Alexithymia in multiple sclerosis: Clinical and radiological correlations

BackgroundAlexithymia, meaning no words for emotions is a common problem that could affect up to 53% of patients in multiple sclerosis (MS).ObjectivesTo determine the frequency of alexithymia in MS and investigate MS-related abnormalities in structural magnetic resonance imaging (MRI) and their associations with fatigue and cognitive functions.MethodsNinety-five patients at all stages of the disease were examined: 21 with clinically isolated syndromes (CIS), 30 with relapsing-remitting MS (RRMS), 21 with primary (PP) and 23 with secondary progressive MS (SPMS). Alexithymia was measured with the Toronto alexithymia scale (TAS-20) and correlated to cognitive functions, depression, and fatigue. Voxel-based morphometry MRI was analyzed to determine lesion load, cerebral and regional atrophy.ResultsFifty-seven of patients had alexithymia with no significant difference between the clinical phenotypes. Alexithymic patients differed from non-alexithymic patients on fatigue, depression and information processing speed. Compared to non-alexithymic patients, alexithymic patients had decreased volumes of cerebral and cerebellar white matter and there was a significant relationship between alexithymia and decreased brainstem, thalamic and corpus callosum volume.ConclusionRegardless of the phenotype of MS, alexithymia is associated with atrophy of cerebral and cerebellar white matter, brainstem, corpus callosum, and thalami.     

Alexithymia and links with depression and anxiety in multiple sclerosis

OBJECTIVES: This study evaluates the prevalence of alexithymia in multiple sclerosis and examines the links between alexithymia, depression and anxiety. METHOD: Sixty-one subjects aged between 18 and 60 years and suffering from multiple sclerosis took part in the study. The psychological assessment consisted of an interview with a psychologist and three questionnaires: the Toronto Alexithymia Scale (TAS), the State-Trait Anxiety Inventory (STAI), the Beck Depression Inventory (BDI). RESULTS: The prevalence of alexithymia was 42.5%, 34.4% for depression and 44.3% for anxiety (high and moderate level). The alexithymic subjects were more depressed and anxious. Results indicated positive correlations between anxiety (state and trait), depression and alexithymia scores. The various dimensions of alexithymia were found to be diversely correlated with anxiety and depression. CONCLUSIONS: Our results point out the importance of anxiety in multiple sclerosis and the specificity of alexithymia.     

Alexithymia in multiple sclerosis: relationship with fatigue and depression

Objective –  The aim of this study was to investigate the prevalence of alexithymia in a sample of patients with multiple sclerosis (MS) and to further evaluate the association between alexithymia and the occurrence of common disabling MS-related symptoms such as fatigue and depression.
Methods –  Fifty-eight relapsing–remitting MS patients treated with interferon (IFN)-beta-1a underwent a complete neurological evaluation, including Expanded Disability Status Scale score assessment. Alexithymia, depressive symptoms and fatigue were assessed using the 20-item Toronto Alexithymia Scale, Beck Depression Inventory and Fatigue Severity Scale.
Results –  Prevalence of alexithymia was 13.8%, with 27.6% of patients presenting borderline alexithymia. Sixty-seven per cent of the patients complained of fatigue while 29.3% of them were depressed. Higher levels of fatigue and depression were found in alexithymic patients when compared with non-alexithymic patients. Results from logistic regressions showed that alexithymia significantly contributes to the severity of fatigue and depression.
Conclusions –  Alexithymia was associated with increased severity of fatigue and depression.     

Visual object recognition in multiple sclerosis

Deficits in tasks measuring visual processing have been earlier reported in studies of MS. Yet, the nature and severity of visual-processing deficits in MS remains unclear. We used a new method in order to measure the different stages of visual processing in object recognition: shape recognition, familiarity recognition, semantic categorization, and identification with naming. Six two-choice reaction-time tasks were presented to 30 MS patients and 15 healthy controls. The patients were divided into cognitively preserved and cognitively deteriorated study groups according to their cognitive status. The purpose was to find out whether deficits at specific stages of visual processing can be found in cognitively deteriorated MS patients. Cognitively deteriorated MS patients did not perform as well as cognitively preserved MS patients or healthy controls. They were slower already at the early stage of visual processing where discrimination of whole objects from scrambled ones was required. They also had higher error rates in tasks requiring object familiarity detection and object identification with naming. Thus, cognitively deteriorated MS patients had difficulties in visual shape recognition and semantic-lexical processing. However, variation of performances was large within both of the patient groups indicating that even patients without a generalized cognitive decline may have deficits in some stages of the visual processing. We suggest that because of the heterogeneity of the patients, every single case needs to be examined separately in order to identify the possible deficits in visual processing.     

