Restoring bottom-up communication in brain-heart interplay after trauma-focused psychotherapy in breast cancer patients with post-traumatic stress disorder.

BACKGROUND: The psychological impact of breast cancer (BC) is substantial, with a significant number of patients (up to 32 %) experiencing post-traumatic stress disorder (PTSD). Exploring the emotional aspects of PTSD through the functional brain-heart interplay (BHI) offers valuable insights into the condition. BHI examines the functional interactions between cortical and sympathovagal dynamics. This study aims to investigate changes in functional directional BHI after trauma-focused (TF) psychotherapy, specifically Eye Movement Desensitization and Reprocessing (EMDR), in comparison to treatment as usual (TAU) among BC patients with PTSD. To our knowledge, this study represents the first examination of such changes. METHODS: We enrolled thirty BC patients who met the criteria for a PTSD diagnosis, with fourteen receiving EMDR and fifteen receiving TAU over a two- to three-month period. We analyzed changes in the emotional response during a script-driven imagery setting. Quantification of the functional interplay between EEG and sympathovagal dynamics was achieved using the synthetic data generation model (SDG) on electroencephalographic (EEG) and heartbeat series. Our focus was on the difference in the BHI index extracted at baseline and post-treatment. RESULTS: We found statistically significant higher coupling in the heart-to-brain direction in patients treated with EMDR compared to controls. This suggests that the flow of information from the autonomic nervous system to the central nervous system is restored following EMDR-induced recovery from PTSD. Furthermore, we observed a significant correlation between improvements in PTSD symptoms and an increase in functional BHI after EMDR treatment. CONCLUSIONS: TF psychotherapy, particularly EMDR, appears to facilitate the restoration of the bottom-up flow of interoceptive information, which is dysfunctional in patients with PTSD. The application of BHI analysis to the study of PTSD not only aids in identifying biomarkers of the disorder but also enhances our understanding of the changes brought about by TF treatments.

Prevalence and features of peripheral neuropathy in Parkinson's disease patients under different therapeutic regimens.

BACKGROUND: Recent reports suggest increased frequency of peripheral neuropathy (PN) in Parkinson's disease (PD) patients on levodopa compared with age-matched controls particularly during continuous levodopa delivery by intestinal infusion (CLDII). The aim of this study is to compare frequency, clinical features, and outcome of PN in PD patients undergoing different therapeutic regimens. METHODS: Three groups of consecutive PD patients, 50 on intestinal levodopa (CLDII), 50 on oral levodopa (O-LD) and 50 on other dopaminergic treatment (ODT), were enrolled in this study to assess frequency of PN using clinical and neurophysiological parameters. A biochemical study of all PN patients was performed. RESULTS: Frequency of PN of no evident cause was 28% in CLDII, 20% in O-LD, and 6% in ODT patients. Clinically, 71% of CLDII patients and all O-LD and ODT PN patients displayed a subacute sensory PN. In contrast, 29% of CLDII patients presented acute motor PN. Levodopa daily dose, vitamin B12 (VB12) and homocysteine (hcy) levels differed significantly in patients with PN compared to patients without PN. CONCLUSIONS: Our findings support the relationship between levodopa and PN and confirm that an imbalance in VB12/hcy may be a key pathogenic factor. We suggest two different, possibly overlapping mechanisms of PN in patients on CDLII: axonal degeneration due to vitamin deficiency and inflammatory damage. Whether inflammatory damage is triggered by vitamin deficiency and/or by modifications in the intestinal micro-environment should be further explored. Proper vitamin supplementation may prevent peripheral damage in most cases.