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In some patients with occupational noise-induced hearing loss, a significant aspect of the handicap concerns the concomitant tinnitus; thus, this disorder must be considered in evaluating a disability percentage in the insurance context. In clinical practice, tinnitus is a fairly common symptom in patients with chronic acoustic trauma and noise-induced hearing loss (NIHL) [1].
The method proposed in this article is based on a rational, ranked progression in decision making: At each of four steps, a fairly large number of elementary (cellular) decisions, easily made and reproducible among different experts, leads to a higher decision level (Fig. 3.2 Besides reporting the tinnitus, does the patient also demonstrate an occupational hearing loss? In case of one or more nonaffirmative responses, the expert must judge whether to come to a final positive or negative decision for each question of level 3.
2.5 Does the hearing loss show the characteristics of NIHL at a functional hearing assessment? 2.7 Is the anamnesis and is the history of complaints suggestive of progressive occupational hearing loss? 2.8 Does the functional assessment of tinnitus (tinnitometry) suggest the etiology of cochlear noise damage? 2.9 Does the medical history demonstrate compatibility of tinnitus with the etiology of cochlear noise damage? 2.10 Is the anamnesis and is the history of complaints suggestive of tinnitus related to progressive occupational hearing loss?
2.11 Are there convincing objective elements for the nature and severity of impairment, disability, or handicap?
2.12 Are there convincing subjective elements for the nature and severity of impairment, disability, or handicap? To check for agreement among different experts of first-level decisions and for concordance in higherlevel decisions, we selected 10 exemplary files from among the patient material of the Institute of Occupational Disorders.
A variant of Cohen's Kappa [4] was applied, as this statistical test takes into account the possibility of chance agreement among raters (as no more than three choices are possible). Tinnitus is frequently associated with occupational hearing loss and can be an additional item of claim in countries applying a specific insurance system for occupational disorders. This research was presented at the Thirty-First Congress of the Neurootological and Equilibriometric Society, Bad Kissingen, Germany, March 25-27, 2004. How to cite this article Alpini D, Kohen-ratz R, Braun R, Burstin A, Tesio L, Pugnetti L, Mendozzi L, et al.
In elderly people, owing to a perturbation at several levels, including the motor, sensory and cognitive levels, a condition of dizziness and unsteadiness complicated by frequent falls often appears. Generally speaking, falls in the elderly typically are caused by multiple deficits that can add up to produce disability disproportionate to their individual contributions [5, 6].
An initial period was dedicated to developing a specific questionnaire aimed at identifying aged subjects with increased risk of mobility-related accidents. The questionnaires were evaluated by means of Rasch analysis [7], a statistical model based on item response theory. The revised FRI was proposed to general practice doctors (GPs) for use in select subjects with a high risk of falls.
Postural control of a standing individual can be partly considered as a dynamic feedback control involving somatosensory, cervical proprioceptive, vestibular, and visual information [8].
Synchronization is the most innovative aspect of posturography and is peculiar to tetraataxiometry. In nonfalling subjects, there was no correlation or a negative correlation between age and instability, whereas in falling subjects, age correlated positively with instability, as might be expected (Fig.
Hazardous noise can destroy the ability to hear clearly and can also make it more difficult to hear sounds necessary for working safely, such as instructions or warning signals. Audiovestibular symptoms are the first and often the only clinical signs of vertebrobasilar insufficiency. Audiovestibular symptoms are the first and often the only clinical signs of vertebrobasilar insufficiency (VBI).
Anatomical and physiological investigations of blood supply of the vestibular analyzer and vestibular receptors show that these structures are found in most dysfunctional circulatory situations, as anastomotic links are absent and ischemic damage is possible [5-8].
Above-threshold vestibular provocation was registered by ENG, and asymmetrical reactions for duration, amplitude, frequency, and establishment of the slow-phase speed (SPS) were evaluated, assuming as asymmetry differences of more than 20% between the two labyrinths.
Evaluation of the ENG according to duration (in seconds) is made by stop-stimulation until nystagmus strokes having an amplitude of 2 mm are registered or until the direction of nystagmus converts.
Caloric tests (for examining each labyrinthine irritation) are conducted 10 minutes after the rotatory tests, as the received nystagmus reactions are registered by the ENG at the same calibration as in the rotatory provocations. On ENG registration, the curve of spontaneous nystagmus shows that the relative share of people with spontaneous nystagmus increases in accordance with increasing age: Among the primary group of patients 40-49 years old, 30% (3 of 10 men) exhibited nystagmus, whereas in the 50- to 59-year-old group, 72% (18 of 25 men) demonstrated nystagmus. The presence of spontaneous nystagmus noted on ENG recordings in patients in the primary group who had no vertigo complaints, however, indicates blood pressure dimensions leading to vestibular dysfunction.
In caloric tests, in contrast to rotatory tests, only one labyrinth in each subject was examined. It is the opinion of many authors that directional nystagmus is a symptom of vestibular sys~m disturbance and is a sign of this system's central damage.
The aforementioned, previously observed asymmetry indices-especially the SPS, duration, and amplitude indices of subjects in the primary group-showed statistically based increases relative to increasing subject age. In caloric tests and rotatory investigations, important differences between the two groups were observed at an SPS asymmetry of more than 20% and frequent asymmetry of more than 20% at culmination. In comparing the results of CP and DP asymmetry, we found that CP asymmetry is predominant at all indices, as the most important differences are determined in SPS asymmetry. Tinnitus has been defined as the perceptual correlate of altered spontaneous neural activity occurring without an external auditory stimulus. Tinnitus is a serious clinical symptom that may affect 30-40 million individuals nationally [1,2]. Our understanding of the functional biochemistry of the medial efferent olivocochlear system has advanced at a steady rate [22-24], whereas comparatively little in the way of function is known of the lateral efferent olivocochlear system.
Opioid peptides and their unique receptors exhibit a widespread distribution in central and peripheral nervous system structures involved in vision, audition, olfaction, and somatic sensation.
The activation of opioid receptors by endogenous opioid substances produces alterations in intercellular ionic conductances, resulting in either neural inhibition or neural excitation l50,66]. In contrast to their more widely studied inhibitory properties, opioid peptides also produce neural excitation [70,73,74). As indicated, dynorphin-and enkephalin-like immunoreactivities have been found in the terminal varicosities of lateral efferent neurons in some species, indicating the presence of these neuroactive peptides in mammalian cochleas [27]. Intravenous (IV) administration of the opioid κ-receptor drug agonist (-) pentazocine produces an enhancement in auditory sensitivity and intensitydependent amplitude changes in the auditory nerve compound action potential (CAP) in chinchillas [83). The initiation of auditory signaling in the mammalian cochlea is highly dependent on the release of excitatory neurotransmitter from the IHCs. However, evidence supports the gene expression of NMDA receptor subunits in the adult guinea pig cochlea [106]. Approximately 40% of the radial type I afferent dendrites form two morphologically and functionally distinct groups that contact the modiolar-oriented surface of each IHC.
As is well-known, peripheral tissue inflammation produces functional changes in neurons of the spinal cord dorsal horn. Recently, a pathophysiological analogy was constructed between chronic nociception (pain) and chronic tinnitus [124]. Overstimulation of NMDA receptors constitutes a major mechanism in glutamate-induced neurotoxicity; for this reason, NMDA receptor antagonists have been used as neuroprotectants in the prevention of excitotoxic cell injury [120,121]. Higher-than-normal levels of reactive anxiety have been reported in tinnitus sufferers, and some speculate that certain individuals may have a greater psychological predisposition or susceptibility to tinnitus than do others [134,135]. Therefore, how might endogenous dynorphins be used in the auditory periphery to modulate or maintain the aversive qualities of excessive (or even abnormally synchronous) auditory neural activity? Type I afferent dendrites innervating cochlear IHCs are themselves innervated by lateral efferent axons [31,32] and, as indicated, some evidence suggests that the lateral efferent system modulates auditory neural sensitivity [36,37]. Peripheral inflammation also is associated with peripheral (and central) receptive field enlargement [116]. Intracochlear perfusion of glutamate or aspartate at high doses has been reported to reduce the discharge of auditory units during the presentation of sound [150]. Consistent with this hypothesis are the intensitydependent biphasic changes in neural amplitude recently observed after a cochlear RW administration of the κ-receptor ligands U-50488H (see Fig. Similar intensity-dependent changes in neural amplitude have been observed consistently after IV administrations of (-) pentazocine [79,80,83]. As indicated, some 80% of tinnitus sufferers have problems that can be traced to, or associated with, changes occurring in the inner ear [1]. Tinnitus may, in some cases, be the immediate source of a stressful experience, though many individuals report that they begin to notice their tinnitus only during periods of high stress [167]. Results from an early investigation of cochlear neurotransmitter candidates in guinea pig perilymph (though excluding an analysis of perilymphatic dynorphin-like neuropeptides) indicated that exposure to intense and presumably stressful wide-band noise (80-115 dB SPL) significantly elevates levels of [Met5]-enkephalin-like opioid peptides, relative to control values obtained in quiet [168,169].
A physiological shift of the auditory periphery into a temporary state of vigilance is, in our view, synonymous with the production of a " hyperacusic" state, whereby most auditory stimuli are amplified.
Alternatively, depending on NMDA receptor sensitivity (or susceptibility) or on the reactivity of the lateral efferent system to the stressor, dynorphins released into an uncompromised cochlea nevertheless could result in the generation of spectral alterations in the ensemble spontaneous discharge (Fig.
At higher levels of the neuraxis, of course, response selection would become advantageously limited or narrowed, as all the enhanced signals from the auditory periphery, including the aberrant activity interpreted as tinnitus, are assigned a significant though equal motivational saliency. A detailed account of the NMDA receptor-dynorphin peptide distribution in the central nervous system is beyond the scope and intent of this article.
First is the evidence supporting the existence of lateral efferent projections to the cochlear nuclear complex [31].
Furthermore, both pharmacological [174,175] and in situ hybridization investigations [176,177] have provided evidence for the existence of NMDA and nonNMDA receptors in the mammalian cochlear nuclear complex. Finally, a likely certainty is that the mechanisms involved in the generation and maintenance of tinnitus are represented neither simply nor narrowly in central auditory pathways or in the auditory periphery (or in both). In a pilot study involving cochlear whole-mount preparations, we have observed dense immunohistochemical staining for CGRP in the IHC region of the organ of Corti in this species. We have presented a biochemical model to explain one possible cause of the phenomenon called tinnitus.
