TY - JOUR
T1 - 1H-magnetic resonance spectroscopy in social anxiety disorder
AU - Howells, Fleur M.
AU - Hattingh, Coenraad J.
AU - Syal, Supriya
AU - Breet, Elsie
AU - Stein, Dan J.
AU - Lochner, Christine
N1 - Publisher Copyright:
© 2014 Elsevier Inc.
PY - 2015/4/3
Y1 - 2015/4/3
N2 - Background: Social anxiety disorder (SAD) is characterized by excessive anxiety about social interaction or performance situations, leading to avoidance and clinically significant distress. A growing literature on the neurobiology of SAD has suggested that the reward/avoidance basal ganglia circuitry in general and the glutamatergic system in particular may play a role. In the current study, we investigated 1H-magnetic resonance spectroscopy (1H-MRS) concentrations in cortical, striatal, and thalamic circuitry, as well as their associations with measures of social anxiety and related symptoms, in patients with primary SAD. Methodology: Eighteen adult individuals with SAD and 19 age- and sex- matched controls participated in this study. 1H-MRS was used to determine relative metabolite concentrations in the anterior cingulate cortex (ACC) using single voxel spectroscopy (reporting relative N-acetyl-aspartate (NAA), N-acetyl-aspartate with N-acetyl-aspartyl-glutamate (NAA+NAAG), glycerophosphocholine with phosphocholine (GPC+PCh), myo-inositol, glutamate (Glu), and glutamate with its precursor glutamine (Glu+Gln)), and the caudate, putamen and thalami bilaterally using two dimensional chemical shift imaging (reporting relative NAA+NAAG and GPC+PCh). Relationships between metabolite concentrations and measures of social anxiety and related symptoms were also determined. Measures of social anxiety included symptom severity, blushing propensity, and gaze anxiety/avoidance. Results: We found, first, decreased relative glutamate concentration in the ACC of SAD and changes in myo-inositol with measures of social anxiety. Second, NAA metabolite concentration was increased in thalamus of SAD, and choline metabolite concentrations were related to measures of social anxiety. Lastly, choline metabolite concentration in the caudate and putamen showed changes in relation to measures of social anxiety. Conclusion: These findings are consistent with evidence that the reward/avoidance basal ganglia circuitry, as well as the glutamatergic system, play a role in mediating SAD symptoms.
AB - Background: Social anxiety disorder (SAD) is characterized by excessive anxiety about social interaction or performance situations, leading to avoidance and clinically significant distress. A growing literature on the neurobiology of SAD has suggested that the reward/avoidance basal ganglia circuitry in general and the glutamatergic system in particular may play a role. In the current study, we investigated 1H-magnetic resonance spectroscopy (1H-MRS) concentrations in cortical, striatal, and thalamic circuitry, as well as their associations with measures of social anxiety and related symptoms, in patients with primary SAD. Methodology: Eighteen adult individuals with SAD and 19 age- and sex- matched controls participated in this study. 1H-MRS was used to determine relative metabolite concentrations in the anterior cingulate cortex (ACC) using single voxel spectroscopy (reporting relative N-acetyl-aspartate (NAA), N-acetyl-aspartate with N-acetyl-aspartyl-glutamate (NAA+NAAG), glycerophosphocholine with phosphocholine (GPC+PCh), myo-inositol, glutamate (Glu), and glutamate with its precursor glutamine (Glu+Gln)), and the caudate, putamen and thalami bilaterally using two dimensional chemical shift imaging (reporting relative NAA+NAAG and GPC+PCh). Relationships between metabolite concentrations and measures of social anxiety and related symptoms were also determined. Measures of social anxiety included symptom severity, blushing propensity, and gaze anxiety/avoidance. Results: We found, first, decreased relative glutamate concentration in the ACC of SAD and changes in myo-inositol with measures of social anxiety. Second, NAA metabolite concentration was increased in thalamus of SAD, and choline metabolite concentrations were related to measures of social anxiety. Lastly, choline metabolite concentration in the caudate and putamen showed changes in relation to measures of social anxiety. Conclusion: These findings are consistent with evidence that the reward/avoidance basal ganglia circuitry, as well as the glutamatergic system, play a role in mediating SAD symptoms.
KW - Anterior cingulate cortex (ACC)
KW - Glutamate
KW - N-acetyl-aspartate (NAA)
KW - Striatum
KW - Thalamus
UR - https://www.scopus.com/pages/publications/84922014105
U2 - 10.1016/j.pnpbp.2014.12.008
DO - 10.1016/j.pnpbp.2014.12.008
M3 - Article
C2 - 25549832
AN - SCOPUS:84922014105
SN - 0278-5846
VL - 58
SP - 97
EP - 104
JO - Progress in Neuro-Psychopharmacology and Biological Psychiatry
JF - Progress in Neuro-Psychopharmacology and Biological Psychiatry
ER -