ABSTRACT
BACKGROUND: Cutaneous neuropraxia is the most common complication following distal biceps tendon repair (DBTR). Currently, no patient demographic factors have been implicated in its occurrence, course, or resolution. The purpose of this study is to explore various patient demographics and their association with postoperative neuropraxia. Further it investigates how mental health scores correlate with patient-reported outcomes, and whether occurrence of neuropraxia alters this association. METHODS: This retrospective review evaluates a consecutive series of patients who underwent distal biceps repair with a single-incision cortical button technique. Patients with reported outcome data at a minimum of 1 year (n = 47) were included for analysis. Demographic data including age, sex, body mass index (BMI), diabetes, smoking status, and occurrence of neuropraxia were recorded. Patient-reported outcome measures (PROMs) include the American Shoulder and Elbow Surgeons-Elbow (ASES-E) score, Single Assessment Numeric Evaluation (SANE) score, Visual Analog Scale (VAS) for pain, Disabilities of the Arm, Shoulder, and Hand Score (QuickDASH), and Veterans RAND 12 (VR-12) Mental Component Score (MCS) and Physical Component Score (PCS) quality-of-life assessment. RESULTS: Postoperative neuropraxia of any duration occurred in 45% (21/47) of patients in this cohort following DBTR. Of these, 62% (13/21) reported resolution of symptoms by the latest follow-up. Mean time to resolution of neuropraxia was 148 days. Patient age, BMI, smoking history, time to surgery, tear thickness, and increasing surgeon experience across the study period were not significantly associated with the incidence or time to resolution of postoperative neuropraxia. Scores for patient satisfaction, VAS, ASES, QuickDASH, SANE, VR-12 MCS, VR-12 PCS, and flexion ROM did not differ significantly between patients with and without postoperative neuropraxia. CONCLUSION: Patient satisfaction following DBTR was not significantly associated with postoperative neuropraxia. Patient and surgical characteristics did not influence the occurrence or time to resolution of neuropraxia. The occurrence of postoperative neuropraxia did not result in significant functional limitations.
ABSTRACT
Valproic acid (VPA) is an antiepileptic, bipolar, and migraine medication, which is associated with embryonic dysmorphology, more specifically neural tube defects (NTDs), if taken while pregnant. One mechanism by which VPA may cause NTDs is through oxidative stress that cause disruption of cell signaling. However, mechanisms of VPA-induced oxidative stress are not fully understood. Since VPA is a deacetylase inhibitor, we propose that VPA promotes mitochondrial superoxide dismutase-2 (SOD2) acetylation, decreasing SOD2 activity and increasing oxidant levels. Using the pluripotent embryonal carcinoma cell line, P19, VPA effects were evaluated in undifferentiated and neurodifferentiated cells. VPA treatments increased oxidant levels, oxidized the glutathione (GSH)/glutathione disulfide (GSSG) redox couple, and decreased total SOD and SOD2 activity in undifferentiated P19 cells but not in differentiated P19 cells. VPA caused a specific increase in mitochondrial oxidants in undifferentiated P19 cells, VPA did not alter respirometry measurements. Immunoblot analyses demonstrated that VPA increased acetylation of SOD2 at lysine68 (AcK68 SOD2) in undifferentiated P19 cells but not in differentiated P19 cells. Pretreatments with the Nrf2 inducer, dithiol-3-thione (D3T), in undifferentiated P19 cells prevented increased oxidant levels, GSH/GSSG redox oxidation and restored total SOD and SOD2 activity, correlating with a decrease in AcK68 SOD2 levels. In embryos, VPA decreased total SOD and SOD2 activity and increased levels of AcK68 SOD2, and D3T pretreatments prevented VPA effects, increasing total SOD and SOD2 activity and lowering levels of AcK68 SOD2. These data demonstrate a potential, contributing oxidizing mechanism by which VPA incites teratogenesis in developing systems. Moreover, these data also suggest that Nrf2 interventions may serve as a means to protect developmental signaling and inhibit VPA-induced malformations.