2015
DOI: 10.1016/j.jad.2015.03.008
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Decreased thalamic glutamate level in unmedicated adult obsessive–compulsive disorder patients detected by proton magnetic resonance spectroscopy

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Cited by 40 publications
(32 citation statements)
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“…In the present study, although the positive correlation between decreased VMHC in the thalamus and compulsion disappeared after Bonferroni correction, we speculate that the impaired intrinsic interhemispheric functional homotopy in the thalamus might be associated with the regulation of compulsive behavior. Previous studies have also demonstrated increased gray matter volume, decreased regional spontaneous neuronal activity and homogeneity, and reduced glutamate level in the thalamus, which were also related to the clinical symptoms of OCD [3,6,7,12,42]. Taking these findings together, we have reason to speculate that the anatomical and functional abnormalities in the thalamus are widely implicated in OCD, and our findings provide new evidence that abnormalities in the CSTC circuitry underlie the pathophysiological mechanisms of OCD.…”
Section: Research Ping LIsupporting
confidence: 77%
“…In the present study, although the positive correlation between decreased VMHC in the thalamus and compulsion disappeared after Bonferroni correction, we speculate that the impaired intrinsic interhemispheric functional homotopy in the thalamus might be associated with the regulation of compulsive behavior. Previous studies have also demonstrated increased gray matter volume, decreased regional spontaneous neuronal activity and homogeneity, and reduced glutamate level in the thalamus, which were also related to the clinical symptoms of OCD [3,6,7,12,42]. Taking these findings together, we have reason to speculate that the anatomical and functional abnormalities in the thalamus are widely implicated in OCD, and our findings provide new evidence that abnormalities in the CSTC circuitry underlie the pathophysiological mechanisms of OCD.…”
Section: Research Ping LIsupporting
confidence: 77%
“…Also, an estimated 30% of patients do not adequately respond to first‐line treatments and complete functional recovery is rare. Varied individual response rates to SSRIs as well as the possible benefit of augmentation therapy with other agents such as antipsychotics further implicate role of other neurobiologic factors in pathophysiology of OCD …”
Section: What Is Known and Objectivementioning
confidence: 99%
“…Recent evidence suggests that abnormalities of the glutamatergic system may play role in the pathophysiology of OCD . In this regard, dysregulation of the cortico‐striatale‐thalamocortical (CSTC)may be a key component, as disruption of glutamatergic transmission – the main excitatory transmitter of this circuitry – has been reported in several studies of patients with OCD.…”
Section: What Is Known and Objectivementioning
confidence: 99%
“…According to five independent family based‐association studies, as well as a case‐control study, the SLC1A1 gene is most consistently associated with OCD . Disruption of glutamatergic transmission in the cortico‐striatal‐thalamo‐cortical (CSTC) circuitry plays a role in OCD pathogenesis . Higher glutamate concentrations in cerebrospinal fluid of patients with OCD compared to control groups have been reported .…”
Section: What Is Known and Objectivementioning
confidence: 99%
“…[6][7][8][9][10][11] Disruption of glutamatergic transmission in the cortico-striatal-thalamo-cortical (CSTC) circuitry plays a role in OCD pathogenesis. 12,13 Higher glutamate concentrations in cerebrospinal fluid of patients with OCD compared to control groups have been reported. 14 Moreover, a decreased amount of glutamate in the anterior cingulate cortex of children with OCD has been observed.…”
Section: What Is K Nown and Objec Tivementioning
confidence: 99%