Alexithymia in multiple sclerosis: Clinical and radiological correlations.

BACKGROUND: Alexithymia, meaning no words for emotions is a common problem that could affect up to 53% of patients in multiple sclerosis (MS). OBJECTIVES: To 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. METHODS: Ninety-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. RESULTS: Fifty-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. CONCLUSION: Regardless of the phenotype of MS, alexithymia is associated with atrophy of cerebral and cerebellar white matter, brainstem, corpus callosum, and thalami.

Thalamic atrophy correlates with dysfunctional impulsivity in multiple sclerosis.

BACKGROUND: Recent studies highlight the central role of thalamic atrophy in Multiple Sclerosis (MS) related disorders. Behavioural aspects of (MS) are rarely explored but their investigation is of high interest. Dickman's Impulsiveness Inventory (DII) allows distinguishing functional impulsivity (FI) which is the ability to react fast and properly when necessary, from dysfunctional impulsivity (DI) which is a behavioural symptom corresponding to the tendency to miss forethought before acting. OBJECTIVE: This paper aims to explore whether MS patients show significantly high and pathological DI, and to evaluate the impulsivity frequency in the different forms of MS including at the early stage of the Clinically Isolated Syndrome. Furthermore, this study focused on the factors that may induce abnormal impulsivity, and the link between thalamic atrophy and dysfunctional impulsivity in patients with MS. METHODS: 95 patients with demyelinating diseases including 21 Clinically Isolated Syndrome (CIS), 30 Relapsing-Remitting MS (RRMS), 23 Secondary Progressive MS (SPMS) and 21 Primary Progressive MS (PPMS) were prospectively recruited, and covered by extensive cognitive evaluation including the BCCogSEP (French version of the Brief Repeatable Battery for Neurological disease), the CSCT (Computerized Speed Cognitive Test) for processing speed of information (PSI), the DII to measure FI and DI, the Fast BDI to evaluate depression, and the EMIF-SEP scale to study physical, cognitive and social fatigues. 3D T2-FLAIR and 3D T1-weighted MRI were analyzed using automatic segmentation tools to quantify the T2 lesion load and to measure the whole and regional brain atrophy. RESULTS: 7% showed a pathologically high DI. The level of DI tended to differ significantly depending on the MS phenotype. There was no significant difference between RRMS, SPMS and PPMS, but RRMS showed significantly higher DI than CIS patients. Cognitive fatigue (r:-0.27, p<.01), depression (r:-0.21, p=.04) but mainly PSI (r:.33, p<.001) showed a significant correlation with DI. Among the brain regions of interest, the strongest significant correlation with DI was with thalamic atrophy (r:.33, p<.001). CONCLUSION: Some MS patients show a pathologically high DI, mainly RRMS compared to CIS. Previous study highlighted impulsive traits in MS patients only in relation with the presence of depression. The present study demonstrates that depression tends to correlate with DI, but that cognitive fatigue, and mainly slowing of PSI, which is the most early and severe cognitive impairment in MS, have a stronger impact on the rise of pathological impulsive behaviour. DI in MS is linked to frontal regions but even more strongly to thalamus atrophy. This is in line with the hypothesis of a disconnection syndrome in MS that causes cognitive impairment to trigger and could have the same impact on behaviour. Hence, impulsive behaviour should be evaluated and taken into account in the care of patients with MS.