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Fatigue is one of the most common symptoms in neurology, especially in MS patients with a prevalence of 65%. It is described as the most disabling symptom by 40% of MS patients. This study aimed to validate the Functional Assessment of Chronic Illness Therapy fatigue version (FACIT-F) and the F-2-MS scale, a new tool to distinguish between fatigue and fatigability.One hundred and fifteen patients with relapsing-remitting MS were enrolled. All patients completed a comprehensive neuropsychological battery, previously validated in MS. Fatigue was evaluated using the Fatigue Severity Scale (FSS), the Modified version of the Fatigue Impact Scale (MFIS), the Functional Assessment of Chronic Illness Therapy measure system (fatigue version) (FCIT-F), and a new tool for the assessment of fatigue and fatigability: the F-2-MS scale. Internal consistency was estimated with Cronbach's Alpha. For intergroup comparisons, Student's t-test and Pearson's chi-squared test were used. Pearson's correlation test was calculated for quantitative variables. Cohen's d was calculated to evaluate the effect size. Binary logistic regression was performed, considering the presence of fatigue as a criterion variable, and the FACIT-F and F-2-MS scores were added as predictor variables. ROC curves were also estimated. We conducted a confirmatory factor analysis for the F-2-MS scale, considering two latent factors.FACIT-F and F-2-MS showed high internal consistency. Both scales were highly correlated with MFIS and FSS, and showed a low correlation with Symbol Digit Modalities Test. There were significant differences between fatigued and non-fatigued patients on FACIT-F and F-2-MS scores with large effect sizes. Both scales showed AUC 0.90 and achieved a correct classification87%. Confirmatory factor analysis showed moderate evidence of two dimensions on the F-2-MS scale.The FACIT-F and F-2-MS scales showed appropriated psychometric properties to be used as fatigue measures in clinical and research settings, allowing a correct distinction between patients with and without fatigue, and contributing to the understanding of the complexities of fatigue in MS.

Oligodendrocyte precursor cell (OPC) migration is a mechanism involved in remyelination, these cells migrate from niches in the adult CNS. However, age and disease reduce the pool of OPCs, as a result, the remyelination capacity of the CNS decreases over time. Several experimental studies have introduced OPCs to the brain via direct injection or intrathecal administration. In this study, we used the nose-to brain pathway to deliver oligodendrocyte lineage cells (human oligodendroglioma (HOG) cells), which behave similarly to OPCs in vitro. To this end, we administered GFP-labelled HOG cells intranasally to experimental animals, which were subsequently euthanised at 30 or 60 days. Our results show that the intranasal route is a viable route to the CNS and that HOG cells administered intranasally migrate preferentially to niches of OPCs (clusters created during embryonic development and adult life). Our study provides evidence, albeit limited, that HOG cells either form clusters or adhere to clusters of OPCs in the brains of experimental animals.

Introduction: AQP4 (aquaporin-4)–immunoglobulin G (IgG)-mediated neuromyelitis optica spectrum disorder (NMOSD) is an inflammatory demyelinating disease that affects the central nervous system, particularly the spinal cord and optic nerve, remyelination capacity in neuromyelitis optica is yet to be determined, as is the role of AQP4–IgG in cell differentiation. Material and Methods: We included three groups—a group of patients with AQP4–IgG-positive neuromyelitis optica, a healthy group, and a sham group. We analyzed differentiation capacity in cultures of neurospheres from the subventricular zone of mice by adding serum at two different times: early and advanced stages of differentiation. We also analyzed differentiation into different cell lines. Results and Conclusions: The effect of sera from patients with NMOSD on precursor cells differs according to the degree of differentiation, and probably affects oligodendrocyte progenitor cells from NG2 cells to a lesser extent than cells from the subventricular zone, however, the resulting oligodendrocytes may be compromised in terms of maturation and possibly limited in their ability to generate myelin. Furthermore, these cells decrease in number with age. It is very unlikely that the use of drugs favoring the migration and differentiation of oligodendrocyte progenitor cells in multiple sclerosis would be effective in the context of neuromyelitis optica, but cell therapy with oligodendrocyte progenitor cells seems to be a potential alternative.