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Neuroplasticity (NPL), neuromodulation (NM), and neuroprotection (NPT) are ongoing biophysiological processes that are linked together in sensory systems, the goal being the maintenance of a homeostasis of normal sensory function in the central nervous system. Keywords: tinnitus, neuroplasticity, neuromodulation, neuroprotection, electrical stimulation, inhibition, auditory and somatosensory cortex. The biophysiological processes of NPL, NM, NPT are considered in our experience to provide a "bridge for continuity of function" between both a sensation and its transformation into one of behavior and affective and somatomotor response.
It is hypothesized that when the balance between excitatory-inhibitory action is broken in sensory systems, predominantly due to neuromodulatory activity with reduced induced inhibition and excitation predominates, sensory circuits become plastic with adaptation at synaptic levels to environmental inputs. In this manuscript, tinnitus refers to a predominantly central type subjective idiopathic tinnitus of the severe disabling type (SIT).Tinnitus an aberrant auditory sensation, for all clinical types, is clinically considered to reflect a failure of NPL, NM, and NPT to maintain normal auditory function at synaptic levels in sensory cortex and projected downstream to levels in the central auditory system and sensorineural elements in ear.
Clinically, the tinnitus sensation becomes behaviorally manifest with varying degrees of annoyance, reflecting a principle of sensory physiology that each sensation has components, i.e.
Sensory inputs to brain are considered to have resulted in the phylogenetic development of multiple brain functions for survival of the species.
A global arousal system (GA) has been proposed that involves the activation of all vertebrate behaviors in response to all brain inputs. A physiological process of significance for NPL and NPT is hypothesized to be inhibition and as reflected in pharmacological and approaches attempting tinnitus relief1,11-15. Both the somatosensory and auditory systems demonstrate "plasticity" changes with respect to behavior.
Clinically the translation of sensory physiology for tinnitus has resulted in the identification of a discipline tinnitology, principles of tinnitology, a theory for all clinical types of tinnitus, an accuracy for the tinnitus diagnosis and a combined tinnitus targeted therapy (TTT) approach for attempting tinnitus relief17-20. Clinically fundamental for all sensory systems is the relationship between structure and function and the identification in neuroanatomic substrates of the underlying involved processes and mechanisms.
The significance and intimacy of brain function and sensation was recognized as early as the first century AD by the Roman philosopher and politician Lucius Aenneus Seneca (*c. The dilemma which faces both the tinnitus patient and professionals attempting tinnitus relief is the one posed originally by Descartes R, i.e. The terminologies of NPL, NM, NPT have increasingly been introduced into the tinnitus lexicon as advances in understanding the physiology of normal brain function and pathophysiology underlying brain function for specific diagnostic categories is being investigated. Our ongoing clinical experiences with SIT at SUNY Downstate since 1979 has an increased relevance for tinnitus diagnosis and treatment when integrated with evidence connecting synaptic plasticity to functional plasticity, perceptual learning and memory, and the emergence of a neurobiology for sensation and perception. The focus specifically on neural plasticity and tinnitus was initially presented from the perspective of a basic science sensorineural approach with animal physiology studies of normal and abnormal predominantly peripheral and central auditory function24-26. Increasingly, and ongoing since mid 1980s, advances in sensory physiology, neuroscience and auditory science, have included evidence for understanding that a linkage exists between sensory biophysiological processes of neural synchrony, dysynchrony, neural plasticity, neuromodulation, thalamocortical oscillation, thalamocortical dysrhythmia and neuroprotection, all of which underlies and results in central auditory and nonauditory brain function. Tinnitus is marked clinically by its heterogeneity for etiolgy, clinical type and subtype, factors influencing its clinical course, and response to treatment.
The underlying biophysiology, originally reported in 1991, is considered to be epileptiform activity in auditory and nonauditory multiple regions of interest in brain2,32. It has been hypothesized that commonalities and differences in both developmental and adult plasticity exist in sensory cortices.
Significant to be considered as demonstration of a commonality in sensory systems are inhibitory plasticity experiences reported in the visual and auditory systems with deprivation.
In the auditory system an auditory deprivation effect for the unfitted ears of the subjects with monaural hearing aids has been reported40. The term "deprivation" is used in its everyday sense to refer to the bilateral absence of acoustic stimulation.
Increased sensory cortical plasticity and improvement in perception and the behavioral response are hypothesized to result by targeting the cortical interneurons and neuromodulatory centers43. This hypothesis is supported by reports demonstrating control over cognititive and emotional behavioral performance by optogenetic and pharmacogenetic targeting of different types of inhibitory and excitatory interneurons or neuromodulatory neurons and for different aspects of auditory perception by targeting the cholinergic system44-46.
