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R H Nodar

Publications and source records attributed to R H Nodar.

At least 19 recordsLinked to original sources
PubMed2001

A biochemical model of peripheral tinnitus.

Subjective tinnitus may be defined as the perceptual correlate of altered spontaneous neural activity occurring in the absence of an externally evoking auditory stimulus. Tinnitus can be caused or exacerbated by one or more of five forms of stress. We propose and provide evidence supporting a model that explains, but is not limited to, peripheral (cochlear) tinnitus. In this model, naturally occurring opioid dynorphins are released from lateral efferent axons into the synaptic region beneath the cochlear inner hair cells during stressful episodes. In the presence of dynorphins, the excitatory neurotransmitter glutamate, released by inner hair cells in response to stimuli or (spontaneously) in silence, is enhanced at cochlear N-methyl-D-aspartate (NMDA) receptors. This results in altered neural excitability and/or an altered discharge spectrum in (modiolar-oriented) type I neurons normally characterized by low rates of spontaneous discharge and relatively poor thresholds. It is also possible that chronic exposure to dynorphins leads to auditory neural excitotoxicity via the same receptor mechanism. Finally, the proposed excitatory interactions of dynorphins and glutamate at NMDA receptors need not be restricted to the auditory periphery.

Animals↗
PubMed1999

Endogenous dynorphins: possible role in peripheral tinnitus.

Tinnitus has been defined as the perceptual correlate of altered spontaneous neural activity occurring without an external auditory stimulus. Hyperacusis, defined as a collapse of tolerance to sound, is present in 40-86% of those who suffer from disabling forms of tinnitus. Both phenomena often are induced or exacerbated by physical or psychological stress. Biological systems known to regulate the body's overall response to stress use and release endogenous neuroactive opioid peptides. These stress-related neuromodulators consist of products derived from three genetically distinct precursor hormones. Two of these precursor hormones are proenkephalin and prodynorphin. Enkephalin and dynorphin-related peptides exist within the efferent olivocochlear systems (lateral and medial) of several mammalian species, including humans. Prodynorphin derivatives, however, may be restricted exclusively to lateral efferent neurons. Descending lateral efferent axons terminate solely on primary (type I) auditory dendrites innervating cochlear inner hair cells in most species. This action indicates that they play an important role in modulating auditory nerve sensitivity and spontaneous discharge. 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. 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.

Cochlea↗
PubMed1996

Tinnitus reclassified; new oil in an old lamp.

This article represents a compilation of study, research, and patient care during a 30-year period. Its development was based on two tenets: (1) keep it simple and (2) be inclusive. The purpose of the classification system was to provide professionals with a vehicle for describing tinnitus and its location, probable cause, loudness, degree of annoyance, and pitch. The system uses two mnemonics to follow the word tinnitus: (1) A, B, or C for tinnitus Aurium, Binaural, or Cerebri; and C-CLAP for Cause, Composition, Loudness, Annoyance, and Pitch. Four descriptions are presented on how this classification system may be used in the clinician's report.

Abbreviations as Topic↗
PubMed1996

Naloxone blockade of (-)pentazocine-induced changes in auditory function.

OBJECTIVE: In a previous report, we found that intravenous (i.v.) (-)pentazocine improved auditory sensitivity and significantly altered compound action potential (CAP) amplitudes. Its sigma (sigma)-receptor-selective optical isomer (+)pentazocine administered at the same dose was without effect, suggesting that the observed auditory neural effects might be mediated by an opioid receptor. To directly test this hypothesis, in the present investigation we attempted to antagonize the auditory neural effects of (-)pentazocine using the pure, nonspecific drug antagonist naloxone. DESIGN: In 25 normal-hearing, male, pigmented chinchillas, amplitude and latency changes in the click-evoked auditory nerve CAP (N1) and cochlear microphonic (CM) were tracked at six stimulus intensities during a baseline period and after the postbaseline administration of the opioid drug agonist (-)pentazocine (16 mg/kg; i.v.). In separate groups of chinchillas, (-)pentazocine was given alone or administered in combination with the standard opioid receptor antagonist naloxone administered at two doses. RESULTS: Robust changes in CAP amplitudes after (-)pentazocine occurred in the absence of measurable alterations in CAP response latencies, CM amplitudes, or blood chemistries and were significantly antagonized when naloxone (5 mg/kg) was added to the i.v. infusion. CONCLUSIONS: The observed blockade clearly indicates that the agonist effects of (-)pentazocine are opioid receptor-mediated and suggests a connection between opioid receptors and auditory neural function. Mechanisms of action and the connection between an opioid modulation of auditory function and stress, hyperacusis, and tinnitus are discussed.