对多发性硬化的再认识

中枢神经系统(CNS)脱髓鞘疾病特指一组病因不明确,通常认为与免疫相关的CNS炎症性疾病,多发性硬化(MS)是最典型的代表.既往研究认为,该疾病病理上主要累及CNS的白质,由髓鞘蛋白致敏的自身活化的CD4+T细胞导致髓鞘脱失和(或)髓鞘形成细胞的破坏,产生脱髓鞘斑块,而神经元和轴索相对保留.     

Immunopathological recognition of autoantigens in multiple sclerosis

Although the aetiology of multiple sclerosis (MS) has not been established, circumstantial evidence points to the involvement of both cell-mediated and humoral immune responses in the formation of demyelinating lesions. In view of the current controversy regarding the reactivity of T lymphocytes from MS patients to myelin basic protein (MBP), we reassessed T cell reactivity in MS using a sensitive and specific indicator of cell-mediated immune response. No significant difference in the reactivity to MBP was observed between MS patients and healthy subjects. Interestingly, significant reactivity to MBP was detected in the control group comprising patients with other diseases. Nevertheless, our demonstration that polymorphism in T cell receptor (TcR) alpha chain are related to MS and that, in demyelinating lesions, TcR usage is limited, suggests that T cells may recognise particular epitopes of a critical antigen involved in this disease. The search for a specific MS antigen recognised by the intrathecally synthesized immunoglobulins typical of MS has so far been unsuccessful. However, recent work, which has focused more particularly onto myelin components with externally located epitopes accessible to the immune response, appears to be more promising. One such antigen, myelin-oligodendrocyte glycoprotein (MOG), is clearly a target for immune attack. Indeed, highly specific antibodies to MOG have been shown to cause demyelination not only in vivo but also in vitro, as demonstrated by our study of the demyelinating effects of a monoclonal anti-MOG antibody on aggregating fetal rat brain cell cultures.(ABSTRACT TRUNCATED AT 250 WORDS)     

Early recognition and diagnosis of multiple sclerosis

Multiple sclerosis (MS) is an autoimmune disorder associated with inflammation and demyelination in the brain, optic nerve, and spinal cord. Patients with MS may present with a wide range of clinical symptoms, either monofocal or multifocal, all of which are related to the central nervous system. Although several strategies for the early recognition of MS are available, diagnostic criteria call for MRI of the brain and spinal cord due to its specificity in identifying white matter lesions disseminated in time and space. The course of MS is unpredictable, but 4 clinical subtypes have been described: relapsing-remitting, secondary progressive, primary progressive, and progressive relapsing. Prevalence rates for MS vary depending on geography, and susceptibility for MS appears to be influenced by both environmental and genetic risk factors.     

Elementary neurocognitive function, facial affect recognition and social-skills in schizophrenia

Social-skill deficits are pervasive in schizophrenia and negatively impact many key aspects of functioning. Prior studies have found that measures of elementary neurocognition and social cognition are related to social-skills. In the present study we selected a range of neurocognitive measures and examined their relationship with identification of happy and sad faces and performance-based social-skills. Fifty-three patients with schizophrenia or schizoaffective disorder participated. Results revealed that: 1) visual vigilance, problem-solving and affect recognition were related to social-skill; 2) links between problem-solving and social-skill, but not visual vigilance and social-skill, remained significant when estimates of verbal intelligence were controlled; 3) affect recognition deficits explained unique variance in social-skill after neurocognitive variables were controlled; and 4) affect recognition deficits partially mediated the relationship of visual vigilance and social-skill. These results support the conclusion that facial affect recognition deficits are a crucial domain of impairment in schizophrenia that both contribute unique variance to social-skill deficits and may also mediate the relationship between some aspects of neurocognition and social-skill. These findings may help guide the development and refinement of cognitive and social-cognitive remediation methods for social-skill impairment.     

Gait abnormalities in minimally impaired multiple sclerosis patients.