In our clinical experiences since 1979 the commonalities and differences are reflected in the clinical heterogeneity of different clinical types of tinnitus. The cited publication by Carcea & Froemke is recommended reading to tinnitus professionals and patients for understanding the complexity of tinnitus and projection to the future for tinnitus diagnosis and treatment1.
The following is a brief edited summary of what the authors of this manuscript consider in their tinnitus experience to be fundamental and essential of what is known at this time for cortical plasticity and for its translation to tinnitus diagnosis and treatment. Basal forebrain- cholinergic, gabaergic and glutaminergic projection neurons and local GABAergic interneurons.Locus Coeruleus-noradrenergic neurons innervate forebrain including sensory cortices. 2) cholinergic inputs trigger disinhibition in the upper cortical layers by activation of nicotinic receptors on layer 1 inhibitory neurons51.
Thalamo cortical dysrhythmia - a pathophysiologic model of brain wave activity of brain function is proposed for neurogenic pain, tinnitus, abnormal movements, epilepsy, and neuropsychiatric disorders. A lesion results in deafferentation of excitatory inputs on thalamic relay cells which initiates tinnitus.
It is hypothesized for tinnitus that the spontaneous and constant gamma band of hyperactivity causes tinnitus. Neural plasticity, clinically, is a reorganization in brain structure and or function in response to constant, single or repetitive, internal and or external stimulation e.g.
Brain plasticity has been defined by "the father of sensory substitution and brain plasticity as the adaptive capacities of the central nervous system - its ability to modify its own structural organization and functioning57". Neuromodulation in neuroscience, is considered to be a complex biology of physiological process(es) which exerts a positive or negative influence on an existing neural signal input or output, but does not eliminate the existing neural signal. In our tinnitus experience, neural plasticity can result in or be accompanied by neuromodulation and neuroprotection. Neuroprotection: refers to processes that protect neuronal function from injury or that improve such function after injury.
Pharmacological agents that are considered to be neuroprotective have been identified and include calcium channel blockers, free radical scavengers, corticosteroids, antagonists of glutamate at N-methyl-Daspartate (NMDA) and non-NMDA receptors, and various thrombolytic agents.
A review of the NPL NM NPT literature finds translation and significance for tinnitus of all clinical types for basic science, clinical medicine, diagnosis and treatment. Varied changes in spectral content in the EEG of patients were reported with tinnitus throughout the frontal and temporal lobes. Tinnitus related distress was correlated with an abnormal pattern of spontaneous activity in particular in right temporal and left frontal brain areas77. With the electroencephalogram (EEG), an increase of band power and local field potential (LFP) signals is typically interpreted as an increase in neuronal synchronization in terms of coincident firing within a neuronal population78.
An inverse relationship has been reported with PET between thalamic activity and EEG alpha power in depressed and healthy patients, i.e. Clinically, this paper is cited for future neuromodulatory pharmacological approaches attempting treatment of the affect component of tinnitus.
Functional brain imaging, metabolic with Cerebral F-18 2-deoxy-fluoroglucose (FDG) Positron Emission Tomography (PET) and electrophysiologic with quantitative electroencephalography (QEEG) was recommended to a cochlear implant patient (CI) age 74, who reported in 2008 an increase in tinnitus intensity and decreased hearing function with the CI ON of 6 months duration.
PET data was acquired in 3D mode with a Siemens Exact 47 HR + after administration of weight adjusted doses of F-18 2-deoxy-fluoroglucose. Preselected regions of interest (ROIs) in this report include medial temporal lobe, frontal, primary auditory cortex and thalamus. In addition it is hypothesized that the activated ROIs reflect metabolic correlates of the underlying biophysiological processes in brain of NPL, NM and NP.
Electroencephalographic functional brain imaging provides a quantitative demonstration of the spectral analysis of the raw EEG brain wave activities (QEEG)73 c): Low resolution brain electromagnetic tomography (LORETA) is a family of analyses which provides a 3D demonstration of the distribution of the generating electric neuronal activity. Thalamus: The SUV% asymmetry between rt and lt metabolic activity of the thalamus with the new cochlear implant CI #2 reveals a reduction but persistence of SUV asymmetry.
With activation asymmetries reduced thalamus lt > rt, primary auditory cortex absent asymmetry rt lt, reduced asymmetry medial temporal lobes lt > rt. With deactivation asymmetries reduced thalamus rt > lt, primary auditory cortex absent asymmetry rt lt, medial temporal lobe increased reduction asymmetry lt > rt. The results of the QEEG include reference database comparisons for relative power Z scores at 1-Hz intervals in the frequency domain, in a numerical table from which topographical maps are derived.