Portions of this manuscript were presented at the Second International Tinnitus Think Tank: The Neurochemistry of Tinnitus, Martha Entenmann Tinnitus Research Center and The State University of New York Health Sciences Center at Brooklyn, NY, November 5-6, 1998. Since ancient times, have been prized and physical recovery from illness during or after childbirth.
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Subsequently, TP was studied in terms of its physiological mechanism [4-9], nystagmic eye movements produced in response to intense sound [6,10-12], and the performance on a force platform with an acoustically stimulated vestibular system [10,13-15]. The presence of the TP was noted also in normal subjects (guinea pigs, monkeys, and humans) [19,20] and later even was found to be ubiquitous in normal subjects [21]. Previous reports show that the TP is provoked by a wide range of acoustic stimuli in terms of modes of delivery, intensity, and frequency. Most authors agree that the middle frequencies are the most effective in producing the TP in patients with inner ear pathology (Table 1) [6,12,14,15,24-26]. Vestibular dysfunction has been characterized in terms of deficits in the vestibuloocular reflex system and the vestibulospinal reflex system.
Posturography is an approach to the assessment of vestibular dysfunction that uses a force platform and provides various measures that reflect postural stability, such as the amount of body sway.
The TP has been studied only by nystagmographic methods and by static posturography, as mentioned.
The changes in postural stability were monitored by CDP when subjects attempted to maintain balance on the platform under stimulation with sound. A pure-tone sound of 110 dB at 1,000 Hz generated by a portable audiometer was delivered by air conduction in continuous mode through earphones. The extent of otological disease was established and documented in every case by history, physical examination, and audiometry.
In addition, most subjects with audiovestibular disorders (groups A and B) underwent ENG with sound stimulation for the detection of spontaneous nystagmus, as in the classic method for the detection of the TP.
The three study groups were matched in terms of age; consequently, differences between ages were not significant when compared statistically, as shown in Table 3. The subjects in this study were not matched in terms of quantitative results of diagnostic tests; therefore, the gravity of their disorder did not constitute a prerequisite for their selection.
The 40 patients investigated first were classified according to their clinical diagnosis (Table 4). Patients' medical history focused on two pertinent symptoms: tinnitus and dizziness (Table 5), with special stress on severity, duration, and precipitating factors. Table 6 exhibits the results of audiological tests: pure-tone audiometry, speech reception thresholds, and performance intensity function for phonetically balanced words (speech discrimination scores).
For the statistical approach of the results obtained in CDP before, during, and after acoustic stimulation, we calculated the means of the composite equilibrium scores and the mean individual sensory ratio scores for each study group in each trial. For purposes of simplicity and a better expression, we preferred to plot the mean composite score and mean vestibular ratio obtained by the three study groups, instead of the individual scores achieved by each subject. Because the composite score is an average of all sensory conditions, it reflects the overall on-feet stability of the subject.
The variation among the three study groups was examined by means of one-way ANOVA followed by Bonferroni multiple range test (Table 9).
Because in the study of the TP we were interested in both the overall equilibrium and the vestibular system in particular, the vestibular ratio score given by the CDP software was investigated next. Once again the one-way ANOVA followed by the Bonferroni mUltiple range test (Table 11) analyzed the variation among the three study groups. The vision preference is one of the sensory ratios provided by the sensory analysis of the CDP's software.
The sensory analysis revealed a variety of disequilibrium types or sensory organization patterns according to the specific sensory system responsible for imbalance (Table 13). A more intriguing pattern-the combined vestibular and vision dysfunction-was observed in some group A patients on trials 2 and 3 (20% and 25%, respectively). A last sensory organization pattern observed on sound delivery in two patients in group A was a vestibular dysfunction combined with vision preference. The current study focused on the postural stability of normal subjects and patients with otological impairments and on a third group of patients with similar otological disorders accompanied by a history of sonovestibular symptoms.
Hadj-Djilani [14,15] studied the performance on the force-plate under sound stimulation with exactly the same sound stimulus that we delivered in our work (1,000 Hz, 110 dB SPL). Our normal subjects and the patients with inner ear impairments without a medical history of Tullio symptoms showed no significant change in postural stability.
The occurrence of vestibular disturbance complicated by vision dysfunction during exposure to strong acoustic stimuli in patients suffering from Tullio symptoms is not surprising, given the exposure of the hyperirritable "Tullio" ears to intense noise as a general excitation and discomfort. The diagnosis of vestibular malfunction related to sound exposure may be of crucial clinical significance, beyond the obvious medicolegal implications.
An additional goal of this study had been to evaluate and compare the sensitivities of CDP and ENG in detecting vestibular impairment in the study participants. CDP and ENG were compared in a retrospective study of a mixed population of 375 patients with complaints of dizziness and imbalance [34]. Two additional retrospective studies [35,36] compared CDP and ENG results in patients with confirmed vestibular system deficits. Because of the nonoverlapping nature of the two tests, the foregoing three studies concluded that both vestibuloocular and vestibulospinal tests were essential components in the diagnostic workup.
We have managed to learn since the inception of this study that many patients who experience attacks of vertigo when exposed to loud noise complain of these symptoms solely in circumstances of noisy environment. A 43-year-old active ambulance driver was referred to the Otolaryngology Department of Bnai-Zion Medical Center 2 years before his admission to the current study. A constant, very disturbing tinnitus of alternately low and high pitch had been complicating his condition ever since. The pure-tone audiogram exhibited a bilateral hearing loss of notched configuration in the higher frequencies, typical of NIHL (Fig. Prior to his admission to this study, the patient underwent ENG that revealed neither spontaneous nor gaze nor positional nystagmus, with no evidence of any vestibular pathology. His temporary unsteadiness provoked by sound occurred because of an underlying vestibular dysfunction, as indicated by sensory analysis: The vestibular ratio is very low (Fig 6).
This work constitutes the final wrap-up of the preliminary study presented at the Twenty-Fourth Neurootological and Equilibriometric Society Congress, 1997, and subsequently published in the International Tinnitus Journal 3:2, 1997. In a medicolegal context, tinnitus is mostly a subsidiary item of claim, additional to that for NIHL.
The essentially subjective nature of tinnitus renders very difficult - at least in some patients - the choice of equitable medicolegal decisions about the presence and severity of tinnitus. The four progressive levels of decision making (1-4), consisting of 65, 12, 4, and 1 decision, respectively. Adequate decision making, even at an elementary level, requires exhaustive and encyclopedic knowledge of otoneurology.
Note: If tinnitus is accepted, the expert must define the percentage of impairment or invalidity. A positive decision about all four of these essential aspects is requested for acknowledging the tinnitus as a part of the occupational disease and for providing compensation. Similarly, documents proving that the patient has sought relief of tinnitus before making any claim for compensation are highly relevant in this context (repeated medical consultation, acupuncture, purchase of tinnitus maskers, etc.).
All files were examined by four different medical specialists (otorhinolaryngologists) interested in legal and forensic medicine. Fund for Occupational Diseases, Brussels, Belgium and Institute of Phoniatrics, Utrecht University Medical Center, the Netherlands.
They are particularly important because they impair the social autonomy of the aged and often are the cause of falls. In this article, we aim to present clinical and instrumental tools connected with accidental falls. An earlierversion falling risk inventory questionnaire (FRI) consisting of 87 items was administered to 57 randomly selected subjects (29 women and 28 men) distinguished only on the basis of age (older than 65 and younger than 80 years).
It assumes that the probability of a given subject-item interaction is governed only by the item's difficulty and the subject's ability. The measurement of body movements during stance are used to assess postural control objectively, which has led to the development of posturography. Patients were evaluated by means of the interactive balance system Tetrax platform, which consists of a pair of sensor platforms subdivided into a heel and a toe part.
It reflects the correlation between the oscillations of the left part of the body with respect to the right and the correlation between the oscillations of the anterior part of the body (toes) and the posterior (heels). Correlations between chronological age and stability among Italian (A) and Israeli (B) subjects. Electronystagmographic and Caloric Investigation Data About V ascular-Vestibular Dysfunction Among Patients with Vertebrobasilar Insufficiency. The aim of our investigation was to analyze the results of caloric and electronystagmographic investigation of vascular-vestibular disorders among patients with vertebrobasilar insufficiency.
The complicated perception of position of the body and its parts in space is a result of analyzed and synthesized impulses by the vestibular analyzer, by superficial and deep proprioception, and by the ocular analyzer, as the vestibular receptors play the main part in this system [1-4]. With the exception of arterial hypertonia or atherosclerosis (or both), pathological changes in the cervical spine (cervical osteoporosis) may lead to disturbances in blood supply of the labyrinth and brainstem. All examined patients were divided into two groups according to their age: 40-49 years and 50-59 years. The average amplitude (in degrees) and frequency (in Hertz) have been calculated at a definite part of the ENG, wherein the nystagmus strokes are maximally expressive, coinciding according to time and distance in the left and right labyrinth.
Among the control group, 0% of 40- to 49-year-olds and 10% of 50- to 59-year-olds (l of 10 men) were found to have nystagmus.
As a whole, the reactions show hyporeflection, which correlates with the data of rotatory tests. In comparing the results of CP and DP asymmetry, we found that CP asymmetry is predominant in all groups at all indices, as the most significant differences -are determined in SPS asymmetry. The differences between the two examined groupssubjects and controls-are statistically important for indices of more than 25% asymmetry, relative to the exaggerated vascular disorders in the vertebrobasilar system and especially in the a. As regards DP results, the most important index was SPS asymmetry (DP) of more than 20%, followed by frequent asymmetry. In both rotatory and caloric tests, this index was shown to provide the most information about functions of the vestibular analyzer. Hyperacusis, defined as a collapse of tolerance to sound, is present in 40-86% of those who suffer from disabling forms of tinnitus. In approximately 10 million individuals, the symptom is severe enough to compromise the quality of life significantly [1].
