Chalah et al. Neurophysiological, radiological and neuropsychological evaluation of fatigue in multiple sclerosis. Mult Scler Relat Disord. 2018 Dec 21;28:145-152.
The questions that need to be asked is alexithymia irreversible; or is it potentially reversible as has been shown with other cognitive impairments in MS? Is there a specific part of the brain where a single lesion can cause alexithymia; in other words can a single MS lesion in a strategic area cause alexithymia as part of a relapse?
Alexithymia is associated with damage to the limbic system and cortical areas of the left hemisphere including the anterior cingulate, inferior, middle, and superior frontal regions, insula, and supplementary motor areas. It appears that alexithymia is another cognitive symptom that is associated with MS-related damage. Therefore, to prevent developing alexithymia we need to treat MS early and effectively; i.e. to turn off the shredder before it causes irreversible damage.
BACKGROUND: Fatigue is a multifactorial symptom frequently reported by multiple sclerosis (MS) patients. To date, the pathophysiology of MS fatigue remains poorly understood and little is known about the relationship between this symptom and various clinical, neuropsychological, neurophysiological and radiological data. The aim of this work is to understand the underlying mechanisms of MS fatigue by means of a multidimensional evaluation.
METHODS: Fatigued (n = 21) and non-fatigued (n = 17) MS patients were enrolled based on the Modified Fatigue Impact Scale. They underwent clinical (disability score and disease duration), neuropsychological (scales of depression, anxiety, alexithymia, sleep, and Symbol Digit Modalities Test), neurophysiological (corticospinal excitability measures using transcranial magnetic stimulation), and radiological (volume-based morphometric magnetic resonance imaging) evaluations. The normality of data distribution was studied by the Kolmogorov-Smirnov test. Group comparison was performed using the Mann-Whitney or Student t test (quantitative data) and the exact Fisher's test (qualitative data). Correlation analysis was done using Pearson and Spearman tests.
RESULTS: Fatigued patients had higher depression (p = 0.02), anxiety (p = 0.02) and alexithymia (p = 0.04) scores compared to non-fatigued patients. On the neurophysiological and radiological evaluations, they also had higher short-interval intracortical inhibition (p = 0.04), larger caudate nuclei (p ≤ 0.01) and smaller left parietal cortex (p = 0.01). These findings were in line with the correlation analyses results.
CONCLUSION: The neuropsychological findings suggest common underlying mechanisms as well as bi-directional relationships between fatigue and each of anxiety, depression, and alexithymia. The neurophysiological findings may reflect maladaptive neuroplasticity processes and an aberrant GABAergic transmission in the generation of fatigue. The radiological findings could be interpreted in the light of the 'dysfunctional hypertrophy' or 'compensatory hypertrophy' hypotheses.