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PubMed2004

Acute endolymphatic hydrops generated by exposure of the ear to nontraumatic low-frequency tones.

Low-frequency sounds presented at high nontraumatizing levels induce temporary hyperacusis in humans and animals. One explanation of this finding is that the basilar membrane operating point may be disturbed by an endolymph volume change. This possibility was investigated using volume and flow markers iontophoresed into the endolymphatic space of guinea pigs. Marker concentrations were measured with ion-selective microelectrodes placed apically and basally to the iontophoresis site during exposure of the ear to low-frequency tones. Concentration changes were interpreted quantitatively using a finite-element model of the endolymphatic space that allowed changes of endolymph cross-sectional area and flow to be derived. Stimulation with a 200 Hz tone at 115 dB SPL for 3 min produced marker concentration changes consistent with the induction of transient endolymphatic hydrops and a basally directed displacement of endolymph. Endocochlear potentials were greater than normal after the exposure when hydrops was present. During identical tone exposures of animals without marker, we found that action potential (AP) threshold changes and endolymph potassium changes associated with the hydropic state were small. Marker concentration changes were compared with changes in endocochlear potential and AP thresholds for a range of exposure frequencies and levels. AP hypersensitivity occurred with 200 Hz exposure levels below those inducing endolymph volume disturbances. Endolymph volume changes are thought to be the result of, rather than the cause of, changes in operating point of the cochlear transducer. The observations that auditory threshold and endolymph potassium changes are minimal under conditions where substantial endolymphatic hydrops is present is relevant to our understanding of the hearing loss in patients with Meniere's disease.

Acute Disease↗
PubMed1984

Benzodiazepine dependence.

Dependence to benzodiazepines is difficult to induce in animals but has been induced by high doses in man. Case reports of benzodiazepine dependence are rare compared with the usage of these drugs, but provide no proper epidemiological framework for the estimation of risk. Patients taking these drugs for four months or more may develop symptoms on withdrawal, characterized by anxiety, dysphoria, malaise, depersonalization, and by perceptual changes such as hyperacusis and unsteadiness. In our first study we compared four patients withdrawing from high doses of benzodiazepines with six patients withdrawing from therapeutic doses. In all patients the typical withdrawal syndrome was noted and was equal in intensity in both groups. In the second study, long-term, normal-dose benzodiazepine treatment was discontinued in 24 patients believed to be dependent on their medication. The withdrawal was gradual, placebo-controlled and double-blind. All experienced some form of withdrawal reaction, which ranged from anxiety and dysphoria to moderate affective and perceptual changes. Symptom ratings rose as the drugs were discontinued, but usually subsided to pre-withdrawal levels over the next two to four weeks. Electroencephalograhic (EEG) changes comprised marked reduction in fast-wave activity as the drugs were withdrawn, and an improvement in psychological performance was noted. It is concluded that a risk of dependencies present in all patients taking benzodiazepines even in therapeutic doses for more than a few months. Caution is urged in the prescribing of these drugs.

Animals↗
PubMedDate not supplied

Tay-Sachs disease: B1 variant.

This first child of non-Jewish parents had nystagmus at 4 months of age, bilateral cherry-red macular spots at 7 months of age, and hyperacusis at 8 months of age; the patient has deteriorated progressively following a clinical course typical of Tay-Sachs disease B variant. Total beta-N-acetylhexosaminidase assayed with 4-methylumbelliferyl-beta-glucosamine (4 MU GlcNAc) as substrate was within the normal range in plasma and cultured dermal fibroblasts and 2/3 the normal mean in leukocytes. The hexosaminidase A activity, assayed with the same substrate in plasma and cultured fibroblasts, approximated Tay-Sachs disease heterozygote levels; however, the activity of hexosaminidase A assayed with 4 MU Glc NAc-6-sulfate in the plasma, leukocytes, and cultured fibroblasts was less than 8, 2, and 1%, respectively of the control mean. This female infant with the B1 variant of Tay-Sachs disease demonstrated an earlier onset and more rapidly progressive course than was observed in 4 of the 5 previously reported patients with this Tay-Sachs disease variant.

Female↗
PubMed1996

Acephalgic migraines of childhood.

