Mult Scler. 2004 Apr;10(2):165-9
Flachenecker P, Bihler I, Weber F, Gottschalk M, Toyka KV, Rieckmann
P.
Department of Neurology, Julius-Maximilians University of Wurzburg,
Josef-Schneider-Strasse 11, D-97080 Wurzburg, Germany
BACKGROUND:
Fatigue is one of the most common disabling symptoms in patients with multiple sclerosis (MS), but the putative role of proinflammatory cytokines remains to be elucidated.
METHODS:
Thirty-seven patients (27 women, 10 men) with relapsing remitting (n = 29) and secondary progressive (n = 8) MS, aged 41.0 +/- 10.2 years, were studied.
Fatigue was assessed by Krupp's Fatigue Severity Scale (FSS).
Cytokine mRNA expression for interferon (IFN)-gamma tumor necrosis factor (TNF)-alpha and interleukin (IL)-10 were measured by real time RT PCR.
Autonomic function was evaluated by standard tests for parasympathetic and sympathetic function, as well as by serum levels of norepinephrine and epinephrine.
RESULTS:
Median levels of TNF-alpha mRNA expression were significantly higher in MS patients with (FSS > or = 4.0 and > or = 5.0, n = 26 and n = 14, respectively) than in those without fatigue (FSS < 4.0, n = 11).
No differences were seen for IFN-gamma and IL-10 mRNA expression.
Cytokine levels were not correlated to autonomic tests or to serum catecholamine levels.
CONCLUSIONS:
These results suggest that TNF-alpha, as a principal proinflammatory mediator, is associated with MS-related fatigue.
This is in support of a pathogenic role of the MS-related inflammatory process in the development of fatigue.