The coronavirus disease 2019 (COVID-19) crisis has greatly affected human lives across the world. Uncertainty and quarantine have been affecting people’s mental health. Estimations of mental health problems are needed immediately for the better planning and management of these concerns at a global level. A rapid scoping review was conducted to get the estimation of mental health problems in the COVID-19 pandemic during the first 7 months. Peer-reviewed, data-based journal articles published in the English language were searched in the PubMed, Medline, and Google Scholar electronic databases from December 2019 to June 2020. Papers that met the inclusion criteria were analyzed and discussed in this review. A total of 16 studies were included. Eleven studies were from China, two from India, and one from Spain, Italy, and Iran. Prevalence of all forms of depression was 20%, anxiety 35%, and stress 53% in the combined study population of 113,285 individuals. The prevalence rate of all forms of depression, anxiety, stress, sleep problems, and psychological distress in general population was found to be higher during COVID-19 pandemic.

WHAT IS ALREADY KNOWN ABOUT THIS SUBJECT • The SCN1A and SCN2A genes encode α subunits of the neuronal voltage‐gated sodium channel, which are targets for various antiepileptic drugs such as carbamazepine, phenytoin, valproate and others. • Recent studies have demonstrated that various genetic variants of these channel genes play important role in the pathogenesis and therapy of epilepsy. WHAT THIS STUDY ADDS • This study demonstrates a significant association between the SCN1A c.3184 A→G; AG genotype and epilepsy. • However SCN2A c.56 G→A; allele ‘A’ was significantly associated with multiple drug resistance in epilepsy in north Indian population. AIMS To evaluate sodium channel genes as candidates for epilepsy susceptibility and their role in therapeutic efficacy, we screened coding single‐nucleotide polymorphism of SCN1A p. Thr 1067 Ala or c.3184 A→G (rs2298771) and SCN2A p.Arg19Lys or c.56 G→A (rs17183814) in north Indian epilepsy patients. METHODS The genotyping was performed in 160 control subjects and 336 patients with epilepsy, of whom 117 were drug resistant and 219 were drug responsive. Therapeutic drug monitoring for phenytoin, carbamazepine, phenobarbital and valproate was also performed in 20% of the patients to confirm compliance. RESULTS AG genotype of SCN1A 3184 A→G polymorphism was significantly higher and associated in epilepsy patients [P= 0.005; odds ratio (OR) 1.76, 95% confidence interval (CI) 1.19, 2.61], whereas A variant of SCN2A c.56 G→A was associated with multiple drug resistance in north Indian patients with epilepsy (P= 0.03; OR 1.62, 95% CI 1.03, 2.56). CONCLUSIONS Overall, results indicate a differential role of genetic polymorphisms of sodium channels SCN1A and SCN2A in epilepsy susceptibility and drug response.

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In epilepsy, there is a tendency towards recurrent unprovoked seizures. Seizures result due to the excessive electrical misfiring in the brain between neurons and disturbance in neurotransmitter release. Several gene products affect the behavior of these neurons by regulating neurotransmission via several mechanisms. One such gene, Synapsin-2 (SYN2), involved in synaptogenesis is also reported to regulate the neurotransmitter release. We hypothesized that SYN2 gene and its polymorphisms could affect the process of epileptogenesis and therapeutic response in humans. In this hospital-based study, we enrolled 372 patients with epilepsy and 199 control subjects. We selected rs3773364 A>G polymorphism in SYN2 gene and analyzed its distribution in north Indian patients with epilepsy and control subjects. Genotyping was carried out by polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) method. According to the results obtained, SYN2 "AG" genotype frequency was significantly higher in patients with epilepsy versus control subjects in north Indian population (P = 0.02, OR = 1.55, 95% CI = 1.06-2.26). After subclassification, we observed higher frequency of AG genotype in idiopathic patients as compared to control subjects (P = 0.01, OR = 1.67, 95% CI = 1.08-2.56). There were no significant differences in genotypic (AG: OR = 0.80, P = 0.377; GG: P = 0.628, OR = 1.17) or allelic (P = 0.86, OR = 1.03) frequency distributions in patients with multiple drug resistance versus patients with drug-responsive epilepsy. Results from our study indicate the involvement of SYN2 gene polymorphism in conferring risk to epilepsy; however, the genetic variant does not seem to modulate drug-response in epilepsy pharmacotherapy.