Migraine aura without headache (acephalgic migraines) is a recognized subset of migrainous phenomena in the adult population. No reports of its prevalence or characteristics in a series of children exists. Using diagnostic criteria for migraine aura without headache established by the International Headache Society, a retrospective review of a computerized database of all patients referred over a 4-year period (July 1991 to June 1995 inclusive) to a single university-based pediatric neurologist was performed. Fourteen patients were identified, representing 2% of all patients with a primary diagnosis of migraine. Nine were females and 13 had a strong family history of migraines. Age of onset of symptoms ranged from 5 to 12 years with a mean of 8 years. Symptoms were episodic in all, varying in frequency from weekly to more typically monthly, lasting generally less than 10 min. In 9 patients the aura described was that of often colorful photopsias or scintillating scotomas. Two had micropsia, one had temporal distortion (time "speeded up"), one had hyperacusis, and the final patient had a vague sense of disconnection from her surroundings. Only 2 patients had a headache occasionally associated with the described aura. In addition to the acephalgic migraines, 9 patients had either common or classical migraines, the latter typically featuring aura distinct from those observed in these patients' acephalgic episodes. Neurologic examination, electrophysiologic investigation (EEG/evoked potentials), and neuroimaging were noncontributory in all instances. Migraine aura without headache is a recognizable benign migraine syndrome of late childhood.

Child↗
PubMed1994

Anxiolytic drugs: dependence, addiction and abuse.

The concepts of dependence, addiction and abuse comprise overlapping clinical phenomena. The earlier anxiolytic drugs, in particular the barbiturates, were prone to abuse, i.e., non-medical use, and to high-dose misuse. Their modern counterparts, the benzodiazepines, are abused in a patchy way and are sometimes taken in regularly high doses. However, the main problem is physical dependence as manifested by a withdrawal syndrome on discontinuation of the drug. The withdrawal syndrome has been carefully described and comprises physical and psychological features. In particular, perceptual symptoms such as photophobia, hyperacusis and feelings of unsteadiness may predominate. The syndrome may come on during dosage reduction but generally starts 2-10 days after cessation of the benzodiazepine, depending on its elimination half-life. About a third of long-term users suffer a recognisable syndrome even after a tapered withdrawal, its duration usually being only a few weeks. A few patients go on to a prolonged withdrawal syndrome, often characterised by muscular spasm. The treatment of the withdrawal syndrome is supportive and non-specific. A few patients started on benzodiazepine therapy escalate the dose. They tend to show the characteristic 'passive-dependent' personality features and may previously have misused other CNS depressants such as the barbiturates and alcohol. Abuse of benzodiazepines occurs in a rather varied way from country to country. Worldwide, flunitrazepam has caused concern but, in the UK, the main problem has been the intravenous use of temazepam. The molecular pharmacology of the benzodiazepine receptor has been extensively studied and is undoubtedly complex.(ABSTRACT TRUNCATED AT 250 WORDS)

Anti-Anxiety Agents↗
PubMed2005

Does sound stimulation have additive effects on cognitive-behavioral treatment of chronic tinnitus?

Psychological and physiological habituation are major goals in the treatment of patients suffering from chronic tinnitus. This study evaluates whether sound stimulation provided by use of low level white noise generators (NG) enhances the effects of cognitive-behavioral treatment (CBT). 124 outpatients with tinnitus of >6 months received manualized group treatment and were randomly assigned to the NG/no NG conditions. Those with moderate tinnitus-related distress obtained four sessions focusing on education, while severely distressed subjects were treated according to a full 10-session CBT program. Outcome was assessed at post-treatment and at 6- and 18-month follow-up. No additive effects due to the NGs could be demonstrated. All groups improved significantly on measures of tinnitus-related distress, dysfunctional cognitions, general psychopathology, depression, hypochondriasis and psychosocial functioning. Beneficial effects of the NGs were only observed for patients with concurrent tinnitus and hyperacusis. As systematic physical stimulation of the auditory system does not further improve the effects of CBT, the importance and strength of psychological interventions are emphasized. The clinical relevance of recently developed "retraining" approaches accentuating physical stimulation should be reconsidered.

Acoustic Stimulation↗
PubMed2006

Death following tonsillectomy in a child with Williams syndrome.

Williams syndrome (WS) is an uncommon genetic syndrome due to a deletion of several genes on chromosome 7. The syndrome is associated with dysmorphic facies, neurological manifestations, idiopathic hypercalcemia, and cardiac abnormalities, particularly supravalvular aortic stenosis (SVAS). Children with Williams syndrome may have chronic serous otitis media and/or obstructive sleep apnea. Hyperacusis is also commonly seen in these children. We report a case of sudden death at the time of tonsillectomy/adenoidectomy and bilateral tympanostomy tube placement in a child with Williams syndrome. All children with Williams syndrome should have a thorough cardiac evaluation before undergoing general anesthesia for any otolaryngologic procedure.

