Socioeconomic status in neurological disorders: a modifiable risk factor?

Socioeconomic status (SES) is known to play a substantial role in health outcomes and disease frequency, although the bulk of current evidence is derived from vascular disease, infectious diseases, and cancer. More recently, the impact of SES on non-vascular neurological disease has been an increasing focus for researchers with implications for health care providers, government policy, clinical study design, as well as individual patient care. Although SES has been historically considered a risk factor with limited scope for modification at an individual level, recent innovative social policy pilot studies have contested this. Such interventions are highly political, but may bring about novel ways of improving patient outcomes. The first paper discussed this month is a large epidemiological study of incident cases of epilepsy in children under three years of age in Scotland. The second paper identifies differences in MRI measures of neurodegeneration in cohorts of African Americans and Caucasian individuals. The final paper discusses initial results from a randomised trial of an unconditional cash transfer to new mothers

A role for the Epstein–Barr virus in multiple sclerosis aetiology?

The association between Epstein–Barr virus (EBV) and multiple sclerosis (MS) has been known for many years. EBV seropositivity in MS has been reported as 99.5–100% compared with ~ 94% in healthy adults, and MS is over twice as common in people who have had symptomatic infectious mononucleosis. Furthermore, patients with MS also have elevated antibodies to EBV nuclear antigens (EBNAs), and EBV has been isolated from MS demyelinating plaques. However, a causal relationship has yet to be fully established. The first paper discussed this month reports a striking temporal relationship between EBV seroconversion and MS onset in a large US military cohort. In the second paper, evidence is presented that suggests clonally expanded B cells in the CSF produce oligoclonal bands, as well as antibodies that cross-react with proteins expressed by EBV and oligodendrocytes. The final paper discussed this month reports that an EBV transcription factor occupies a large number of the MS genetic risk variants and this may at least partly explain how EBV infection and genetic risk intersect to cause MS

Supplementary Material for: Modelling Disease progression of Multiple Sclerosis in a South Wales Cohort

Objectives: To model multiple sclerosis (MS) disease progression and compare disease trajectories by sex, age of onset, and year of diagnosis. Study Design and settings: Longitudinal EDSS scores were collected since 1985 for relapse-onset MS patients at MS clinics in South Wales and modelled using a multilevel model (MLM). The MLM adjusted for baseline covariates (sex, age of onset, year of diagnosis, and disease modifying treatments (DMTs)), and included interactions between baseline covariates and time variables. Results: The optimal model was truncated at 30 years after disease onset and excluded EDSS recorded within 3 months of relapse. As expected, older age of onset was associated with faster disease progression at 15 years (effect size (ES): 0.75; CI: 0.63, 0.86; P: 2011) progressed more slowly than those diagnosed historically (<2006); (ES: -0.46; CI: -0.75, -0.16; P: 0.006) and (ES: -0.95; CI: -1.20, -0.70; P: <0.001), respectively. Conclusion: We present a novel model of MS outcomes, accounting for the nonlinear trajectory of MS and effects of baseline covariates, validating well-known risk factors (sex and age of onset) associated with disease progression. Also, patients diagnosed more recently progressed more slowly than those diagnosed historically