Archival ReportEvidence of Cortical Inhibitory Deficits in Major Depressive Disorder
Section snippets
Subjects
This study included 60 right-handed patients (mean age = 47.17 years ± 11.20 years, 22 men and 38 women) with a DSM-IV diagnosis of MDD confirmed by the Structured Clinical Interview for DSM-IV (SCID) (18) and 25 healthy right-handed volunteers (mean age = 43.84 years ± 8.95 years, 12 men and 13 women). Healthy subjects were screened for psychopathology with a modified SCID (18). Exclusion criteria included a self-reported comorbid medical or neurological illness, a history of drug or alcohol
Results
Across all four groups of patients with MDD and healthy control subjects, there was no significant difference in the percentage of male subjects (χ2 = 2.65, p = .10) or in age [ANOVA: F(84) = 1.30, p = .28] (Table 1). Vis-à-vis psychiatric symptoms, group-wise comparisons among TRD and unmedicated MDD patients did not reveal significant differences in HAMD17 scores [t(39) = 1.53, p = .13]; however, as anticipated, there were significant differences between TRD patients and unmedicated MDD
Discussion
Our results suggest that all patients with MDD, regardless of symptom or medication state, demonstrated significant CSP deficits compared with healthy subjects. By contrast, only TRD patients demonstrated SICI deficits. Taken together these data suggest that MDD is associated with deficits in neurophysiological indexes of GABAB receptor-mediated inhibitory neurotransmission, whereas patients with TRD demonstrated deficits in neurophysiological indexes of both GABAB and GABAA receptor-mediated
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