Initially a high beta with was recorded bilateral essentially equal from all recording electrodes. The neural plasticity process is dramatically demonstrated in the alteration in activity between the thalamus and frontal cortex in the PET CT images with CI #1 on and off. The neuromodulation process, both positive and negative is clinically considered to be reflected in the sequential QEEG relative power Z scores.
The neuroprotective process is clinically demonstrated by the efficacy of cochlear implant #2 in the both PETCT images and QEEG recordings. The focus of this manuscript has been on biophysiological processes in brain of NPL, NM, and NPT and their translation for tinnitus.
Evidence has been presented linking synaptic plasticity, functional activity and learning1. The neuroscience evidence underlying NPL NM PNPT is contributing to an evolving neurobiology for the diagnosis and treatment of all clinical types of tinnitus by linking synaptic plasticity, not only with functional activity, and learning but also memory, sensory perception and behavior.
The original sensorineural approach for understanding tinnitus with a focus predominantly on the ear and also brain reflected what had been known in the past of auditory and brain function.
Significant is considered the correlation of the data between nuclear medicine brain imaging (PET CT) and electrophysiology quantitative electroencephalography (QEEG).
Specifically, the metabolic activity in ROIs of thalamus and primary auditory cortex with the ES CI #1 and CI #2, is hypothesized to reflect a reorganization in both with ES On and OFF i.e.
Significant metabolic improvement in the thalamus, primary auditory cortex and medial temporal lobe with both conservative therapy and new CI #2 electrical stimulation. It is hypothesized that the SUV result in the primary auditory cortex clinically reflects the neuroprotective effect of the ES CI #2 for the sensory component of the SIT. The interconnectivity between medial temporal lobe and frontal lobes are clinically considered to reflect process(es) underlying neuromodulation. The clinical recommendation of functional brain imaging, metabolic with F-18 PET brain, and electrophysiology quantitative electroencephalography (QEEG) provide an objectivity for improvement of the accuracy of the tinnitus diagnosis and provide a rationale for treatment. The significant elimination of asymmetry with CI #2 in primary auditory cortex is not reflected in the degree of change in the F-18 FDG PET SUV hypometabolic activity in the medial temporal lobe.
3) The neuronal interconnectivity between thalamus, primary auditory cortex and medial temporal lobe reflect a medical significance other than limited to tinnitus.
Clinically the correlation of tinnitus relief with the reduction in SUV asymmetry between the F-18 FDG PET and QEEG reduction in excess brain activity in delta and beta demonstrate the NM and NPT function of CI #2 ES. The neuroprotective process is clinically demonstrated by the efficacy of cochlear implant #2 in the both F18- FDG PET CT images, SUV, and QEEG recordings. Clinically significant is considered the correlation between the metabolic F18 FDG PET PET SUV in the thalamus, primary auditory cortex, mesial temporal lobes and the relative power Z-scores from the recording sites of the QEEG. The perception of tinnitus has clinically been considered to be a "phantom sensory phenomenon90", i.e.
A phantom symptom is physiologically defined as the lack of or inability to identify a underlying neural substrate. Clinically the authors of this manuscript have recommended since 1989 that subjective idiopathic tinnitus of all clinical types and subtypes no longer be considered a "phantom" sensory auditory percept. Evidence has been accumulating since 2004 that an imbalance between excitation and inhibition in multiple neuroanatomic substrates in brain underlies NPL NM NPT1,4,41. Synaptic plasticity has been reported to be reduced in adult brain compared to developmental brain1. Identification in the clinical history of factors influencing the clinical course of the tinnitus, and treatment as appropriate, can result in tinnitus relief in individual tinnitus patients23,86,90.
The responses to modalities of treatment are clinically oreflective of positive NPL, NM and NPT. The elimination of the negative effect of the ES of CI #1 and the positive effect ES of CI #2 is a clinical manifestation of NPL NM NPT underlying the reported subjective tinnitus relief. The ultimate goal is to identify multiple targets of tinnitus activity and develop multimodal tinnitus treatment approaches for all clinical types and subtypes of tinnitus, eg. Functional brain imaging results presented in this manuscript provided clinical objective demonstration of the positive and negative effects of ES. The authors gratefully express their appreciation to the Department of Otolaryngology, SUNY Downstate, Richard M.


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It is hypothesized that when the balance between excitatory - inhibitory action is broken in sensory systems, predominantly due to neuromodulatory activity with reduced induced inhibition and excitation predominates, sensory circuits become plastic with adaptation at synaptic levels to environmental inputs1. The cognitive brain function of "memory" is the predominant brain function that is hypothesized to bind the two together2. The resulting alterations in synaptic transmission and neuronal network function depend on the extent of calcium signaling and NMDA activation in response to different patterns of stimulation1,3,4. The roles of excitatory amino acids, specifically glutamate, and calcium as mediators of excitotoxicity has been reported with resultant cellular neuronal death.
