Impairments of thalamic resting-state functional connectivity in patients with chronic tinnitus

Wang

et al. 2017

Front. Hum. Neurosci.

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Purpose: The neural mechanisms that give rise to the phantom sound of tinnitus have not been fully elucidated. Neuroimaging studies have revealed abnormalities in resting-state activity that could represent the neural signature of tinnitus, but there is considerable heterogeneity in the data. To address this issue, we conducted a meta-analysis of published neuroimaging studies aimed at identifying a common core of resting-state brain abnormalities in tinnitus patients.Methods: A systematic search was conducted for whole-brain resting-state neuroimaging studies with SPECT, PET and functional MRI that compared chronic tinnitus patients with healthy controls. The authors searched PubMed, Science Direct, Web of Knowledge and Embase databases for neuroimaging studies on tinnitus published up to September 2016. From each study, coordinates were extracted from clusters with significant differences between tinnitus subjects and controls. Meta-analysis was performed using the activation likelihood estimation (ALE) method.Results: Data were included from nine resting-state neuroimaging studies that reported a total of 51 distinct foci. The meta-analysis identified consistent regions of increased resting-state brain activity in tinnitus patients relative to controls that included, bilaterally, the insula, middle temporal gyrus (MTG), inferior frontal gyrus (IFG), parahippocampal gyrus, cerebellum posterior lobe and right superior frontal gyrus. Moreover, decreased brain activity was only observed in the left cuneus and right thalamus.Conclusions: The current meta-analysis is, to our knowledge, the first to demonstrate a characteristic pattern of resting-state brain abnormalities that may serve as neuroimaging markers and contribute to the understanding of neuropathophysiological mechanisms for chronic tinnitus.

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Resting-State Brain Abnormalities in Chronic Subjective Tinnitus: A Meta-Analysis

Wang

et al. 2017

Front. Hum. Neurosci.

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“…The amygdala receives and sends auditory information directly or indirectly to the medial geniculate body and auditory cortex and is well-positioned to relay emotional attributes of a sound to the auditory cortex [Chen et al, 2012;LeDoux, 2007]. Prior resting-state fMRI studies have revealed aberrant functional coupling between auditory cortex and amygdala in tinnitus patients [Kim et al, 2012;Maudoux et al, 2012b;Moller, 2006;Zhang et al, 2015] as well as rats with salicylate-induced tinnitus [Chen et al, 2015a]. Infusion of salicylate directly into amygdala increases sound-evoked activity in the auditory cortex, illustrating the potent modulatory effect that the amygdala exerts on auditory processing carried out by the auditory cortex [Chen et al, 2012].…”

Section: Disrupted Effective Connectivity From and To The Amygdalamentioning

confidence: 99%

“…Neuroimaging studies have suggested that abnormal coupling between the frontal cortex and other regions contributes to tinnitus disability [Chen et al, 2014[Chen et al, , 2015cLanting et al, 2016;Leaver et al, 2016b;Mirz, 2000;Schlee et al, 2009a;Vanneste and De Ridder, 2012;Vanneste et al, 2010a;Zhang et al, 2015]. Rauschecker et al developed a model to demonstrate structural and functional differences in ventromedial prefrontal cortex that were associated with tinnitus subjective loudness, indicating the contribution of frontal cortex to certain perceptual features of tinnitus [Rauschecker et al, 2010].…”

Section: Disrupted Effective Connectivity From and To The Amygdalamentioning

confidence: 99%

Tinnitus distress is linked to enhanced resting‐state functional connectivity from the limbic system to the auditory cortex

