Facial and bodily emotion recognition in multiple sclerosis: the role of alexithymia and other characteristics of the disease.

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.

Opportunities and Obstacles Associated With Sequential Immune Reconstitution Therapy for Multiple Sclerosis: A Case Report.

Cladribine is an effective disease-modifying treatment for relapsing-remitting multiple sclerosis that acts as an immune reconstitution therapy and is administered in a pulsed manner. Despite its efficacy, severe disease reactivation early after treatment represents a serious clinical problem, and clear evidence to guide the management of such a situation is lacking. Here, we describe the case of a patient experiencing considerable disease activity during the 1st year after the initiation of cladribine treatment. The patient was switched to alemtuzumab and, therefore, received double immune reconstitution therapy. Data regarding this approach are lacking, and real-world observations may be of interest. Despite achieving good control of disease activity, we observed several serious infectious complications. Our results suggest that sequential immune reconstitution therapies may be effective; however, at the price of higher susceptibility to infections.

Innate immunity modulates autoimmunity: type 1 interferon-beta treatment in multiple sclerosis promotes growth and function of regulatory invariant natural killer T cells through dendritic cell maturation.

Type 1 interferon-beta (T1IFN-beta) is an innate cytokine and the first-choice therapy for multiple sclerosis (MS). It is still unclear how T1IFN-beta, whose main function is to promote innate immunity during infections, plays a beneficial role in autoimmune disease. Here we show that T1IFN-beta 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-beta treatment significantly increased the percentages of Valpha24(+) NKT cells in peripheral blood mononuclear cells of MS patients. Furthermore, iNKT cells of T1IFN-beta-treated individuals showed a dramatically improved secretion of cytokines (interleukins 4 and 5 and interferon-gamma) in response to antigenic stimulation compared to iNKT cells isolated from the same patients before T1IFN-beta treatment. The effect of T1IFN-beta on iNKT cells was mediated through the modulation of myeloid dendritic cells (DCs). In fact, DCs modulated in vivo or in vitro by T1IFN-beta were more efficient antigen-presenting cells for iNKT cells. Such a modulatory effect of T1IFN-beta 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-beta in MS.

Nerve fibre layer analysis with GDx with a variable corneal compensator in patients with multiple sclerosis.

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.

Pramipexole-treated Parkinson's disease during pregnancy.

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.