ABSTRACT
Although an electrohypersensitivity (EHS) is reported in numerous studies, some authors associate hyperfrequencies (HF)-related pains with a nocebo effect while others suggest a biological effect. Therefore, we aimed to suggest hypotheses about the complex mechanisms of headaches related to HF-exposure. We crossed basic features of headaches with relevant studies (from the year 2000 up to 2018) emphasizing on the HF effects that may lead to pain genesis: neuroglial dysmetabolism, neuroinflammation, changes in cerebral blood perfusion, blood-brain barrier dysfunction and electrophysiological evidences of hyperexcitability. We privileged studies implying a sham exposure (for in vivo studies) and a specific absorption rate lower than 4 W/Kg. HF-induced headaches may involve an indirect inflammatory process (neurogenic, magnetogenic or thermogenic) as well as a direct biophysical effect (thermogenic or magnetogenic). We linked inflammatory processes to meningeal dysperfusion or primary neuroglial dysfunction triggered by non-thermal irradiation or HF-induced heating at thermal powers. In the latter case, HF-induced excitoxicity and oxidative stress probably play a crucial role. Such disorders may lead to vascular-trigeminal activation in predisposed people. Interestingly, an abnormal oxidative stress predisposition had been demonstrated in overall 80% of EHS self-reporting patients. In the case of direct effects, pain pathways’ activation may be directly triggered by HF-irradiation (heating and/or transcranial HF-induced ectopic action potentials). Further research on HF-related headaches is needed.
Declarations of interest
The authors report no conflicts of interest.
Acknowledgement
Authors would like to thank Dr Ali Kassab for helping to review the final proof of this paper.