The reported role of NMDA receptors as the predominant molecular mechanism for the control of synaptic plasticity and memory function7. Clinically, the excitatory hypothesis is considered significant for the development of an auditory memory, hypothesized to be "paradoxical" for tinnitus8. The biophysiological processes of NPL, NM, NPT are ongoing and considered to have been and are critical in this development. It has also been hypothesized that the neuroanatomical, neurophysiological and molecular properties of reticular neurons within the nucleus gigantocellularis (NGC) of the mammalian medulla, have a major role in GA.
When a stimulus is cognitively associated with reinforcement, its cortical strength is strengthened and enlarged. Specifically, a hypothesis that attempts to explain how an aberrant auditory sensory stimulus becomes transformed into one of affect and somatosensory (motor) response(s).
Initially the focus was on the sensorineural approach to understand tinnitus, limited predominantly to the ear, reflective of what was known of the cochleovestibular system. Basic science investigations and clinical efforts for the diagnosis and treatment of all clinical types of tinnitus have been and continue to be grounded in translation of principles of sensory physiology for tinnitus.
These advances have been integrated into expansion and supplementation of the predominant peripheral and original sensorineural theoretical approach for tinnitus based predominantly on the ear and brain to a focus on both brain and ear, which has found translation for tinnitus theory, diagnosis and treatment18,27-29.
Interference in the precision, specificity involved in synaptic transmission for normal and interneuronal function reflects the complexity of the tinnitus symptom. Common to both is considered to be a "transient" imbalance between inhibition and excitation. In the visual system inhibitory plasticity has been considered to be important in circuit refinement that can contribute both to the compensatory forms of circuit plasticity in the early stages of development and to the pathological loss of function induced by visual deprivation during the critical period.
The multiple biophysiological processes of NPL, NM, NPT reflect adaptation in neuroanatomic brain substrates and interconnectivities between neural circuits internal and external environments. Neural plasticity, NM, NP are biophysiological processes, linked together to assure structural maintenance and modification of neuronal ensembles with their synapses and circuitries, in response to internal and external sensory stimulation. The sensory cortex responds to behavioral stimuli by different neuromodulators which control plasticity in the human brain by coordination of modifications at selected sets of neuronal synapses45. Synaptic transmission and network function are dependent on which neuromodulatory systems are activated and on the extent to which intracellular Ca2+ signaling and NMDA receptor activation are engaged in stimulus patterns1.
The correlation between excitatory and inhibitory inputs may dictate the stability of synaptic fields in the developing auditory cortex. The relationship between the strength and timing of excitatory and inhibitory currents control input integration48. Sensory maps reflect the development of synaptic and spiking receptive fields at a neuronal population level49.
Developmental windows called critical periods, are characteristic for most sensory cortices and structures important for emotion, eg Amygdala50.
The relationship between synaptic plasticity and excitatory-inhibitory balance is consistent in the adult sensory cortex. Activation of various modulatory systems can alter excitatory- inhibitory balance and enable experience -dependent modifications. Neuromodulators, single or multiple including - acetylcholine, dopamine, serotonin or peptide modulators eg oxytocin result in activation different behavioral states, i.e.
N-methyl-D- aspartate receptor, a glutamate receptor, is the predominant molecular device to control synaptic plasticity and memory function7. Failure to establish a synchrony of activity in response to the dysynchronous auditory stimulus may become clinically manifest by seizure activity, other neuropsychiatric symptoms, behavioral abnormalities, and tinnitus. It is hypothesized that common etiological agents that cause injury to the CNS have similar effects on the inner ear It is hypothesized that common etiological agents that cause injury to the CNS have similar effects on the inner ear. Neural plasticity is reported to be "considerable" in healthy individuals across life spans. Aging is associated with progressive losses in function across multiple systems, including sensation, cognition, memory, motor control, and affect. Behavioral training has been demonstrated in a reliable training gain for (intra modal) auditory but not for the (across-modal) visual transfer task. Cognitive training was reported to be to be a potential tool for investigation of basic mechanisms of adaptive behavior, neuronal functioning, and design training69-72.
Significantly in this study patients with impaired hearing identified with audiometry were excluded from this study73. Alpha band power was significantly reduced, whereas delta and gamma band power was significantly increased in the temporal regions74. These data suggest that a physiologic link exists between the EEG and cerebral metabolism during anesthesia that is mathematically quantifiable80. Clinically, to illustrate this point, are the reports of significant tinnitus relief with instrumentation, i.e.
