BackgroundThe neurophysiological mechanisms underlying tinnitus perception are not well understood. Surprisingly, there have been no group studies comparing abnormalities in ongoing, spontaneous neuronal activity in individuals with and without tinnitus perception.Methods and FindingsHere, we show that the spontaneous neuronal activity of a group of individuals with tinnitus (n = 17) is characterised by a marked reduction in alpha (8–12 Hz) power together with an enhancement in delta (1.5–4 Hz) as compared to a normal hearing control group (n = 16). This pattern was especially pronounced for temporal regions. Moreover, correlations with tinnitus-related distress revealed strong associations with this abnormal spontaneous activity pattern, particularly in right temporal and left frontal areas. Overall, effects were stronger for the alpha than for the delta frequency band. A data stream of 5 min, recorded with a whole-head neuromagnetometer under a resting condition, was sufficient to extract the marked differences.ConclusionsDespite some limitations, there are arguments that the regional pattern of abnormal spontaneous activity we found could reflect a tinnitus-related cortical network. This finding, which suggests that a neurofeedback approach could reduce the adverse effects of this disturbing condition, could have important implications for the treatment of tinnitus.

Tinnitus is defined by an auditory perception in the absence of an external source of sound. This condition provides the distinctive possibility of extracting neural coding of perceptual representation. Previously, we had established that tinnitus is characterized by enhanced magnetic slow-wave activity (ϳ4 Hz) in perisylvian or putatively auditory regions. Because of works linking high-frequency oscillations to conscious sensory perception and positive symptoms in a variety of disorders, we examined gamma band activity during brief periods of marked enhancement of slow-wave activity. These periods were extracted from 5 min of resting spontaneous magnetoencephalography activity in 26 tinnitus and 21 control subjects. Results revealed the following, particularly within a frequency range of 50 -60 Hz: (1) Both groups showed significant increases in gamma band activity after onset of slow waves. (2) Gamma is more prominent in tinnitus subjects than in controls. (3) Activity at ϳ55 Hz determines the laterality of the tinnitus perception.Based on present and previous results, we have concluded that cochlear damage, or similar types of deafferentation from peripheral input, triggers reorganization in the central auditory system. This produces permanent alterations in the ongoing oscillatory dynamics at the higher layers of the auditory hierarchical stream. The change results in enhanced slow-wave activity reflecting altered corticothalamic and corticolimbic interplay. Such enhancement facilitates and sustains gamma activity as a neural code of phantom perception, in this case auditory.

Prenatal exposure to maternal stress can have lifelong implications for psychological function, such as behavioral problems and even the development of mental illness. Previous research suggests that this is due to transgenerational epigenetic programming of genes operating in the hypothalamic–pituitary–adrenal axis, such as the glucocorticoid receptor (GR). However, it is not known whether intrauterine exposure to maternal stress affects the epigenetic state of these genes beyond infancy. Here, we analyze the methylation status of the GR gene in mothers and their children, at 10–19 years after birth. We combine these data with a retrospective evaluation of maternal exposure to intimate partner violence (IPV). Methylation of the mother's GR gene was not affected by IPV. For the first time, we show that methylation status of the GR gene of adolescent children is influenced by their mother's experience of IPV during pregnancy. As these sustained epigenetic modifications are established in utero, we consider this to be a plausible mechanism by which prenatal stress may program adult psychosocial function.

A broad consensus within the neuroscience of tinnitus holds that this audiologic condition is triggered by central deafferentation, mostly due to cochlear damage. The absence of audiometrically detectable hearing loss however poses a challenge to this rather generalizing assumption. The aim of this study was therefore to scrutinize cochlear functioning in a sample of tinnitus subjects audiometrically matched to a normal hearing control group. Two tests were applied: the Threshold Equalizing Noise (TEN) test and a pitch scaling task. To perform well on both tasks relatively normal functioning of inner hair cells is a requirement. In the TEN test the tinnitus group revealed a circumscribed increment of thresholds partially overlapping with the tinnitus spectrum. Abnormal slopes were observed in the pitch scaling task which indicated that tinnitus subjects, when presented with a high-frequency stimulus, relied heavily on input derived from lower-frequency inner hair cells (off-frequency listening). In total both results argue for the presence of a deafferentation also in tinnitus subjects with audiometrically normal thresholds and therefore favour the deafferentation assumption posed by most neuroscientific theories.

In this chapter we will present support for the hypothesis that synchronous neuronal activity of cell assemblies within the auditory cortex could be the underlying neural code of tinnitus. Such synchronous activity is reflected in the ongoing oscillatory activation pattern that can be recorded non-invasively using MEG and EEG techniques. We conclude that such an oscillatory model of tinnitus can explain many different observations regarding tinnitus.