BACKGROUND: Depression and anxiety (DA) are common in persons with brain tumor (PBT) and are associated with neurocognitive deficits. The terms DA and affective disorders are often used interchangeably in this study. Objective: This was a pilot study, conducted with the purpose of better assessing DA symptoms in association with socioeconomic and clinical characteristics in PBT. METHOD: A cross-sectional study was conducted on a sample of PBT (N = 102), recruited from a neurosurgical department. The tools employed were the Beck Depression Inventory-II (BDI-II) and the Hospital Anxiety and Depression Scale (HADS). The self-rating instruments proved feasible and reliable in screening for the severity of DA symptoms. The HADS is designed to measure the severity of anxiety and depressive symptoms in non-psychiatric hospital outpatients and does not assess the common somatic symptoms of these two disorders. The BDI-II evaluates the severity of depressive symptoms with items related to physical symptoms. RESULTS: Although our study did not, for the most part, yield results of statistical significance, it, however, demonstrated that anxiety and depressive disorders existed in PBT, showing a relatively higher rate in age groups 30–49 years. CONCLUSION: It was unclear whether these symptoms were invalidated by response bias, participant’s functional status, natural reaction to a fearing situation or just presentation of pseudodepression arose as a result of organic deficits. There is a need for further research to examine these factors.
Background Epilepsy, a serious chronic neurological condition effecting up to 100 million people globally, has clear genetic underpinnings including common and rare variants. In Saudi Arabia the prevalence of epilepsy is high and caused mainly by perinatal and genetic factors. No whole-exome sequencing (WES) studies have been performed to date in Saudi Arabian Epilepsy cohorts. This offers a unique opportunity for the discovery of rare genetic variants impacting this disease as there is a high rate of consanguinity amongst large tribal pedigrees. Results We performed WES on 144 individuals diagnosed with epilepsy, to interrogate known Epilepsy related genes for known and functional novel variants. We also used an American College of Medical Genetics (ACMG) guideline based variant prioritization approach in an attempt to discover putative causative variants. We identified a 32 potentially causative pathogenic variants across 30 different genes in 44/144 (30%) of these Saudi Epilepsy individuals. We also identified 232 variants of unknown significance (VUS) across 101 different genes in 133/144 (92%) subjects. Strong enrichment of variants of likely pathogenicity were observed in previously described epilepsy-associated loci, and a number of putative pathogenic variants in novel loci are also observed. Conclusion Several putative pathogenic variants known to be epilepsy-related loci were identified for the first time in our population, in addition to several potential new loci have been identified which may be prioritized for further investigation.
Background Epilepsy, a serious chronic neurological condition effecting up to 100 million people globally, has clear genetic underpinnings including common and rare variants. In Saudi Arabia, the prevalence of epilepsy is high and caused mainly by perinatal and genetic factors. No whole-exome sequencing (WES) studies have been performed to date in Saudi Arabian epilepsy cohorts. This offers a unique opportunity for the discovery of rare genetic variants impacting this disease as there is a high rate of consanguinity among large tribal pedigrees. Results We performed WES on 144 individuals diagnosed with epilepsy, to interrogate known epilepsy-related genes for known and functional novel variants. We also used an American College of Medical Genetics (ACMG) guideline-based variant prioritization approach in an attempt to discover putative causative variants. We identified 32 potentially causative pathogenic variants across 30 different genes in 44/144 (30%) of these Saudi epilepsy individuals. We also identified 232 variants of unknown significance (VUS) across 101 different genes in 133/144 (92%) subjects. Strong enrichment of variants of likely pathogenicity was observed in previously described epilepsy-associated loci, and a number of putative pathogenic variants in novel loci are also observed. Conclusion Several putative pathogenic variants in known epilepsy-related loci were identified for the first time in our population, in addition to several potential new loci which may be prioritized for further investigation.
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