Aim: To study the prevalence of psychiatric comorbidities in patients of multiple sclerosis and their association to the degree of disability.
Method: Psychiatric symptoms were assessed in 90 patients of multiple sclerosis using GHQ-12, MMSE, HADS, Beck Depression Inventory and AUDIT. Neurological disability was assessed using Expanded Disability Status Scale. Correlations were determined between EDSS scores and psychiatric scale scores.
Result: 61% of patients had significant psychological distress. Depression was most common (38.8%) which was followed by anxiety symptoms (27.8%). Cognitive functioning was relatively intact in patients with mild to moderate neurological disability. Alcohol abuse was mostly restricted to male gender.
Conclusion: Psychiatric illness is highly prevalent in patients of multiple sclerosis leading to poor quality of life and significant distress. Psychiatric disability was higher in patients who had greater deterioration in neurological function. All cases of MS should be assessed for psychiatric morbidities as can be alleviated by appropriate intervention.
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http://dx.doi.org/10.1016/j.pjnns.2018.09.003 | DOI Listing |
J Neuroinflammation
January 2025
Department of Neurology, Division of Neuroimmunology, School of Medicine, Johns Hopkins University, Baltimore, MD, 21287, USA.
Chronic innate immune activation in the central nervous system (CNS) significantly contributes to neurodegeneration in progressive multiple sclerosis (MS). Using multiple experimental autoimmune encephalomyelitis (EAE) models, we discovered that NLRX1 protects neurons in the anterior visual pathway from inflammatory neurodegeneration. We quantified retinal ganglion cell (RGC) density and optic nerve axonal degeneration, gliosis, and T-cell infiltration in Nlrx1 and wild-type (WT) EAE mice and found increased RGC loss and axonal injury in Nlrx1 mice compared to WT mice in both active immunization EAE and spontaneous opticospinal encephalomyelitis (OSE) models.
View Article and Find Full Text PDFActa Neurol Belg
January 2025
Ziekenhuis Oost Limburg, Genk, Belgium.
With the increasing use of disease modifying therapies as treatment for multiple sclerosis, knowledge of the rare but possibly severe adverse events becomes increasingly important. We present a case of Varicella-Zoster virus associated vasculopathy in a young male multiple sclerosis patient, treated with dimethyl fumarate. We aim to address this rare but potentially deadly complication of varicella-Zoster virus infection and spread awareness about the increased risk in this patient population.
View Article and Find Full Text PDFSci Rep
January 2025
Department of Clinical Neuroscience, Karolinska Institutet, Stockholm, Sweden.
Multiple sclerosis (MS) unfavorably affects working capacity. The Comprehensive International Classification of Functioning, Disability and Health Core Set for MS (cICF-MS), issued by the World Health Organization, has not yet been extended to evaluate working capacity level (WCL). To evaluate the relative importance of cICF-MS categories in relation to WCL.
View Article and Find Full Text PDFRev Neurol (Paris)
January 2025
Clinical Neuroscience Centre, CIC_P1414 Inserm, University Hospital, Rennes, France. Electronic address:
Neurobiol Dis
January 2025
Office of the Saskatchewan Multiple Sclerosis Clinical Research Chair, University of Saskatchewan, Saskatoon, SK S7K 0M7, Canada; Neurology Division, Department of Medicine, University of Saskatchewan, Saskatoon, SK S7N 0X8, Canada. Electronic address:
RNA binding protein dysfunction is a pathogenic feature of multiple neurological diseases, including multiple sclerosis (MS). Neurodegeneration (the loss of, or damage to neurons and axons) is the primary driver of disease progression in MS. Herein, we utilized a novel, neuron-specific model of neurodegeneration by transducing primary mouse neurons with mutant forms of the RNA binding protein heterogeneous nuclear ribonucleoprotein A1 (hnRNP A1) identified from MS patients, including one within the M9-nuclear localization sequence of hnRNP A1 (A1(P275S)) and a second in the prion-like domain of hnRNP A1 (A1(F263S)) to test the hypothesis that neuronal hnRNP A1 dysfunction drives neurodegeneration in MS.
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