
Contributions
Abstract: P606
Type: Poster
Abstract Category: Pathology and pathogenesis of MS - 23 Neurophysiology
Objectives: Fatigue is a common symptom in patients with multiple sclerosis (MS). Despite its invalidating nature, its physiopathology remains ill-defined and seems to be multifactorial [1]. Transcranial magnetic stimulation (TMS) is an emerging technique that allows, through double pulse paradigms, the exploration of cortical inhibitory and excitatory mechanisms. The alteration of the latter could underlie various neuropsychiatric disorders. In the context of MS fatigue, few studies have addressed these measures and their results remain controversial.
Methods: 38 MS patients were recruited and divided into two groups: non-fatigued (n = 17) and fatigued (n = 21) according to the Modified Fatigue Impact Scale (MFIS) score. The neurophysiological evaluation consisted in testing the following parameters: resting motor threshold, amplitude of motor evoked potentials, short-interval intracortical inhibition (SICI), intracortical facilitation (ICF), cortical silence period and interhemispheric inhibition [2].
Results: SICI was significantly higher in fatigued compared to non-fatigued patients, especially for the 2 ms inter-stimulus interval (35.0 ± 40.8 vs. 63.9 ± 20.9, p = 0.04). SICI at 2 ms was significantly correlated with MFIS scores (total score: r = 0.4, p < 0.01, cognitive subscale score: r = 0.4, p < 0.01, psychosocial subscale score: r = 0.3, p = 0.04).
Conclusion: Fatigued MS patients had increased intracortical inhibition compared to non-fatigued patients. This could reflect an alteration of the GABAergic/glutamatergic balance at the detriment of the facilitatory mechanisms [3]. In other words, there is an apparent link between the integrity of the facilitatory mechanisms and the ability to cope with functional decline and subsequent generation of fatigue in these patients.
References:
[1] Chalah MA, et al. Fatigue in Multiple Sclerosis: Neural Correlates and the Role of Non-Invasive Brain Stimulation. Front Cell Neurosci. 2015; 9:460.
[2] Ayache SS, et al. Relapses in multiple sclerosis: effects of high-dose steroids on cortical excitability. Eur J Neurol. 2014; 21:630-6.
[3] Ayache SS, Chalah MA. Cortical excitability changes: A mirror to the natural history of multiple sclerosis? Neurophysiol Clin. 2017. pii: S0987-7053(17)30005-9. doi: 10.1016/j.neucli.2017.02.001. [Epub ahead of print]
Keywords: Multiple sclerosis, cortical excitability, intracortical inhibition, transcranial magnetic stimulation, TMS.
Disclosure: This research did not receive any funds.
SSA declares having received travel grants or compensation from Genzyme, Biogen, Novartis and Roche.
AC gave expert testimony for CSL Behring, Novartis, received grants from Biogen, Novartis, CSL Behring, GE Neuro, Octapharma, and gave lectures for Genzyme.
JPL and MAC: Nothing to disclose.
Abstract: P606
Type: Poster
Abstract Category: Pathology and pathogenesis of MS - 23 Neurophysiology
Objectives: Fatigue is a common symptom in patients with multiple sclerosis (MS). Despite its invalidating nature, its physiopathology remains ill-defined and seems to be multifactorial [1]. Transcranial magnetic stimulation (TMS) is an emerging technique that allows, through double pulse paradigms, the exploration of cortical inhibitory and excitatory mechanisms. The alteration of the latter could underlie various neuropsychiatric disorders. In the context of MS fatigue, few studies have addressed these measures and their results remain controversial.
Methods: 38 MS patients were recruited and divided into two groups: non-fatigued (n = 17) and fatigued (n = 21) according to the Modified Fatigue Impact Scale (MFIS) score. The neurophysiological evaluation consisted in testing the following parameters: resting motor threshold, amplitude of motor evoked potentials, short-interval intracortical inhibition (SICI), intracortical facilitation (ICF), cortical silence period and interhemispheric inhibition [2].
Results: SICI was significantly higher in fatigued compared to non-fatigued patients, especially for the 2 ms inter-stimulus interval (35.0 ± 40.8 vs. 63.9 ± 20.9, p = 0.04). SICI at 2 ms was significantly correlated with MFIS scores (total score: r = 0.4, p < 0.01, cognitive subscale score: r = 0.4, p < 0.01, psychosocial subscale score: r = 0.3, p = 0.04).
Conclusion: Fatigued MS patients had increased intracortical inhibition compared to non-fatigued patients. This could reflect an alteration of the GABAergic/glutamatergic balance at the detriment of the facilitatory mechanisms [3]. In other words, there is an apparent link between the integrity of the facilitatory mechanisms and the ability to cope with functional decline and subsequent generation of fatigue in these patients.
References:
[1] Chalah MA, et al. Fatigue in Multiple Sclerosis: Neural Correlates and the Role of Non-Invasive Brain Stimulation. Front Cell Neurosci. 2015; 9:460.
[2] Ayache SS, et al. Relapses in multiple sclerosis: effects of high-dose steroids on cortical excitability. Eur J Neurol. 2014; 21:630-6.
[3] Ayache SS, Chalah MA. Cortical excitability changes: A mirror to the natural history of multiple sclerosis? Neurophysiol Clin. 2017. pii: S0987-7053(17)30005-9. doi: 10.1016/j.neucli.2017.02.001. [Epub ahead of print]
Keywords: Multiple sclerosis, cortical excitability, intracortical inhibition, transcranial magnetic stimulation, TMS.
Disclosure: This research did not receive any funds.
SSA declares having received travel grants or compensation from Genzyme, Biogen, Novartis and Roche.
AC gave expert testimony for CSL Behring, Novartis, received grants from Biogen, Novartis, CSL Behring, GE Neuro, Octapharma, and gave lectures for Genzyme.
JPL and MAC: Nothing to disclose.