Figure 1.

a–c, Cortical map reorganization (a, b) and psychoacoustic properties (c) of tinnitus. a, In the normal-hearing cat (◊), the characteristic frequency tuning of neurons at low sound intensity shows an orderly gradient from low to high frequencies across the surface of A1 (tonotopy). In cats exposed to noise trauma (+), neurons in the hearing loss region (above ∼8 kHz in this example) responded preferentially to sound frequencies at the edge of normal hearing (from Eggermont and Komiya, 2000, with permission). b, Model for map reorganization in primary auditory cortex. The dashed lines represent diminished thalamocortical input to cortical cells in the hearing loss region. A few inhibitory feedforward connections are indicated (one is labeled i) that suppress the same cells receiving thalamic inputs after one synaptic delay. Feedback inhibition is indicated by one example (ii). Hearing loss reduces excitation and feedforward inhibition arising from thalamocortical pathways, such that the affected neurons begin to respond preferentially to inputs from their unaffected neighbors via horizontal connections in the tonotopic map. The output of the affected neurons remains intact and is heard in terms of their original cochleotopic tuning as the tinnitus percept (from Eggermont and Roberts, 2004, with permission). c, The group-averaged audiogram, tinnitus spectrum, and RI function in 47 participants with chronic bilateral tinnitus. To obtain the tinnitus spectrum, participants rated each of 11 sounds differing in center frequency for similarity to their tinnitus (a likeness rating >40 indicated a sound beginning to resemble tinnitus). The RI function shows the suppression of tinnitus reported after cessation of band-limited noise sounds differing in center frequency (−5 equaled “tinnitus gone;” 0, no change; +5, tinnitus worse). The RI function is plotted negative up to show its similarity to the tinnitus spectrum. WN, white noise (from Roberts et al., 2008, with permission).