Adenoidectomy↗
PubMed2005

Noise-induced cell death in the mouse medial geniculate body and primary auditory cortex.

Noise-induced effects within the inner ear have been well investigated for several years. However, this peripheral damage cannot fully explain the audiological symptoms in noise-induced hearing loss (NIHL), e.g. tinnitus, recruitment, reduced speech intelligibility, hyperacusis. There are few reports on central noise effects. Noise can induce an apoptosis of neuronal tissue within the lower auditory pathway. Higher auditory structures (e.g. medial geniculate body, auditory cortex) are characterized by metabolic changes after noise exposure. However, little is known about the microstructural changes of the higher auditory pathway after noise exposure. The present paper was therefore aimed at investigating the cell density in the medial geniculate body (MGB) and the primary auditory cortex (AI) after noise exposure. Normal hearing mice were exposed to noise (10 kHz center frequency at 115 dB SPL for 3 h) at the age of 21 days under anesthesia (Ketamin/Rompun, 10:1). After 1 week, auditory brainstem response recordings (ABR) were performed in noise exposed and normal hearing animals. After fixation, the brain was microdissected and stained (Kluever-Barrera). The cell density in the MGB subdivisions and the AI were determined by counting the cells within a grid. Noise-exposed animals showed a significant ABR threshold shift over the whole frequency range. Cell density was significantly reduced in all subdivisions of the MGB and in layers IV-VI of AI. The present findings demonstrate a significant noise-induced change of the neuronal cytoarchitecture in central key areas of auditory processing. These changes could contribute to the complex psychoacoustic symptoms after NIHL.

Acoustic Stimulation↗
PubMed2004

TFII-I, a candidate gene for Williams syndrome cognitive profile: parallels between regional expression in mouse brain and human phenotype.

The gene for TFII-I, a widely expressed transcription factor, has been localized to an interval of human chromosome 7q11.23 that is commonly deleted in Williams syndrome (WS). The clinical phenotype of WS includes elfin facies, infantile hypercalcemia, supravalvular aortic stenosis, hyperacusis and mental retardation. The WS cognitive profile (WSCP) is notable for the differential impairment of visual-spatial abilities with relative sparing of verbal-linguistic function. Fine mapping of individuals with WS has revealed a close association between deletion of TFII-I and the WSCP. To determine the plausibility of the hypothesis that hemizygous deletion of TFII-I contributes to the WSCP, we have examined the anatomic distribution of TFII-I RNA and protein isoforms in brains from adult and embryonic mice. Our studies show that early in development, TFII-I expression is widespread and nearly uniform throughout the brain. In adult brain, TFII-I protein is present exclusively in neurons. Highest levels of expression are observed in cerebellar Purkinje cells and in hippocampal interneurons. TFII-I immunoreactivity is distinct from that of the related protein, TFII-IRD1, which is also localized to the region of human chromosome 7 deleted in WS. The expression pattern of TFII-I in mouse brain parallels regions in human brain which have been shown to be anatomically and functionally altered in humans with WS. These observations are consistent with the hypothesis that deletion of the gene for TFII-I contributes to the cognitive impairments observed in WS.

Animals↗
PubMed2005

[Physiopathological mechanisms in tinnitus generation and persistence].

Progress in neuroscience research has given birth to new theories for tinnitus generation. From a point of view where cochlear dysfunctions would be considered as the origin and maintenance mechanisms, it has been introduced the important role of compensation systems from the central auditory pathways. They could act as the most relevant factor for chronic persistent tinnitus after a peripheral aggression. Unmasking of silent synapses or sprouting of new ones activate cortical reorganization for frecuencial areas nearby the non-stimulated ones through brain plasticity. Connections to associative cortex and limbic-amigdala area using the non-classical auditory system explain the presence of hyperacusis, anxiety or depression, factors that increase the severity of tinnitus. Implementation of these physiopathological theories reinforces the tinnitus neurophysiological model. The development of an aversive response through the survival reflex and the participation of negative emotional response are the responsible for signal persistence and vegetative reactions from the autonomous nervous system. Implications of this knowledge for tinnitus treatment involve the central auditory system approach through the combination of medical counselling for reduction of the aversive reaction and sound therapy to diminish its perception.

Cochlea↗
PubMed2003

Pathophysiology of tinnitus.

