Book Summary: Tinnitus: A Multidisciplinary Approach provides a broad account of tinnitus and hyperacusis, detailing the latest research and developments in clinical management, incorporating insights from audiology, otology, psychology, psychiatry and auditory neuroscience. It promotes a collaborative approach to treatment that will benefit patients and clinicians alike. The 2nd edition has been thoroughly updated and revised in line with the very latest developments in the field. The book contains 40% new material including two brand new chapters on neurophysiological models of tinnitus and emerging treatments; and the addition of a glossary as well as appendices detailing treatment protocols for use in an audiology and psychology context respectively.

No description available.

No description available.

L’hyperacousie est définie comme une hypersensibilité aux sons d’intensité modérée. Il s’agit d’un trouble de la perception auditive qui a des répercussions néfastes sur la qualité de vie des patients. Un mécanisme impliquerait la modification du gain central des neurones auditifs centraux sous l'influence des régions cérébrales non auditives. Toutefois, la question de l'endroit où ces anomalies surviennent dans le système auditif reste ouverte, plus particulièrement lorsque l'hyperacousie survient sans perte auditive neurosensorielle. Nous avons utilisé un modèle animal d’hyperacousie réversible et sans perte audiométrique, induit par injection aigue de salicylate. Nous avons observé un raccourcissement significatif de la latence des ondes III et IV des PEA aux fréquences inférieures à 10 kHz corrélé à une diminution de 15 dB du seuil de réflexe de sursaut acoustique à basses fréquences. La diminution de l’efficacité du réflexe musculaire de l’oreille moyenne suite à l’injection de salicylate semble trop modérée pour expliquer l'hyperacousie, qui semble plutôt être causée par une altération du codage temporo-spatial de la sonie dans le tronc cérébral. L’hyperacousie fait partie des troubles de perception retrouvés dans la migraine, nous avons étudié les changements physiologiques auditifs dans un modèle animal de migraine induit par administration extradurale de soupe inflammatoire. Dans un contexte migraineux, aucun des paramètres modifiés par le salicylate n'est affecté de sorte que l'hypersensibilité au son est plutôt une phonophobie, réponse émotionnelle au son résultant d’une activation anormale du système limbique et du système nerveux autonome. / Hyperacusis is a disorder of loudness perception defined as decreased tolerance to ordinary environmental sounds that are felt as disagreeable, or even, unbearably painful. The idea that hyperacusis is underpinned by an increase in central auditory gain is now widely invoked. Besides, the neural bases of this gain abnormality remain unclear, as well as more generally the mechanisms of loudness perception. We used an animal model of reversible and hearing-loss-free hyperacusis induced by acute salicylate injection. We observed a significant shortening of the latency of ABR waves III and IV at frequencies below 10 kHz correlated to a 15 dB decrease of the threshold of acoustic startle reflex at low frequencies and without sensorineural hearing loss. The decreased effectiveness of middle ear muscle reflex following salicylate injection seems too moderate for explaining hyperacusis, which is more likely produced by impaired temporo-spatial loudness coding with a brainstem origin. Hyperacusis is one of the perceptual disorders found in migraine. We studied auditory physiological changes in an animal model of migraine induced by extradural administration of inflammatory soup. In a migraine context, none of the salicylate-induced changes was observed so that the reaction to sound is likely closer to phonophobia, an emotional response to sound resulting from abnormal activation of the limbic system and the autonomic nervous system.

No description available.

No description available.

Embora hiper-reatividade auditiva (HRA) e/ou hiperacusia (HPA) sejam manifestações frequentes no Transtorno do Espectro Autista (TEA) são poucos os estudos que investigaram este sintoma com medidas fisiológicas ou exploraram os mecanismos auditivos neurais que podem estar associados a esta característica. O principal objetivo deste trabalho foi estudar a queixa subjetiva (o sintoma) e o desconforto observável (o sinal) da HPA no TEA e avaliar a relação com o efeito inibitório do complexo olivococlear medial (EICOCM). Foram recrutadas 13 crianças e adolescentes com TEA (idade média = 7,2 anos) de ambos os sexos, e 11 crianças e adolescentes com desenvolvimento típico (idade média = 7,2 anos) de ambos os sexos. Para avaliar a HPA, todos os sujeitos responderam a um questionário de caracterização desse sintoma. As medidas psicoacústicas e eletroacústicas permitiram a determinação da sensibilidade auditiva, do funcionamento coclear, do nível de desconforto auditivo e do campo dinâmico da audição. Para a avaliação da via eferente, o EICOCM foi investigado pelas emissões otoacústicas evocadas transientes com ruído contralateral. Os resultados mostraram que o grupo com TEA apresentou desconforto em intensidades mais baixas nas frequências de 1 kHz, 2 kHz e 4 kHz (1 kHz, t = 1,99, p = 0,059; 2 kHz, t = 2,16, p = 0,042; 4 kHz, t = 2,37, p = 0,028), e menor faixa dinâmica auditiva em comparação com o grupo controle, sendo que nas frequências de 0,5 kHz, 4 kHz e 8 kHz houve diferenças estatisticamente significantes (respectivamente: 0,5 kHz p = 0,03; 4 kHz p = 0,01 e 8 kHz p = 0,03). As emissões otoacústicas evocadas transientes evidenciaram amplitudes de resposta coclear semelhante entre os grupos, porém, o efeito inibitório não: o grupo com TEA apresentou valores menores em comparação ao grupo controle (F(4;76) = 3,49, p = 0,01). Houve correlação positiva entre o EICOCM e a medida do campo dinâmico da audição. Crianças e adolescentes com TEA apresentaram maior ocorrência de hiperacusia, o que pode indicar que esse sinal está relacionado a um déficit no EICOCM / Although auditory hyper-responsiveness (AHR) and/or hyperacusis is a frequent manifestation in Autism Spectrum Disorder (ASD), few studies have investigated this symptom with physiological measures or explored the neural auditory mechanisms that may be associated with this characteristic. The main objective was to study the complains (symptom) and the evident discomfort (sign) of hyperacusis in ASD and to evaluate its relationship with the inhibitory effect of the medial olivocochlear bundle (MOCB). Two groups, one of 13 children and adolescents with ASD (mean age = 7.2 years) of both sexes, and other with 11 children and adolescents typically developed (mean age = 7.2 years) of both sexes, were recruited. To assess hyperacusis, all subjects answered a questionnaire characterizing this symptom. The psychoacoustic and electroacoustic measurements allowed the determination of auditory sensitivity, cochlear functioning, level of auditory discomfort and auditory dynamic range. For the evaluation of the efferent pathway, the inhibitory effect of the MOCB was assessed by transient evoked otoacoustic emissions with contralateral noise. The results showed that the group with ASD presented discomfort at lower frequencies in the frequencies of 1, 2 and 4 kHz (1 kHz, t = 1.99, p = 0.059; 2 kHz, t = 2.16, p = 0.042; 4 kHz, t = 2.37, p = 0.028), and lower auditory dynamic range in comparison with the control group, while for the frequencies of 0, 5, 4 and 8 kHz, a statistically significant difference was found (respectively: 0.5 kHz p = 0.03; 4 kHz p = 0.01 and 8 kHz p = 0.03). Transient evoked otoacoustic emissions showed similar cochlear response amplitudes between groups, while the inhibitory effect did not: the group with ASD presented lower values in comparison to the control group (F(4;76) = 3.49, p = 0,01). There was a positive correlation between the inhibitory effect of the MOCB and the auditory dynamic range measurement. Children and adolescents with ASD had a higher occurrence of hyperacusis, which may point out that this sign is associated with a deficit in the inhibitory effect of MOCB