Pain is a subjective experience that is influenced by genetics, gender, social, cultural and personal parameters. Opposed to chronic pain, which by definition has to last for at least 3 months, acute pain is mostly because of trauma, acute medical conditions or treatment. The link between mood disorders and acute pain has proven to be increasingly significant since the link is bi-directional, and both act as risk factors for each other. Depression and anxiety are associated with increased perception of pain severity, whereas prolonged duration of acute pain leads to increased mood dysregulation. Although both depression and anxiety have a proven association with acute pain, the link between depression and acute pain is more thoroughly studied. Pain can be the presenting or sole complaint in depressed patients who present to primary care practices and is often overlooked by clinicians. However, reports on the perception of experimentally-induced pain in depressed patients are mixed, showing both an increased and decreased pain threshold and pain tolerance across various studies. Although less data is published about anxiety and pain, the relationship is consistent across studies as increased anxiety leads to increased severity of pain perceived and decreased pain tolerance. Anxiety as well as fear, stress, and catastrophizing are also shown to be mediators in the causal pathway between pain and disability.

Understanding of the basis of osteoarthritis (OA) has seen some interesting advancements in recent years. It has been observed that cartilage degeneration is preceded by subchondral bone lesions, suggesting a key role of this mechanism within the pathogenesis and progression of OA, as well as the formation of ectopic bone and osteophytes. Moreover, low-grade, chronic inflammation of the synovial lining has gained a central role in the definition of OA physiopathology, and central immunological mechanisms, innate but also adaptive, are now considered crucial in driving inflammation and tissue destruction. In addition, the role of neuroinflammation and central sensitization mechanisms as underlying causes of pain chronicity has been characterized. This has led to a renewed definition of OA, which is now intended as a complex multifactorial joint pathology caused by inflammatory and metabolic factors underlying joint damage. Since this evidence can directly affect the definition of the correct therapeutic approach to OA, an improved understanding of these pathophysiological mechanisms is fundamental. To this aim, this review provides an overview of the most updated evidence on OA pathogenesis; it presents the most recent insights on the pathophysiology of OA, describing the interplay between immunological and biochemical mechanisms proposed to drive inflammation and tissue destruction, as well as central sensitization mechanisms. Moreover, although the therapeutic implications consequent to the renewed definition of OA are beyond this review scope, some suggestions for intervention have been addressed.

Objectives: The aim of this ecological study was to investigate what the impact of digital learning due to the COVID-19 pandemic was on the burnout and overall mental health (MH) of medical students. Background: During the unprecedented era of the COVID-19 pandemic, the majority of countries worldwide adopted very strong measures. Universities closed their doors, and education continued through digital learning lectures. Methods: An anonymous questionnaire was administered to all 189 eligible candidates before and during the COVID-19 pandemic. Mental health was assessed via the MH domain of the 36-item Short Form Health Survey (SF-36) and burnout with the Maslach Burnout Inventory—Student Survey (MBI-SS). Results: The overall response rate was 81.5%. The overall burnout prevalence did not differ significantly between the two periods (pre-COVID-19 18.1% vs. COVID-19 18.2%). However, the burnout prevalence dropped significantly in year 4 (pre-COVID-19 40.7% vs. COVID-19 16.7%, p = 0.011), whereas it increased significantly in year 6 (pre-COVID-19 27.6% vs. COVID-19 50%, p = 0.01). When looking at each MBI-SS dimension separately, we found that emotional exhaustion decreased significantly in year 4 but increased in year 6, and cynicism increased in all years. The overall MH deteriorated significantly between the two periods (pre-COVID-19 58.8 ± 21.6 vs. COVID-19 48.3 ± 23, p < 0.001). Conclusions: Digital learning in medical studies carries significant risks. Not only does the MH deteriorate, but cynicism levels also increase. Emotional exhaustion was found to increase particularly in final year students, who struggle with the lack of clinical experience just before they start working as qualified junior doctors.

The primary aim of this systematic review was to establish the prevalence, character, and risk factors of peripheral neuropathy amongst chronic alcohol abusers and to identify the most appropriate management strategies. In this review, possible pathogenetic mechanisms are also discussed. A systematic, computer-based search was conducted using the PubMed database. Data regarding the above parameters were extracted. 87 articles were included in this review, 29 case–control studies, 52 prospective/retrospective cohort studies and 2 randomised control trials, 1 cross sectional study, and 3 population-based studies. The prevalence of peripheral neuropathy amongst chronic alcohol abusers is 46.3% (CI 35.7– 57.3%) when confirmed via nerve conduction studies. Alcohol-related peripheral neuropathy generally presents as a progressive, predominantly sensory axonal length-dependent neuropathy. The most important risk factor for alcohol-related peripheral neuropathy is the total lifetime dose of ethanol, although other risk factors have been identified including genetic, male gender, and type of alcohol consumed. At present, it is unclear what the pathogenetic mechanisms for the development of neuropathy amongst those who chronically abuse alcohol are, and therefore, it is unknown whether it is attributed to the direct toxic effects of ethanol or another currently unidentified factor. There is presently sparse data to support a particular management strategy in alcohol-related peripheral neuropathy, but the limited data available appears to support the use of vitamin supplementation, particularly of B-vitamin regimens inclusive of thiamine.

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.

Alzheimer’s Disease (AD) accounts for 60-70% of all dementia cases, and clinical diagnosis at its early stage is extremely difficult. As several new drugs aiming to modify disease progression or alleviate symptoms are being developed, to assess their efficacy, novel robust biomarkers of brain function are urgently required. This study aims to explore a routine to gain such biomarkers using the quantitative analysis of Electroencephalography (QEEG). This paper proposes a supervised classification framework which uses EEG signals to classify healthy controls (HC) and AD participants. The framework consists of data augmentation, feature extraction, K-Nearest Neighbour (KNN) classification, quantitative evaluation and topographic visualisation. Considering the human brain either as a stationary or a dynamical system, both frequency-based and time-frequency-based features were tested in 40 participants. Results: a) The proposed method can achieve up to 99% classification accuracy on short (4s) eyes open EEG epochs, with the KNN algorithm that has best performance when compared to alternative machine learning approaches; b) The features extracted using the wavelet transform produced better classification performance in comparison to the features based on FFT; c) In the spatial domain, the temporal and parietal areas offer the best distinction between healthy controls and AD. The proposed framework can effectively classify HC and AD participants with high accuracy, meanwhile offering identification and localisation of significant QEEG features. These important findings and the proposed classification framework could be used for the development of a biomarker for the diagnosis and monitoring of disease progression in AD.