t realise it’s happening.
In 1984 she discovered Sound Therapy and wrote the original book on her discoveries: Sound Therapy for the Walkman. I am part of a project in New Zealand to set up a permaculture village, designed for resilience. The latter often end up in a vicious circle of sleep disorders, and some even suffer from depression. The only condition is that you provide a direct link to the specific article you use on the page where you quote us. For this reason, subjective tinnitus is often referred to as a phantom auditory perception.
Both acute (short-lasting or temporary) and chronic (long-term) tinnitus often begins with or follows an episode of stressful acoustic over-stimulation.
The Type-I auditory neurons are responsible for all or most of the auditory input that initially and ultimately reaches the auditory cortex. DYNs can interfere with the rate of extracellular GLU uptake by glial cells, and hence, can significantly increase the extracellular availability of GLU.
DYNs exhibit pharmacological actions that closely resemble those of the excitatory, and sometimes cytotoxic drug, sodium salicylate (aspirin). During periods of psychological (non-auditory) stress, the same mechanism could selectively enhance Type-I auditory neural activity at low or possibly negligible levels of an auditory stimulus. These nuclei receive abundant axonal projections from norepinephrine (NE)-rich axons of another brainstem nucleus, the locus coeruleus (LC).
FDA-approved drugs are available that can safely be used to antagonize the properties of DYNs. Sahley, PhD, CCC-A, is currently an associate professor in the School of Health Sciences at Cleveland State University. In order to post comments, please make sure JavaScript and Cookies are enabled, and reload the page. Localization of brain action is now possible and is being investigated with both Positron Emission Tomography (PET) and Single Photon Emission Computer Tomography (SPECT) brain imaging. The transition is acknowledged to be complex, involving an integration of multiple neuronal networks within the brain.
The underlying mechanism is that of dysynchronization, that is, a lack of synchrony or interference in timing of the discharge rate and phase locking of the auditory signal having a location peripheral, central or both.
To date 48 patients were selected for SPECT imaging of the brain identified with the MATPP to have severe disabling tinnitus of the central type. The clinical application of this hypothesis for present and future tinnitus diagnosis and treatment is conside d significant. It includes the subcallosal, cingulate, and parahippocampal gyri, the hippocampal formation, and the dentate gyrus.
The temporal lobe connects with the hippocampus (AMMONS horn) via the temporoammonic tract. The entorhinal cortex is a major source of projections at the hippocampus and in turn receives input from adjacent perirhinal, parahippocampal cortices.
Final Common Pathway for Tinnitus - The Medial Temporal Lobe System (Presentation at the Charles Univ.
It is hypothesized based on our tinnitus experience that in the normal auditory system a sequence of auditory images, results first in establishment of an auditory memory for a sensory input, both short and long term; and secondarily a positive affective behavioral response. It is possible that there may be further or additional localization for a particular sensation. Feldmann reported the difference in interaction of signal and masker in patients with and without tinnitus by masking curves.
SPECT findings at this time suggest a common neural pathway and not an abstract algorithmic description. The FCP is a biological model which is an outgrowth of our ongoing attempts to integrate the basic sciences with our clinical experience for the diagnosis and treatment of all types and subtypes of tinnitus. Presented at the Fourth International Seminar Inner Ear Medicine and Surgery, July 1994, Snowmass, Colorado.
Observations of simultaneous auditory brainstem responses with monaural stimulation in the tinnitus patient.
On the Functional State of Central Vestibular Structures in Monaural Symptomatic Tinnitus Patients.
The other is to purchase through one of our Independent Consultants, who sell our Synergy brand. Dystonia is “a movement disorder that causes the muscles to contract and spasm involuntarily,” according to the dystonia foundation. Her mission is to make Sound Therapy and the discoveries of Dr Tomatis widely available to everyone who needs it. Many diseases are on the rise, including cancer, chronic fatigue, chemical sensitivity and tinnitus. People of calmer disposition and a general sense of well-being suffer far fewer psychological effects from the continuous buzzing or ringing in the ears. Approximately 25.3% of the general population (or 50 million adults) in the United States experiences the disorder.
Acoustic over-stimulation is at times followed by an acute or a chronic reduction in hearing sensitivity that may or may not be accompanied by an acute or chronic tinnitus. DYNs also potentiate the excitatory properties of GLU at postsynaptic GLU-sensitive neural receptors.
Sodium salicylate is well known and is well-studied for its capacity to produce a transient, dose-dependent neural-generated tinnitus when administered systemically. Normally, such an increase in auditory sensitivity during periods of vigilance would be considered appropriate and adaptive.
The LC exhibits high activity levels during periods of emotional stress, increased behavioral vigilance, anxiety, and generally in response to autonomic (sympathetic) arousal.
