ABSTRACT
Introduction: The hippocampus plays a key role in depressive disorder, and the amygdala is involved in depressive disorder through the key role that it plays in emotional regulation. Electroconvulsive therapy (ECT) may alter the microstructure of these two regions. Since mean diffusivity (MD), is known to be an indirect marker of microstructural integrity and can be derived from diffusion tensor imaging (DTI) scans, we aim to test the hypothesis that treatment-resistant depression (TRD) patients undergoing bilateral (BL) ECT exhibit a decrease of MD in their hippocampus and amygdala. Methods: Patients, between 50 and 70 years of age, diagnosed with TRD were recruited from the University Hospital of Toulouse and assessed clinically (Hamilton Depression Rating Scale, HAM-D) and by DTI scans at three time points: baseline, V2 (during treatment), and V3 within 1 week of completing ECT. Results: We included 15 patients, who were all responders. The left and right hippocampi and the left amygdala showed a significant decrease in MD at V3, compared to baseline [respectively: ß = -2.78, t = -1.97, p = 0.04; ß = -2.56, t = -2, p = 0.04; ß = -2.5, t = -2.3, p = 0.04, false discovery rate (FDR) corrected]. MD did not decrease in the right amygdala. Only the left amygdala was significantly associated with a reduction in HAM-D (ρ = 0.55, p = 0.049, FDR corrected). Conclusion: MD is an indirect microstructural integrity marker, which decreases in the hippocampus and the left amygdala, during BL ECT in TRD populations. This could be interpreted as a normalization of microstructural integrity in these structures.
ABSTRACT
INTRODUCTION: 20-30% of depressed patients experience Treatment Resistant Depression (TRD). Electroconvulsive Therapy (ECT) remains the treatment of choice for TRD. However, the exact mechanism of ECT remains unclear. We aim to assess grey matter changes in patients with TRD undergoing bilateral ECT treatment at different points during and after treatment. METHODS: Patients are recruited at the University Hospital of Toulouse. Eligibility criteria include a diagnosis of TRD and an age between 50 and 70 years old. Patients received clinical assessments (Hamilton Depression Rating Scale) and structural scans (MRI) at three points: baseline (within 48â¯h before the first ECT); V2 (after the first ECT considered effective); and V3 (within 1 week of completing ECT). RESULTS: At baseline, controls had significantly higher cortical thickness than patients in the fusiform gyrus, the inferior, middle and superior temporal gyrus, the parahippocampal gyrus and the transverse temporal gyrus (respectively: t(35)=2.7, pâ¯=â¯0.02; t(35)=2.89, pâ¯=â¯0.017; t(35)=3.1, pâ¯=â¯0.015; t(35)=3.6, pâ¯=â¯0.009; t(35)=2.37, pâ¯=â¯0.031; t(35)=2.46, pâ¯=â¯0.03). This difference was no longer significant after ECT. We showed an increase in cortical thickness in superior temporal gyrus between (i) baseline and V3 (t(62)=-3.43 pâ¯=â¯0.009) and (ii) V2 and V3 (t(62)=-3.42 pâ¯=â¯0.009). We showed an increase in hippocampal volume between (i) baseline and V3 (t(62)=-5.23 p < 0.001) and (ii) V2 and V3 (t(62)=-5.3 p < 0.001). CONCLUSION: We highlight that there are grey matter changes during ECT treatment in a population with TRD compared to a healthy control population. These changes seem to occur after several rounds of ECT.
Subject(s)
Depressive Disorder, Treatment-Resistant/pathology , Depressive Disorder, Treatment-Resistant/therapy , Electroconvulsive Therapy , Gray Matter/pathology , Adult , Aged , Brain/diagnostic imaging , Brain/pathology , Depressive Disorder, Treatment-Resistant/diagnostic imaging , Female , Gray Matter/diagnostic imaging , Hippocampus/diagnostic imaging , Hippocampus/pathology , Humans , Magnetic Resonance Imaging , Male , Middle Aged , Parahippocampal Gyrus/diagnostic imaging , Parahippocampal Gyrus/pathology , Temporal Lobe/diagnostic imaging , Temporal Lobe/pathologyABSTRACT
Posttraumatic stress disorder (PTSD) is commonly acknowledged to be associated with reduced specificity of autobiographical memory (AM). However, very few studies have assessed AM in the peritraumatic phase. The aim of the present study was to examine whether the AM impairment reported in PTSD is present a few days after a traumatic event. We assessed AM in 41 participants who had recently been exposed to trauma, and 34 controls who had never experienced a traumatic situation. The trauma-exposed participants also completed the Impact of Event Scale-R (IES-R), the Inventory of Peritraumatic Distress, and the Peritraumatic Dissociative Experiences Questionnaire. Results showed that autobiographical memories cued by negative words were significantly less specific in the group of trauma-exposed participants than in the control group (p = .008; d = 0.40). Thus, mild AM impairment was already present three days after trauma exposure, long before acute PTSD set in.