Summary: The positive and negative subjective results reported with multimodalities attempting tinnitus relief are clinically considered to reflect degree of success or failure of underlying biophysiological processes of NPL, NM, NPT.
Routine PET processed standard uptake value data (SUV) was in turn analyzed by the NeuroQ program which provided a comparative three dimensional quantitative normative data base with statistical analysis of 240 neurologically appropriate ROIs normalized to whole brain counts after spatial morphing of subject data to the standardized 3D template. To obtain objective evidence of activation of regions of inters(ROIs)t in brain by electrical stimulation with the implanted cochlear implant ear rt reported by the patient to result in an increased tinnitus severity. Visual interpretation of the PET images and QEEG data demonstrate a significant association between the thalamus and frontal lobes.
Cerebral F-18 FDG Positron - CT brain Tomography color images represent greater to lesser relative ROI metabolic activity reconstructed from red (greater SUV) to blue (lesser SUV) multicolor display. Treatment recommendations included diuretic therapy for presumed secondary endolymphatic hydrops lt; Gabapentin 300 mg bid, and Klonopin 5 mg hs for control. Color images identify clinically critical regions of thalamus (A), posterior frontal cortex (B), primary auditory cortex (C), and medial temporal lobe (D). All results reported are based on an analysis of the data referenced to Z scores in the database described88,89. The QEEG clinically provides an electrophysiological correlate of brain wave of activity of multiple brain functions in the presence of the tinnitus signal. Specifically, demonstration of a correlation between metabolic reduction in asymmetries in and between regions of interest in brain and electrophysiologic reduction in relative power Z-scores with cochlear implant #2 compared to cochlear implant #1. The complexities involved in NPL, NM, NPT are hypothesized to be reflected clinically in the heterogeneity of all clinical types and subtypes of tinnitus, and to underlie an ongoing attempt to maintain a normal homeostasis of function in underlying neuroanatomical substrates in brain. Advances in sensory physiology, auditory science, neuroscience of brain function, results of functional brain imaging technology all have dramatically shifted the focus for tinnitus to the brain. The FCP is suggested to be expanded for and to have clinical application for all sensations. Demonstration of evidence of tinnitus suppression in multiple brain ROIs with ES and pharmacological therapy.
Positive and negatives effects of electrical stimulation (ES) clinically are demonstrated with functional brain imaging. These are two different metrics which demonstrate and support the recommendation of clinical translation of these technologies particularly for SIT for improvement of accuracy for the tinnitus diagnosis and a monitor for treatment efficacy. Reversal in the pattern of for activation and deactivation of the thalamus with activation and deactivation the CI #1 and CI #2. Correlation of the subjective tinnitus complaint with the alteration in SUV values is greatest in the order of the primary auditory cortex > thalamus, > medial temporal lobe.
The difference in SUV uptake values between the therapy and no ES CI #1 and CI #2 is highest in the significant reduction in the primary auditory cortex. The mild FDG-18 PET SUV asymmetry % in the thalamus with CI #2 on and off is clinically hypothesized to reflect a lack of total tinnitus suppression at the level of the thalamus - But-total tinnitus suppression at the level of the primary auditory cortex. The Inter-connectivity between thalamus and primary auditory cortex, are clinically considered to reflect the process (es) underlying neuromodulation and reflected in the FDG -18 PET SUV% asymmetry indices. It is hypothesized that the brain functions of affect, behavioral response and memory functions, are in response to the presence of the tinnitus signal in brain and are reflected to the limits of this examination by the interconnectivity between medial temporal and frontal lobes. The tinnitus relief reported with the activation and use of CI #2 is an example of the neuroprotective function of electrical stimulation (ES). The hypo metabolic function in the medial temporal lobe is a reflection of the low level of metabolism associated with the low frequency brain wave activity. The striking feature in the FDG -18 PET SUV% asymmetry indices is the absence of asymmetry in the primary auditory cortex with the CI #2 on and off, and the marked reduction in asymmetry in the thalamus, primary auditory cortex, and medial temporal lobe with CI #2 and therapy including elimination CI #1 electrical stimulation. The F-18 FDG PET and QEEG brain data provide objective evidence that CI #1 was a cochlear implant soft failure in this patient. The QEEG clinically provides an electrophysiological correlate of multiple brain wave activities accompanying multiple brain functions in the presence of the tinnitus signal. The identification of the biophysiology underlying NPL NM NPT for all tinnitus types and subtypes. Identification of similarities and differences, based on etiologies of tinnitus, in the neurobiology underlying the biophysiological processes of NPL, SD, NPT, and its linkage with functional plasticity, affect behavior, learning auditory perception and memory. Specifically, the development of a tinnitopharmacology reflective of the molecular genetic code of the individual tinnitus patient, i.e. What is 'common' and shared for all clinical types of tinnitus in sensory auditory and non auditory for NPL NM NPT cortices and what is different, "special" for a particular clinical type of tinnitus, with "top down" or "bottom up" processing?