Tinnitus is not a single entity but a rather diverse group of disorders. Despite symptoms that indicate the ear is the site of the pathology, there is strong evidence that most forms of severe tinnitus are caused by functional changes in the central nervous system. The changes are induced through expression of neural plasticity, some of which may have been caused initially by abnormalities in the ear or the auditory nerve. The involvement of the nonclassical ascending auditory pathway with its subcortical connections to limbic structures (the amygdala) may explain some of the symptoms of some forms of tinnitus including hyperacusis and affective disorders, such as phonophobia and depression, which often accompany severe tinnitus.

Auditory Pathways↗
PubMed2006

Neural plasticity in tinnitus.

Two distinctly different kinds of tinnitus occur: objective and subjective tinnitus. Objective tinnitus is caused by sounds generated in the body while subjective tinnitus is caused by abnormal neural activity that is not evoked by sound. This chapter discusses subjective tinnitus. Subjective tinnitus has many forms. In most forms of tinnitus the anatomical location of the physiological abnormality is in the central nervous system, although the sensation is often referred to one ear or both ears. The cause of most forms of subjective tinnitus is the changes that have occurred as a result of expression of neural plasticity, thus a form of reprogramming of the brain that is not to the benefit of the individual person. Tinnitus often occurs together with hearing loss, indicating that the expression of neural plasticity has been evoked by deprivation of input. Tinnitus is often accompanied by hyperacusis, and sometimes phonophobia and depression, indicating altered processing of auditory information or rerouting of information. Several studies have brought evidence that some forms of tinnitus are associated with an abnormal involvement of the nonclassical (extralemniscal, diffuse, or polysensory) auditory pathways that bypass the primary auditory cerebral cortex and provide subcortical connections to limbic structures among others. There is no general treatment for tinnitus, but there are several treatments that can alleviate or reduce the tinnitus in some patients.

Humans↗
PubMed2002

Bilateral cholesteatoma and habitual sniffing.

OBJECTIVE: To examine the clinical findings of acquired bilateral cholesteatoma with special reference to incidence of habitual sniffing and sniff-related negative middle ear pressure. METHODS: Eighty-eight fresh cases of unilateral cholesteatoma and 33 fresh cases of bilateral cholesteatoma, which were operated on at Department of Otolaryngology, Hyogo College of Medicine, were examined in this study. Responses to a detailed questionnaire were obtained from the patients concerning about the habit of habitual sniffing to relieve aural symptoms such as aural fullness, autophonia or hyperacusis. The same questionnaire was obtained from unilateral cholesteatoma patients to compare the incidence of habitual sniffing with that of patients with bilateral cholesteatoma. We measured the negative middle ear pressure at the time of sniffing by using TTAG (tubo-tympano aerodynamic graphy, Nagashima Co. Ltd, Tokyo). We also compared the positive percentage of the sniff test in bilateral cholesteatoma with in unilateral cholesteatoma and normal controls. Sniff test was performed in 30 patients with bilateral cholesteatoma, 20 patients with unilateral cholesteatoma and 20 normal controls. RESULTS: In 33 patients with bilateral cholesteatoma (66 ears), 57 ears had the pars flaccida type (86.4%) and 9 ears had the pars tensa type (13.6%). Cholesteatoma of pars flaccida type were predominant in bilateral cholesteatoma. The rate of habitual sniffing of bilateral cholesteatoma (23/33, 69.7%) was significantly higher than that of unilateral cholesteatoma (21/88, 23.9%). The incidence of positive sniff test in bilateral cholesteatoma (19/30, 63.3%) was significantly higher than in unilateral one (6/20, 30%) and normal control (3/20, 15%). CONCLUSIONS: Habitual sniffing was closely related to the pathogenesis of bilateral cholesteatoma, especially in cases with bilateral pars flaccida type.

Adolescent↗
PubMed1990

Audiological manifestations of Ramsay Hunt syndrome.

Ramsay Hunt syndrome is known to cause audiological signs and symptoms, including sudden, unexpected hearing loss. We carried out a retrospective review of the audiological manifestations of 186 patients with Ramsay Hunt syndrome, measuring their hearing loss patterns, hyperacusis, tinnitus, herpetic rash, facial paralysis, pain and vertigo. Statistical correlations of these parameters were equated with prognosis. Prognosis for eventual hearing recovery is, in general, excellent. Prognostic indicators of poor hearing recovery include advanced age, retrocochlear hearing loss, male gender, vertigo, and speech frequency hearing loss.