Animals↗
PubMed1996

Blockade of opioid-induced changes in auditory function at the level of the cochlea.

OBJECTIVE: We have previously investigated the auditory neural effects of the kappa-opioid receptor agonist, (-)pentazocine. When administered intravenously (i.v.), this drug temporarily alters auditory nerve compound action potential (CAP) amplitudes. To test the hypothesis that the observed neural effects of i.v. (-)pentazocine occur via kappa-receptor interactions within the cochlea, we attempted to block these effects by employing a specific kappa-opioid receptor antagonist applied directly to the cochlear round window (RW) membrane. DESIGN: In 31 normal-hearing, male pigmented chinchillas, amplitude changes in the click-evoked auditory CAP (N1) were tracked at six stimulus intensities during a baseline and a postbaseline period in which i.v. (-)pentazocine (8 mg/kg) was administered. (-)Pentazocine administration was preceded by the delivery to the cochlear RW membrane of an artificial perilymph solution given alone or containing the kappa-opioid receptor selective antagonist, norbinaltorphimine (Nor-BNI), which was administered at two concentrations in separate groups of animals. RESULTS: The amplitude increase in the CAP after (-)pentazocine was significantly reduced when i.v. (-)pentazocine was preceded by RW-administered Nor-BNI (4 mM). CONCLUSIONS: The reversibility of agonist effects by Nor-BNI indicates direct or indirect opioid kappa-receptor-mediated auditory neural effects at the level of the cochlea and suggests a connection between kappa-receptors and auditory neural function.

Animals↗
PubMed1996

Hearing and Sjögren's syndrome.

Immune sensorineural hearing loss is manifested in several systemic immune diseases. Although hearing loss has been previously documented in patients with Sjögren's syndrome (SS), the effect of SS on hearing is unclear. This prospective study was designed to assess the presence of hearing loss in 14 patients with SS and, if sensorineural hearing loss was present, to determine if the hearing loss was immune-mediated. Patients were evaluated with basic audiologic tests as well as for cellular immune inner ear reactivity as measured by the lymphocyte transformation test (LTT). Three patients had evidence of sensorineural hearing loss. Two patients had a positive LTT without evidence of sensorineural hearing loss. This preliminary study suggests that SS may not directly cause sensorineural hearing loss, immuno-mediated or otherwise.

Adult↗
PubMed1994

Improvement in auditory function following pentazocine suggests a role for dynorphins in auditory sensitivity.

The pharmacologic specificity of potentially beneficial drug effects on the auditory system were investigated. Changes in auditory sensitivity were evaluated in chinchillas following the infusion of an opioid narcotic. This drug (pentazocine) mimics endogenous opioid peptides (dynorphins), postulated to be chemical neurotransmitters (or neuromodulators) within the mammalian cochlea. In this study, two pentazocine enantiomers were investigated over a range of stimulus intensities. Significant baseline-relative changes in compound action potential (CAP) amplitudes were observed following intravenous administration of the kappa-opioid agonist (-)pentazocine (8 mg/kg). The sigma-receptor drug agonist (+)pentazocine (8 mg/kg) produced no measurable auditory effects. The magnitude of the (-)pentazocine effects were inversely related to stimulus intensity, up to 10 dB above threshold (i.e., 10 dB SL). Consistent with the observed amplitude doubling, auditory sensitivity was also improved an average 5-7 dB sound pressure level (SPL) following the administration of (-)pentazocine, while CAP response latencies and cochlear microphonic (CM) amplitudes remained unchanged. Results indicate stereospecific kappa-receptor mediated actions of pentazocine at the auditory nerve, and suggest an auditory role for neuroactive dynorphin peptides contained within the lateral efferent olivocochlear neurons.

Animals↗
PubMed1988

Long-term histologic study of a new carbon-carbon ossicular replacement prosthesis.

