Multiple sclerosis (MS) may be associated with impaired perception of facial emotions. However, emotion recognition mediated by bodily postures has never been examined in these patients. Moreover, several studies have suggested a relation between emotion recognition impairments and alexithymia. This is in line with the idea that the ability to recognize emotions requires the individuals to be able to understand their own emotions. Despite a deficit in emotion recognition has been observed in MS patients, the association between impaired emotion recognition and alexithymia has received little attention. The aim of this study was, first, to investigate MS patient's abilities to recognize emotions mediated by both facial and bodily expressions and, second, to examine whether any observed deficits in emotions recognition could be explained by the presence of alexithymia. Thirty patients with MS and 30 healthy matched controls performed experimental tasks assessing emotion discrimination and recognition of facial expressions and bodily postures. Moreover, they completed questionnaires evaluating alexithymia, depression, and fatigue. First, facial emotion recognition and, to a lesser extent, bodily emotion recognition can be impaired in MS patients. In particular, patients with higher disability showed an impairment in emotion recognition compared with patients with lower disability and controls. Second, their deficit in emotion recognition was not predicted by alexithymia. Instead, the disease's characteristics and the performance on some cognitive tasks significantly correlated with emotion recognition. Impaired facial emotion recognition is a cognitive signature of MS that is not dependent on alexithymia.

Summary Type 1 interferon‐β (T1IFN‐β) is an innate cytokine and the first‐choice therapy for multiple sclerosis (MS). It is still unclear how T1IFN‐β, whose main function is to promote innate immunity during infections, plays a beneficial role in autoimmune disease. Here we show that T1IFN‐β promoted the expansion and function of invariant natural killer (iNKT) cells, an innate T‐cell subset with strong immune regulatory properties that is able to prevent autoimmune disease in pre‐clinical models of MS and type 1 diabetes. Specifically, we observed that T1IFN‐β treatment significantly increased the percentages of Vα24+ NKT cells in peripheral blood mononuclear cells of MS patients. Furthermore, iNKT cells of T1IFN‐β‐treated individuals showed a dramatically improved secretion of cytokines (interleukins 4 and 5 and interferon‐γ) in response to antigenic stimulation compared to iNKT cells isolated from the same patients before T1IFN‐β treatment. The effect of T1IFN‐β on iNKT cells was mediated through the modulation of myeloid dendritic cells (DCs). In fact, DCs modulated in vivo or in vitro by T1IFN‐β were more efficient antigen‐presenting cells for iNKT cells. Such a modulatory effect of T1IFN‐β was associated with up‐regulation on DCs of key costimulatory molecules for iNKT (i.e. CD80, CD40 and CD1d). Our data identified the iNKT cell/DC pathway as a new target for the immune regulatory effect of T1IFNs in autoimmune diseases and provide a possible mechanism to explain the clinical efficacy of T1IFN‐β in MS.

There are few reports about drug-related effects on PD pregnancy. We describe the case of a woman affected by PD treated with pramipexole monotherapy during pregnancy. The child, born by caesarean delivery, is healthy, whereas motor disability of the mother progressively increased to the point that levodopa therapy was necessary.

We describe a patient with ophthalmoplegic migraine and left sixth nerve palsy, in whom disease's onset occurred at middle age.

Purpose: To evaluate the ability of GDx with variable corneal compensator (VCC) compared to visual-evoked potentials (VEPs) and standard automated perimetry (SAP) in the detection of early optic nerve damage in patients with multiple sclerosis (MS). Methods: 46 eyes of 23 MS patients were included. Ten of them had a history of acute retrobulbar optic neuritis. A control group of 20 normal subjects was also included. All subjects underwent a complete ophthalmological examination and testing with SAP, GDx VCC and VEPs. Results: 19 eyes (41.3%) were abnormal with GDx VCC compared to 38 eyes (82.6%) with SAP and 31 (64.4%) with VEPs. In the optic neuritis group, 9 eyes (69.2%) had optic nerve pallor; SAP was abnormal in 8 of these eyes (61.5%) while VEPs and GDx VCC were abnormal in 6 eyes (46.1%). 2/20 eyes (10.0%) in the control group gave a false-positive abnormal result with SAP. GDx VCC and VEP were normal for all the eyes in the control group. Conclusions: GDx VCC is less able to detect early defects in MS patients compared to the currently used standard techniques of SAP and VEPs.