Cortical excitability and transcallosal inhibition in chronic tinnitus: transcranial magnetic study

It has been proposed that tinnitus may be caused by maladaptive plasticity of processing in the central auditory pathways, and that this may be due in part to a generalised deficit in NMDA-dependent glutamatergic synapses.

To test this hypothesis, we used transcranial magnetic stimulation to assess the excitability of a number of well-defined synaptic connections in the motor cortex of patients with tinnitus.

Thirty-seven patients with chronic tinnitus and 12 normal age- and sex-matched volunteers were used as a control group. We measured resting and active motor thresholds (rMT/aMT) and the duration of the contralateral and ipsilateral cortical silent periods (CSP and ISP). Short interval intracortical inhibition (SICI) and intracortical facilitation (ICF) were evaluated using a paired pulse stimulation paradigm in the left (dominant) hemisphere.

There was no difference between patients and healthy subjects in rMT or aMT or the onset latency of the ISP. The CSP was shorter in patients (P=0.046) whereas the ISP was longer than in healthy subjects (P=0.048) but there was no difference between the hemispheres nor any relation to tinnitus side in patients with predominantly unilateral symptoms. There was no difference in the time course of SICI/ICF between patients and control groups and no significant correlation between tinnitus handicap inventory (THI) score and any of the measures of cortical excitability.

There are small changes incortical excitability in patients with chronic tinnitus. However, given the number of factors we examined in each individual, such minor changes seem unlikely to be an important factor in development of clinical symptoms.