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Aging is an inevitable process and represents the accumulation of bodily alterations over time. Depression and chronic pain are highly prevalent in elderly populations. It is estimated that 13% of the elderly population will suffer simultaneously from the two conditions. Accumulating evidence suggests than neuroinflammation plays a critical role in the pathogenesis of both depression and chronic pain. Apart from the common pathophysiological mechanisms, however, the two entities have several clinical links. Their management is challenging for the pain physician; however, both pharmacologic and nonpharmacologic approaches are available and can be used when the two conditions are comorbid in the elderly patients.

Introduction: Vitamin B6 is a water-soluble vitamin that is naturally present in many foods and is accessible in many dietary supplements. The three natural forms are pyridoxine, pyridoxal, and pyridoxamine. Both vitamin B6 deficiency and high B6 intake have been described as risk factors for developing peripheral neuropathy (PN). The aim of this systematic review is to characterize and comprehensively describe B6-related PN. Method: A systematic, computer-based search was conducted using the PubMed database. Twenty articles were included in this review. Results: Higher vitamin B6 levels, which usually occur following the taking of nutritional supplements, may lead to the development of a predominantly, if not exclusively, sensory neuropathy of the axonal type. After pyridoxine discontinuation, such patients subjectively report improved symptoms. However, although low vitamin B6 levels can be seen in patients suffering from peripheral neuropathy of various etiologies, there is no firm evidence that low B6 levels have a direct causal relationship with PN. Many studies suggest subjective improvement of neuropathy symptoms in patients suffering from PN of various etiologies after receiving B6 supplementation; however, no data about B6 administration as a monotherapy exist, only as part of a combination treatment, usually with other vitamins. Therefore, the potential therapeutic role of B6 cannot be confirmed to date. Supplementation with vitamin B6, even as part of a nutritional multivitamin supplement, has not been proven harmful at permitted daily doses in patients who already suffer from PN. Conclusion: Current scientific evidence supports a neurotoxic role of B6 at high levels. Although some studies suggest that low B6 is also a potential risk factor, further studies in this area are needed.

Objective. Neuropathic pain is a common presenting complaint of patients with peripheral neuropathy (PN) and is considered one of the most disabling neuropathic symptoms, with detrimental effects on patients’ quality of life (QoL). The aim of this review was to overview the current literature that focuses on QoL in painful PN of various aetiologies. We sought to clarify the direct effect of pain and its treatment on patients’ QoL. Methodology. A systematic computer-based literature search was conducted using the PubMed database to search for papers on QoL in painful PN. Information was extracted regarding prevalence, demographics, and response to treatment where relevant. Results. We identified 66 articles eligible for inclusion. The vast majority of studies (n=47) focused on patients with diabetic PN. Other aetiologies of painful PN where QoL has been studied to date include gluten, immune-mediated, HIV, chemotherapy-induced, and chronic idiopathic axonal polyneuropathy. Pharmacological treatment is the mainstay in managing pain and has a direct positive and independent effect on the overall QoL. Other nonpharmacological approaches can also be of benefit, either alone or as adjuvant treatments, and are discussed. Conclusion. The findings demonstrate that QoL is impaired in painful PN and should not be neglected in clinical practice. Patients’ pain management and subsequent impact on QoL should routinely be assessed and monitored.

Neuropathic pain describes a range of unpleasant sensations caused by a lesion or disease of the somatosensory nervous system. The sensations caused by neuropathic pain are debilitating and improved treatment regimens are sought in order to improve the quality of life of patients. One proposed treatment for neuropathic pain is vitamin B12, which is thought to alleviate pain by a number of mechanisms including promoting myelination, increasing nerve regeneration and decreasing ectopic nerve firing. In this paper, the evidence for B12 as a drug treatment for neuropathic pain is reviewed. Twenty four published articles were eligible for inclusion in this systematic review in which a range of treatment regimens were evaluated including both B12 monotherapy and B12 in combination with other vitamins or conventional treatments, such as gabapentinoids. Overall, this systematic review demonstrates that there is currently some evidence for the therapeutic effect of B12 in the treatment of post-herpetic neuralgia (level II evidence) and the treatment of painful peripheral neuropathy (level III evidence).

Peripheral neuropathy (PN) is a common disease affecting about 5% of the general population after the age of 50. Causes of PN are numerous and include genetic, diabetes, alcohol, vitamin deficiencies, and gluten sensitivity among others. This systematic review aimed to study the association between oxidative stress and PN in an attempt to better understand PN pathogenesis. A computer-based, systematic search was conducted on the PubMed database, and ensuing data from included articles was analyzed and discussed in this review. Sixty-nine papers were eligible and were used for this review. Peripheral neuropathy is associated with an increase of reactive oxygen species and a decrease in endogenous antioxidants. Genetic predisposition to oxidative damage may be a factor. Antioxidant treatment is promising regarding treatment. Though further research is necessary to better understand the underlying mechanism, it is evident that oxidative stress is implicated in the pathogenesis of – or is at least systematically present in – PN.

