SUMMARY: Parvovirus B19 has been linked with various clinical syndromes including neurological manifestations. However, its role in the latter remains not completely understood. Although the last 10 years witnessed a surge of case reports on B19‐associated neurological aspects, the literature data remains scattered and heterogeneous, and epidemiological information on the incidence of B19‐associated neurological aspects cannot be accurately extrapolated. The aim of this review is to identify the characteristics of cases of B19‐associated neurological manifestations. A computerized systematic review of existing literature concerning cases of B19‐related neurological aspects revealed 89 articles describing 129 patients; 79 (61.2%) were associated with CNS manifestations, 41 (31.8%) were associated with peripheral nervous system manifestations, and 9 (7.0%) were linked with myalgic encephalomyelitis. The majority of the cases (50/129) had encephalitis. Clinical characteristic features of these cases were analyzed, and possible pathological mechanisms were also described. In conclusion, B19 should be included in differential diagnosis of encephalitic syndromes of unknown etiology in all age groups. Diagnosis should rely on investigation of anti‐B19 IgM antibodies and detection of B19 DNA in serum or CSF. Treatment of severe cases might benefit from a combined regime of intravenous immunoglobulins and steroids. To confirm these outcomes, goal‐targeted studies are recommended to exactly identify epidemiological scenarios and explore potential pathogenic mechanisms of these complications. Performing retrospective and prospective and multicenter studies concerning B19 and neurological aspects in general, and B19 and encephalitic syndromes in particular, are required. © 2014 The Authors. Reviews in Medical Virology published by John Wiley & Sons, Ltd.

Background: Patients with multiple sclerosis (MS) frequently reveal social behavior disturbance. Nevertheless, little is known regarding the impact of MS on social cognition, particularly theory of mind (ToM), and its neural basis. Objectives: To explore how ToM is affected in MS and its neural correlates. Methods: Enrolled 60 consecutive MS patients and 60 healthy controls (HC) matched on age, sex, and education. Participants underwent ToM testing (Eyes Test, Videos Test) and 3 T brain magnetic resonance imaging (MRI). Using Freesurfer software, cortical and subcortical gray matter (GM) volumes were calculated. Results: MS patients performed worse on Eyes Test (58.7% ± 13.8% vs 81.9% ± 10.4%, p < 0.001) and Videos Test (75.3% ± 9.3% vs 88.1% ± 7.1%, p < 0.001). Eyes Test performance in MS was positively correlated with the volume of subcortical structures (amygdala, putamen) and cortical regions (entorhinal cortex, fusiform gyrus, superior temporal gyrus, superior parietal gyrus, supramarginal gyrus, medial orbitofrontal cortex, anterior and posterior cingulate gyrus). In regression analysis, amygdala volume was the single predictor of performance ( R² change = 0.064, p = 0.031), and a mediation analysis indicated that it contributes for the differences observed between MS and HC. Conclusion: Patients with MS have impairment on social cognition. Amygdala atrophy was the main predictor probably due to its central position within the “social brain” network.

This study investigates the utility of the Portuguese version of Montreal Cognitive Assessment (MoCA) as a screening-method for identifying cognitive dysfunction (CD) in multiple sclerosis (MS). The 118 participants with comprehensive neuropsychological assessment were divided into two subgroups: (I) MS group (n = 59) and (II) control group (n = 59). The MS patients were classified as cognitively intact (n = 26) or impaired (n = 33, 56%). The results indicated that the MoCA is a psychometrically valid instrument in assessment of MS patients. The Multiple Linear Regression analyses highlighted the significant influence of Modified Fatigue Impact Scale and Irregular Word Reading Test on MoCA performance. The MoCA total score showed a good discriminative capacity between cognitively impaired and cognitively intact subjects. In addition, there were significant differences in MoCA cognitive domain scores between groups. The MoCA total score cut-off point for identifying CD in MS patients was a score below 26 points (AUC = 0.837, CI = 0.736–0.937). A proposed EM-MoCA-Subscore for identifying the MS-related cognitive impairment (max. score = 19 points, cut-off <17 points, AUC = 0.871, CI = 0.784–0.958), can reduce administration time for cognitive screening in clinical settings. The MoCA is a useful and sensitive instrument to identify the MS-related cognitive impairment.

Objective: To assess the contribution of microstructural normal-appearing white matter (NAWM) damage to social cognition impairment, specifically in the theory of mind (ToM), in multiple sclerosis (MS). Methods: We enrolled consecutively 60 patients with MS and 60 healthy controls (HC) matched on age, sex, and education level. All participants underwent ToM testing (Eyes Test, Videos Test) and 3T brain MRI including conventional and diffusion tensor imaging sequences. Tract-based spatial statistics (TBSS) were applied for whole-brain voxel-wise analysis of fractional anisotropy (FA) and mean diffusivity (MD) on NAWM. Results: Patients with MS performed worse on both tasks of ToM compared to HC (Eyes Test 58.7 ± 13.8 vs 81.9 ± 10.4, p < 0.001, Hedges g −1.886; Videos Test 75.3 ± 9.3 vs 88.1 ± 7.1, p < 0.001, Hedges g −1.537). Performance on ToM tests was correlated with higher values of FA and lower values of MD across widespread white matter tracts. The largest effects (≥90% of voxels with statistical significance) for the Eyes Test were body and genu of corpus callosum, fornix, tapetum, uncinate fasciculus, and left inferior cerebellar peduncle, and for the Videos Test genu and splenium of corpus callosum, fornix, uncinate fasciculus, left tapetum, and right superior fronto-occipital fasciculus. Conclusions: These results indicate that a diffuse pattern of NAWM damage in MS contributes to social cognition impairment in the ToM domain, probably due to a mechanism of disconnection within the social brain network. Gray matter pathology is also expected to have an important role; thus further research is required to clarify the neural basis of social cognition impairment in MS.