No abstract

Although fatigue is common among multiple sclerosis (MS) patients, evaluation of this symptom is difficult due to the subjectivity and variability of the complaint. We proposed the Fatigue Descriptive Scale (FDS) as a tool to evaluate the severity and quality of fatigue in a group of patients suffering from MS. As a way to demonstrate the usefulness of this scale we applied the FDS in a group of 155 patients (105 women and 50 men) with clinically-definite multiple sclerosis, as outlined according to Poser's criteria. Age was 36.2 +/- 11.1 years (range 12-62) and time of evolution was 8.3 +/- 9.4 years (range 1-44). The Fatigue Severity Scale (FSS) was also used. Descriptive statistics techniques and techniques for nonparametric distribution (Spearman Rank, Kruskal-Wallis ANOVA) were used. One hundred and eighteen patients reported fatigue (73 spontaneously, 45 when questioned). All descriptions of fatigue were ranked according to FDS categories. Eighty-five patients defined the symptom as fatigue with exercise, 26 as asthenia and seven as the worsening of other symptoms. Fatigue by itself produced limited or disrupted activity in 78 patients; work-related functions were limited in 48 patients; social relations were limited in 29 patients; and self-care difficult for one patient. Fifty-six patients suffered fatigue daily. FDS score was 4.9 +/- 3.9 (range 0-13). FSS was 3.1 +/- 1.7 (range 0.2-6.6). FDS and FSS of Krupp were highly correlated (R = 0.87, p < 0.001). Therefore, in comparison with other scales, the FDS shows remarkable usefulness in classifying, periodicity, and severity of fatigue in MS patients. The high correlation with the FSS implies that it is a valid method to measure the severity of fatigue, as was demonstrated in our paper proposing the FDS. The importance of this new scale is its ability to inform the clinicians in a very quick, easy, and at the same time complete way, how severe the fatigue really is and how it affects the patient.

The Spanish FAMS is a psychometrically valid instrument that allows clinicians and clinical researchers the ability to measure the QOL concerns of MS patients in Spain.

Although different factors are probably involved in the etiology of fatigue in multiple sclerosis patients, no definite mechanism has been proposed. We have proposed that fatigue is a complex symptom that includes three clinical different entities (asthenia, fatigability and worsening of symptoms with effort). The goal of this study is to demonstrate if there is a peculiar mechanism for each of the different varieties of fatigue. A control sample of 155 patients (105 women, 50 men) with clinically definite MS was studied. Fatigue was measured using the Fatigue Descriptive Scale (FDS) and the Fatigue Severity Scale (FSS). Treatment, depression, anxiety, sleep and cellular immune status were studied too. Fatigue was a symptom in 118 patients (76.13%); 26 patients (22.03%) described it as asthenia (fatigue at rest); 85 patients (72.03%) as fatigability (fatigue with exercise), and seven patients (5.9%) as worsening of symptoms. The severity of pyramidal involvement was significantly more severe in patients suffering from fatigue; some immunological parameters were associated with fatigue as well. The discriminant analysis of the data shows that some of the immunoactivation parameters are associated with asthenia (F=21.5, P<0.001), and pyramidal tract involvement is associated with fatigability (F=10.5, P<0.001). Sleep disorders, anxiety and depression were linked with fatigue in a few patients. No relationship with treatment was proven. In conclusion, fatigue in MS seems to be a heterogeneous entity. Asthenia and fatigability may be different clinical entities. Certain immunoactivation parameters correlate with the presence of asthenia while pyramidal involvement is associated with fatigability.

Loss-of-function SPG11 mutations are the major cause of autosomal recessive hereditary spastic paraparesis with thin corpus callosum in Southern Europe, even in apparently sporadic cases. Decreased thalamic metabolism was consistently a phenotypical SPG11 mutation hallmark.