Journal of Clinical and Diagnostic Research aims to publish findings of doctors at grass root level and post graduate students, so that all unique medical experiences are recorded in literature.

Background and aims: Despite its inclusion in the 11th revision of the International Classification of Diseases, there is a virtual paucity of high-quality scientific evidence about compulsive sexual behavior disorder (CSBD), especially in underrepresented and underserved populations. Therefore, we comprehensively examined CSBD across 42 countries, genders, and sexual orientations, and validated the original (CSBD-19) and short (CSBD-7) versions of the Compulsive Sexual Behavior Disorder Scale to provide standardized, state-of-the-art screening tools for research and clinical practice.Method: Using data from the International Sex Survey (N = 82,243; M_age = 32.39 years, SD = 12.52), we evaluated the psychometric properties of the CSBD-19 and CSBD-7 and compared CSBD across 42 countries, three genders, eight sexual orientations, and individuals with low vs. high risk of experiencing CSBD.Results: A total of 4.8% of the participants were at high risk of experiencing CSBD. Country- and gender-based differences were observed, while no sexual-orientation-based differences were present in CSBD levels. Only 14% of individuals with CSBD have ever sought treatment for this disorder, with an additional 33% not having sought treatment because of various reasons. Both versions of the scale demonstrated excellent validity and reliability.Discussion and conclusions: This study contributes to a better understanding of CSBD in underrepresented and underserved populations and facilitates its identification in diverse populations by providing freely accessible ICD-11-based screening tools in 26 languages. The findings may also serve as a crucial building block to stimulate research into evidence-based, culturally sensitive prevention and intervention strategies for CSBD that are currently missing from the literature.

The second year of the COVID-19 (coronavirus disease) pandemic has seen the need to identify and assess the long-term consequences of a SARS-CoV-2 infection on an individual’s overall wellbeing, including adequate cognitive functioning. ‘Cognitive COVID’ is an informal term coined to interchangeably refer to acute changes in cognition during COVID-19 and/or cognitive sequelae with various deficits following the infection. These may manifest as altered levels of consciousness, encephalopathy-like symptoms, delirium, and loss of various memory domains. Dysexecutive syndrome is a peculiar manifestation of ‘Cognitive COVID’ as well. In the previous major outbreaks of viruses like SARS-CoV, MERS-CoV and Influenza. There have been attempts to understand the underlying mechanisms describing the causality of similar symptoms following SARS-CoV-2 infection. This review, therefore, is attempting to highlight the current understanding of the various direct and indirect mechanisms, focusing on the role of neurotropism of SARS-CoV-2, the general pro-inflammatory state, and the pandemic-associated psychosocial stressors in the causality of ‘Cognitive COVID.’ Neurotropism is associated with various mechanisms including retrograde neuronal transmission via olfactory pathway, a general hematogenous spread, and the virus using immune cells as vectors. The high amounts of inflammation caused by COVID-19, compounded with potential intubation, are associated with a deleterious effect on the cognition as well. Finally, the pandemic’s unique psychosocial impact has raised alarm due to its possible effect on cognition. Furthermore, with surfacing reports of post-COVID-vaccination cognitive impairments after vaccines containing mRNA encoding for spike glycoprotein of SARS-CoV-2, we hypothesize their causality and ways to mitigate the risk. The potential impact on the quality of life of an individual and the fact that even a minor proportion of COVID-19 cases developing cognitive impairment could be a significant burden on already overwhelmed healthcare systems across the world make it vital to gather further evidence regarding the prevalence, presentation, correlations, and causality of these events and reevaluate our approach to accommodate early identification, management, and rehabilitation of patients exhibiting cognitive symptoms.

Background: Obstructive sleep apnea (OSA) and type 2 diabetes mellitus (T2DM) are two interacting epidemics both with high prevalence and morbidity. Both epidemiologic and clinical studies suggest that the majority of patients with T2DM also have OSA and untreated OSA in these patients results in poor glycemic control leading to acceleration of diabetes-related complications. Objectives: To assess the prevalence and severity of OSA in T2DM patients and to assess the impact of OSA treatment on presenting symptoms and hemoglobin A1c (HbA1c). Methods: We performed polysomnography (PSG) studies and measured HbA1c in 62 consecutive patients with T2DM that were referred from various subspecialty clinics from July 2011 to August 2013. Results: In our 62 diabetic patients, 59 (95.2%) had abnormal PSG. Based on Apnea–Hypopnea Index (AHI) score, 3 (5.1%) patients had mild, 28 (47.5%) had moderate, and 28 (47.5%) had severe OSA. The mean AHI of diabetic patients was significantly more than nondiabetic patients, i.e., 25.7 versus 19.7 (P = 0.001). Variables that significantly correlated with the presence of OSA include age, gender, body mass index (BMI), hypertension, diabetes, and cardiovascular disease (P < 0.05); however, on logistic regression only BMI, hypertension, and nocturia correlated with OSA. Overall, 59% of diabetic patients showed improvement in their glycemic control as measured by HbA1c with continuous positive airway pressure (CPAP) treatment. Significant, moderate, and mild categories of treatment response were respectively observed in 7%, 20%, and 32% of patients. Conclusion: Treatment of OSA with CPAP reduces HbA1c in a significant number of diabetics.