Background The hippocampus is likely involved in mood disorders but in vivo evidence for the role of anatomically distinct hippocampal subregions is lacking. Multiple sclerosis (MS), an inflammatory disease of the CNS, is linked to a high prevalence of depression as well as hippocampal atrophy and may thus provide important insight into the pathological correlates of medical depression. Here, we examine the role of subregional hippocampal volume for depression in relapsing-remitting (RR) MS. Methods Anatomically defined hippocampal subregional volumes (Cornu Ammonis 1 (CA1), CA2–CA3 and the Dentate Gyrus (CA23DG), Subiculum, Entorhinal Cortex) were measured using a high resolution T2-weighted magnetic resonance imaging (MRI) sequence in 29 RRMS patients and 20 matched healthy controls. Diurnal salivary cortisol was assessed at awakening, 4pm and 9pm on two consecutive days. Subjects also completed the Beck Depression Inventory (BDI-II). Results MS patients showed smaller hippocampal volumes compared to controls, particularly in the CA1 and Subiculum subregions. In addition, MS patients with depressive symptoms (BDI-II > 13) also showed smaller CA23DG volumes and higher cortisol levels. Within the MS group, CA23DG volume was correlated with depressive symptoms and cortisol levels. There were no associations with number of previous steroid treatments, global atrophy, or disease duration. Conclusions This report provides in vivo evidence for selective association of smaller CA23DG subregional volumes in the hippocampus with cortisol hypersecretion and depressive symptoms in MS.

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Introduction A novel approach of in‐advance preparatory respiratory training and practice for deep inspiration breath holding (DIBH) has been shown to further reduce cardiac dose in breast cancer radiotherapy patients, enabled by deeper (extended) DIBH. Here we investigated the consistency and stability of such training‐induced extended DIBH after training completion and throughout the daily radiotherapy course. Methods Daily chestwall motion from real‐time surface tracking transponder data was analysed in 67 left breast radiotherapy patients treated in DIBH. Twenty‐seven received preparatory DIBH training/practice ( prep Trn) 1–2 weeks prior to CT simulation, resulting in an extended DIBH ( ext DIBH) and reduced cardiac dose at simulation. Forty had only conventional immediate pre‐procedure DIBH instruction without prep Trn and without extended DIBH (non‐Trn group). Day‐to‐day variability in chestwall excursion pattern during radiotherapy was compared among the groups. Results The average of daily maximum chestwall excursions was overall similar, 2.5 ± 0.6 mm for prep Trn/ ext DIBH vs. 2.9 ± 0.8 mm for non‐Trn patients ( P = 0.24). Chestwall excursions beyond the 3‐mm tolerance threshold were less common in the prep Trn/ ext DIBH group (18.8% vs. 37.5% of all fractions within the respective groups, P = 0.038). Among patients with cardiopulmonary disease those with prep Trn/ ext DIBH had fewer chestwall excursions beyond 3 mm (9.4% vs. 46.7%, P = 0.023) and smaller average maximum excursions than non‐Trn patients (2.4 ± 0.3 vs. 3.0 ± 0.6 mm, P = 0.047, respectively). Conclusion Similar stability of daily DIBH among patients with and without preparatory training/practice suggests that the training‐induced extended DIBH and cardiac dose reductions were effectively sustained throughout the radiotherapy course. Training further reduced beyond‐tolerance chestwall excursions, particularly in patients with cardiopulmonary disease.

The case presented describes a 24-year-old female with mitochondrial myopathy, encephalopathy, lactic acidosis, and stroke (MELAS) who was diagnosed with anorexia nervosa (AN) and treated for the eating disorder for two years before her mitochondrial cytopathy was detected. Upon closer scrutiny of her symptoms, she did not have body image disturbance and thus did not meet criteria for AN despite a body mass index (BMI) of 12 and significant reduction of food intake. Additionally, neurological and gastrointestinal symptoms, for which an eating disorder could not account, were present, prompting a broadening of the differential leading to the correct diagnosis. Eating disorder symptoms have been documented to occur comorbidly with a mitochondrial cytopathy but not as a presenting syndrome in the absence of an eating disorder as defined by the Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition, Text Revision (DSM-IV-TR).