Multiple chemical sensitivity (MCS) is characterized by somatic distress upon exposure to odors. As in other idiopathic environmental intolerances, the mechanisms behind the reported hypersensitivity are unknown. Using the advantage of the well-defined trigger (odor), we investigated whether subjects with MCS could have an increased odor-signal response in the odor-processing neuronal circuits. Positron emission tomography (PET) activation studies with several different odorants were carried out in 12 MCS females and 12 female controls. Activation was defined as a significant increase in regional cerebral blood flow (rCBF) during smelling of the respective odorant compared to smelling of odorless air. The study also included online measurements of respiratory frequency and amplitude and heart rate variations by recording of R wave intervals (RR) on the surface electrocardiogram. The MCS subjects activated odor-processing brain regions less than controls, despite the reported, and physiologically indicated (decreased RR interval) distress. In parallel, they showed an odorant-related increase in activation of the anterior cingulate cortex and cuneus-precuneus. Notably, the baseline rCBF was normal. Thus, the abnormal patterns were observed only in response to odor signals. Subjects with MCS process odors differently from controls, however, without signs of neuronal sensitization. One possible explanation for the observed pattern of activation in MCS is a top-down regulation of odor-response via cingulate cortex.
(c) 2006 Wiley-Liss, Inc.