Xia

et al. 2017

Human Brain Mapping

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101

The phantom sound of tinnitus is believed to be triggered by aberrant neural activity in the central auditory pathway, but since this debilitating condition is often associated with emotional distress and anxiety, these comorbidities likely arise from maladaptive functional connections to limbic structures such as the amygdala and hippocampus. To test this hypothesis, resting-state functional magnetic resonance imaging (fMRI) was used to identify aberrant effective connectivity of the amygdala and hippocampus in tinnitus patients and to determine the relationship with tinnitus characteristics. Chronic tinnitus patients (n = 26) and age-, sex-, and education-matched healthy controls (n = 23) were included. Both groups were comparable for hearing level. Granger causality analysis utilizing the amygdala and hippocampus as seed regions were used to investigate the directional connectivity and the relationship with tinnitus duration or distress. Relative to healthy controls, tinnitus patients demonstrated abnormal directional connectivity of the amygdala and hippocampus, including primary and association auditory cortex, and other non-auditory areas. Importantly, scores on the Tinnitus Handicap Questionnaires were positively correlated with increased connectivity from the left amygdala to left superior temporal gyrus (r = 0.570, P = 0.005), and from the right amygdala to right superior temporal gyrus (r = 0.487, P = 0.018). Moreover, enhanced effective connectivity from the right hippocampus to left transverse temporal gyrus was correlated with tinnitus duration (r = 0.452, P = 0.030). The results showed that tinnitus distress strongly correlates with enhanced effective connectivity that is directed from the amygdala to the auditory cortex. The longer the phantom sensation, the more likely acute tinnitus becomes permanently encoded by memory traces in the hippocampus. Hum Brain Mapp 38:2384-2397, 2017. © 2017 Wiley Periodicals, Inc.

“…On the other hand, ReHo may be more sensitive at Cellular Physiology and Biochemistry Cellular Physiology and Biochemistry detecting regional brain abnormalities than ALFF. The combination of the ALFF and ReHo may provide a more comprehensive pathophysiological assessment of human brain dysfunctions than either method alone or other combinations [26][27][28], indicating that the coexisting neural intensity and coherence abnormalities in specific brain regions may represent more severe brain changes than those revealed by a single method. Thus, we utilized these two common methods as well as FC analysis to identify whole-brain spontaneous neural activity and connectivity in T1DM.…”

Section: Xindao Yinmentioning

confidence: 99%

Decreased Spontaneous Brain Activity and Functional Connectivity in Type 1 Diabetic Patients Without Microvascular Complications

Xia¹,

Chen²,

Luo³

et al. 2018

Cell Physiol Biochem

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Background/Aims: Type 1 diabetes mellitus (T1DM) has been proven to be associated with an increased risk of cognitive dysfunction. In this study, we aimed to investigate whether disrupted spontaneous activity and functional connectivity (FC) exist in T1DM patients using resting-state functional magnetic resonance imaging (rs-fMRI) and to detect the relationships of these parameters with cognitive impairment. Methods: T1DM patients (n=35) were compared with age-, sex-, and education level-matched healthy controls (n=50) through rs-fMRI. Using rs-fMRI professional software, we calculated the amplitude of low-frequency fluctuation (ALFF), regional homogeneity (ReHo), and seed-based FC in the posterior cingulate cortex (PCC) to measure the spontaneous neural activity in the groups. The relationship between rs-fMRI data and cognitive performance was further investigated. Results: Compared with the healthy controls, T1DM patients showed significantly decreased ALFF values in the PCC and right inferior frontal gyrus (IFG), decreased ReHo values in the right middle frontal gyrus (MFG) and reduced FC between the PCC and the right MFG. Furthermore, a positive correlation was found between decreased ALFF values in the PCC and Rey-Osterrieth Complex Figure Test (CFT)-delay scores in T1DM patients (r=0.394, p=0.026). Moreover, the Trail Making Test-B (TMT-B) scores showed negative correlations with decreased ReHo values in the right MFG (r=-0.468, p=0.007) and reduced FC between the PCC and right MFG (r=-0.425, p=0.015). Conclusion: Our combined analyses revealed decreased spontaneous activity and FC mainly within the default mode network, which was correlated with specific impaired cognitive functioning in T1DM. This study thus elucidates the neurophysiological mechanisms underlying T1DM-related cognitive impairment and may serve as a reference for future clinical diagnosis.