Reversing pathologically increased EEG power by acoustic coordinated reset neuromodulation

Abstract

Acoustic Coordinated Reset (CR) neuromodulation is a patterned stimulation with tones adjusted to the patient's dominant tinnitus frequency, which aims at desynchronizing pathological neuronal synchronization. In a recent proof-of-concept study, CR therapy, delivered 4–6 h/day more than 12 weeks, induced a significant clinical improvement along with a significant long-lasting decrease of pathological oscillatory power in the low frequency as well as γ band and an increase of the α power in a network of tinnitus-related brain areas. As yet, it remains unclear whether CR shifts the brain activity toward physiological levels or whether it induces clinically beneficial, but nonetheless abnormal electroencephalographic (EEG) patterns, for example excessively decreased δ and/or γ. Here, we compared the patients' spontaneous EEG data at baseline as well as after 12 weeks of CR therapy with the spontaneous EEG of healthy controls by means of Brain Electrical Source Analysis source montage and standardized low-resolution brain electromagnetic tomography techniques. The relationship between changes in EEG power and clinical scores was investigated using a partial least squares approach. In this way, we show that acoustic CR neuromodulation leads to a normalization of the oscillatory power in the tinnitus-related network of brain areas, most prominently in temporal regions. A positive association was found between the changes in tinnitus severity and the normalization of δ and γ power in the temporal, parietal, and cingulate cortical regions. Our findings demonstrate a widespread CR-induced normalization of EEG power, significantly associated with a reduction of tinnitus severity.

The neural correlates of cognitive dysfunction in phantom sounds

“…This finding corroborates with previous studies that indicate that the amount of gamma band activity is correlated to the subjectively perceived tinnitus loudness (van der Loo et al, 2009;Vanneste et al, 2012) and a decrease in alpha power is associated with an increase in gamma power in tinnitus (Adamchic et al, 2012;Adamchic et al, 2014;Lorenz et al, 2009;Ramirez et al, 2009). To a certain extent this fits with the concept of thalamocortical dysrhythmia (Llinas et al, 2005;Llinas et al, 1999).…”

Abnormal cross-frequency coupling in the tinnitus network

“…Furthermore, reduction of oscillatory power in the delta/theta and gamma frequency ranges and increase of the oscillatory power in the alpha band in this area is associated with reduction of tinnitus loudness (Kahlbrock and Weisz, 2008; De Ridder et al, 2011b; Adjamian et al, 2012; Tass et al, 2012; Adamchic et al, 2014). The thalamocortical dysrhythmia model provides an explanation for the emergence and persistence of such a pattern of oscillatory activity as a result of sensory differentiation (Llinas et al, 1999).…”

Desynchronization boost by non-uniform coordinated reset stimulation in ensembles of pulse-coupled neurons

“…This is because neurons have to be active in order to unlearn their pathological synaptic connectivity. In this way sustained long-lasting desynchronization is induced, and, as predicted computationally (Tass and Majtanik, 2006; Hauptmann and Tass, 2007; Tass and Popovych, 2012), therapeutic effects were observed in rat hippocampal slice experiments in the context of epilepsy (Tass et al, 2009) as well as in a clinical proof of concept study in tinnitus patients treated with acoustic CR stimulation (Tass et al, 2012a), where both pathological neuronal synchrony (Adamchic et al, 2013) and pathological effective connectivity (Silchenko et al, 2013) considerably decreased. In addition, in parkinsonian (MPTP) monkeys it was shown that unilateral CR stimulation delivered to the subthalamic nucleus (STN) for only 2 h per day during 5 days leads to significant and sustained therapeutic aftereffects for at least 30 days, while standard 130 Hz DBS has no aftereffects (Tass et al, 2012b).…”