Background: Balance and proprioception are essential elements in postural control and injury prevention. Proprioception, the body’s sense of position and movement, is closely tied to balance, which depends on input from the visual, vestibular, and somatosensory systems. This article explores the link between trauma experiences and proprioceptive dysfunction, emphasizing how heightened muscle tone, dissociation, and altered sensory processing contribute to balance issues and the risk of injury. Method: The study included 48 participants, aged 18–25. Participants completed the Emotional Regulation Scale, Dissociative Experiences Scale II, and Childhood Trauma Questionnaire, after which they had to stand on a BTrackS Balance Plate while being exposed to images that are designed to evoke emotions from the OASIS image set. The balance plate software calculated outcomes of the participants’ postural sway (total sway, sway area, root mean square (RMS) to the mediolateral (ML) and anteroposterior (AP) way, and excursion to ML and AP ways). Results: Dissociative experience shows significant correlation with RMS ML when viewing positive pictures (rτ = 0.207, p = 0.045) and when viewing negative pictures again; scores with RMS ML (rτ = 0.204, p = 0.049) but also with RMS AP (rτ = 0.209, p = 0.042) and with Excursion ML (rτ = 0.200, p = 0.049) were significant. Experiences of physical abuse affected certain indicators of postural sway when viewing positive images compared to participants with no such experience (sway area: U = 374.50, p = 0.027; RMS AP: U = 383.50, p = 0.016; Excursion ML: U = 397.00, p = 0.007). Similarly, physical neglect affected postural sway during viewing of negative images (sway area: U = 366.50, p = 0.003; RMS AP: U = 371.00, p = 0.004; Excursion ML: U = 347.00, p = 0.034; and Excursion AP: U = 353.00, p = 0.010). Conclusions: The study highlights that dissociation disrupts balance in trauma survivors, especially under emotional stress which highlights the potential for motor-based treatments.

Ethanol is a known neurotoxic agent that induces endoplasmic reticulum (ER) stress and apoptosis in nerve cells. The transcription factor CREB is crucial for cell survival under stress; however, its involvement in ethanol-induced endoplasmic reticulum (ER) stress remains poorly understood. We examined the effects of ethanol on wild-type PC12 cells and CREB-overexpressing PC12-CREB cells. Cell viability was evaluated by ATP assays, apoptosis was detected by Hoechst staining, and key proteins involved in ER stress and apoptotic signaling were analyzed by Western blot analysis. Ethanol treatment decreased cell viability and increased apoptosis in wild-type PC12 cells in a time-dependent manner. In contrast, PC12-CREB cells-maintained viability and showed significantly lower apoptotic cell numbers. Ethanol activated markers of ER stress (BiP, CHOP, ATF6) and pro-apoptotic pathways (phosphorylation of JNK and p38 MAPK) in wild-type cells. In CREB-overexpressing cells, CHOP induction and JNK activation were decreased, while the expression of the anti-apoptotic protein Mcl-1 was increased. CREB overexpression protects against ethanol-induced ER stress and apoptosis. This protective effect is mediated through modulation of unfolded protein response (UPR) signaling and regulation of pro-and anti-apoptotic gene expression. These findings underscore a potential role for CREB in attenuating ethanol-induced neurotoxicity.