Magnetic
Bio-Stimulation
in Painful Diabetic Peripheral Neuropathy: A Novel
Intervention - A Randomized, Double-Placebo Crossover
Study
by Michael I. Weintraub, MD, FACP
Volume: AJPM Vol. 9 No. 1 January 1999 pgs 8-17
Abstract:
The pathophysiology of diabetic peripheral neuropathy
(DPN) is complex
and poorly understood. Despite the current state of
technology,
dysesthetic pain in the extremities of diabetics and
other patients
with neuropathies remains a refractory problem.
Conventional treatment
is largely symptomatic, somewhat arbitrary, and often
ineffective.
Prior preliminary studies suggested that the application
of magnetic
foot pads may be a modifiable factor in intractable
neuropathic pain
syndromes. The primary objective of this randomized,
double-placebo
control, crossover trial was to test the effectiveness
of
magnetotherapy in neuropathic pain and also to assess
the role of
placebo. Secondary objectives were to quantify nerve
conduction
electrophysiologic changes and neurologic examination
changes over a
4-month period. Of 24 initial patients, 19 completed the
4-month trial.
There were 10 patients with advanced and refractory DPN
(Stage II/III)
and 9 non-DPN. Improvement was significantly more
pronounced in the
diabetic cohort, 90% versus 33%, at the end of four
months (p <
0.02). During the first month, the placebo response was
noted to be the
same in both groups (22%) for symptoms of burning and
numbness and
tingling, whereas in the second month, the placebo
effect was greater
in the DPN cohort (38% versus 22%). This was felt to
represent an
overshoot phenomenon. At the end of 4 months,
improvement was
significantly more pronounced in the diabetic cohort for
burning (p
< .05) and numbness and tingling reduction (p <
.05).
Neuropathologic differences identified severe axonal
damage principally
in the diabetic cohort (absent CMAP 60%, absent SNAP
100%), whereas
mild demyelinating changes were seen principally in the
N-DPN group.
These severe axonal changes were strongly predictive of
clinical
success and responsiveness. There were no significant
serial changes in
the neurologic examination or electrodiagnostic studies.
Painful
dysesthesias associated with C-fiber dysfunction in the
diabetic cohort
responded dramatically to exposure to static magnetic
fields. The most
plausible explanation of benefit and suppression of
symptoms was that
the K+ internal rectifying channels were stimulated
producing
repolarization and/or hyperpolarization. Despite the
uncertainty
regarding the precise mechanism of this novel approach,
the results are
impressive and suggest that a legitimacy exists for
magnetotherapy as a
safe and unique therapy in neuropathic diabetic foot
pain. These
preliminary data need to be validated by a larger
longitudinal study.