Dynorphin-like and enkephalin-like opioid peptides are codistributed within lateral efferent brainstem nuclei, in their descending fiber bundles and, in lateral efferent terminal varicosities, in the cochlea of such species as the guinea pig and rat [25-27]. The axons of descending, lateral efferent brainstem neurons [30] are well-known to terminate on the auditory spiral ganglion type I dendrites that, in turn, innervate the cochlear in-ner hair cells [31,32].
These three identified peptide families are (1) proopiomelanocortin (2) proenkephalin (proenkephalin A), and (3) prodynorphin (proenkephalin B). This fact has underscored their neurotransmitter-neuromodulatory role in the filtering of sensory information and in the enhancement and fine tuning of the regulatory functions exerted by other neurotransmitters or hormones [53-58]. As with most neuropeptides, the receptor-activated ion-channel properties of opioid peptides are mediated by a class of membranebound, pertussis toxin-sensitive "G" -proteins [50,61,66]. As is often the case in the central nervous system [69], the ion channel actions of opioid-receptor linked G-proteins are mediated by the regulation of adenylate cyclase that catalyzes the synthesis of the second messenger, cyclic adenosine 3',5'-monophosphate (cAMP) [47,6 1). For instance, opioid receptors can be linked to a Gs-protein that, when stimulated, activates adenylate cyclase and increases cAMP [61,67].
In that investigation, the nonopioid (+) pentazocine, administered at an equivalent IV dose and concentration, was without effect (Fig. Biphasic intensity-dependent amplitude changes after administration of the κ-receptor drug agonist U-50488H (50 mM) delivered to the cochlear round window (RW) in five animals. Though some uncertainty still exists [99], many investigators have argued that glutamate is the afferent neurotransmitter in the mammalian cochlea [27,100-104]. In addition, alpha-amino-3 hydroxy-5-methyl-isoxazol-propionic acid-induced excitotoxicity and degeneration of cochlear spiral ganglion neurons is accompanied by a neurotropic NMDA receptor action of glutamate in this species [100]. Here, the overall synaptic density of afferents generally is greater as compared to the density of dendrites on the pillar surfaces of the THCs. These changes consist of alterations in SDR, a lowering of thresholds, and an enlargement of receptive fields, producing an increased sensitivity to both noxious and innocuous stimuli [73,114-116]. More specifically, it was constructed between the wind-up phenomena and the associated hyperalgesia observed in chronic pain, and the auditory symptoms of hyperacusis and chronic tinnitus [125].
Noteworthy is that nonNMDA receptors also can mediate neurotoxicity, especially during prolonged or widespread insults [120,132].
A reasonable assumption is that constitutional differences exist with respect to individual reactivities to environmental and physical stress.
The opioid effects of μ-receptor ligands, however, often are accompanied by emotional states of dysphoria, disorientation, or depersonalization [59,98,138], and whether dynorphins are capable of producing any form of antinociception is questionable [74,139]. Does any evidence support that a neuropharmacological link exists between endogenous μ-receptor-sensitive dynorphins (or enkephalins) and neural excitability? The preceding review seems to clarify that only a few studies have investigated the potential effects of specific opioid receptor agonist-antagonist substances on the discharge of the auditory nerve. Endogenous dynorphins have been reported to interact with glutamate-sensitive NMDA receptors in rat cortical neurons [143], though the precise mechanism is not yet understood [144]. In addition, peripheral inflammation leads to a large increase in prodynorphin gene expression (increased mRNA) in dorsal horn neurons, and this central nervous system increase parallels the development of hyperalgesia [74,146]. However, in these investigations, neural suppression never was observed at higher stimulus levels.
Endogenous opioids have been suggested to modulate excitation at NMDA receptors [147] by (1) increasing the affinity of the ligand for the receptor (2) decreasing the degree of dissociation of the ligand from the receptor, or (3) by producing a change in the second messenger response to receptor activation. However, as with all perceptions (and especially those that involve aversion), the experience of tinnitus certainly must involve central auditory pathways and cortical regions and non auditory cortical-subcortical regions.
According to one view, tinnitus results from the stress-induced central enhancement and magnification of abnormal but weak triggering signals passing from the auditory periphery to the auditory cortex, where they are perceived [1]. Intense emotional stress has been reported also to improve auditory thresholds temporarily in guinea pigs [l70], and we have observed improved auditory thresholds after the cochlear administration of opioid κ-receptor ligands [19]. The amplitude enhancement of weak auditory patterns characterizing tinnitus and hyperacusis has been suggested to be part of an evolutionary survival reflex [171]. Individual constitutional differences naturally would dictate the degree to which peripheral (and central) dynorphin systems are activated (and consequently the severity of the subjective hyperacusis). In the long term, the consequence of this prolonged vigilant state is expected to produce a vicious feed-forward cycle. Investigations designed to determine the distribution of κ-receptors and dynorphins in specific brainstem auditory pathways and in cell layers of critical auditory nuclei have yet to be performed. Opioid prodynorphin (and proenkephalin) derivatives have been detected throughout the medullary brainstem, in regions that have included the separate divisions of this nuclear complex [54,172,173]. Additionally, a considerable number of prodynorphin-positive neurons have been detected within the inferior colliculus [173]. For instance, the release of excitatory amino acids (and therefore the observed hyperexcitability at NMDA receptors in neurons of the spinal cord dorsal horn) is facilitated by the release of the calcitonin gene-related peptide (CGRP) [73]. Such evidence raises the possibility that a dynorphin modulation of neural excitability through, perhaps, an enhancement of glutamate effects at NMDA receptors may occur at serial locations along the auditory pathway. Recognizing that this symptom represents a broad spectrum of auditory experiences, we acknowledge the possibility of an equally broad spectrum of auditory generators.
Monaghan DT, Bridges RJ, Cotman CWo The excitatory amino acid receptors:their classes, pharmacology, and distinct properties in the function of the central nervous system. Effect to improve the disorder of the autonomic nervous system has worked to produce a substance called serotonin in essential amino acids to adjust autonomic tryptophan is one thing and the arch-enemy of Tinnitus can be expected.
There many are possible in case of dizziness, sickness, is the most common cause of ear disease. It is to communicate that information to the brain by brain keep body balance body to the directive. Tinnitus is only the patient himself listening for no more than the discomforts and understanding people around harder, always sounds listening is a serious problems lead to poor concentration and poor quality of life, such as insomnia, irritability, mental stress and anxiety caused by exceeding. The percentage of people who feel the tinnitus with age each to increased, even hearing loss progresses with aging. The Tullio phenomenon evaluated by computed dynamic posturography (CDP) under acoustic stimulation is reflected in postural unsteadiness, rather than in the classic nystagmus.

This establishes the described method as a sensitive testing technique for validating the existence of the Tullio phenomenon in patients with a variety of disorders of the inner ear, especially chronic noise-induced hearing loss and acute acoustic trauma. In his early works on labyrinthine physiology, Pietro Tullio [1-3] described how sound stimuli caused pigeons to sway in the plane of the horizontal semicircular canals when minute holes were created in these canals. Blecker and deVries [4] showed that a microphonic, analogous to the cochlear microphonic, can be recorded from the cristae of the fenestrated semicircular canal of the pigeon and that the frequency response of this crystal microphonic parallels the frequency response curve for the TP. No difference in body sway was observed according to whether sound was delivered with monaural or binaural stimulation [13]. Lowfrequency noise (50-400 Hz) was shown also to induce responses in the vestibular neurons [9] by direct influence on vestibular end organs [3,9], and its influence on vestibular function was studied with infrasound stimuli of 25, 50, and 63 Hz at 130-132 dB [13,17]. Tests of the vestibuloocular reflex system-caloric irrigation, vertical axis rotation of the entire body, and ENG evaluations of spontaneous and positional nystagmus -provide information about the symmetry of a vestibular lesion affecting the horizontal semicircular canals. One of the latest versions, computed dynamic posturography (CDP) (Equitest), attempts to ferret out the effects of various sensory inputs to the brain and to relate them to overall on-feet balance and stability [27-29]. We could not find any study of vestibular responsiveness to acoustic stimulation evaluated by CDP in the literature.
Mean composite equilibrium scores in three consecutive sensory organization tests; the second trial was carried out with acoustic stimulation In conditions 5 and 6. From the wide range of acoustic stimuli used to provoke a sonovestibular response, we favored one of low intensity that efficiently, yet safely, elicits a Tullio response.
Some patients were investigated by imaging studies (computed tomography or magnetic resonance imaging). Informed consent was obtained from the subjects, and the experimental protocol was approved by the local Ethics (Helsinki) Committee and the Israeli Ministry of Health. The only criteria in our choice were the established diagnosis of an audiovestibular disease and an accurate medical history concerning the presence or absence of sonovestibular complaints.
The two dominating categories in this study, comprising a majority of 80% (70% in group A and 90% in group B), were patients demonstrating hearing loss caused by noise. By definition, all patients with sonovestibular complaints (clustered in group A) had to be suffering from either lightheadedness, true vertigo, or plain disequilibrium, with or without nausea and vomiting. The binaural hearing loss percentage was based on the pure-tone thresholds at the speech frequencies of SOO, 1,000, 2,000, and 3,000 Hz and were calculated according to the formula used by the American Medical Association [32]. For a more accurate evaluation of hearing loss, basic statistical tests were run on several audiometric parameters.
This was accomplished by the alternate binaural balance test administered to patients with a difference of 2S dB or more between the hearing thresholds of the two ears at the test frequency. As we have seen, this presumption about the nonsimilarity of the two sets of subjects with otological disorders eventually was proved partially correct.
Vestibular ratios scores obtained in computed dynamic posturography in three consecutive sensory organization tests, the second under stimulation with sound. Switching to this representation is correct as long as the mean follows the trend of most individual values in the group. The trend over repeated trials of SOT was studied by ANOVA for repeated measurements, followed by the Bonferroni test for repeated measurements, applied to the average composite score (Tables 7,8).
The trend over repeated trials of SOT was again studied by making use of the ANOVA for repeated measurements, followed by the Bonferroni test for repeated measurements (Table 10; see also Table 8).
It reflects the degree to which affected patients rely on visual information to maintain balance, even when the information is incorrect.
In this pattern, the sensory ratio of condition 4 to condition 1 is abnormal, whereas those of the remaining pairs are within the normal range (the equilibrium scores for condition 4 are abnormally low relative to the scores on condition 1).
