Review Article

A Brain Centred View of Psychiatric Comorbidity in Tinnitus: From Otology to Hodology

Table 3

Tinnitus-related alterations “beyond” auditory pathways.

Methods Alterations observedReferences

fMRIIncreased connectivity in extra-auditory regions (brainstem, basal ganglia/NAc, cerebellum, parahippocampal, and right prefrontal, parietal, and sensorimotor areas); reduced connectivity in right primary auditory cortex, left prefrontal, left fusiform gyrus, and bilateral occipital regions.[42]
Reduced grey matter volume in bilateral insula.[43]
Significant grey matter decrease in right IC and left hippocampus.[44]
Hyperactivity in the anterior cingulate cortex, midcingulate cortex, posterior cingulate cortex, left middle frontal gyrus, retrosplenial cortex and insula. [65]
Highly significant volume loss in the subcallosal area; significant increase of grey-matter density in the posterior thalamus.[66]
Activation of primary auditory cortices, associative auditory cortices, and left hippocampus. [67]

PETHyperactivity of NAc and primary auditory cortex; increased gray matter and decreased white matter concentrations in the ventromedial PFC.[68]
Increased metabolic activity in temporal and parietal brain regions (in female tinnitus patients) and in frontal and occipital regions (in male tinnitus patients) associated with significantly increased metabolic activity in the left primary auditory cortex.[53]

DTIDecreased FA in the left frontal arcuate fasciculus and the right parietal arcuate fasciculus.[69]
Increased FA in the inferior frontooccipital fasciculus and superior longitudinal fasciculus; decreased FA in the superior longitudinal fasciculus of the left parietal lobe.[70]
Disrupted white matter integrity in tracts involving the connectivity of PFC, temporal lobe, thalamus, and limbic system.[71]

EEG Increased alpha activity in both left and right anterior insula in patients with severe tinnitus-related distress who can or cannot cope with these phantom sounds.[72]
In the right anterior insula increased delta and gamma activity related to increased tinnitus distress; in the left anterior insula decreased theta and gamma activities.[58]
Gamma-band activity in the parahippocampal area contralateral to the tinnitus lateralization.[72]

MEGMarked reduction in alpha (8–12 Hz) power associated with enhancement in delta (1.5–4 Hz) neuronal activity particularly in right temporal and left frontal areas[56]
In patients with significant tinnitus-related distress, more synchronized alpha activity in subcallosal anterior cingulate cortex, insula, parahippocampal area, and amygdala; less synchronized alpha activity in posterior cingulate cortex, precuneus, and DLPFC. [58]
Tinnitus-related distress correlated with a right sided connectivity increase between the anterior cingulate and the frontal and parietal cortices.[46]
Altered role of frontal cortex in the modulation of sensory inputs.[73]

IC: Inferior Colliculus
NAc: Nucleus Accumbens
PFC: Prefrontal Cortex
DLPFC: Dorsolateral Prefrontal Cortex
FA: Fractional Anisotropy.