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Static, Low-Frequency, and Pulsed Magnetic Fields
that MRI examinations, even in ultra-high-field scanners, do not seem to have any
persisting influence on the attention networks of human cognition immediately after
exposure.
3.3.1.3 Occurrence of Analgesia
Specific SMFs, ELF-EMFs, and pulsed EMFs (PEMFs) have been shown to induce analgesia (antinociception) in snails, rodents, and healthy human volunteers. In particular,
the effects of ELF-EMFs on analgesia have been reviewed in detail by Prato, Thomas, and
Cook (2005). However, evidence concerning the effects of magnetic fields on nociceptive
or pain sensation processes is contradictory in the literature probably due to differences
in species, characteristics of the magnetic fields, and duration of the exposure.
Prato et al. (2005) showed that repeated daily exposures for 1 hour to an ambient
magnetic field–shielded environment induce analgesia (antinociception) in mice. The
exposures were carried out in the dark during the mid-light phase of the diurnal cycle.
However, when the mice were exposed in the presence of visible light (400–750 nm) the
analgesic effects of shielding were eliminated. The Prato research group later showed
that the analgesic effect of magnetic field shielding in mice is light-intensity and wavelength dependent (Prato et al. 2009). Introduction of red light (peak wavelength at
635  nm) had little or no effect, presumably because mice do not have photoreceptors
sensitive to red light above 600 nm in their eyes. By contrast, introduction of ultraviolet
light (peak wavelength at 405 nm) abolished this effect, presumably because mice do
have ultraviolet A receptors. Blue light exposures (peak wavelength at 465 nm) of different intensities demonstrated that the effect has an intensity threshold of 12% of the blue
light in the housing facility.
Sándor et al. (2007) examined the action of acute exposure to a gradient SMF (B max of
389 mT, 39 T/m, for 30 minutes) on acute visceral and somatic chemonociception and
inflammatory mechanical hyperalgesia in mice. The SMF exposure significantly diminished the number of acetic acid- or MgSO 4 -induced abdominal contractions (acute visceral nociception), the number of formalin-evoked paw lickings and liftings in both
phase I (acute somatic nociception) and phase II (acute inflammatory nociception),
and mechanical hyperalgesia evoked by intraplantar (i.pl.) injection of carrageenan as
well as a capsaicin receptor TRPV1 agonist (resiniferatoxin). Selective inactivation of
capsaicin-sensitive sensory fibers by high-dose resiniferatoxin pretreatment decreased
nocifensive behaviors in phase II of the formalin test to a similar extent, suggesting
that pro-inflammatory neuropeptides such as substance P and calcitonin gene–related
peptide released from these fibers are involved in this inflammatory reaction. They
found that significant inhibitory effects of SMF on formalin-induced nociception and
carrageenan-evoked hyperalgesia were absent in resiniferatoxin-pretreated mice. The
findings indicate that capsaicin-sensitive nerves are involved in the SMF-induced antinociceptive action. The same research group reported that analgesic effect is induced
by whole-body exposure to the same gradient SMF as in the previous study in mice
(László et al. 2007). As a result, the authors found a magnet arrangement recipe that
achieves an analgesic effect of over 80% in the writhing test. The same research group
further reported that SMF (B max of 330 mT, 13.2 T/m, for 30 minutes) increased thermal pain threshold (TPT) and reduced within-block thermal habituation in healthy