In this pattern, the sensory ratios on both SOT condition 5 to condition 1 and condition 4 to condition 1 are abnormal, with normal 2 to 1 and 3 and 6 to 2 and 5 ratios. Our two sets of pathological patients were picked by definition with regard to the medical history of inner ear disease and to the exclusion of neurological (somatosensory), orthopedic, and vision dysfunction. Both the ratio for conditions 5 and 1 and the paired analysis of conditions 3 and 6 relative to conditions 2 and 5 were abnormal.
Accomplishing that would have enabled a correct parallel and eventual contrast between the results and effectiveness of the two vestibular tests in evaluating the TP. The postural responses were monitored on the Equitest (the CDP) in three consecutive sensory organization tests, with the second performed partially under binaural delivery of sound (1 IO dB at 1,000 Hz). This establishes the described method as a sensitive testing technique for validating the existence of the TP in patients with a variety of disorders of the inner ear, especially chronic noise-induced hearing loss and phonal trauma, even when employing stimuli of harmless intensities (110 dB) and short durations (6 × 20 sec). Three sensory systems are involved in the maintenance of balance: vestibular, visual, and somatosensory. As mentioned, ENG recordings were not made in some cases for a multitude of reasons, and the testing protocols were not identical in the remaining subjects. CDP abnormalities were documented in 55% of the cases, whereas ENG revealed abnormality in only 26% of the patients. In these more homogenous groups of 46 and 52 patients, ENG and CDP abnormalities were equally prevalent and occurred in approximately 50% of the cases.
The contrast between ENG findings and CDP findings in the particular case of patients with sonovestibular symptoms, however, is an interesting aspect and remains one of our objectives for the future. Others may suffer anyway, but their symptoms are significantly exacerbated during sound stimulation. He presented with a history of dizziness attacks triggered suddenly by noise, such as loud music or at weddings, or the whine of jet engines on aircraft flying at low altitude. He had been an otherwise healthy person, except for a peptic ulcer, silent at the time of our investigation, for which he had been administered antacids and H2-receptor blockers in the past. ENG with acoustic stimulation included a 60-second continuous recording of ocular movements during binaural stimulation with the pure tone of 110 dB at 1,000 Hz. Individual and composite scores obtained from a patient with noise-induced hearing loss and the Tullio phenomenon in the sequence of three consecutive computed dynamic posturography sensory organization tests (SOTs). Sensory ratio scores obtained from the same patient as in Figure 5 (with noise-induced hearing loss and the Tullio phenomenon) in the sequence of three consecutive computed dynamic posturography sensory organization tests . To reach a maximum of medicolegal objectivity, a system was developed within the Belgian Institute of Occupational Disorders (Brussels) in the form of a four-level decision structure, after exhaustive but noninvasive assessment of patients.
This difficulty implies that assessment must involve a large set of parameters combining subjective and objective items [3]. The four levels are worked through in progression from level 1 to level 4 and consist of 65,12,4, and 1 decision, respectively. Each specialist was required to make his or her decision according to the pathway proposed in this protocol. The test reveals a Kappa value of 0.74, demonstrating a high interrater consistency at the first level. A decision - making system based on an exhaustive assessment and a four - level decision structure proves to be helpful. The posturographic findings show that the falling subjects, to maintain postural control, are highly dependent on somatosensory inputs and have a weaker "systeme postural fin" (fine postural system), according to Gagey. Starting from the matrix of raw scores, difficulty and ability are both estimated in true interval units along the shared continuum made up by the underlying variable (in this case, the risk of falling). Tetraataxiometry (Tetrax, Tel Aviv, Israel) is the last developed posturographic set, consisting of two pairs of single piezoelectric sensor platforms that record posturographic right and left heel and toe applied forces on the ground. The oscillations may be in phase and defined as coactive synchronization or opposite in phase and defined as compensatory synchronization.
Falling elderly subjects are less stable than non falling elderly subjects during a standing test on pads. This situation seems to indicate that among elderly persons is a subpopulation that, for unknown reasons, is immune from destabilization and, hence, from falls. Age is correlated to instability only in falling subjects, whereas a paradoxical negative correlation is evident in nonfalling subjects, regardless of their nationality. Knowledge and perception of fall-related risk factors and fall-reduction techniques among communitydwelling elderly individuals.
According to various authors [2,3,5,9-14], chronic irritation of the sympathetic nerve plexus around the vertebral and basilar arteries provokes reflex changes in blood supply of the inner ear, which leads to vertigo, noise in the ears, and a feeling of hearing loss. The signal is valid for the following parameters: a lO-mm graphic view of the fast site of the nystagmus in a 10-degree angle diversity of the eyes, for left or right to center. Therefore, this index must be applied in routine neurootological practice, especially in vascularvestibular disorders. The results of that objective investigation show that receptor damages of the vestibular analyzer prevail over the central ones in people with vascular-vestibular dysfunction at ages between 40 and 49 years. Tinnitus has been described as the perceptual correlate of altered spontaneous neural activity occurring in the absence of an external auditory stimulus [3-6]. Though the existence of prodynorphin peptides has yet to be shown in the human auditory system, products of proenkephalin synthesis have been detected in the lateral efferent terminal varicosities of the human cochlea [28]. The axodendritic innervation pattern of these dynorphin-containing terminals suggests that the lateral efferent system participates in modulating auditory neural sensitivity [33-35].
Neuroactive opioid peptides modulate sensory input through separate and often distinct opioid receptors. Antinociception (analgesia) is the most familiar and most intensively investigated property of such opioid substances as morphine; by definition, all opioids are analgesics [49,59].
The G-proteins derive their name from the fact that they bind the guanine nucleotides, guanosine triphosphate, and guanosine diphosphate [67].
Therefore, the binding of opioid ligands to their respective receptors often activates a Gi-protein that inhibits adenylate cyclase and decreases cAMP [61,67). Nevertheless, specific receptor subtypes that bind endogenous enkephalins and dynorphins (a and κ, respectively) have yet to be identified in the cochlea of any mammalian species. Each plotted point represents the mean percentage of amplitude change relative to a grand baseline amplitude mean (±SE) obtained during each of six 30-minute recording periods. Each plotted point represents the mean percentage of amplitude change relative to a grand baseline amplitude mean (±SE) for the two dependent measures, obtained during each of six 30-minute recording periods. 3) produces increased auditory sensitivity and intensity-dependent amplitude changes in the auditory nerve CAP when administered intracochlearly [93,19]. Each plotted point represents the mean percentage of amplitude change relative to a grand baseline amplitude mean (±SE) obtained during each of six 30-minute recording periods recorded at the six stimulus intensities indicated.
Adding to the complexity is the fact of even less certainty regarding the receptor type activated by putative excitatory afferent neurotransmitters in the cochlea [99]. Furthermore, a significant body of pharmacological evidence supports a functional auditory role for glutamate-sensitive NMDA receptors in the adult guinea pig cochlea [101-104, 107-109].
Tn general, the modiolar-oriented units are characterized by relatively lower spontaneous discharge rates (SDRs), higher auditory thresholds, smaller fiber diameters, and lower mitochondrial densities [33,110-112]. According to Moller [125], both pain and tinnitus involve neural sensitization that leads to a reduction in threshold or increased levels of neural excitability (or both). Characteristically, NMDA receptor-gated activity produces an influx of extracellular Ca++, which in excess activates a variety of potentially destructive processes [120,121]. Equally reasonable is the expectation of individual differences with regard to the degree to which certain endogenous biochemical systems are likely to become activated during stressful events. Also endogenous dynorphins have been demonstrated to potentiate, rather than to suppress, behavioral changes induced by stressful events [63]. The results of those investigations indirectly have supported the existence of opioid receptor subtypes in the cochlea. Unlike previously reported δ-receptor ligand effects [142], dynorphins do not appear to interact with excitatory non-NMDA receptors [143], though potential interactions between these substances and glutamate-sensitive NMDA and non-NMDA receptors have yet to be demonstrated in the mammalian cochlea.
Dynorphins have been implicated also in the wind-up-like activation of NMDA receptors, leading ultimately to neurotoxicity [147]. A tempting speculation is to envision the changes that high concentrations of cochlearly administered κ-receptor drug agonists would produce on auditory neural discharge as an auditory stimulus is progressively increased in intensity from threshold. At threshold and at relatively lower stimulus levels, these substances each promoted or enhanced neural excitation.
Whether these changes reflect actions at glutamate-sensitive NMDA, non-NMDA, or both receptor types, or at some other nonopioid receptor requires further investigation. Nevertheless, a peripherally generated tinnitus can result from any number of insults to the inner ear, ranging from advancing age to excessive noise exposure [2,151]. Our position however, is that during stressful episodes, these abnormal signals (triggers) are not weak but are in fact abnormally amplified in the periphery. Therefore, we are proposing that a stress-induced release of neuroactive dynorphin-like opioid peptides from the lateral efferent terminals located beneath the IHCs contributes to an increase in auditory neural sensitivity and to spectral alterations in the ensemble spontaneous discharge activity of the auditory nerve. However, those auditory (type I) neurons innervating a cochlea having sustained weakened or damaged OHCs (and therefore preordained to generate aberrant spectral discharge patterns) would be additionally susceptible to stress. Therefore, under certain stressful conditions, dynorphins alone may serve as a trigger for tinnitus. Step 1: Excitatory neurotransmitter (glutamate) is released by the inner hair cell (A) during the presentation of a stimulus or (B) spontaneously during periods of quiet and binds to glutamate-sensitive (possibly N-methyl-D aspartate) receptors located postsynaptically on the type I auditory dendrites. This hypothesized feedforward cycle is similar conceptually to the wind-up phenomenon, which could serve to advance the organism to a state of peripheral and central auditory neural excitotoxicity and neurotoxicity.