Endogenous dynorphins, glutamate and N-methyl-D-aspartate receptors may participate in a stress-mediated Type-I auditory neural exacerbation of tinnitus. Modulation of cochlear afferent responses by the lateral olivocochlear system: activation via electrical stimulation of the inferior colliculus. Repair of inner hair cell-auditory nerve synapse and recovery of function after an excitotoxic injury.
Choline acetyltransferase, glutamate decarboxylase, tyrosine hydroxylase, calcitonin gene-related peptide and opioid peptides coexist in lateral efferent neurons of rat and guinea-pig.
Underlying mechanisms are hypothesized to exist and to be highlighted by a diminution of inhibition mediated by gamma aminobutyric acid (GABA) due to disconnection from excitatory (glutamate) inputs.

It is considered to transcend the classica thinking of tinnitus as an auditory signal restricted to the auditory pathway. The limbic system is a term used to include the limbic lobe and associated subcortical nuclei (amygdaloid complex, septal nuclei, hypothalamus, epithalamus and other thalamic nuclei). The frontal, temporal, parietal lobes project to the perirhinal, parahippocampal cortices from unimodal and polymodal areas.
A paradoxical memory modulates the transition between the sensory and behavioral component of tinnitus. It is speculated that for tinnitus the amygdala is significant for the alteration in emotional behavior described by the patient. It is speculated that the primary auditory cortex projects to the hippocampus and amygdaloid complex. The masking curves "can be thought of as contour lines of the neural elements involved in processing signal and masker."34 Tinnitus is believed to produce or reflect a instability or interruption in auditory masking function. The future is to identify neural networks and to create idealized computer simulates of groups of neurons.
For auditory perception this includes the inner ear and Organ of Corti; transmission within the ascending auditory system to registration of impulses within the auditory cortex.
Over-exposure to loud, intense environmental sounds often results in tinnitus when the auditory stimuli last for prolonged periods of time.
In the cochlea, glutamate (GLU) is the excitatory neurotransmitter that activates the Type-I auditory neurons.
Indeed, the excitatory, neurotoxic GLU-receptor mediated actions of low concentrations of DYNs are well documented. For this reason, salicylate-induced tinnitus has historically served as a reliable, highly controlled pharmacological model for naturally occurring, neural-generated tinnitus. However, in a neurologically compromised inner ear, a psychological stress-induced DYN-mediated increase in receptor sensitivity to GLU could result in, or contribute to an exacerbation of a pre-existing (chronic) condition of tinnitus and neural inflammation, perhaps resulting as well in the generation of hyperacusis.
Sahley also holds an adjunct appointment in the Department of Biological, Geological, and Environmental Sciences (BGES). Blockage of GABA mediated inhibition results in Tinnitogenesis, a epileptiform auditory phenomena. The clinical manifestations of the affective behavior of the tinnitus patient can be considered to be components of the FCP for tinnitus.
Physiologic evidence suggests functional differences between the various components although most are related to visceral or behavioral activities (Fig. The mamillary body connects with the anterior nucleus of the thalamus via the mamillothalamic tract. Severe memory impairment associated with hippocampal and amygdala lesions were attributed not to the addition of the amygdala to the hippocampal lesion but instead to the addition of cortical regions that lie adjacent to the amygdala and that are necessarily damaged when the amygdala is removed or impaired. This sequence of events is hypothesized to exist in general for other sensory systems and specifically for the cocheovestibular system.
The central efferent system at a cortical and subcortical level at brainstem is speculated to control the masking capability of the auditory system. Acoustic over-exposure and the subsequent Type I auditory-neural trauma that follows, is the result of an excessive, excitotoxic accumulation of GLU. More notably, DYNs are well known to exist within important anatomical microstructures within the cochlea. Sodium salicylate has been shown, in repeated investigations, to potentiate the Type-I neural excitatory properties of the auditory neurotransmitter, GLU. Hyperacusis, which is often associated with tinnitus, is usually defined as increased sensitivity, intolerance, and an abnormally strong reaction to ordinary, low intensity-level environmental sounds, that are neither threatening nor uncomfortably loud. Application of NE to LOC brainstem nuclei produces Type-I neural activity changes in response to sound that closely resemble those that follow systemic or cochlear administrations of drugs that mimic DYNs.
In the future, as the clinical experience of multiple disciplines increases for the symptom of tinnitus, it is predicted that additional components will be identified. The anterior nucleus of the thalamus connects with the cingulate gyrus via the superior thalamic peduncle, thus completing the circuit.