In a variety of structural forms, carbon possesses certain properties that render it suitable for implantation in the human body. This report analyzes biocompatibility of a new carbon-carbon prosthesis following long-term middle ear implantation in a prospective, controlled animal study. The prosthesis was placed in the left ear of 20 healthy guinea pigs and in the dorsal subcutaneous tissues for control. The right ear also served as control. Preoperative and postoperative auditory evoked potentials were recorded and compared. Samples of tissue from all three sites were evaluated at 3 and 6 months by light microscopy. The implants also were evaluated by scanning electron microscopy. Samples of lymph nodes, liver, spleen, and lungs also were examined. Fourteen animals (70%) demonstrated no change in auditory evoked potentials postoperatively. One animal developed unilateral dysfunction and three others developed bilateral dysfunction for unexplained reasons. No significant tissue destruction or inflammation of the tissues and no digestion or erosion of the implants were observed. No passage of carbon particles into the reticuloendothelial system was identified. These preliminary results suggest that this new carbon-carbon prosthesis may be biocompatible at 6 months follow-up in the guinea pig and encourage further investigation.

Animals↗
PubMed1983

Hearing loss in multiple sclerosis.

Hearing loss in an uncommon symptom in multiple sclerosis (MS). In nine patients with MS, seven with unilateral hearing loss and two with bilateral impairment, accompanying symptoms and signs included facial numbness, hemifacial paresis or spasms, ipsilateral limb ataxia, nystagmus, vertigo, tinnitus, and spastic-ataxic gait. Central auditory dysfunction was suggested by audiometric findings and/or by brainstem auditory evoked potentials in all nine patients. Clinical improvement in two was accompanied by return toward normal in the results of audiometric or electrophysiologic studies. Hearing impairment should be sought in patients with MS and appropriate studies pursued.

Adult↗
PubMed1983

Analysis of test-retest variability in facial electroneurography.

Facial electroneurography is an objective electrophysiologic measurement of a muscle compound action potential used to assess prognosis for recovery from facial paralysis. In the present study, test precision is accompanied by a test-retest variability of 6.2%. The primary source of this variability is trigeminal nerve artifact, but submaximal nerve stimulation, changing skin resistance, and inherent nerve properties may also influence results. An ideal stimulus intensity that avoids patient discomfort and trigeminal nerve artifact but attains maximal nerve response is not possible in every patient.

Action Potentials↗
PubMed1982

Brainstem dysfunction in the infant apnea syndrome.

Thirty-six infants identified as infant apnea syndrome (IAS) and 25 controls with a comparable age distribution were evaluated with Brainstem Auditory Evoked Potential (BAEP) testing. There was a significant predilection for leftsided BAEP abnormalities in IAS patients. Fifteen IAS patients had bilateral abnormalities, and of the 21 IAS patients with unilateral abnormalities, 17 had abnormalities on the left side (p less than 0.01 by McNemar's test). Significant differences (p less than 0.05 by analysis of covariance adjusting for age) between normal controls and IAS infants were found for peak latencies I, III, and V, and amplitude III. Linear regression analyses of the above parameters versus age in months for normal controls were constructed with 68% and 95% prediction interval bands to permit analysis of individual data points. Data points from the IAS infants with bilateral BAEP abnormalities have been plotted on these linear regression curves. No single measurement of latency or amplitude is abnormal in the majority of IAS infants, but many of the individual points fall outside of the 95% prediction curve.

Brain Stem↗
PubMed1980

Brain stem auditory evoked potentials in determining site of lesion of brain stem gliomas in children.

Brain stem auditory evoked potential (BAEP) test results are reported on seven children (2 1/2-13 years) with brain stem neoplasms. In each case, the BAEP test results clearly indicated the site of lesion as determined by computerized tomography and observation during surgery. Seven criteria for the assessment of BAEP test results are also presented: 1. Peak latency, 2. Intra-peak latency, 3. Inter-peak latency, 4. Response stability, 5. Amplitude, 6. Waveshape, and 7. Peak presence. Six children had positive indications on at least four of the seven criteria described, while one child had two positive indications. However, dramatic abnormality on any single criterion warrants serious investigation.

Adolescent↗
PubMed1980

The contralateral effects of large tumors on brain stem auditory evoked potentials.

Brain stem auditory evoked potential (BAEP) testing has been demonstrated to be a useful diagnostic tool in the presence of severe or complete sensorineural hearing loss. From a series of 38 patients with tumors in the vicinity of the VIIIth nerve, 13 patients with tumors larger than 2 cm had abnormal BAEP results contralateral to the involved side. The abnormalities observed on the noninvolved side included prolonged peak latencies, reduced amplitudes, poor wave shape and poor response stability. The significance of these findings is twofold: 1. Large tumors may disrupt BAEP test results on the side contralateral to the lesions, 2. Important information may be obtained on patients having complete sensorineural hearing loss on the involved side.

Adult↗