Subclinical evidence of gait abnormalities were identified in a group of seven patients with multiple sclerosis, EDSS scored 0 - 2, without functional limitations. A movement analysis technique was used to identify gait parameters indicative of impaired motor function during walking. Abnormalities related primarily to time-distance parameters (reduced speed of progression, shorter strides, prolonged double support phase) and muscular function (premature recruitment of gastrocnemius and late relaxation of tibialis anterior during stance phase) were identified regardless the severity of the clinical score. The gait analysis procedure was able to provide the clinician with evidence of motor abnormalities prior to functional disturbance observable by a trained physician. These minimal dysfunctions may have resulted from reflex mechanisms impaired by delayed transmission through long loop pathways or else as a result of a nonspecific protective gait strategy to improve balance control. The technique described in this study may be useful to identify earlier starting points for follow-up and physiotherapy.     

Impaired recognition of affect in facial expression in depressed patients.

Measures of recognition of seven affects in facial and verbal expressions to 17 depressed patients and 31 controls were administered. Depressed patients were significantly impaired in the recognition of affect in the facial, but not verbal, expressions. Among the seven affects examined, depressed patients made significantly or near significantly fewer correct matches for sad, happy, and interested face items. The performance of the depressed patients was similar to that observed by Kolb and Taylor in patients with right, but not left, hemisphere cortical excisions. The neurobiology of facial recognition is reviewed, and the relevance of the observed perceptual deficit in depressed patients to the pathophysiology and symptomatology of depression is discussed.     

Differential impairments of facial affect recognition in schizophrenia subtypes and major depression

The goal of this study was to assess facial affect recognition abilities in subjects with various schizophrenia subtypes and subjects with major depression. A total of six disorganized, 21 paranoid and 18 residual subjects with schizophrenia (DSM-IV criteria) were compared with 21 subjects with major depression (DSM-IV criteria) and 30 matched healthy control subjects. Two experimental tasks requiring the sorting and rating of emotional facial expressions were applied. Disorganized and paranoid subjects showed strong impairments in the sorting of emotional facial expressions. Depressive subjects displayed only minor deficits, and residual subjects were unimpaired. Subjects with disorganized schizophrenia rated emotional facial expressions as more aroused, and depressive subjects rated them as less aroused, than the other study groups. Our study demonstrates strong deficits in facial affect recognition in subjects with schizophrenia and pronounced disorganized or psychotic symptoms. Deficits in facial affect recognition are specific to schizophrenia. They may be considered as a state marker of schizophrenia.     

Deficits in facial affect recognition among antisocial populations: a meta-analysis

Individuals with disorders marked by antisocial behavior frequently show deficits in recognizing displays of facial affect. Antisociality may be associated with specific deficits in identifying fearful expressions, which would implicate dysfunction in neural structures that subserve fearful expression processing. A meta-analysis of 20 studies was conducted to assess: (a) if antisocial populations show any consistent deficits in recognizing six emotional expressions; (b) beyond any generalized impairment, whether specific fear recognition deficits are apparent; and (c) if deficits in fear recognition are a function of task difficulty. Results show a robust link between antisocial behavior and specific deficits in recognizing fearful expressions. This impairment cannot be attributed solely to task difficulty. These results suggest dysfunction among antisocial individuals in specified neural substrates, namely the amygdala, involved in processing fearful facial affect.     

Neuroanatomical correlates of impaired decision-making and facial emotion recognition in early Parkinson's disease

Decision-making and recognition of emotions are often impaired in patients with Parkinson's disease (PD). The orbitofrontal cortex (OFC) and the amygdala are critical structures subserving these functions. This study was designed to test whether there are any structural changes in these areas that might explain the impairment of decision-making and recognition of facial emotions in early PD. We used the Iowa Gambling Task (IGT) and the Ekman 60 faces test which are sensitive to the integrity of OFC and amygdala dysfunctions in 24 early PD patients and 24 controls. High-resolution structural magnetic resonance images (MRI) were also obtained. Group analysis using voxel-based morphometry (VBM) showed significant and corrected ( P  < 0.05 FEW-small volume correction) gray matter (GM) loss in the right amygdala and bilaterally in the OFC in PD patients. Volumetric analyses were also performed but did not yield significant differences between groups. Left lateral GM volume in OFC showed a slight correlation with the IGT, and bilateral OFC GM was strongly correlated with Ekman test performance in PD patients. We conclude that: (i) impairment in decision-making and recognition of facial emotions occurs at the early stages of PD, (ii) these neuropsychological deficits are accompanied by degeneration of OFC and amygdala, and (iii) bilateral OFC reductions are associated with impaired recognition of emotions, and GM volume loss in left lateral OFC is related to decision-making impairment in PD.