The entorhinal cortex was suggested to be the principle route by which information from the neocortex reaches the hippocampus. Other aberrant sensations experienced by patients include hyperacusis, dysacusis, vertigo, etc. For tinnitus such abilities may reflect cumulative changes in perceptual and response systems and for the development of new skills and habits personified by increasing attention to tinnitus and inability to "cope" with tinnitus. The reciprocal projections between the entorhinal cortex, hippocampus and amygdala result in an emotional response. The degree of inhibition regulated by GABA function is hypothesized to be reflected in the degree of development of the paradoxical memory for tinnitus.
Kassirer stated it well in discussing a visual image in clinical medicine that "often we are creating mental models of physical models. Acoustic over-exposure to loud sounds is often stressful to the nervous system in general, and often traumatizes the inner ear, in particular. GLU is well known for its selective neurotoxicity and exacerbation of injury when present in excessive amounts in the nervous system. Specifically, DYNs are localized within the organized bundle of descending lateral (efferent) olivocochlear (LOC) axon terminals that directly innervate the dendrites of Type-I auditory neurons.
The salicylate-induced potentiation of GLU, and resulting well-known neural-generated tinnitus, is mediated by the same class of GLU-sensitive receptors that are known to interact with DYNs. Hyperacusis, like tinnitus, is often associated with or is worsened by physical fatigue or emotional stress.
Hence, LOC-induced alterations in Type-I auditory responses to sound may well be regulated by sympathetic input from the LC, and possibly mediated in the cochlea by a presynaptic release of DYNs. Additional feeding pathways to the circuit were described to include the septal and olfactory regions and amygdala.
Increasing attention and a probable relationship to sleep phenomena also is considered to be a reflection or projection from the amygdala to sleep areas in cortex.
Current opinion holds that neural events that give rise to the perception or exacerbation of tinnitus are likely to begin with anomalous or altered neural activity that originates from within the inner ear (cochlea), beginning with a preliminary lesion or insult to the peripheral sensory neural machinery (Type-I neurons) innervating the cochlear end-organ.
The GLU-mediated Type-I auditory neural (dendritic) swelling and inflammation that often follows from acoustic over-stimulation is symptomatically associated with tinnitus. Moreover, in the cochlea, the Type-I auditory dendrites that bear this class of GLU-sensitive receptor are situated in such a way that places them in very close proximity to high concentrations of presynaptic, DYN-bearing axon terminals. Given that DYNs are involved in the regulation of biological responses to all forms of stress, what possible connection might exist between environmental or psychological stressors, and the release of DYNs from the LOC axon terminals within the cochlea? The reciprocal interconnections between primary and secondary associated auditory cortices and vestibular cortices of the cochleovestibular system reflect multiple neuronal networks which have the capability to adapt to changes reflecting alteration in sensory input and output due to different factors influencing neuronal activity of the cochleovestibular system and other systems at a cortical and subcortical levels. In response to auditory stimuli, Type I auditory neurons are normally excited by the release, from the base of the IHCs, of the neurotransmitter GLU. Young (1991) considered for depression that the location of cortisol control to be not in the hypothalamus but rather in the hippocampus.26 It is proposed for tinnitus that a cycle can be established wherein reciprocal projections between hippocampus, amygdala, entorhinal cortex and hypothalamus vary in the degree of control of cortisol levels resulting in further strengthening of an already established paradoxical memory with resultant additional negative affect behavioral manifestations of emotion, fear, anxiety, depression, etc. In the chronic form, altered peripheral input from the cochlea, resulting from insult, injury, or peripheral Type-I neural damage, is the most common event that activates central neural plasticity changes that many believe, lead to an eventual neural reorganization of parts of the central auditory pathways. Type I neural excitation is initiated at the dendrites, via postsynaptic GLU-sensitive receptors. Neuronal networks are hypothesized to exist which in the past were identified as primary and secondary areas. Central neural plasticity changes only then, generate and perpetuate the actual phantom auditory perception, known as (chronic) subjective tinnitus. Hence, the presynaptic DYN-bearing LOC axon terminals that innervate Type I auditory dendrites are in very close physical (and synaptic) proximity to the (postsynaptic) GLU-sensitive receptors located within the same dendrites. This close proximity between GLU-sensitive receptors and the DYN-bearing LOC axon terminals greatly increases the likelihood of a DYN-GLU-receptor interaction within the cochlea.
Such an interaction would conceivably occur in the event that conditions favored a presynaptic release of DYNs from the LOC axon terminals. It is conceived that the excitatory action of the amino acid glutamate may result in more than one physiological function.
Under carefully controlled experimental conditions, we have repeatedly observed that auditory sensitivity to very soft sounds is enhanced when drugs that mimic the effects of DYNs are administered either systemically, or placed directly into the cochlea. That is, following the administration of such drugs, the excitatory, receptor-mediated actions of GLU are potentiated in the cochlea. It is speculated that the GABAergic inhibition and resultant glutamate excess produces a disruption in calcium homeostasis.

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