What significance is the etiology of the tinnitus in the activation of neuromodulator(s) at different neuromodulatory centers? Is the neurobiology underlying each of the four components of a particular type of tinnitus the same or different for the processes of NPL, NM, and NPT? How can the present evidence connecting synaptic plasticity to functional plasticity, perceptual learning and memory be translated to an increased accuracy for tinnitus diagnosis and efficacy for treatment for all clinical types and subtypes of tinnitus? Is the neurobiology the same for each of the four components of a particular type of tinnitus? Evidence has been presented connecting synaptic plasticity with functional plasticity, affect behavior, learning, auditory memory and perception and the underlying biophysiological processes of NPL, NSD, NPT. It is hypothesized that an imbalance between excitatory and inhibitory inputs at synaptic neuronal circuits in brain triggers synaptic plasticity, functional plasticity and the biophysiological processes of NPL ND and NPT. Neural plasticity, NM, NPT are biophysiological processes, linked together to maintain structure, maintain a homeostasis of normal function and reflect modification of selected neuronal ensembles with their synapses and circuitries, in response to internal and external sensory stimulation. The degree of efficacy of modalities of treatment attempting tinnitus relief are clinically considered to reflect varying degrees of activity of the biophysiological processes of NPL, NM, and NP. The clinical implications of Cerebral F-18 FDG PET CT SUV are multiple and highlighted by the significant absence of asymmetry at primary auditory cortex and reduction in the asymmetries for the non auditory thalamus and medial temporal lobes with CI #2. Functional brain imaging is recommended to be considered for the clinical identification of a cochlear implant soft failure (CISF) in a predominantly central type subjective idiopathic tinnitus of the severe disabling type92.
It is hypothesized that the input and output from the Olivary System in brain has a significant influence on normal and aberrant auditory function and maintenance of a balance between excitation and inhibition at sensory auditory cortex and the resulting biophysiological processes of NPL, NM and NPT93.


It is a great alternative for brand and generic Cialis offered with Mango and Orange flavours. It is usually given after other blood pressure medications have been tried without successful treatment. It is also used to treat the manic phase of bipolar disorders(manic-depressive illness) and to prevent migraine headaches. It interferes with the metabolism of alcohol resulting in unpleasant effects when alcohol is consumed. Just login and point your mouse at any content block on the page and an editor will come up allowing you to change or delete it. Tinnitus an aberrant auditory sensation, for all clinical types, is clinically considered to reflect a failure of NPL, NM, and NPT to maintain normal auditory function at synaptic levels in sensory cortex and projected to downstream levels in the central auditory system in brain and sensorineural elements in ear. Modalities of tinnitus therapies, eg instrumentation, pharmacology, surgery, target a particular component of tinnitus, with resultant activation of neuromodulators at multiple neuromodulatory centers in brain and ear. The neuronal circuits of control and regulation of the GA are considered central to understanding the origin and motivated behaviors e.g.
The changes are caused by both the sensation and "learning of the sensory experience, particularly when associated with reward and classical conditioning behaviors16". The hypothesis of the FCP for tinnitus and the identified neuroanatomical substrates, highlighted by hypometabolism in the medial temporal lobe, and structures in the pontomesencephalic region of brain including the nucleus accumbens, when viewed in terms of the physiology of sensory processing, is considered to be expanded and broader in its application for all sensations, normal or aberrant2.
Investigations for tinnitus, both clinical and basic science, attempting to answer this question for tinnitus are resulting in advances in the understanding of the ear and brain function, of the peripheral and central cochleovestibular system, translated for tinnitus diagnosis and treatment. Neurotologic complaints of hearing loss, tinnitus, vertigo, ear blockage, hypercusis, alone or in combination, are a reflection of and associated with a damaged hearing system, but not tinnitus severity. Neuroanatomic substrates associated with tinnitus have been identified in brain with nuclear medicine single photon emission computerized tomography (SPECT) since 1989, which precludes by definition consideration of subjective idiopathic tinnitus to be a "phantom phenomenon2,6,8,32-34". Inhibitory plasticity as an important player in circuit refinement can contribute both to the compensatory forms of circuit plasticity in the early stages of development and to the pathological loss of function induced by visual deprivation during the critical period39. Outcomes also show acclimatization in the form of significant improvements in performance over time after implantation41. Developmental abnormalities in synaptic plasticity result in abnormal connectivity, functional disintegration and immaturity of auditory cortical areas, the smearing of feature representations in the auditory system, cross-modal recruitment of some auditory areas for non-auditory functions, and the reorganization of cognitive functions due to absence of auditory input42.
