Contributions
Abstract: EP1566
Type: ePoster
Abstract Category: Pathology and pathogenesis of MS - 23 Neurophysiology
Objectives: Alexithymia is frequently encountered in patients with multiple sclerosis (MS). It is a multicomponent personality construct featuring difficulty in identifying feelings or describing them, and an externally oriented thinking. Recent evidence proposes defective GABAergic transmission and deficits in interhemispheric transfer behind its occurrence. Such mechanisms could be explored using transcranial magnetic stimulation (TMS). To the best of our knowledge, no single TMS study has been performed in the context of alexithymia in MS patients.
Methods: 10 alexithymic and 12 non-alexithymic patients with progressive MS were enrolled based on the 20-item Toronto Alexithymia Scale score (TAS). TMS was used to record the cortical silent period (CSP) and interhemispheric inhibition at different inter-stimulus intervals. Clinical (i.e. Expanded Disability Status Scale, disease duration, progressive phase duration), socio-demographic (age, gender, education level, marital status), and neuropsychological data (i.e. Fatigue Severity Scale, Symbol Digit Modalities Test, Hospital Anxiety and Depression Scale, Epworth Sleepiness Scale) were collected. Group comparison was done using the Mann-Whitney and Fisher's exact tests. In addition, Spearman rank correlation coefficient was used to assess the relationship between TAS scores and each of the cortical excitability measures.
Results: Compared to non-alexithymic patients, alexithymic ones had significantly shorter CSP duration (mean: 159.33 ± 76.96, median: 148.50, vs. mean: 84.34 ± 49.73, median: 91.50, respectively; p=0.03), but did not differ with regards to the remaining excitability data, or clinical, socio-demographic and neuropsychological variables. In addition, a significant inverse correlation was found between TAS scores and CSP (r= -0.59; p= 0.004).
Conclusion: This study offers for the first time insights into the neurophysiological mechanisms of alexithymia in MS. Defective GABAergic transmission, particularly that mediated by GABA receptors type B, seems to be associated with alexithymia. Although interesting, these findings warrant further screening in large-scale studies.
Keywords: Multiple sclerosis, alexithymia, Toronto alexithymia scale, cortical silent period, cortical excitability, transcranial magnetic stimulation.
Disclosure: This research did not receive any specific grant from funding agencies in the public, commercial, or not-for-profit sectors. AC gave expert testimony for CSL Behring, Novartis, received grants from Biogen, Novartis, CSL Behring, GE Neuro, Octapharma, and gave lectures for Genzyme. SSA declares having received travel grants or compensation from Genzyme, Biogen, Novartis and Roche. The remaining authors declare no conflict of interest.
Abstract: EP1566
Type: ePoster
Abstract Category: Pathology and pathogenesis of MS - 23 Neurophysiology
Objectives: Alexithymia is frequently encountered in patients with multiple sclerosis (MS). It is a multicomponent personality construct featuring difficulty in identifying feelings or describing them, and an externally oriented thinking. Recent evidence proposes defective GABAergic transmission and deficits in interhemispheric transfer behind its occurrence. Such mechanisms could be explored using transcranial magnetic stimulation (TMS). To the best of our knowledge, no single TMS study has been performed in the context of alexithymia in MS patients.
Methods: 10 alexithymic and 12 non-alexithymic patients with progressive MS were enrolled based on the 20-item Toronto Alexithymia Scale score (TAS). TMS was used to record the cortical silent period (CSP) and interhemispheric inhibition at different inter-stimulus intervals. Clinical (i.e. Expanded Disability Status Scale, disease duration, progressive phase duration), socio-demographic (age, gender, education level, marital status), and neuropsychological data (i.e. Fatigue Severity Scale, Symbol Digit Modalities Test, Hospital Anxiety and Depression Scale, Epworth Sleepiness Scale) were collected. Group comparison was done using the Mann-Whitney and Fisher's exact tests. In addition, Spearman rank correlation coefficient was used to assess the relationship between TAS scores and each of the cortical excitability measures.
Results: Compared to non-alexithymic patients, alexithymic ones had significantly shorter CSP duration (mean: 159.33 ± 76.96, median: 148.50, vs. mean: 84.34 ± 49.73, median: 91.50, respectively; p=0.03), but did not differ with regards to the remaining excitability data, or clinical, socio-demographic and neuropsychological variables. In addition, a significant inverse correlation was found between TAS scores and CSP (r= -0.59; p= 0.004).
Conclusion: This study offers for the first time insights into the neurophysiological mechanisms of alexithymia in MS. Defective GABAergic transmission, particularly that mediated by GABA receptors type B, seems to be associated with alexithymia. Although interesting, these findings warrant further screening in large-scale studies.
Keywords: Multiple sclerosis, alexithymia, Toronto alexithymia scale, cortical silent period, cortical excitability, transcranial magnetic stimulation.
Disclosure: This research did not receive any specific grant from funding agencies in the public, commercial, or not-for-profit sectors. AC gave expert testimony for CSL Behring, Novartis, received grants from Biogen, Novartis, CSL Behring, GE Neuro, Octapharma, and gave lectures for Genzyme. SSA declares having received travel grants or compensation from Genzyme, Biogen, Novartis and Roche. The remaining authors declare no conflict of interest.