Association of tinnitus and electromagnetic hypersensitivity: hints for a shared pathophysiology?
From: PLoS ONE. 2009;4(3):e5026. Epub 2009 Mar 27
Tinnitus is a frequent condition with high morbidity and impairment in quality of life. The pathophysiology is still incompletely understood. Electromagnetic fields are discussed to be involved in the multi-factorial pathogenesis of tinnitus, but data proofing this relationship are very limited. Potential health hazards of electromagnetic fields have been under discussion for long. Especially, individuals claiming themselves to be electromagnetic hypersensitive suffer from a variety of unspecific symptoms, which they attribute to electromagnetic fields exposure. The aim of the study was to elucidate the relationship between electromagnetic field exposure, electromagnetic hypersensitivity and tinnitus using a case-control design.
Tinnitus, the perception of sound in the absence of an external sound, is a frequent disorder of auditory perception, which is very difficult to treat. Tinnitus as a phantom perception of a meaningless sound has to be differentiated from auditory hallucinations which mainly occur in the context of psychiatric diseases and are characterized by e.g. the perception of voices. About 10–20% of the adult population experiences some degree of tinnitus. Many learn to ignore the sounds and experience no major effects, but for about 1 in 100 adults, the noise interferes significantly with daily life. In those patients, tinnitus is frequently associated with neuropsychiatric co-morbidity such as depression, anxiety or sleep disorders, which underlines the clinical and socio-economic importance.
Even if the pathophysiology of tinnitus remains incompletely understood, there is growing evidence that dysfunctional neuroplastic processes in the brain are involved. In particular, it is assumed that tinnitus might be the correlate of maladaptive neuroplastic changes due to distorted sensory input. Accordingly functional imaging studies demonstrated neuroplastic alterations in the central auditory system. However tinnitus related alterations of neural functioning are not limited to the central auditory system, but also encompass non-auditory regions such as frontal and limbic areas.
There has been an ongoing debate, whether tinnitus might be related to exposure to electromagnetic fields. One previous study found a tinnitus prevalence of 14% in a sample of electromagnetic hypersensitive subjects. Whereas electromagnetic hypersensitivity per se is not a proxy variable for electromagnetic field exposure, substantial evidence from electrophysiological studies has shown electromagnetic fields and especially mobile phone emissions to influence cognitive function and neuronal processing in the central auditory system. These might represent potential mechanisms by which electromagnetic fields could contribute to the development of tinnitus. However, two recent epidemiological studies from a student and a the general population, respectively, did not demonstrate a significant relationship between mobile phone use and tinnitus.
Besides the hypothesized involvement in the generation of tinnitus, electromagnetic field exposure has also been related to a variety of unspecific health symptoms (e.g., dizziness, fatigue, headache, sleep disturbances, etc.). Despite a huge amount of studies investigating the health impact of electromagnetic fields, no clear relationship between electromagnetic field exposure and these unspecific health symptoms could be established and the majority of provocation studies failed to demonstrate such a relationship. Based on the fact that some individuals suffer from a variety of symptoms, which they attribute to electromagnetic fields exposure, whereas the overwhelming majority does not experience any symptoms under the same electromagnetic field exposure, the concept of “subjective electromagnetic hypersensitivity” evolved. This subjective electromagnetic hypersensitivity is characterized by health complaints, which interfere with daily living and are subjectively attributed to electromagnetic fields of named emission sources (e.g., mobile phone base stations, hot spots, TV-sets, etc.). Very recent data from an epidemiological case-control study suggest that this subjective electromagnetic hypersensitivity is characterized by dysfunctional cognitions, reduced discrimination ability for sensory stimuli and increased sensitivity of a cortical network encompassing the anterior cingulate and insular cortex.
Due to the large sample size, the detailed clinical and neurobiological characterization and the control group, which was matched for age, gender and either living surroundings or workplace (as very rough proxies for electromagnetic field exposure), this study population was well suited to investigate the relationship between tinnitus, subjective electromagnetic hypersensitivity and electromagnetic field exposure. In detail, we addressed the following questions: 1.) Do subjective electromagnetic hypersensitive people suffer more often from tinnitus than controls? 2.) Are there clinical characteristics that point to potential common pathological mechanisms?
With the failure to prove a causal relationship between electromagnetic field exposure and symptoms in subjectively electromagnetic hypersensitive patients, research is focusing increasingly on neuronal mechanisms involved in symptom formation. Recent results suggest an individual vulnerability of these patients against environmental stressors especially affecting the autonomic nervous system. A pilot study investigating possible alterations of central nervous system excitability found evidence for alterations of the glutamatergic system, which may be an indicator of reduced adaptation abilities of these patients. These results have been replicated in a larger study population underlining the robustness of these findings. Furthermore, specific dysfunctional cognitions dealing with different aspects of electromagnetic fields were identified to play a pivotal role in the generation of subjective electromagnetic hypersensitivity. The importance of these cognitive processes is supported by the efficacy of cognitive behavioral therapy for the treatment for electromagnetic hypersensitivity. In addition, functional imaging revealed the involvement of anterior cingulate and insular cortex in symptom generation. These areas, which are part of a neural network conveying distress and avoidance in pain perception, seem also to play a pivotal role in subjective electromagnetic hypersensitivity or other functional somatic syndromes like e.g. multiple chemical sensitivity. With respect to tinnitus, the increased prevalence in electromagnetic hypersensitive patients could be due to the increased sensitivity of this cortical distress network, which has been repeatedly shown to be involved in the pathophysiology of tinnitus.
The dysfunctional over-activation of this cortical neural network might be related to a disturbed representation of external and internal perceptions, which in turn could explain the reduced ability to discriminate real from sham electromagnetically evoked stimuli of electromagnetic hypersensitive patients as well as in subjects experiencing tinnitus.
Taken together these results point to a shared pathophysiology of subjective electromagnetic hypersensitivity and tinnitus. It may be hypothesized that these changes represent a key feature of somatoform disorders, which should be addressed in future studies.
In conclusion, this study has shown that tinnitus is much more frequent among subjective electromagnetic hypersensitive patients whereas there is no hint for a relationship between tinnitus and exposure to electromagnetic fields. Rather, the correlation between tinnitus and electromagnetic hypersensitivity might be due to an individual vulnerability. Neurobiological characteristics of this increased vulnerability such as an oversensitive cortical distress network and an impaired discrimination ability for electromagnetically evoked sensory stimuli might be involved in the pathophysiology of both tinnitus and electromagnetic hypersensitivity and possibly also in other related perception disorders. Nevertheless, this hypothesis derived from our epidemiological study has to be confirmed in further studies by e.g. intervention studies aiming for a normalization of the postulated over-activated distress network in subjectively electromagnetic hypersensitive (e.g. cognitive behavioral therapy, which has been shown to be successful in electromagnetic hypersensitivity and tinnitus patients).