GABA (gamma-amino butyric acid) receptors have always been an inviting target in the etiology and treatment of epilepsy because of its role as a major inhibitory neurotransmitter in the brain. The aim of our study was to find out the possible role of single nucleotide polymorphisms (SNPs) present in GABRA1 IVS11+15 A>G (rs2279020) and GABRG2 588C>T (rs211037) genes in seizure susceptibility and pharmaco-resistance in northern Indian patients with epilepsy. A total of 395 epilepsy patients and 199 control subjects were enrolled for present study. The genotyping was done by PCR-RFLP methods. The GABRA1 IVS11+15 A>G polymorphism conferred high risk for epilepsy susceptibility at genotype 'AG' (P=0.004, OR=1.77, 95% CI=1.20-2.63), 'GG' (P=0.01, OR=1.80, 95% CI=1.15-2.80) and G allele level (P=0.001, OR=1.50, 95% CI=1.16-1.92). Moreover this polymorphism was also associated with multiple drug resistance in patients with epilepsy for homozygous variant 'GG' genotype (P=0.031, OR=1.84, 95% CI=1.05-3.23) and G allele (P=0.020, OR=1.43, 95% CI=1.05-1.95). However GABRG2 588C>T polymorphism was not found to be associated either with epilepsy susceptibility or with drug resistance. Overall results indicate differential role of different subunits of GABA(A) receptor subtypes in epilepsy susceptibility and pharmacotherapy.

Background:The Indian population suffers with significant burden of mental illness. The prevalence rate and its association with age and other demographic indicators are needed for planning purpose.Objective:This study attempted to calculate age-wise prevalence of mental illness for rural and urban settings, and its association with age.Materials and Methods:Data published in National Sample Survey Organization (2002) report on disability is used for the analysis. Spearman correlation for strength of association, z-test for difference in prevalence, and regression statistics for predicting the prevalence rate of mental illness are used.Result:Overall population have 14.9/1000 prevalence of mental illness. It is higher in rural setting 17.1/1000 than urban 12.7/1000 (P < 0.001). There is a strong correlation found with age in rural (ϱ = 0.910, P = 0.001) and urban (ϱ = 0.940, P = 0.001).Conclusion:Results of this study confirm other epidemiological research in India. Large-population epidemiological studies are recommended.

Background. The coexistence of psychiatric disorders in people with intellectual disability (ID) is common. This study determined the prevalence of psychiatric disorders in children with ID in Barwani, India. Method. A total of 262 children with ID were evaluated for psychiatric disorders using the diagnostic criteria outlined in the International Classification of Diseases (ICD-10). Results. Psychiatric disorders appeared in study participants at the following rates: attention deficit hyperactivity disorder (ADHD), 6.5%; autism, 4.2%; anxiety, 2.7%; bipolar disorder, 1.1%; delusional disorder, 0.8%; depression, 2.3%; obsessive-compulsive disorder, 0.8%; schizophrenia, 1.9%; enuresis, 10.3%; epilepsy, 23.7%; and behavioral problems, 80.9%. The prevalence of psychiatric disorders was statistically higher in severely intellectually disabled children (IQ ≤ 49) than mildly intellectually disabled children (IQ ≥ 50). Conclusions. There is a higher prevalence of psychiatric disorders in children with ID when their IQ ≤ 49 compared with ID children whose IQ ≥ 50.

A polymorphism in the promoter region of uncoupling protein 2 gene -866 G/A has been associated with its expression levels, the risk of obesity, and metabolic abnormalities. We aimed to investigate the associations of uncoupling protein (UCP)2 gene variants with obesity and related traits. A total of 440 subjects, 200 obese, and 240 non-obese individuals were included in this case-control study. Hormone and glucose levels were estimated using standard protocols. Genotyping of UCP-2 gene polymorphism for all subjects was performed by the PCR-RFLP polymerase chain reaction (PCR) method. Higher Systolic blood pressure, Diastolic blood pressure, Waist to hip ratio, Leptin, Insulin, and blood glucose levels were observed in obese than non-obese (P < 0.05). The distributions of genotype (0.001) and allele (0.003) were significantly different between the non-obese and the obese groups. In the obese group, subjects with the A allele showed significant high insulin levels (<0.001) in comparison with A allele non-carriers. In conclusion, our results suggest that the -866 AA genotype and A allele of the UCP2 gene is associated with obesity and A allele associated with hyperinsulinemia in obese subjects.