The goal is functional maintenance of an ongoing homeostasis of normal function to assure survival.
Synaptic transmission and network function is dependent on which neuromodulatory systems are activated and on the extent to which intracellular Ca2+ signaling and NMDA receptor activation are engaged in stimulus patterns.
The critical window is considered to exist not only for different modalities of treatment but for different functions of the same sensory system.
Neuromodulatory systems can differ one from the other with significant effects on functional maps and sensory performance52. Multiple ongoing processes and levels of activity are involved at organ, tissue, cellular, synaptic and molecular genetic locations.
It involves and reflects adaptive and maladaptive changes in neuronal activity at cortical and subcortical levels of neuronal activity.
The chief etiologies to be considered include ischemia, trauma, or hemorrhage, and neurodegenerative disease. Alterations in local excitatory circuitry increase the spread of spared representations into deprived cortical regions61.
The mechanisms involved are reported to support cognition and are influenced by normal ageing, particularly in the medial temporal lobe and prefrontal cortex, changes in which can clinically demonstrate interference in behavior62-67. Training-induced activation decreases in the auditory transfer task were found in two regions in the right inferior frontal gyrus. Given the heterogeneity reported apparently other conditions must modify the EEG content in these tinnitus patients75,76. A widespread inverse relationship of delta power to metabolism was found between various regions; additionally, delta power was negatively correlated to cerebral glucose metabolism in individual regions. C-R neuromodulation, a potential significant advance for all clinical types of tinnitus treatment objective electrophysiological evidence is demonstrated of improvement in particular neural circuitry(ies) neuroanatomical substrates of brain functions, and resultant reported tinnitus84.
In rodents, an increase in dopamine neurons in the nucleus accumbens modulated the neural encoding of depression related behaviors, suggesting that processes affecting depression symptoms may involve alterations in neural encoding action in the limbic system85. Before and after activation of cochlear implant sequential FDG scan coronal images reveal that following activation of cochlear implant which produced greater tinnitus especially of the right side (R), FDG activity is markedly elevated in ipsilateral right thalamus and primary auditory cortex. The impedance measured at each electrode site with respect to the reference was less than 5,000 Ohms. Multicolor display for each study is designed to maximize visualization of relative functional ROI asymmetry and not absolute activity as expressed in standard uptake value (SUV).
With removal of cochlear implant #1 and reimplantation with cochlear implant #2 the brain wave activities for all frequencies returned within the normal range. Tinnitus is a symptom of neurotologic disease in which ear and brain functions are of equal significance.
The metabolic activity between thalamus and frontal cortex clinically is hypothesized to reflect a thalamocortical oscillation and dysrhythmia.
Specifically with the new CI #2, the patient reported significant subjective tinnitus relief ear rt and improvement hearing. Significant is considered the absence of asymmetry with ES CI #2 in the primary auditory cortex. Clinically the PET SUV values are considered to reflect the metabolic effects of neuroplasticity (NPL), neuromodulation (NM), and neuroprotection (NPT) associated with electrical stimulation. Clinically, the thalamo cortical interconnectivity may have a dynamic range of activity greater for overall sensory function than that between the temporal and frontal lobes.
The affect, behavioral response to the presence of the tinnitus and memory functions are individual for each tinnitus patient for all clinical types of tinnitus. The tinnitus relief is a clinical manifestation of the linkage between the biophysiological processes of NPL, NM, NPT. This is correlated with the delta frequency of brain wave activity demonstrated in the QEEG. Clinically this provides objective evidence in support of the recommendation for attempting tinnitus relief by identification and treatment of factors influencing the clinical course of all clinical types of tinnitus, individual for each tinnitus patient.
The recommendations to specify, alone or in combination, which component(s) of the aberrant tinnitus sensation, is being targeted by a particular modality of tinnitus treatment. The goal short and long term is functional maintenance of an ongoing homeostasis of normal function for survival.
Clinically, this result is demonstration of the specificity of ES for the sensory component of the tinnitus as well as the affect behavior, i.e. D, Professor and Chairman, and the Martha Entenmann Tinnitus Research Center, Inc., for support of this educational and research effort. Final common pathway for tinnitus: theoretical and clinical implications of neuroanatomical substrates.