However, an important note is that though the focus of this article has been the auditory periphery, the possibility also exists for concurrent interactions of endogenous dynorphins with NMDA receptors at locations within the central auditory system. We have found CGRP immunoreactivity in a significant number of cells in the dorsal cochlear nucleus and in neurons of the ventromedial region of the lateral superior olive (LSO) [178]. This possibility and the precise relationship of κ-receptor ligands to NMDA receptor-activated neural discharge in the inner ear will be the focus of future investigations. However, we are compelled to conclude that when a human organism is confronted with any number of stressful events, conditions are optimal for the overall release of neuroactive opioid substances and the generation and perception of tinnitus. Neural mechanisms of tinnitus: the pathological ensemble spontaneous activity of the auditory system. Changes in the auditory neural response following cochlear administration of U-50488H and (-) pentazocine. Modulation of synaptic efficacy as a basis for tinnitus:hints suggested from the effects of quinine and aspirin on cochlear neurotransmission. Effects of electrical stimulation of efferent olivocochlear neurons on cat auditory-nerve fibers: I.
Effects of electrical stimulation of efferent olivocochlear neurons on cat auditory-nerve fibers:II. Coexistence of putative neuroactive substances in lateral olivocochlear neurons in guinea pig and rat. Prodynorphin peptides are co-localized within auditory structures of the Chinchilla brainstem. Efferent innervation of the inner hair cell region:origins and terminations of two lateral olivocochlear systems.
Efferent synapses in the inner hair cell area of the cat cochlea:an electron-microscopic study of serial sections.
Physiology of cochlear efferent and afferent neurons:direct comparisons in the same animal.
Acetylcholine potentiation of glutamate-induced response in guinea pig spiral ganglion cells. Long-term physiological consequences of cutting the olivocochlear bundle (OCB) in neonatal animals.
Partial characterization of the mRNA that codes for enkephalins in bovine adrenal medulla and human pheochromocytoma. Molecular cloning establishes proenkephalin as precursor of enkephalin-containing peptides.
Cloning and sequence analysis of cON A for porcine β-neoendorphinl dynorphin precursor. Immunohistochemical localization of the cloned κl receptor in the rat CNS and pituitary. Endogenous opioid peptides acting at μ-opioid receptors in the dorsal horn contribute to midbrain modulation of spinal nociceptive neurons. Opioid peptide modulation of circulatory and endocrine response to mental stress in humans. Behavioral changes induced by stressful situations:effects of enkephalins, dynorphin, and their interactions. Modulatory effects of Gs-coupled excitatory opioid receptor functions on opioid analgesia, tolerance, and dependence.
Dual opioid modulation of the action potential duration of mouse dorsal root ganglion neurons in culture. Dynorphin prolongs the action potential duration of mouse sensory ganglion neurons by decreasing a K+ conductance whereas the specific kappa opioid, U-50, 488H does so by increasing a Ca2+ conductance.
Dynorphin prolongs the action potential of mouse sensory ganglion neurons by decreasing a potassium conductance whereas another specific kappa opioid does so by increasing a calcium conductance.
Mu, delta, and kappa opioid receptor mRNA expression in the rat CNS:an in situ hybridization study.
Improvement in auditory function following pentazocine suggests a role for dynorphins in auditory sensitivity.
Effects of opioid drugs on auditory evoked potentials suggest a role of lateral efferent olivocochlear dynorphins in auditory function.
Binaltorphimine-related bivalent ligands and their K opioid receptor antagonist selectivity.
Implication of NMDA type glutamate receptors in neural regeneration and neoformation of synapses after excitotoxic injury in the guinea pig cochlea. Receptor pharmacological models for inner ear therapies with emphasis on glutamate receptors:a survey.
The role of glutamate at the afferent synapses of mammalian inner hair cells:a microiontophoretic study. A microiontophoretic study of the role of excitatory amino acids at the afferent synapses of mammalian inner hair cells.
N-methyl-D-aspartate-induced oscillations in excitatory afferent neurotransmission in the guinea pig cochlea. Transient expression of NMDA receptors during rearrangement of AMPA-receptor expressing fibers in the developing ear.
Electrophysiological evidence for the presence of NMDA receptors in the guinea pig cochlea. Morphological differences among radial afferent fibers in the cat cochlea:an electron-microscopic study of serial sections.
Morphometry of intracellularly labeled neurons of the auditory nerve:correlations with functional properties. Response properties of cochlear efferent neurons:monaural vs binaural stimulation and the effects of noise. Contribution of central neuroplasticity to pathological pain:review of clinical and experimental evidence. A comparative study of the changes in receptive-field properties of multireceptive and nociceptive rat dorsal hom neurons following noxious mechanical stimulation. The induction and maintenance of central sensitization is dependent on N-methylD-aspartic acid receptor activation; implications for the treatment of post-injury pain hypersensitivity states. The relation between net calcium, alkali cation and chloride movements in red cells exposed to salicylate.
Concomitant salicylate-induced alterations of outer hair cell subsurface cisternae and electromotility.
Mu agonist induced euphoria as opposed to dysphoria elicited by κ-agonists in humans and experimental animals. Intrathecal dynorphin 1-13 results in an irreversible loss of the tail-flick reflex in rats. A direct non-opiate interaction of dynorphin 1-13 with the N-methyl-D-aspartate NMDA receptor. The influence of sustained opioid receptor blockade in a model of long-term, localized inflammatory pain in rats. In situ hybridization cytochemistry and immunocytochemistry reveal an increase in spinal dynorphin biosynthesis in a rat model of peripheral inflammation and hyperalgesia. Selective potentiation of NMDA-induced activity and release of excitatory amino acids by dynorphin:possible roles in paralysis and neurotoxicity. Norbinaltorphimine protection against N-methyl-D-aspartic acid-induced convulsions and mortality. Acute ultrastructural changes in acollstic trauma:serial-section reconstruction of stereocilia and cuticular plates. Effect of sound stimulation at several levels on concentrations of primary amines, including neurotransmitter candidates, in perilymph of the guinea pig inner ear.
Immunocytochemicallocalization of glycine in a subset of cartwheel cells of the dorsal cochlear nucleus in rats.
Differential expression of N-methyl-D-aspartate receptor in the cochlear nucleus of the mouse. Localization of calcitonin gene-related peptide (CGRP) within auditory structures of the chinchilla brainstem. Dizziness in improving the disorder of the autonomic nervous system and blood flow of the inner ear, tinnitus as well as RID is also valid.
Occasional repeat attacks of vertigo, often people it mental stress or overwork will be attacks.
Actually, is the percentage of people plagued by tinnitus and hearing loss in Japan is targeted to all ages and one about 5 people, aged 65 and over to target and about three to one. With an effective tracking system and insurance program, EMS is able to offer a secure delivery worldwide.
With such a method, the dangerous effects of noise-induced instability can be assessed and prevented.
This vestibular microphonic can be recorded from any of the vestibular end organs and has been observed in many species. A scan of the literature for the different stimuli used in different studies reveals that the sound pressure levels used to elicit a TP in healthy subjects were higher than those used in subjects with pathologies of the ear. These vestibular tests, however, do not characterize the vestibular deficit in terms of patients' functional status (the ability to stand and walk) because such patients are evaluated in "passive" positions in which balance is not required. CDP includes test conditions in which the platform and visual environment are moved to reduce subjects' ability to use visual and proprioceptive information for balance. Static posturography falls short of revealing pure vestibular malfunction, manifested clinically as unsteadiness when standing or walking. This SPL is well within safety limits (Table 2) in accordance with the Illinois Occupational Diseases Act [30] and the Occupational Safety and Health Administration Regulation [31]. All patients with abnormal visual, orthopedic, and neurological function (other than audiovestibular disorders) were excluded from the study. Therefore, patients in group A were intrinsically a "dizzier" and (as demonstrated later) a more "unstable" set of subjects than were those in group B. Single-factor analysis of variance (ANOVA) revealed insignificant differences among hearing loss percentages, speech reception thresholds, and speech discrimination scores of the two pathological groups (see Table 6). These study groups harbor a discrepancy with regard to symptomatology, whereas objective audiometry revealed a similar degree of hearing impairment.
In this way, excessive clutter in the illustration is avoided without generating any statistical error in this case.
Thus, the severity of dizziness in these patients (as indicated by history) found a confirmation in terms of posturography by showing a worse balance even in the absence of sound.
In group A, the vestibular component of the equilibrium again demonstrates a decrease on stimulation with sound (see Fig 3).
Thus, we got a confirmation of what theoretically was expected; the impaired on-feet stability is (at least in part) explained by a flawed vestibular system in patients with TP. The vision preference scores did not show a large variation, either over consecutive trials or across study groups (Table 12).
The initial proportion of vestibular dysfunction increased on acoustic stimulation to 55% in group A but subsequently decreased in the third trial. As we know from the literature, this pattern is not observed commonly in patients with impairment limited to the vestibular system but rather are suggestive of central nervous system pathology, possibly in addition to that of the vestibular system. CDP performances demonstrated that 90% of the 40 subjects (groups A and B) showed either normal balance or vestibular dysfunction solely. In these cases, the average equilibrium scores for conditions 3, 5, and 6 were not only below the normal limits but were abnormally low relative to the scores on conditions 1 and 2.
Regrettably, not all 60 study subjects underwent ENG recording under stimulation with sound, and some of those who did were not evaluated identically in terms of duration of exposure to the acoustic stimulus for various reasons. In comparing our results to those found in previous works in which static posturography methods were used, we must take note of the controversy surrounding the subject in the literature. In these works, they studied the TP using low-frequency sound (25-63 Hz, 130 dB SPL) and observing the change in stability on a static posturograph. This stimulus is well within the noise exposure standards and therefore is safe, with a temporary threshold shift the only unwanted effect it produces. When vestibular damage occurs and remains undiagnosed, the overall function of balance relies only on the other two systems. Conclusions based on such a methodological incongruity of the two diagnostic tests could be erroneous. Hence, CDP provided the only documented evidence of pathology in approximately 30% of the cases.
Both categories, especially the former, undergo extensive and protracted workup as the usual diagnostic tests fail to reveal the gravity of their otoneurological disease. He described these attacks as short (minutes), mainly lasting through the duration of the noise but sometimes beyond that, and always accompanied by nausea. As compared to relatively good overall equilibrium (composite score, 78) and competent sensory systems on the first trial (see Fig. The second trial was performed with acoustic stimulation during conditions 5 and 6, whereas the other two were quiet SOTs in the regular mode. Responses of squirrel monkey vestibular neurons to audiofrequency sound and head vibration. Influence of pressure loading to the external auditory canal on standing posture in normal and pathological subjects. Tullio phenomenon and postural stability: experimental study in normal subjects and patients with vertigo.
