What Causes MCS? Physiological And Psychological Hypotheses
This chapter provides an updated discussion of both physiological and psychological hypotheses regarding MCS. I do not endorse psychological explanations, but review them so that people can be informed.
Except from p. 33-34:A New Generation of “Are They Crazy?” Studies
There are some newer studies that attempt to tease out psychological variables in comparing MCS patients to both normal populations and persons with other health conditions. Kai Österberg and colleagues have done a series of studies of this sort. Österberg, Ørbaek and Karlson (2002) question how persons with MCS can have “neurotoxicologically induced brain dysfunction” when their previous exposures are “as a rule, found to be very faint or nonneurotoxic” (p. 140). The authors gave persons with MCS and matched controls a battery of neuropsychological tests and found differences on only one: a complex reaction time test. They then conclude that “Obviously, neurotoxic brain impairment in the traditional sense is an untenable explanation for the smell intolerance in MCS because of the absence of previous exposure of neurotoxic significance in most cases” (p. 145). (Apparently the authors classify pesticides, solvents, anesthesias, and other sensitizers and “nonneurotoxic,” which seems to fly in the face of the toxicology data.)
In another study published in that same year, Österberg, Karlson, and Ørbaek (2002) compared persons with MCS, patients with toxic encephalopathy (TE), and controls on risk perception, the Karolinska Scales of Personality (KSP), and the Symptom Checklist 90 (SCL-90). There were no differences in risk perception between any of the groups (meaning that persons with MCS did not exaggerate risks). On the Karolinska Scales persons with MCS were elevated on only one of sixteen variables: psychasthenia. On the SCL-90 people with MCS scored higher than controls on Somatization, Depression, and Interpersonal Sensitivity scales, and on the Global Severity Index, a sum total of all of the scales. But the elevations for those with MCS were “moderate” compared with those with TE. The authors then explain that the elevation on the SCL 90 for TE shows that:
“responses in inventories to both mental distress and personality traits may be affected even by very slight neurotoxic brain impairment. In the present context, this suggests that it might be completely misleading to view elevated scores on self-rating scales of mental distress and personality as evidence of primary psychiatric disease in MCS cases” (p. 173).
So it seems that in this study, the researchers move toward admitting to neurological effects in MCS. They go further and give their “impression of MCS cases as a basically non-psychiatric group” (p. 173). But they backslide a bit when they say that people with MCS may have “a somewhat more asthenic personality than most people and . . . more sensitive in social relations, more bothered with bodily perceptions, and more prone to depressive reactions” (p. 173). Clearly having trouble pigeonholing this population, they finally conclude: “The MCS syndrome does not fit into either a somato-immunological or a traditional psychiatric explanation model” (p. 174).
The group gets down to the nitty-gritty in 2003 by using an exposure chamber to expose both women with MCS and control women to n-butyl acetate or toluene. Women with MCS showed more mucous membrane irritation and fatigue (physical indicators), but not greater expectancy effects (psychological indicators). The women with MCS also showed poorer (slower) initial reaction times as well as more deterioration in reaction times than controls and did not show learning on an eye-hand coordination task like the control group did (neurological effects) (Österberg, Ørbaek, Karlson, Åkesson, and Bergendor, 2003). Although the authors are not completely able to renounce the somatization possibility in this study, they state in the abstract “The results offer the most support to an irritative basis for multiple chemical sensitivity” (p. 40).