Background: Functional magnetic resonance imaging (fMRI) is a noninvasive method to detect focal brain activity at high spatial resolution. Acoustic stimulation induces an increase of regional cerebral blood flow in the primary auditory cortex. This entails an increased concentration of diamagnetic oxyhemoglobin in the capillaries and the venous system. The resulting decrease of the local magnetic susceptibility was detected as a signal increase in T2*-weighted images. The central auditory pathways predominantly cross to the contralateral hemisphere in normally hearing subjects. The aim of the present study was to investigate the primary auditory cortex after acoustic stimulation in unilateral deaf patients using fMRI.
Methods: Magnetic resonance images were acquired on a 1.5 T Siemens Vision scanner. For fMRI, a single shot gradient recalled, echo planar imaging (EPI) sequence with decreasing excitation order was used, allowing the aquisition of 9 slices within 1.8 s. The 9 slices covered a slab of 3.6 cm in cranio-caudal extension in the region of the temporal lobes. For statistical processing of the raw image data the SPM96 software package was used. A p-value of p < 0.01 was applied to differentiate between activated and non-activated. The resulting functional activation maps were superimposed onto the EPI scan. The number of activated pixels was used to quantitate the cortical response upon acoustic stimulation. Stimulation consisted of a 1000-Hz sine tone (100 dB SPL at the distal end of the head phone, pulsed at 6 Hz) to which the patients were asked to listen passively. A piezoelectric loudspeaker was mounted on the subject table and connected to a plastic tube system leading to a combination of bilateral ear- and headphones. Auditory paradigms require disentangling experimental excitation from the scanner noise that approximates 90 dB. Headphones suppress noise by approximately 30 dB. To decrease the acoustic background-to-stimulation ratio and to keep background noise constant during stimulation and resting, we employed short scanning (1.8 s) and long resting periods (10.2 s; TR = 12 s). This acquisition mode allows sufficient recovery during off-periods and sufficient excitation during on-periods. 14 unilateral deaf patients were examined. The mean duration of deafness was 22.5 years.
Results: Acoustic stimulation of the deaf ear revealed only weak cortical activation which could be explained by sound transmission via bone conduction to the other ear. A significant increase of BOLD (blood oxygen level dependent)-activation in the primary auditory cortex could be demonstrated in all patients after stimulation of the hearing ear. However, remarkable individual differences were noticed concerning the absolute number of activated pixels. The lateralization ratio was calculated by the number of activated pixels on the hearing side divided by the number of activated pixels on the deaf side. A mean lateralization ratio of 0.9 (Stdv +/- 0.6) was found. The mean lateralization ratio for patients with a right deaf ear (n = 8) and those with a left deaf ear (n = 5) was 1.1 (Stdv +/- 0.7) and 0.6 (Stdv +/- 0.3) respectively. However, the difference was not significant (Wilcoxon test: p = 0.08).
Conclusions: Central-auditory compensation by bilateral cortical activation was demonstrated in unilateral deaf patients. Moreover, a tendency towards a dominance of the left primary auditory cortex was found, although the difference between both hemispheres was not significant. The lateralization ratio in unilateral deaf patients is similar to findings after binaural stimulation in normally hearing subjects.