Effects of increasing intensity levels of intermittent and continuous 1000 Hz tones on human equilibrium. Adaptation to alter support and visual conditions during stance: patients with vestibular deficits.
Effect of visual support surface references upon postural control in vestibular deficit subjects.
Computerized dynamic posturography: its place in the evaluation of patients with dizziness and imbalance. Comparison between dynamic posturography and ENG recordings in patients with peripheral vestibular disorders. An aggregate of multiple-choice responses (affirmative, neutral, negative) to elementary questions leads to a decision of the next level, which in turn determines - together with the other decisions at the same level - the conclusion at a still higher level. Further, as in some cases tinnitus may cause devastating (and objectionable) effects on one's lifestyle and ability to work, it may attract levels of compensation higher than those for hearing loss [2]. The ultimate decision is to accept or reject the tinnitus as a true component of the occupational disorder (noise-induced cochlear damage). An aggregate of multiplechoice decisions (affirmative, neutral, negative) on elementary questions leads to a decision at the next level, which in turn determines - together with the other decisions at the same level - the conclusion at a still higher level. They also show that an elderly subpopulation exists that, for unknown reasons, is immune to destabilization and falls.
There is evidence that aging affects multiple sensory inputs as well as the muscles' , joints', and central nervous system's ability to perform sensorimotor integration [1,2].
The posturographic findings in falling and nonfalling elderly women belonging to two culturally different popUlations, Italian and Israeli, have been compared, and the preliminary results are presented here. 2), indicating a weaker "systeme postural fin" (fine postural system), according to Gagey [9] and probably a weaker postural feed-forward mechanism, anticipating dangers that threaten the body's equilibrium.
Percentage of instability index is displayed on the ordinate axis (low score indicates stable; high score indicates unstable).

Percentage of instability index is displayed on the ordinate axis (0 = normal stability; 100 = fall). Presented at the Symposium of the International Society for Postural and Gait Research, Marseille, France, May 29, 1988.
Standard and electronystagmographic ("Tonnies" type) caloric tests were used to evaluate the human vestibular analyzer.
Our aim in this investigation was to analyze the results of caloric and electronystagmographic (ENG) investigation of vascular-vestibular disorders among patients with VBI. The results obtained by lonkins and Philipson's formula [4] for prevalence in relation to the direction (DP), at the same indices (Fig. Biological systems known to regulate the body's overall response to stress use and release endogenous neuroactive opioid peptides.
Some 80% of tinnitus sufferers have problems that can be traced to or are associated with changes in the inner ear [1].
Preliminary work has indicated also that dynorph in-related derivatives are codistributed within lateral efferent brain stem nuclei of the chinchilla [29], though it remains to be determined whether the descending axons that project into the cochlea also contain dynorphins in this species. Data from recent pharmacologic studies [36,37] and developmental studies [38,39] also suggest an important role for this system in modulating auditory sensitivity.
Also well-known is that opioid peptides function as neurotransmitters or neuromodulators and that they play an important role in modulating nociceptive sensory input [59-61].
In many other instances, the opioid receptor-linked stimulation of a G-protein may regulate a specific type of ion channel directly, such as a potassium (K+) or a calcium (Ca++) channel, independent of adenylate cyclase-cAMP. Furthermore, results of a subsequent investigation [79] indicated that large auditory neural amplitude changes at twice the dose were naloxone-reversible and occurred with no corresponding changes in the hair cell-generated cochlear microphonic potential (Fig. Considerable evidence supports the existence of excitatory non-N-methyl-D-aspartate (NMDA) receptors in the normal adult mammalian cochlea [27,99].
Cochlear NMDA receptors may, however, be restricted to the type I auditory dendrites innervating the modiolar side, as opposed to the pillar side, of the IHCs [109].
Tn approximately 70% of these units (25-30% of the total), the auditory dendrites may be innervated by a range of 1-32 lateral efferent axons (mean, 10).
The enlargement of receptive fields and the ensuing hyperalgesia occur via the facilitation of excitatory amino acid effects at NMDA receptors [73,114]. Recently, inner ear damage from overstimulation was shown to be prevented by the cochlear administration of leupeptin, an inhibitor of intracellular Ca++ -activated cytosolic proteases (calpains) [15,133]. As with pain, what is becoming clear is that tinnitus must consist of both central and peripheral components; certainly, the response of an organism to stress surely involves the entire organism, both its peripheral and central nervous systems. Furthermore, evidence suggests that the aversive motivational properties of endogenous and exogenous opioids are mediated through peripheral κ-opioid receptors [140,141]. Nevertheless, dynorphins have been proposed to playa significant role in pathologies of central and peripheral inflammation [73,115,144,145].
For example, dynorphins produce neurotoxic effects in the spinal cord [139], and the κ-receptor-induced neurotoxicity and neurological dysfunction occur through an enhanced excitotoxic activity at NMDA receptors [73,144,148]. As the stimulus level is increased, glutamate concentrations in the inner ear also would increase but would be potentiated abnormally at each level of increase as a consequence of a κ-receptor facilitation of glutamate at NMDA receptors.
The OHCs appear to be the inner ear structures most susceptible to damage in general and to noise damage in particular [152-155], and often tinnitus is associated with OHC dysfunction [3,156,157].
Though signal enhancement or increased synchronicity (or both) may occur at any location in the auditory system during extreme episodes of anxiety or stress [1], the initial neural changes involved in most forms of tinnitus begin in the auditory periphery [127]. Therefore, as part of an overall response to stress during actual or perceived life-threatening situations (as in extreme anxiety), endogenous neuroactive dynorphin peptides are released into the mammalian cochlea at axodendritic synapses beneath the IHCs and are released throughout the central nervous system. The release of dynorphins and perhaps the subsequent enhanced neural sensitivity to excitatory neurotransmitter activation [73, 148] would result in amplified spectral alterations in the ensemble spontaneous discharge activity associated with tinnitus [4], thereby exacerbating or revealing the preexisting symptom.
This event might occur in a manner that perhaps is similar to that described after receipt of sodium salicylate [4,5,21], shown recently to potentiate glutamate effects at NMDA receptors in the mammalian cochlea (20). Step 2: Endogenous dynorphin-related opioid peptides released from lateral efferent terminals tonically, or during physical or emotional stress, interact with N-methyl-D-aspartate receptors located postsynaptically on the type I auditory dendrites, to potentiate the excitatory properties of glutamate. Presently unknown is whether this group of LSO neurons projects specifically to the chinchilla cochlea as palt of the lateral efferent system. In Abstracts of the Twenty-Second Midwinter Meeting of the Association for Research in Otolaryngology 836:209-210, 1999. In Abstracts of the Twenty-First Midwinter Meeting of the Associationfor Research in Otolaryngology, 447, 1998.
In Abstracts of the Eighteenth Midwinter Meeting of the Associatiollfor Research in Otolaryngology, 679:170, 1995. In Abstracts of the Twentieth Midwinter Meeting of the Associationfor Research in Otolaryngology, 600:20,1997. In Abstracts of the Twentieth Midwinter Meeting of the Association for Research in Otolaryngology, 213:54, 1997. In GJ Siegel, BW Agranoff, RW Albers, SK Fisher, MD Uhler (eds), Basic Neurochemistry (6th ed).
In JG Hardman, LE Limbird, PB Molinoff, et al.(eds), Goodman and Gilman's The Pharmacological Basis of Therapeutics (9th ed). In R Quirion, K Jhamandas, C Gianoulakis (eds), Progress in Clinical and Biological Research: The International Narcotics Research Conference INRC '89. Proceedings of the Second International Tinnitus Think Tank: The Neurochemistry of Tinnitus. In AG Gilman, TW Rail, AS Nies, P Taylor (eds), Goodman and Gilman's The Pharmacological Basis of Therapeutics (8th ed). In GE Reich, JA Vernon (eds), Proceedings of the Fifth International Tinnitus Seminar, 1995.
In Abstracts of the Nineteenth Midwinter Meeting of the Associationfor Research in Otolaryngology, 469:118, 1996. Also helps to relieve stress, become causes of hearing loss, tinnitus, Vertigo and bee child contains arginine and lysine,. You can track your package with the tracking code provided and it will be delivered within a week. This should be carried out preferably by means of CDP with acoustic stimulation for an objective corroboration of their complaint before continuing activity in a noisy environment, thus preventing dangerous loss of balance when exposed to noise. Tullio observed the currents created in the labyrinthine fluids in response to sound by watching the motion of dye particles introduced into the endolymph and perilymph.
Furthermore, information gathered from these studies may indicate that the vestibular response-evoking threshold intensity varies with the frequency of the stimulus: Normal subjects evidence sonovestibular responses at midfrequency range (l,000 Hz) over 120 dB [23]. CDP constitutes a comprehensive sensorial function test of the equilibrium by virtue of its inherent feature of isolating the vestibular, visual, and somatosensory contribution to overall balance, unlike older posturography techniques that served as mere systemic balance tests. We deem CDP a very appropriate technique for investigating the interaction between balance and sound within the labyrinth. According to these noise exposure safety standards, subjects can be exposed safely to 110 dB for a half-hour daily before any otological damage would occur. Subsequently, we summarized all the relevant medical information supplied by history and the battery of audiological tests. The findings were not suggestive of any correlation between recruitment and the presence or absence of sonovestibular symptoms. This is not surprising, considering that abnormal sensory preference is, in essence, the effect of a central pathology (arising from the vestibular nuclei or their higher connections), whereas all the subjects in this study were patients suffering from peripheral disease exclusively (arising from the labyrinth or vestibular nerve).
The vestibular dysfunction percentages remained constant in the other two groups on repeated trials.
The significance of this disclosure of a disturbance in the central connections responsible for equilibrium, triggered by acoustic stimulation in the patients with sonovestibular symptoms, has yet to be interpreted.
Only 10% (two subjects in group A on trial 1 and two in group B on trial 3) revealed an inability to use input from the visual system to maintain balance. In general, patients with this kind of pattern are unable to use vestibular system inputs and are abnormally destabilized by orientationally inaccurate visual stimuli.
Not only did the intense sound have no deleterious effect on the balance of normal subjects but they improved their postural stability during sound stimulation, probably through the alerting response. Thus, it can be used routinely for detecting this disturbing and potentially dangerous phenomenon in patients who complain of sudden dizziness or report protean descriptions of feeling bad when they happen to be exposed to intense noise at a concert hall, discotheque, airfield, or work.
