NEUROLOGIC, MR-IMAGING, AND MR SPECTROSCOPIC FINDINGS IN EOSINOPHILIA-MYALGIA-SYNDROME

BACKGROUND AND PURPOSE: Eosinophilia myalgia syndrome (EMS), a multisy stemic disease induced by exposure to L-tryptophan, may result in seri ous CNS abnormalities. The purpose of this study was to determine the pattern of neurologic characteristics, MR imaging abnormalities, and b rain neurometabolites in EMS. METHODS: Sixteen patients with EMS and C NS abnormalities (CNS-EMS) and 12 control subjects underwent evaluatio n, including medical and neurologic examination, proton MR spectroscop y, and MR imaging. RESULTS: Neurologic findings that were increased in CNS-EMS included minor depression (100%), amnesia (88%), and intermit tent confusion (38%), although fatigue (31%), motor disorders (31%), r ecurrent headache (19%), major depression (13%), and dementia (6%) als o occurred, but at a lesser significance, Self-reported disability was markedly increased in CNS-EMS, MR imaging findings included subcortic al focal lesions, focal lesions in deep white matter, cortical atrophy , ventricular dilatation, and diffuse and periventricular white matter abnormalities. MR spectroscopic findings established two distinct spe ctral patterns: 1) increased choline-containing compounds, decreased N -acetylaspartate, and increased lipid-macromolecules, consistent with inflammatory cerebrovascular disease; and 2) increased glutamine, decr eased myo-inositol, and decreased choline, consistent with acute CNS i njury or metabolic encephalopathy, CONCLUSION: Neurologic abnormalitie s, self-reported disability, brain lesions, and MR spectroscopic abnor malities are common in CNS-EMS, The pattern of cerebral lesions and ne urometabolites is consistent with widespread inflammatory cerebrovascu lar disease. However, a subgroup of patients with CNS-EMS have neurome tabolic changes consistent with a metabolic encephalopathy identical o r similar to hepatic encephalopathy. The neurologic abnormalities in E MS and related hypereosinophilic syndromes should be interpreted cauti ously, with the recognition that both cerebrovascular injury and secon dary metabolic encephalopathies may be involved.