TY - JOUR
T1 - Human auditory cortex neurochemistry reflects the presence and severity of tinnitus
AU - Sedley, William
AU - Parikh, Jehill
AU - Edden, Richard A.E.
AU - Tait, Valerie
AU - Blamire, Andrew
AU - Griffiths, Timothy D.
N1 - Publisher Copyright:
© 2015 Sedley et al.
PY - 2015/11/4
Y1 - 2015/11/4
N2 - It is not known why tinnitus occurs in some cases of hearing damage but not others. Abnormalities of excitation-inhibition balance could influence whether tinnitus develops and its severity if it does. Animal models of hearing damage, which also produce tinnitus based on behavioral evidence, have identified abnormalities of GABA ergic inhibition, both cortically and sub cortically. However, the precise relationships of GABA inhibitory changes to tinnitus itself, as opposed to other consequences of hearing damage, remain uncertain. Here, we used magnetic resonance spectroscopy to non-invasively quantify GABA in the left (LAC) and right (RAC) auditory cortices of a group of 14 patients with lateralized tinnitus (eight left ear) and 14 controls matched for age, sex, and hearing. We also explored the potential relationships with other brain metabolites (i.e., choline, N-acetylaspartate, and creatine). The presence of tinnitus was associated with a reduction in auditory cortex GABA concentration. Regardless of tinnitus laterality, post hoc testing indicated reductions that were significant in RAC and nonsignificant in LAC. Tinnitus severity and hearing loss were correlated positively with RAC choline but not GABA. We discuss the results in the context of current models of tinnitus and methodological constraints.
AB - It is not known why tinnitus occurs in some cases of hearing damage but not others. Abnormalities of excitation-inhibition balance could influence whether tinnitus develops and its severity if it does. Animal models of hearing damage, which also produce tinnitus based on behavioral evidence, have identified abnormalities of GABA ergic inhibition, both cortically and sub cortically. However, the precise relationships of GABA inhibitory changes to tinnitus itself, as opposed to other consequences of hearing damage, remain uncertain. Here, we used magnetic resonance spectroscopy to non-invasively quantify GABA in the left (LAC) and right (RAC) auditory cortices of a group of 14 patients with lateralized tinnitus (eight left ear) and 14 controls matched for age, sex, and hearing. We also explored the potential relationships with other brain metabolites (i.e., choline, N-acetylaspartate, and creatine). The presence of tinnitus was associated with a reduction in auditory cortex GABA concentration. Regardless of tinnitus laterality, post hoc testing indicated reductions that were significant in RAC and nonsignificant in LAC. Tinnitus severity and hearing loss were correlated positively with RAC choline but not GABA. We discuss the results in the context of current models of tinnitus and methodological constraints.
KW - Auditory cortex
KW - Choline
KW - GABA
KW - MR spectroscopy
KW - Tinnitus
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U2 - 10.1523/JNEUROSCI.2695-15.2015
DO - 10.1523/JNEUROSCI.2695-15.2015
M3 - Article
C2 - 26538652
AN - SCOPUS:84946430611
SN - 0270-6474
VL - 35
SP - 14822
EP - 14828
JO - Journal of Neuroscience
JF - Journal of Neuroscience
IS - 44
ER -