Adolescent↗
PubMedDate not supplied

Lyme borreliosis and facial paralysis--a prospective analysis of risk factors and outcome.

PURPOSE: To evaluate the incidence of Lyme borreliosis in patients with acute idiopathic facial paralysis with special emphasis on the risk factors that explain the poor outcome of facial paralysis and occurrence of Lyme borreliosis. MATERIALS AND METHODS: During a 2-year period, we prospectively studied 503 consecutive patients with acute idiopathic facial paralysis for the presence of Lyme borreliosis. We screened the patients for antibodies to Borrelia burgdorferi and for symptoms or signs related to Lyme borreliosis. Chi-square and logistic regression tests were used for the statistical analysis. Special attention was paid to strict criteria for the diagnosis of Lyme borreliosis. RESULTS: Eleven (2.2%) of the 503 patients with facial paralysis had Lyme borreliosis. Fever, headache, pharyngalgia, enlarged cervical lymph nodes, bilateral paralysis, and arthralgia were more common in patients with Lyme borreliosis than in those without it. In the logistic regression modeling the best combination of explanatory variables for predicting the occurrence of Lyme borreliosis included summer season at the onset of facial paralysis, presence of enlarged cervical lymph nodes, and arthralgia. The best combination of explanatory variables to predict the poor outcome of facial paralysis was total paralysis of facial nerves, recurrent facial paralysis, and hyperacusis. CONCLUSIONS: Lyme borreliosis is an important infectious cause of facial paralysis. In our study, 11 of 503 patients with acute idiopathic facial paralysis had Lyme borreliosis. The screening for serum antibodies in addition to the thorough evaluation of the history of the patient and of the patient's clinical signs or symptoms possibly linked with Lyme borreliosis, are essential when diagnosing Lyme borreliosis.

Acute Disease↗
PubMed1995

Neurobehavioral and physiologic effects of trifluoromethane in humans.

Nuclear magnetic resonance (NMR) imaging shows promise in the measurement of human cerebral blood flow (CBF) in that nonradioactive indicators may be used. Our earlier investigations with trifluoromethane (FC-23) gas have shown that this compound can be used to safely and effectively measure CBF in anesthetized animal models. In this Phase I dose-escalation study we set out to determine the maximal tolerated concentration (MTC) of FC-23 in normal healthy male volunteers and to assess its feasibility as an NMR indicator. Five subjects were exposed in a blinded fashion to escalating concentrations of FC-23 between 10% and 60%, randomly interleaved with exposures to both room air and 40% nitrous oxide. On each study day, the subjects breathed the test gas for eight pulses of 3 min each with 2-min clearance periods between the pulses. The subjects underwent intensive physiologic and neurobehavioral monitoring throughout the study period. The first subject experienced an anesthetic response to 60% FC-23, and the second subject experienced "discomfort" and requested discontinuation at the initiation of 40% FC-23. The MTC was subsequently determined to be 30% FC-23 (all subjects tolerated the gas), although a small (37.6 vs. 40.5) but statistically significant retention of carbon dioxide was found (p = .003). When one subject received 30% FC-23 during an NMR imaging study, a pronounced anesthetic effect with intolerable hyperacusis was demonstrated. Human studies of FC-23 have been discontinued in our laboratory.

Administration, Inhalation↗
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

Effects of acclimatization and deprivation on non-speech auditory abilities.

This article reviews the evidence for acclimatization and deprivation with respect to non-speech auditory abilities. Although this subject has not been studied extensively, clear evidence exists for acclimatization and/or deprivation effects on intensity discrimination, binaural masking level difference, and auditory localization and lateralization. There is also some argument for such effects with regard to changes in tolerance for intense sounds or preferred levels of amplification. However, the main evidence for these effects, changes in loudness discomfort levels with repeated testing, may reasonably be explained as procedural or task-related effects rather than changes in auditory abilities. On the other hand, the successful use of tinnitus maskers to treat hyperacusis suggests that particularly low tolerance levels may be improved by exposure to certain types of auditory stimulation. Overall, this retrospective review of changes in non-speech auditory abilities, associated with the presence or absence of listening experience, indicates that acclimatization or deprivation effects may have influenced the results of some of the experiments reviewed. This suggests that experiments designed to study acclimatization or deprivation are timely and useful. In addition, acclimatization and deprivation are potential variables that should be considered, and preferably controlled, within experiments on auditory abilities. Clinically, the review adds weight to the argument for considering acclimatization and/or deprivation in hearing aid fitting and evaluation.

Functional Laterality↗