Functional somatic syndromes are characterized by high morbidity due to various, fluctuating symptoms without objective somatic findings. There is increasing evidence for the contribution of emotional and cognitive functions to symptom formation, which has been well established in the perception of pain. In addition to their involvement in various other cognitive and emotional processes, the anterior cingulate and insular cortex are thought to contribute to the so-called "pain neuromatrix". Recent data suggest that these areas appear also to be involved in symptom manifestation in multiple chemical sensitivity. Here we used functional Magnetic Resonance Imaging (fMRI) to test whether this network is also involved in the induction of unpleasant perceptions by sham mobile phone radiation in subjectively electrosensitive patients. This design enabled us to completely dissociate the unpleasant subjective perception from any real physical stimulus. Fifteen subjectively electrosensitive patients and 15 age- and gender-matched healthy controls were exposed to sham mobile phone radiation and heat as a control condition. The perceived stimulus intensities were rated on a five-point scale. During anticipation of and exposure to sham mobile phone radiation increased activations in anterior cingulate and insular cortex as well as fusiform gyrus were seen in the electrosensitive group compared to controls, while heat stimulation led to similar activations in both groups. Symptom manifestation during sham exposure to mobile phone radiation was accompanied by specific alterations of cortical activity in anterior cingulate and insular cortex in subjectively electrosensitive patients further supporting the involvement of these areas in the perception of unpleasantness and generation of functional somatic syndromes.
"Several previous studies have demonstrated that sham exposures can elicit symptoms in healthy participants    and people with various forms of IEI  , and that this process might be facilitated by leaflets produced by an IEI support group . However, another study failed to find, probably due to the small sample size and the lack of statistical power, a significant effect of written positive or negative information on expectations, cognitive performance, and symptom reports after a real or sham exposure to an EMF . "
[Show abstract][Hide abstract] ABSTRACT: Medically unsubstantiated 'intolerances' to foods, chemicals and environmental toxins are common and are frequently discussed in the media. Idiopathic environmental intolerance attributed to electromagnetic fields (IEI-EMF) is one such condition and is characterized by symptoms that are attributed to exposure to electromagnetic fields (EMF). In this experiment, we tested whether media reports promote the development of this condition.
Participants (N=147) were randomly assigned to watch a television report about the adverse health effects of WiFi (n=76) or a control film (n=71). After watching their film, participants received a sham exposure to a WiFi signal (15min). The principal outcome measure was symptom reports following the sham exposure. Secondary outcomes included worries about the health effects of EMF, attributing symptoms to the sham exposure and increases in perceived sensitivity to EMF.
82 (54%) of the 147 participants reported symptoms which they attributed to the sham exposure. The experimental film increased: EMF related worries (β=0.19; P=.019); post sham exposure symptoms among participants with high pre-existing anxiety (β=0.22; P=.008); the likelihood of symptoms being attributed to the sham exposure among people with high anxiety (β=.31; P=.001); and the likelihood of people who attributed their symptoms to the sham exposure believing themselves to be sensitive to EMF (β=0.16; P=.049).
Media reports about the adverse effects of supposedly hazardous substances can increase the likelihood of experiencing symptoms following sham exposure and developing an apparent sensitivity to it. Greater engagement between journalists and scientists is required to counter these negative effects.
Journal of psychosomatic research 03/2013; 74(3):206-12. DOI:10.1016/j.jpsychores.2012.12.002 · 2.74 Impact Factor
"However, it should be mentioned that the findings of these earlier studies were highly heterogeneous (for an overview see Table 1). There were single reports for structural changes in thalamus, inferior colliculus , hippocampus, orbitofrontal cortex, corpus callosum , dorsomedial prefrontal gyrus, and supramarginal gyrus (Diesch et al. 2012; Landgrebe et al. 2008a; Leaver et al. 2012; Mahoney et al. 2011). Three publications of one working group showed repeated changes in ventromedial prefrontal cortex (Leaver et al. 2011, 2012; Mühlau et al. 2006). "
[Show abstract][Hide abstract] ABSTRACT: Neuroimaging studies of tinnitus suggest the involvement of wide-spread neural networks for perceptual, attentional, memory, and emotional processes encompassing auditory, frontal, parietal, and limbic areas. Despite sparse findings for tinnitus duration and laterality, tinnitus distress has been shown to be related to changes in non-auditory cortical areas. The aim of this study was to correlate tinnitus characteristics with grey matter volume in two large samples of tinnitus patients. High-resolution brain images were obtained using a 1.5 T magnetic resonance imaging scanner and analysed by means of voxel-based morphometry. In sample one (n = 257), tinnitus distress correlated negatively with grey matter volume in bilateral auditory areas including the Heschl's gyrus and insula, that is, the higher the tinnitus distress the lower the grey matter volume. The effects of this correlation were small, but stable after correction for potential confounders such as age, gender, and audiometric parameters. This negative correlation was replicated in a second independent sample (n = 78). Our results support the notion that the role of the auditory cortex in tinnitus is not restricted to perceptual aspects. The distress observed was dependent on grey matter alterations in the auditory cortex, which could reflect reverberations between perceptual and distress networks.
Brain Structure and Function 02/2013; 218(4). DOI:10.1007/s00429-013-0520-z · 5.62 Impact Factor
"It has recently been proposed that the unified tinnitus percept actually involves multiple parallel dynamically adaptive networks , with each network reflecting a specific aspect of tinnitus, for example distress  . These subnetworks can be non-specific as demonstrated by the fact that the distress network in tinnitus is similar to the distress network observed in pain , asthmatic dyspnea , social rejection  and somatoform disorder . The DLPFC has been proposed as an integrator of emotion and cognition . "
[Show abstract][Hide abstract] ABSTRACT: Both invasive and non-invasive neuromodulation of the dorsolateral prefrontal cortex (DLPFC) are capable of suppressing tinnitus loudness. Repetitive transcranial magnetic stimulation (rTMS) of the DLPFC has an add-on effect for auditory cortex (AC) rTMS in improving tinnitus-related distress. We aimed to investigate whether TMS and rTMS of the DLPFC is capable of reducing tinnitus loudness and what mechanism might be involved. Two TMS studies targeting the right DLPFC were performed. Study 1 investigated 44 tinnitus patients who underwent either 1 or 10 Hz real or sham TMS (200 pulses at 80% motor threshold). In Study 2 we performed rTMS (10 sessions of 600 pulses) in responders of study 1. Changes on the visual analog scale (VAS) loudness were evaluated. All patients underwent a pre-TMS electroencephalography: differences in functional connectivity between responders and non-responders were evaluated using sLORETA. Only 1 Hz TMS was capable of significantly reducing tinnitus loudness for 11 patients with a mean suppression of 39.23%. RTMS for these 11 patients yielded a 21% improvement in VAS loudness, and in 7 of 11 rTMS was successful, with, a mean suppression of 27.13%. The responders were characterized by a difference in lagged linear connectivity in the theta band among the DLPFC, anterior cingulate cortex (ACC), parahippocampus and AC. In summary, 1 H, TMS and rTMS of the right DLPFC can transiently reduce the perceived tinnitus loudness mediated via functional connections between the DLPFC and a network consisting of the ACC, parahippocampus and AC.
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