1. Inner Ear Dysfunction Upcoming Talk: Isabelle Peretz Musical & Non-musical Brains Nov. 22 @ 12 noon + Lunch Rm 2068B South Building

2. Neural Correlates of Stream Segregation  Summation of cortical response hypothesis (DRAW) Will a stimulated area summate with another stimulated area on the tonotopic map?(DRAW) Will a stimulated area summate with another stimulated area on the tonotopic map?  Tetanic + rapid stimulation increases probability of summation (Fishman et al., 2001) ALTERNATIVELY?  Lesions of temporal cortex (in and around primary auditory cortex) (Peretz and colleagues, 1999; 2001) Poster temporal gyrus affects melodic groupingPoster temporal gyrus affects melodic grouping  Intervals, melodic contours Anterior temporal gyrus affects meterAnterior temporal gyrus affects meter  Rhythmic grouping, temporal combinations

3. Tinnitus: It has a certain ring to it (see Mencher pp. 144-145)  What is Tinnitus? Ringing, buzzing, roaring, clicking experienced in one or both earsRinging, buzzing, roaring, clicking experienced in one or both ears  Objective tinnitus Audible to a third partyAudible to a third party  Stethoscope examination  Less than 5% of all tinnitus sufferers  Subjective tinnitus Audible only to the patientAudible only to the patient  Subjective report  Approx. 35% of the population (continuous 15%) Severe in 15% of tinnitus sufferersSevere in 15% of tinnitus sufferers  Incidence increases with age & hearing loss Noise-induced traumaNoise-induced trauma

4. Causes of Tinnitus  Vibratory Acoustic stimulation of cochleaAcoustic stimulation of cochlea  Pulsatile tinnitus: Rhythmic pulsing, heartbeat  Leudet’s tinnitus: crackling of involuntary muscles Jaw & neck positionJaw & neck position  Clicking tinnitus: Clicking sound that may occur with serous otitis media May be objective or subjectiveMay be objective or subjective  Non-vibratory Neurochemical changesNeurochemical changes  Not traced to acoustic stimulation Subjective tinnitusSubjective tinnitus

5. Physiological-subjective tinnitus (Jastreboff, 1990)  Cochlear causes Increased otoacoustic emissionsIncreased otoacoustic emissions  Continuous spontaneous firing (4%) Collapsing tectorial membraneCollapsing tectorial membrane  Chronic bent inner hair cells  Tetanic stimulation of auditory system Reduced outer hair cell populationReduced outer hair cell population  Inability to modulate gain  Chronic higher sensitivity to background noise Hyperacusis: chronic oversensitivity (40% correlation)Hyperacusis: chronic oversensitivity (40% correlation)  Correlation with Sensori-neural hearing loss

6. Higher-level Tinnitus (Lockwood et al., 1998)  Persistent symptoms after transection of auditory pathway Cortical phenomenon?Cortical phenomenon?  fMRI evidence (blood flow) Typical auditory stimulation = bilateral activationTypical auditory stimulation = bilateral activation Tinnitus causes unilateral activationTinnitus causes unilateral activation  Modulation of tinnitus has unilateral effects  Neurochemical change in midbrain or cortex may contribute to tinnitus

7. Summary & Treatments  Variety of contributing pathologies PhysicalPhysical  Pinched blood vessel, loud-noise exposure, muscular activity, stress ToxicityToxicity  Foods (allergic reactions), quinine, aspirin, cigarettes, alcohol, caffeine Multiple causesMultiple causes  Treatments Jaw positionJaw position Cutting cochlear nerve (50% effective)Cutting cochlear nerve (50% effective) Masking noiseMasking noise  Effectiveness of noise suggests no dementia Hearing Aid useHearing Aid use Tinnitus retraining therapyTinnitus retraining therapy  Habituation to tinnitus sound to reduce aversiveness