Àá½Ã¸¸ ±â´Ù·Á ÁÖ¼¼¿ä. ·ÎµùÁßÀÔ´Ï´Ù.
KMID : 0350519950480020579
Journal of Catholic Medical College
1995 Volume.48 No. 2 p.579 ~ p.595
Changes of Spinal Evoked Potentials and Histologic Findings in the Regenerated Rat Sciatic Nerves after Compression Injury


Abstract
In order to investigate the significance of somatosensory evoked potential test in the evaluation of the progress of peripheral nerve regeneration, the changes in spinal evoked potential (SEP) and histologic findings were studied in
experimentally
designed compression neuropathy.
One hundred twenty adult male Wistar rats were divided into two groups : the control group (n=60) was normal rats without anyu injury and the experimental group (n=60) was prepared by compressing the right sciatic nerve using a pressure algometer
with
the pressure of 5 kg/§² for 10 seconds. In both groups, the waveforms, peak latencies and amplitudes of SEP were measured after stimulation distal to the lesion of the right sciatic nerve at 1 hour and 1, 2, 4, 8 and 12th week, respectively,
after
the
compression injury. The distribution of the myelinated nerve fibers (MFs) according to the diaeter were also determined from the specimen of the sciatic nerve distal to the lesion. The data obtained from 120 rats were analyzed and both groups
were
compared statistically.
@ES The results were as follows :
@EN The SEP in control group showed polyphasic potentials composed of 5 peaks of 5 peaks of P1, N1, P2, N2 and P3. The waveforms in experimental group were monophasic or triphasic from 1 hourto 4th week after compression injury and were changed
to
similar waveforms of cnotrol group at the 12th week.
2. The mean P1 and N1 latencies of SEP in the control group were 1.18¡¾0.12 msec and 1.53¡¾0.19 msec, respectively. The latencies in the experimental group were significantly prolonged at 1 hour after the compression injury, and were prologed
most
at
the 2nd week, which were 4.1 and 3.7 times longer than those of the control group. And they began to decrease from the 4th week. The latencies were not significantly differen from those of the control group at the 12th week.
3. The mean P1, N1 amplitude of SEP in the control group was 6.42¡¾3.76§Å. The P1, N1 amplitude in the experimental group began to decrease from 1 hour after compression injury, and decreased most at the 2nd week to be about 12.1% of that of the
control group. Then it increased gradually and reached 68.8% of the control value at the 12th week.
4. The mean number of MFs with diameter above 4§­in the control group was 451.9¡¾6.19/50,000§­*. The number of the MFs in the experimental group significantly decreased except 1 hour after the compression injury, and was about 23.4% of the
control
group at the 1st week, 4.6% at the 2nd week, and then increased gradually to 50.1% at the 8th week, and 83.0% of control group at the 12th week.
5. As the number of MFs with diameter above 4§­incresed from 1st week after the compression injury, the P1 and N1 latencies of SEP were shortened (r=-0.6458 and -0.6538 respectively), and the P1, N1 amplitude was increased (r=0.6051). The P1 and
N1
latencies were more correlated with the number of MFs than the P1, N1 amlitude.
The results of the present study suggest that SEP is valuable in the evaluation of the progress of peripheral nerve regeneration after compression injury.
KEYWORD
FullTexts / Linksout information
Listed journal information