Unilateral cochlear ablation produces greater loss of inhibition in the contralateral inferior colliculus. Electrodiagnostics, Electrotherapeutics, and other Approaches to the management of tinnitus.
Tinnitus dyssynchrony-synchrony theory: a translational concept for diagnosis and treatment.
Effective neuromodulation at sensory neuronal synaptic levels results in NPL in sensory cortex, NPT and tinnitus relief. Specifically for tinnitus this has resulted clinically in an alteration in the definition of tinnitus, theories of hearing and balance, introduction of new concepts of central auditory function, relationship between tinnitus and hearing loss, expansion of existing teachings in neurotology to include principles of sensory physiology for complaints of hearing loss, tinnitus and vertigo; and the translation of concepts of heterogeneity, homeostasis of function for tinnitus diagnosis and treatment. This focus has resulted in an emerging neurobiology for tinnitus reflective of which brain function(s) are elicited in the presence of the tinnitus signal. Whereas alterations during the early development of sensory cortices are very long lasting and frequently permanent37 plasticity in the adult sensory cortex is frequently transient38. Patterned stimulation increased the correlation between excitatory and inhibitory inputs nonspecifically, with improvement in the overall balance47.
The result of the reorganization is a positive or negative alteration in structure and or function from the normal, i.e. A brain-plasticitybased intervention targeting normal age-related cognitive decline may potentially offer benefit to a broad population of older adults68. The right inferior frontal gyrus is frequently found in maintaining modality-specific auditory information. Frontal theta power correlated especially with rostral thalamic central medial nucleus (CMR). Patient ROI count data falling more than 1.65 STD beyond the mean value for a longitudinally validated control group ROI is flagged as abnormal by the NeuroQ analysis. The SUV% asymmetry between rt and lt thalamic metabolic activity is decreased bilateral with activation and deactivation, but reversed asymmetry compared to the old CI #1. This predominance of the ES effect in the primary auditory cortex clinically supports the observation of the high association of "tinnitus" with sensorineural hearing loss but not with severity. The "plasticity" may be of a higher order reflecting an "older "origin of brain structure and function in the hierarchy of phylogenetic development of the brain.
Significantly, the functional brain imaging with FDG -18 PET and the SUV% asymmetry indices correlate with the electrophysiology quantitative electroencephalography (QEEG) relative power scores (Tables 1 and 2).
At synaptic levels in brain, for each component of all sensations, there is an attempt to connect synaptic neuronal plasticity with functional plasticity, affect behavior, somatomotor response, learning and memory. The GA hypothesis is recommended to be considered for translation of the affect behavioral component of all clinical types of tinnitus9. In this case the neurobiology for tinnitus that is being identified in brain is "top down". This is another example of two of the three components of the aberrant tinnitus sensation, i.e. These results might reflect increased neural efficiency in auditory working memory processes. Three hundred (300) epochs were recorded; twenty five (25) were selected as being representative and artifact-free, processed and compared with the normative database.
The SUV for thalamus, primary auditory cortex, medial temporal lobes with CI #1 and CI #2 provide objective data reflective of a reduction in metabolic activation in all three ROIs which correlates with the reduction in the relative power Z scores. The asymmetries and brain location of the PET SUVs for the thalamus clinically are considered to support the thalamocortical and thalamocortical dysrhythmia hypothesis translated for tinnitus. There is a need to differentiate between the dysynchronous signal hypothesized to be tinnitus and the synchrony of neuronal activity at the brain cortex, which is expressed as the function of perception and conscious awareness of tinnitus19. The goal is to attempt to restore and or to maintain a homeostasis of normal neural function in the peripheral and or central nervous system56.
The increasing identification of neuroanatomic substrates in subjective idiopathic tinnitus (SIT) for all clinical types and subtypes of SIT supports consideration that tinnitus no longer be considered to be a "phantom" sensory auditory percept. The raw data EEG results were submitted to the Lexicor Company for analysis, and that firm generated a report called the Datalex report for clinical application (Lexicor Medical Technology, Inc. It is hypothesized that this is reflected clinically in the high incidence of association between sensorineural hearing loss and tinnitus - but - not in the tinnitus severity and auditory brain function of memory. Functional brain imaging, metabolic (PET brain) and electrophysiology quantitative electroencephalography (QEEG) data in a cochlear implant soft failure patient demonstrates what is clinically considered to reflect NPL, NM, NPT. It is considered to provide a clinical objective demonstration of neural electrical activity, neural plasticity, neuromodulation with and without tinnitus treatment e.g. The reader is provided with a rationale for tinnitus diagnosis and treatment, with a focus on ES, reflecting the biology underlying NPL, NM, NPT.




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