The primary aim was to estimate the burnout prevalence among all medical students at the Medical School of the University of Cyprus. Secondary aims were to ascertain the predictors of burnout and its relationship with lifestyle habits, sleep quality and mental health. Burnout in the healthcare sector has drawn significant scientific attention over the last few years. Recent research underscored the large burden of profession-related burnout among medical students. An anonymous questionnaire was administered to all 189 eligible candidates. This included demographic and lifestyle characteristics. Sleep quality was assessed via the Pittsburg Sleep Quality Index, mental health was assessed via the mental health (MH) domain of the 36-item Short Form Health Survey (SF-36) and burnout with the Maslach Burnout Inventory-Student Survey (MBI-SS). Overall response rate was 96.3%. The burnout prevalence was 18.1%. There was a significant linear effect of between the year of studies and the burnout frequency [F(1) = 5.09, p = 0.024], implying that with increasing academic year there were more students with burnout, especially after the 4th year of education which signifies the beginning of clinical education. Students with burnout were more likely to have poor sleep quality (90.9% vs. 60.8%, odds ratio 4.33, p = 0.023) and worse mental health (MH score 40.2 ± 17.7 vs 62.9 ± 20.3, p<0.001). Alcohol consumers had more symptoms of cynicism and less feelings of efficacy than non-alcohol consumers. Moreover, less feelings of efficacy were significantly associated with more alcohol consumption among alcohol consumers. Burnout is prevalent in medical students and increases significantly during the clinical years. Students with burnout have worse sleep and mental health and might use alcohol as a coping mechanism. Implementing prevention strategies of burnout may be beneficial.

Introduction: Autism spectrum disorder (ASD) is a neurodevelopmental condition characterized by social communication difficulties and repetitive behaviors. Emerging evidence suggests a potential link between ASD and celiac disease (CD), possibly mediated by immune dysregulation and nutrient deficiencies. This study explores the shared biological pathways between ASD and CD using an in silico approach. Methods: Gene–disease associations for ASD and CD were retrieved from DisGeNET using MedGen Concept IDs (C1510586 and C0007570, respectively). An over-representation analysis (ORA) was conducted using GeneTrail 3.2 to identify significantly enriched biological pathways, which were then compared for overlap. A false discovery rate (FDR) < 0.05 was considered statistically significant. Results: The gene–disease association analysis identified 536 ASD-related genes and 52 CD-related genes. The ORA revealed several shared biological pathways, including immune pathways, cellular metabolism, and micronutrient processing (e.g., folate, selenium, vitamin A). These findings suggest immune dysfunction and nutrient malabsorption as potential mechanistic links between ASD and CD. Conclusions: The observed pathway overlap supports the hypothesis that immune dysregulation and metabolic disturbances contribute to both ASD and CD. Nutrient deficiencies, driven by CD-associated malabsorption, may exacerbate ASD symptoms. Additionally, sensory processing abnormalities in ASD could impact dietary choices, complicating gluten-free diet adherence. Future studies should validate these findings in clinical cohorts and explore dietary interventions, such as targeted supplementation, to mitigate ASD symptoms in individuals with CD.

Purpose. Burnout is a prolonged response to chronic emotional and interpersonal stressors on the job. The purpose of our cross-sectional study was to estimate the burnout rates among medical residents in the largest Greek hospital in 2012 and identify factors associated with it, based on the job demands-resources model (JD-R). Method. Job demands were examined via a 17-item questionnaire assessing 4 characteristics (emotional demands, intellectual demands, workload, and home-work demands’ interface) and job resources were measured via a 14-item questionnaire assessing 4 characteristics (autonomy, opportunities for professional development, support from colleagues, and supervisor’s support). The Maslach Burnout Inventory (MBI) was used to measure burnout. Results. Of the 290 eligible residents, 90.7% responded. In total 14.4% of the residents were found to experience burnout. Multiple logistic regression analysis revealed that each increased point in the JD-R questionnaire score regarding home-work interface was associated with an increase in the odds of burnout by 25.5%. Conversely, each increased point for autonomy, opportunities in professional development, and each extra resident per specialist were associated with a decrease in the odds of burnout by 37.1%, 39.4%, and 59.0%, respectively. Conclusions. Burnout among medical residents is associated with home-work interface, autonomy, professional development, and resident to specialist ratio.

Keywords: Nocebo, adverse events, trial design

Epilepsy is a risk factor for the development of psychogenic non-epileptic seizures (PNES) and comorbid epilepsy is recognized as a comorbidity in about 10–30% of patients with PNES. The combination of epileptic and nonepileptic seizures poses a particular diagnostic challenge. In patients with epilepsy, additional PNES may be suspected on the basis of their typical semiology. The possibility of additional PNES should also be considered if seizures fail to respond to antiepileptic drug treatment, in patients with frequent emergency admissions with seizures and in those who develop new types of seizures. The description of semiological details by patients and witnesses can suggest additional PNES. Home video recordings can support an initial diagnosis, however, especially in patients with mixed seizure disorders it is advisable to seek further diagnostic confirmation by capturing all habitual seizure types with video-EEG. The clinical features of PNES associated with epilepsy are similar to those in isolated PNES disorders and include longer duration, fluctuating course, asynchronous movements, pelvic thrusting, side-to-side head or body movement, persistently closed eyes and mouth, ictal crying, recall of ictal experiences and absence of postictal confusion. PNES can also present as syncope-like episodes with unresponsiveness and reduced muscle tone. There is no unique epileptological or brain pathology profile putting patients with epilepsy at risk of additional PNES. However, patients with epilepsy and PNES typically have lower educational achievements and higher levels of psychiatric comorbidities than patients with epilepsy alone. Psychological trauma, including sexual abuse, appears to be a less relevant aetiological factor in patients with mixed seizure disorders than those with isolated PNES, and the gender imbalance (i.e. the greater prevalence in women) is less marked in patients with PNES and additional epilepsy than those with PNES alone. PNES sometimes develop after epilepsy surgery. A diagnosis of ‘known epilepsy’ should never be accepted without (at least brief) critical review. This narrative review summarises clinical, electrophysiological and historical features that can help identify patients with epilepsy and additional PNES.