Carpal tunnel syndrome (CTS) alters sensory afferent input and may affect cortical sensorimotor processing. We investigated short-latency afferent inhibition (SAI) and its relationship with fine motor performance in 25 patients with unilateral mild-to-moderate CTS. SAI was assessed using individualized interstimulus intervals based on N20 latency. SAI did not differ between the affected and unaffected sides (p = .539). However, higher SAI values, indicating less inhibition, were associated with poorer fine motor performance, with longer Nine-Hole Peg Test completion times on the affected side (p = .042). These findings suggest that individual variation in afferent inhibition may be related to fine motor hand function in CTS.
Objectives To characterize intraoperative neurophysiological monitoring in pediatric epilepsy surgery in a single tertiary center. Methods We reviewed intraoperative neurophysiological monitoring procedures during pediatric epilepsy surgeries at Meyer Children’s Hospital, Florence, Italy, from 2018 to 2025. Results We analyzed 39 procedures in 37 children with lesional epilepsy. Mean age at surgery was 9.4 years. All patients underwent a comprehensive presurgical workup. Frontal lobe resection was the most frequent surgery, and focal cortical dysplasia was the most common histopathology. Total intravenous anesthesia and neuronavigation were used routinely. Brain activity was monitored using intraoperative electroencephalography; motor function was assessed using motor evoked potentials, direct cortical and subcortical stimulation, and continuous electromyography; somatosensory and visual function were evaluated using somatosensory and visual evoked potentials, respectively. All responses remained stable throughout all procedures. We reached high mean transcranial (164.4 mA) and cortical (21.7 mA) stimulation thresholds, however, we observed only one intraoperative seizure (2.6%) following intraoperative bleeding. Mean follow-up after surgery was 30.9 months. Expected postoperative deficits occurred in 38.5% procedures (permanent in three patients). At last visit 66.7% of patients were seizure-free. Discussion In pediatric epilepsy surgery, intraoperative neurophysiological monitoring is safe even at high stimulation thresholds. Combining presurgical planning and intraoperative neurophysiological monitoring optimizes pediatric epilepsy seizure and functional outcomes.
Smoking and alcohol misuse are associated with reductions in long-chain polyunsaturated fatty acids (PUFA). We investigated plasma fatty acid (FA) profiles and in vivo n-6 PUFA metabolism in male and female participants who either smoked or did not smoke cigarettes. Participants followed self-selected (SS), fish-based (FB), and beef-based (BB) diets for 3 weeks each. Participants diagnosed with an alcohol use disorder (AUD) were included. Individuals received 2H5-18:2n-6 ethyl ester orally. Endogenous FA were analyzed using gas chromatography and the 2H5-n-6 PUFA by gas chromatography–mass spectrometry. The concentration-time curves for the 2H5-n-6 PUFA were fit to a compartmental model. Among nonsmoking individuals, the FB diet elevated plasma 20:5n-3 and 22:6n-3 by 2.5-fold. This was not observed in smokers. Male smokers had higher plasma FA levels on both the SS and BB diets compared to nonsmokers and heightened synthesis of 2H5-20:4n-6. In female smokers, 2H5-20:4n-6 synthesis was suppressed on SS diets. In AUD males, plasma n-3 PUFA were lower compared to smokers, and both AUD males and females had diminished synthesis of 2H5-20:4n-6 compared to smokers. In smokers, turnover of plasma 20:4n-6 was lower relative to nonsmokers. In AUD males, turnover of 18:2n-6 and 20:4n-6 were also lower compared to smokers. Smoking had a major impact on FA profiles in males, but the effects on n-6 PUFA metabolism between males and females were diverse. The FB diet did not elevate plasma n-3 PUFA in smokers compared with nonsmokers. Smoking and alcohol use profoundly altered plasma lipids and n-6 PUFA metabolism in male and female subjects.
High-fat diets (HFDs) are a major modifiable risk factor for intestinal health. Current research focuses primarily on palmitate (C16:0); however, myristate (C14:0, rich in dairy products) has been minimally investigated. HFDs increase ceramide generation, which drives endoplasmic reticulum (ER) stress, with both sphingolipids and ER stress being key contributors to intestinal biology. Whether different fatty acids uniquely impact sphingolipid metabolism and ER stress in intestinal biology has not been well defined. Human colon epithelial cells were utilized to determine the role of ceramide synthases (CerS) 5 and 6 on myristate-induced ER stress using pharmacologic inhibitors and siRNA. Intestinal epithelial cell-specific CerS5 and/or CerS6 knockout mice of both sexes were fed a control, high milk-fat, or high lard-fat diet for 16 weeks. Cells and colon tissues were analyzed for lipids, mRNA, and protein. Myristate treatment increased d18:1/C14:0-ceramide and induced IRE1α-dependent ER stress. Inhibition of CerS suppressed these effects, yet knockdown of CerS5/6, the primary enzymes generating d18:1/C14:0-ceramide, unexpectedly exacerbated IRE1α activation both in vitro and in vivo, potentially due to depletion of dihydro(dh)sphingosine. Altogether, our data suggest that loss of CerS5/6 exacerbates myristate-induced intestinal ER stress in colon epithelial cells and in vivo, and accumulation of dhsphingosine may provide protection.