Even though the functional impact of vestibular and vision dysfunction is limited to noise exposure in such patients, they require a stable support surface reference to maintain balance (somatosensory-dependent) in those instances. When, in addition, other sudden sensory deprivation occurs or if new relationships develop between the sensory systems involved in balance, spatial disorientation may transpire under these circumstances. Among the cases with history of head injury, 100% had CDP abnormalities, whereas ENG results were normal in all of them.
Among patients with abnormal ENG and normal SOT results, the majority had compensated unilateral lesions. Such patients' symptoms seldom improve, because the underlying damage is by and large permanent regardless of etiology. Additionally, he mentioned occasional vertiginous attacks caused by bending forward, always quite suddenly relieved by straightening out.
Speech audiometry found binaural speech reception thresholds and speech discrimination scores of 20 dB and 100% at 55 dB, respectively. 5A), our patient demonstrated a sharp decrease in his overall balance when exposed to the pure tone of 110 dB at 1,000 Hz (composite score, 52) (see Fig. Cited by Erlich MA, Lawson W, The incidence and significance of the Tullio phenomenon in man. A positive outcome on all four level-3 questions is required for recognition of noise-induced hearing loss-related tinnitus as an occupational disorder and for financial compensation (final decision, level 4). Directly related to this decision is a determination of the percentage of disability or impairment that may be attributed to this tinnitus component. When, within an exhaustive assessment, those topics for which a patient's assertion can be objectively controlled systematically demonstrate reliability, a reasonable assumption is that those for which such an objective control is impossible are also credible. A variant of Cohen's Kappa for multiple raters demonstrated high interrater consistency at the first level (10 cases, 4 raters). The elderly are characterized by a perturbation at several levels, including the sensorimotor (decreases in muscle mass, increases in the threshold of vibratory sensations) and the cognitive levels (memory processes, attention span) [3]. According to a logistical model, the more a subject's ability overcomes the item's difficulty, the higher the probability is for the subject to achieve a pass rather than a fail score in that item. Our data from this investigation show that in both rotatory and caloric tests, the slow-phase speed is the most important index about function of the vestibular analyzer. These stress-related neuromodulators consist of products derived from three genetically distinct precursor hormones. Hyperacusis has been defined as a collapse of tolerance to sound, often occurring with no significant loss in hearing sensitivity [7,8]. Consistent with what is currently known regarding neuroactive opioid peptides is our view that auditory neural modulation occurs at axodendritic synapses beneath the IHCs and involves (at least in part) the actions of endogenous opioid substances [40].
In addition to modulating the sensation-perception of pain, opioid peptides exert a wide spectrum of physiological-behavioral effects on autonomic function, affect, mood, attention, and physical or psychological stress [62,63]. In postnatal rats, glutamate-sensitive NMDA receptor subtypes have been reported to appear only transiently in the developing cochlea prior to the onset of hearing [105]. The remaining 33% of the modiolar-oriented units (10-15% of the total) are extremely mitochondria-poor, exhibit very low SDRs, and have the highest auditory thresholds of all the type I auditory units. In addition, chronic (prolonged) pain has been attributed to a gradual increase in action potential discharge and excitability in high-threshold spinal cord neurons in response to repeated peripheral stimulation.
Moreover, patients with severe tinnitus report discomfort from intense auditory stimuli, and repeated exposure to such stimuli actually lowers their tolerance to all sounds [125-127].
Though clearly no single drug panacea exists, neuroprotective drug therapy has been proposed also for the alleviation of tinnitus [15,122,123]. As has been emphasized, endogenous opioid peptides play a role in the fine-tuning and filtering of sensory information and are released from neural systems in response to stress [53,57]. Iontophoretic application of the δ-opioid receptor ligand [Met5]-enkephalin produces a naloxone-reversible reduction in excitatory amino acidinduced auditory neural excitation in the guinea pig cochlea.
For example, in the spinal cord (dorsal horn), dynorphins induce an NMDA receptor antagonist-reversible enlargement of neural receptive fields. The excitotoxic and neurotoxic actions of dynorphins at the NMDA receptor arise through a κ-receptor mediated facilitation of NMDA receptor sensitivity to glutamate or to aspartate [114,147].
Therefore different-even oppositeeffects on neural amplitude would be predicted at each progressive increase in stimulus level from auditory neural threshold. Abnormally elevated spontaneous discharge rates within single auditory neurons often are observed when cochlear noise damage is confined to the OHCs [153,154,158]. The result is to advance an affected organism to a heightened state of auditory vigilance [40], which may be adaptive in the short-term when a rapid fight-or-flight response is required. Step 3A: Neural responses to relatively low levels of an auditory stimulus are enhanced [19]. In the rat, however, the medial limb of the LSO contains a large percentage of efferent neurons [179], suggesting that the CGRP-positive neurons observed in the chinchilla may be part of the lateral efferent system of neurons projecting to the cochlea. Presented at the Martha Entenmann Tinnitus Research Center and the State University of New York SUNY Health Sciences Center at Brooklyn. Proved particularly effects for tinnitus tinnitus, Vertigo and hearing loss in the rate of improvement has been proven in tests of the predominately young bees, etc..
The day 22 nutrients since emerging starts and amassed a predominately young bees is of sprout wings. He noted that these currents were in perfect correspondence with the frequency of the applied tone.
At low frequencies (25-63 Hz), the minimal intensity would be 145 dB [13], whereas at frequencies up to 2,500 Hz, the vestibular responses occur only at a sound pressure level (SPL) exceeding 120-160 dB [19]. This was followed 20 minutes later by a test carried out in quiet stance in SOTs I through 4 and with acoustic stimulation in SOT 5 and SOT 6 (Fig. This duration is more than an order of magnitude larger than the total of 120 seconds for which our subjects were exposed during the sequence of two SOTs (5 and 6) repeated three times each. In vestibular dysfunction, the sensory ratio of condition 5 to condition 1 is abnormal, whereas those of the remaining pairs are within the normal range.
This pattern was observed neither in those in group B nor in normal controls, whether stimulated acoustically or not.
None of the patients demonstrated somatosensory or central pathology, except for the "central" pattern exhibited by those in group A during and after exposure to sound, as discussed in the previous paragraph.
As both the lack of visual and support surface inputs and conflicting visual inputs are destabilizing, these patients are more impaired functionally than are those with either vestibular dysfunction or vision preference alone. In the absence of a stable surface, they do not make effective use of either vestibular or visual inputs [33]. Exposure to intense noise in unusual environmental settings (during flying under changing gravitational forces, diving, physical activity in darkness, or night driving) might produce conditions that in certain circumstances could even be life-threatening.
In contrast, patients with normal ENG and abnormal SOT results had clear positive symptoms of vestibular system disorder. By the nature of his trade, he had been constantly exposed to the wail of the ambulance siren for almost two decades, and this had turned his everyday life for the last 7 years into a desperate condition. Capelli, 1929.) Cited by Erlich MA, Lawson W, The incidence and significance of the Tullio phenomenon in man. We assessed 10 exemplary files on which this system was applied by four experts rating independently. The main goals are to reach an optimal consistency among experts in these decisions and to offer optimal transparency in case of litigation.
Gait stability, especially in women, may be compromised in the elderly by the combination of increased body weight and decreased muscle strength [4]. Once a subject's overall ability and the item difficulty are known, individual missing responses can also be estimated (an otherwise arbitrary procedure with raw scores). Hyperacusis is present in approximately 40-86% of those who suffer from disruptive forms of tinnitus; it also can compromise the quality of life in those individuals so afflicted [7-9]. Indeed, considerable evidence indicates that endogenous opioid peptides are found within, and are released from, neural systems that regulate the body 's overall biological response to stress [53,64,65]. Therefore, in many neural systems, opioid receptors are coupled to either the Gi-or Go-protein, wherein the actions of opioid ligands inhibit adenylate cyclase and K+ or Ca++ channels are regulated [61). Such powerful IV μ-receptor agonists as fentanyl and morphine are without effect on the same auditory measures [84-87]. Tn fact, this smaller subset of modiolar-oriented units exhibits thresholds that are 20-80 dB poorer than are the thresholds of the more numerous type I units innervating the IHC pillar side [33,110,111,113]. The windup phenomenon associated with pain depends on NMDA receptor activation in high-threshold neurons [118]. Some suggested pharmacological therapies have included antianxiolytics, antioxidants, antihistamines, antidepressants, anticonvulsants, antiepileptogenics, diuretics, Ca++ channel blockers, dexamethasone, lidocaine, and (of course) glutamate-receptor antagonists [11,12,15].
Emotional or physical stress is known also to induce potent analgesic effects [53,117,136], and "stress-induced analgesia" is likely to involve multiple opioid systems [65,137].
The δ-receptor effect, however, occurs at both NMDA and glutamate-sensitive non-NMDA receptors, though enkephalin appears to exert a stronger inhibitory effect on non-NMDA receptor-induced auditory neural activity [142]. The receptive field enlargement results in a greater number of stimulated neurons and produces hyperalgesia [73,115]. Moreover, the existence of an activity-dependent neuronal plasticity in response to tissue injury has been hypothesi zed to account for the increased sensitivity and spontaneous pain associated with enhanced dorsal horn excitability at NMDA receptors by endogenous dynorphin peptides [114,73].
Normally, OHCs serve to damp activity in unstimulated regions of the cochlear partition, thereby decreasing the auditory sensitivity at (irrelevant) frequencies corresponding to those regions [153,159-161].
Alternatively, spectral anomalies in the ensemble spontaneous discharge associated with tinnitus may be amplified or generated, as illustrated in step 3B.
The second group (B) included 20 neurootological patients without a history of Tullio phenomenon. He also noted that at higher sound intensities, a nystagmus was produced, the frequency of which corresponded to the oscillations of the internal current.
