The effects of exposure of rats to a 915 MHz electromagnetic field (EMF) on neuropathic pain in an amputation model should be investigated, as few studies (Yuh et al. 1992, Formica et al. 2004 and Colip 2013) have suggested an association between EMF and neuropathic pain.
Neuropathic pain is pain caused by damage of the nervous system, e.g. caused by an amputation.
From a total of 20 rats, 16 were randomly selected to receive a surgical treatment to simulate amputation and generate a neuroma (a neural bulb typically occurring after amputations) at the sciatic nerve (TNT group). The remaining animals (n=4) received sham surgeries (TNT sham group). Both groups were exposed to the electromagnetic field afterwards (remark EMF-Portal: there was no control group and no statistical comparisons to a control condition without exposure were made).
After 4 weeks of exposure, animals from the TNT group were randomly divided into two subgroups (n=8 each): 1) TNT neuroma resection and 2) TNT sham resection. Moreover, 8-week-old neuromas of unspecified origin were investigated.
To check whether the pain response was caused by thermal effects, additional tests with an infrared heat source were conducted.
In parallel, in vitro experiments were conducted on dissociated dorsal root ganglion neurons in the presence and absence of TNF-α (to simulate the conditions of inflammatory injury) in order to determine whether exposure to EMF was sufficient to directly depolarize sensory neurons.
Exposure duration: continuous for 10 minutes once peer week for 8 weeks in a row and once in week 28
in vivo experiments
Exposure duration: continuous for 10 minutes
in vitro experiments
|Exposure duration||continuous for 10 minutes once peer week for 8 weeks in a row and once in week 28|
|Additional info||in vivo experiments|
|Exposure duration||continuous for 10 minutes|
|Additional info||in vitro experiments|
|power density||756 mW/m²||average over time||measured||-||maximum value, ± 8.5 mW/m2|
During exposure to the electromagnetic field, a significant higher pain response was observed in the TNT group compared to the TNT sham group from week 3, what could not be prevented by resection of neuroma bulbs. An injection of lidocaine prevented pain, which indicated a nerve-mediated pain reaction. During exposure in the pretest, the skin temperature increased by 2.1 ± 0.7°C (remark EMF-Portal: the comparability to mobile radio exposure is questionable).
Exposure to the thermal stimulus increased the skin temperature by 4.8 ± 0.4°C and induced a significantly higher pain response in the TNT group compared to the TNT sham group as well. However, this response was lower compared to EMF exposure, indicating a thermal component in EMF-induced pain but also additional mechanisms.
In neuroma bulbs, a significantly increased protein expression of TRPV4 ion channels compared to the contralateral healthy nerve was found. This indicated that EMF-induced postamputation pain may be mediated by activation of TRPV4 ion channels.
In the in vitro experiments, EMF-exposed cells showed significantly higher rates of intracellular calcium peaks compared to the control group, which was interpreted as indicative of an effect on depolarization and activation of the neurons. Administration of TNF-α resulted in a significantly higher percentage of activated neurons during EMF exposure, suggesting an increased sensitivity of sensory neurons through EMF exposure in combination with inflammatory processes.
The authors conclude that exposure of rats to a 915 MHz electromagnetic field might contribute to neuropathic pain in an amputation model.