SPINAL CORD INJURY
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THE SOCIETY OF NEUROLOGICAL SURGEONS
75th Meeting in its 64th Year
New York, New York
April 25-28, 1984
Department of Neurosurgery
New York University
PULSED ELECTROMAGNETIC FIELDS ALTER CALCIUM IN SPINAL CORD
INJURY
Wise Young, Ph.D., M.D., NYU Medical Ctr., New York, NY 10016 |
Two years ago, we demonstrated with extracellular
calcium (Ca) measurements that contusion of the spinal cord
causes massive Ca entry into cells. More recently, using atomic
absorption spectroscopy (AAS), we found that Ca progressively
accumulates in injured spinal cords, so that tissue Ca at the
lesion site doubles by 3 hours and may increase 5-fold within
24 hours. Normally, neural cells maintain intracellular Ca at
very low levels. Entry of Ca into neurons and glia is known
to have deleterious effects on cellular function and survival.
Therefore, we and others have hypothesized that Ca plays a role
in producing the necrotic extension and exonal die - back seen
in spinal cord injury.
To test this hypothesis, we applied pulsed electromagnetic fields
(PEMF) to contused cat spinal cords. Electromagnetic fields
have long been known to alter Ca in central nervous tissues.
Exposure of brain tissues, for example, to even low intensity
fields can significantly increase Ca efflux from cells both
in vivo and in vitro. Although the mechanisms of such field
effects are not well understood, recent work suggests that Ca
changes can result from fields too low in power to heat tissue
significantly, that radiofrequency fields ranging to 147 MHz
may work as well, that a key factor is the induction of tissue
voltage gradients of 10-30 mV/cm, and that modulated fields
enhance the Ca changes. We chose to apply a 27.12 Mhz electromagnetic
field with an instrument (Diapulse), which allows external field
delivery without implanted electrodes. To induce tissue voltage
gradients of 10-30 mV/cm, fields of 3000 mW/sqcm peak power
density were used. To minimize thermal effects, the fields were
applied to 65 usec. pulses 400/sec for an average power of 78
mW/sqcm.
Two standardized contusion spinal injury models were used in
the experiments. One is a standard 20 gm dropped 20 cm onto
T9 cord exposed by laminectomy. This causes paraplegia in 90%
of cats for at least 2-3 months after injury. The other consists
of a 13-gram weight dropped 20 cm onto T9 cord with rigid clamping
of the spinal column. This supported contusion model produces
greater damage to the spinal cord causing unremitting paralysis
and sensory loss in the hind limbs. PEMF was compared against
untreated controls. For ionic studies, spinal cords were
injured, treated and dissected out at 3 hours after injury into
2-3mm segments and then individually analyzed by AAS for Ca,
Na, K and water contents. To assess the effect of PEMF on functional
recovery, cats were evaluated weekly or for a month and then
monthly for 3 months with somatosensory evoked potentials (SEP),
vestibulospinal responses (VSR), and scoring for locomotory
ability. At 4 months after injury, we counted and compared numbers
of axons passing through the contusion sites.
PEMF significantly altered Ca distribution in injured spinal
cords. We compared 2 groups of 10 cats: untreated controls and
cats in which PEMF was applied for 2 hours starting 45 minutes
after injury.
Untreated controls showed a consistent pattern of Ca accumulation
at the contusion site, doubling by 3 hours after injury. Ca
accumulated to even higher levels in cord adjacent to the lesion,
to twice that at the contusion site. Tissue Na increased 120%,
K fell 60%, and water content increased 7% at the contusion
site. PEMF reduced Ca significantly in cord adjacent to but
not at the lesion site. PEMF did not affect Na, K, or water
changes in the contused spinal cords. These findings suggest
that PEMF specifically reduces Ca accumulation.
Cats treated with PEMF showed significantly better recoveries
of SEP. VSR, and ability to locomote independently. We compared
2 groups of 10 cats injured with the l3gm-2Ocm supported contusion.
One group was untreated and served as controls. The other was
treated with PEMF for 4 hours beginning 45 minutes after injury.
In the control group, no cat was able to walk at 4 months after
injury, only 10% recovered SEP, and 20% had some VSR. In the
PEMF group, 50% of the cats were able to walk independently,
60% recovered SEP bilaterally and 50% had VSR. The PEMF group
differed significantly (p<O.Ol, Chi-square test) from the
control group for all three modes of evaluation. Axon counts
suggest that PEMF treated cats have more axons traversing the
lesion.
We then designed the following experimental paradigm to answer
several questions. Can the treatment time be shortened? What
is the optimum time to start applying the PEMF after injury.
How long can PEMF treatment be delayed? Four groups of 10 cats
were injured with the standard 2Ogm-2Ocm contusion model. One
group was untreated and served as control (group C). The remaining
three groups were treated with PEMF for two weeks after injury,
an hour daily. However, one of the groups received an hour of
PEMF starting an hour after injury (P1). In another, PEMF was
started 4 hours (P4). One group was not treated during the first
24 hours (P24). If the PEMF effect were due to the prevention
of progressive Ca entry into cells, the treatment should be
beneficial at 1-4 hours but not 24 hours. The cats were evaluated
for 2 months after injury. The results are listed below in percentages
of cats in each group with definite responses.
SEP
VSR
Walking
Group n days - > 30
60
30
60
30
60
| C |
10 |
0% |
10% |
20% |
30% |
0% |
0% |
| P1 |
20 |
70%*** |
40% |
40% |
70% |
0% |
20% |
| P4 |
10 |
50%*** |
50% |
50% |
50% |
0% |
30% |
| P24 |
10 |
60%*** |
20% |
20% |
40% |
0% |
10% |
| Control vs PEMF group |
(Chi - square): *p<0.05 |
**p<0.01 |
***p.<0.00l |
In conclusion, PEMF applied to spinal cords shortly after contusion
reduces Ca accumulation in cord adjacent to the injury site.
This change in Ca is associated with better recovery of motor
and sensory function in severe spinal injury. PEMF treatment
of lesser duration still improves recovery of neurophysiological
responses but the extent of recovery may be reduced. Delaying
PEMF treatment to 24 hours after injury results in only transient
SEP recoveries. |
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