Bearing in mind that acoustic stimuli in unusual environmental conditions always affect both ears, we preferred to employ a binaural stimulation in the attempt to prove the hypothesized correlations in accordance to the hazards of quotidian reality. Thus, the equilibrium scores for condition 5 only, or for conditions 5 and 6, are abnormally low relative to the scores on condition 1. This abnormal pattern is described as occurring in patients with balance disorders secondary to traumatic head injuries but also was reported in other patient populations. The balance functions during exposure to intense noise in such patients tend to be more impaired than in those with vestibular dysfunction, vision preference, or a combination of these pattems. In these patients, disorders were either more central or were presumed to effect peripheral components other than the horizontal semicircular canals (vestibuloocular system). Consequently, these patients continue to seek medical assistance, and their complaints seem to be psychologically aggravated by frustration accumulated through continual visits, referrals, and failing therapy. On the third (quiet) trial, 20 minutes later, his balance recovered completely (composite score, 80) (see Fig.
A variant of Cohen's Kappa for multiple raters demonstrated high interrater consistency at the first level. In this way, the final medicolegal decision relies on standardized criteria and becomes perfectly transparent in cases of litigation.
The improbability of the response of a subject to the various items accumulates, thus providing a measure of improbability of the whole response set. Enkephalin and dynorphin-related peptides exist within the efferent olivocochlear systems (lateral and medial) of several mammalian species, including humans. In a large percentage of those suffering from both phenomena, the debility has been traced to the auditory periphery [10-12]. In addition to the wide range of observed behavioral responses, a wide range of neurophysiological responses also is produced by the binding of endogenous opioid ligands to their receptors.
Opioid receptor activation of the Gi-or the Go-protein has been linked to neural inhibition through an activation of voltage-or Ca++ dependent, inward-rectifying K+ channel conductances or inhibition of voltage-dependent inward Ca++ channel conductances [61,66,70-72].
From these investigations, some have argued that the observed auditory neural changes after IV (-) pentazocine reflect drug actions within the cochlea [79,80,83].
The dendrites of each of these very low SDR-very high threshold units are innervated by 7-32 lateral efferent axons (mean, 20), an amount twice the number of lateral efferent axons terminating on each of the pillar-oriented type I auditory dendrites [33].
Cochlear NMDA receptors also are activated primarily by the presentation of repetitive or relatively intense auditory stimuli [27, 108].
Therefore, an important component of an organism's response to a real or perceived life-threatening emergency is a reduction in responsiveness to pain. Such evidence is consistent with the widely observed inhibitory properties of enkephalins, and indicates that endogenous enkephalins acting through δ-receptors modulate excitatory neural activity at glutamate-sensitive NMDA and non-NMDA receptors in the mammalian cochlea. Finally, the κ-receptor antagonist norbinaltorphimine has been found to be a potent antagonist of NMDA receptor activity, and a neuroprotective role has been suggested for this agent in the treatment of NMDA-induced convulsions and neurotoxicity [144, 149].
This property of OHCs contributes greatly to the sharp tuning of the cochlear partition [161-164]. In other words, that are about this ????? 21 mark proves you use a high-quality bee kid Chu. Sounds reaching the ear of the animal produced a current in the open canal, also affecting all three semicircular canals simultaneously.
In the latter two tests, subjects had only the vestibular system at their disposal (with inputs from other sensory systems canceled or inaccurate). The functional impact of this pattern dwells in the necessity of either a stable support surface or stable visual field to maintain balance. Indeed, one of our two patients with this disequilibrium pattern mentioned a head injury incurred several years prior to the current investigation (in addition to the NIHL from which he was suffering and for which he was selected).
Preferably, this should be carried out by means of CDP with acoustical stimulation for an objective corroboration of their complaint before continuing activity in a noisy environment, thus preventing dangerous loss of balance when exposed to noise. We deem the description of a typical case of TP pedagogically rewarding and suggestive of the problem and therefore appropriate.
The same holds true for the improbability of the response achieved by a given item from various subjects.
Prodynorphin derivatives, however, may be restricted exclusively to lateral efferent neurons. For instance, in one investigation, hyperacusis was shown to involve the peripheral auditory system in 59% of cases [6]. This finding is suggested by (-) pentazocine's relatively high tissue solubility [88] and relatively low molecular weight [89,90], factors that should permit an easy passage of (-) pentazocine across the blood-labyrinthine barrier.
This anatomical array suggests that the lateral efferent system exerts relatively more influence on type I auditory neurons characterized by very low rates of spontaneous discharge and very high thresholds. NMDA receptor-linked and non-NMDA receptor-linked neurotoxic effects of glutamate or aspartate have been implicated also in a number of severe pathophysiological neurodegenerative disorders [119-121], in auditory neural excitotoxicity [15], in acute ischemia of radial auditory dendrites [27,109] and, of course, in tinnitus [10,11,15,101,122,123].
As indicated, cochlear NMDA receptors appear to be restricted to the much higher threshold, modiolar-oriented type I auditory dendrites [109]. Though such evidence argues that glutamate activation of cochlear NMDA receptors plays a substantial role in inner ear neuroexcitotoxicity and in the etiology, maintenance, or exacerbation of peripheral neural generators of tinnitus, what has become clear also is that stress-related events are more powerful triggers for tinnitus than are strictly auditory-related events [6,7,15,16]. This reaction creates little diffi-culty in envIsioning that in meeting the behavioral demands prompted by such exposure, an animal's normal reactions to pain could prove deleterious [117]. Also fairly likely is that such effects normally are initiated via the lateral efferent system.
Such evidence, taken together with more recent data [19], is consistent with the widely observed excitatory properties of dynorphins, further suggesting the possibility that endogenous dynorphins, acting through κ-receptors, facilitate the excitatory neural actions of glutamate in the inner ear. One popular theory [157,165] is that damaged or dysfunctional OHCs decouple from the tectorial membrane, owing to a loss in their hydrostatic pressure [166] or to stereocilia damage [153]. Effects of electrical stimulation of efferent olivocochlear neurons on cat auditory-nerve fibers: III.
A pure-tone stimulus of I,000 Hz at 110 dB was delivered binaurally for 20 seconds during condition 5 and condition 6 of the CDP sensory organization test.
However, the current was predominant and the cristae more easily displaced in the fenestrated canal, accounting for visible movements only in the plane of this canal.
The sensory analysis of the second patient showed mainly vestibular dysfunction and only a borderline visual preference abnormality. In this way, the final medicolegal decision relies on standardized criteria and becomes perfectly transparent. Rasch analysis of the first release of the FRI allowed us to prepare a definitive version of the FRI (Table 1). Descending lateral efferent axons terminate solely on primary (type I) auditory dendrites innervating cochlear inner hair cells in most species. Furthermore, both auditory phenomena are associated with or are induced or exacerbated by physical fatigue or psychological stress [2,6,13-16]. Naloxone Hel (Narcan), the antagonist drug of choice for opioid intoxication, also is known to pass easily through blood-endothelial barriers [59].
Finally, sodium salicylate, well-known for its anti nociceptive properties and its capacity to produce transient tinnitus, also increases intercellular Ca++ levels in neurons [125] and in cochlear outer hair cells (OHCs) [129]. Consequently, during threatening conditions, reactions to pain would be suppressed in favor of more adaptive behaviors, enabling an organism to escape or defend itself (fight or flight).
The corresponding loss in their normal damping properties leads to an increased production of thermal noise within specified regions of the cochlear partition. The sequence of six sensory organization conditions was performed three times with two intermissions of 15-20 minutes between the trials.
From the different reactions that Tullio observed by stimulating the ears of animals, he proposed that perhaps this was to become a potential diagnostic tool with which one could recognize the seat and nature of lesions in the different parts of the labyrinth. The latter is described in the literature as accountable to, among other causes, a declining performance caused by fatigue or by exacerbation of the patient's symptoms during repeated trials [29].
This action indicates that they play an important role in modulating auditory nerve sensitivity and spontaneous discharge. An association has been drawn also between clinical depression (dysphoria) and severe forms of tinnitus, with an incidence reported as high as 60-80% [16-18].
Alternatively, the observed auditory neural changes subsequent to IV administration of (-) pentazocine or naloxone may have been, at least in part, an indirect reflection of the actions of both drugs in the brainstem, leading to the subsequent release-suppression of dynorphins, or of some other neurotransmitter-modulator at the lateral efferent-type I auditory synapse.
Perhaps more important, however, was the recent demonstration that sodium salicylate potentiates the excitatory effects of glutamate at NMDA receptors in the mammalian inner ear [20], an action consistent with the observations and conclusions made by previous tinnitus investigators [3,130,131]. This added shift in the neural discharge spectra then is interpreted erroneously by the central auditory system as a genuine signal [3,4]. In a fashion similar to that exhibited by the observed excitatory mechanism of action of dynorphins in the spinal cord, sodium salicylate (aspirin) recently was shown to facilitate the excitatory effects of glutamate in the cochlea. As discussed later, opioid κ-receptor ligands administered into the cochlea have been observed to alter auditory neural sensitivity to low-intensity sounds [19]. Whether and to what extent such effects occurred from indirect drug actions in the brainstem or from direct actions in the cochlea cannot be evaluated at present. This was followed 20 minutes by a trial carried out in quiet stance in sensory organizations tests (SOTs) I through 4, and with acoustic stimulation in SOT 5 and SOT 6. This article provides support for a neurochemical model in which endogenous dynorphins may induce hyperacusis and can contribute to the induction, maintenance, or exacerbation of tinnitus in the auditory periphery by altering auditory type I neural excitability to glutamate. In a fashion similar to that of the reported effects of dynorphins in the spinal cord, sodium salicylate recently was shown to facilitate the excitatory effects of glutamate in the cochlea [20]. Still unknown is whether κ-receptors exist in the chinchilla brainstem and whether IV (-) pentazocine effects are eliminated in animals, maintaining ablations to the lateral efferent pathways. Furthermore, salicylate produces tinnitus concomitant with quantifiable spectral alterations in the "ensemble spontaneous discharge activity" of the auditory nerve [4,5,21]. Our position is that endogenous dynorphin peptides are liberated into the inner hair cell (IHC) synaptic region by the lateral efferent olivocochlear system. These neuroactive substances then interact with nearby excitatory neurotransmitter receptors, producing quantifiable alterations in stimulus-evoked and spontaneous auditory neural activity.
During periods of physical or emotional stress, this interaction may be especially pertinent. Furthermore, this hypothesized association may not be restricted only to tinnitus generated at the level of the auditory periphery.

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