The typical changes in the CMAP during compression of a single nerve are shown in figure . Specifically, figure shows changes in amplitude while figure documents the corresponding changes in the CMAP onset latency and duration. This figure illustrates four common findings during hyperacute nerve compression. First, compression to 20 g of tension (P = 370 mmHg) leads to very little acute reduction in CMAP amplitude (~20%, figure ) while compression to 80 g (P = 1470 mmHg) causes significant CMAP amplitude reduction (~60%) but only minimal CMAP latency increases (figure ). Second, there is considerable variation in the CMAP duration but durations typically drop as the CMAP amplitude declines. Third, the CMAP amplitude during the recovery period may exceed that prior to compression. Fourth, at the high pressure levels (>80 g) used in this study, there are very rapid responses to compression.
Figure 2 CMAP parameters and nerve compression tension as a function of time during a typical nerve compression experiment. (A) Changes in CMAP amplitude and CMAP waveform. (B) Changes in CMAP onset latency and duration. In both cases, the applied force is shown (more ...)
Knowing these general properties, it is useful to look at the responses in the entire group of studied nerves. The CMAP amplitude is reduced by 50% for the first time during compression at a tension T = 52.7 g (std 22.7, min 18, max 79) corresponding to a mean pressure of 970 mmHg. The AUC for the CMAP is strongly correlated with the peak to peak amplitude. Linear regression of the normalized AUC on the normalized amplitude yields a slope of 0.95 (+/- .008) with R2 = .74. As expected, the AUC drops to 50% at a tension T = 54.4 g (P = 1001 mmHg), similar to the tension at which the CMAP amplitude drops to 50% of baseline. Figure shows the mean changes in amplitude and AUC during each phase of the experiment averaged over all nerves. The CMAP amplitude and AUC reductions first reach statistical significance during the phase in which the nerve is subjected to compression at a tension of 80 g. Figure shows the mean changes in velocity and duration of the CMAP during cycles of compression and recovery. Nerve conduction velocity changes minimally until levels of compression significant enough to reduce the CMAP amplitude to less than 20% of its initial value are attained. Although small, the 5% reduction in conduction velocity seen during the 80 g compression is statistically significant. Figure also confirms the decline in CMAP duration during compression. There is much variability in this measure and significant differences are not seen until the terminal compression phase. Figure demonstrates that the CMAP onset and mean latency, do not change significantly during the early phases of compression. Significant change is only observed at the terminal compression phase. Although the latency variance does increase during compression and decrease during recovery, this effect does not reach statistical significance until the terminal compression phase. We also investigated whether any combination of the above parameters show statistically significant changes earlier in the experiment. These included products of the primary parameters discussed earlier in such combinations as amplitude*velocity, amplitude*velocity*duration, amplitude*velocity* τs. However, none of these derived parameters showed statistically significant changes in the CMAP at an earlier point than either the CMAP amplitude or velocity alone. It should be noted that similar results were obtained using both the parametric and non-parametric ANOVA testing.
Figure 3 (A) Changes in amplitude and area under the curve at various points during the compression and recovery cycles. (B) Changes in nerve conduction velocity and CMAP duration during the various stages of nerve compression. (C) Changes in CMAP onset latency, (more ...)
In all cases where a CMAP was recordable, the maximum velocity was never less than half of its initial value. In order to better elucidate the changes in the CMAP, figures and show the normalized CMAP velocity and CMAP duration respectively from each recorded potential as a function of the normalized CMAP amplitude. In both of these cases, no change in the measured parameters greater than 10% occurs until the CMAP amplitude is reduced by over 80%. Similar effects of the mean latency and latency variance are noted.
Figure 4 Changes in relative CMAP velocity as a function of relative CMAP amplitude. In each case, relative CMAP values are derived from the raw measured values of that parameter by dividing the raw values by the mean value of the given parameter in the baseline (more ...)
Changes in relative CMAP duration as a function of relative CMAP amplitude.
An examination of the behavior of individual nerves shows that the CMAP amplitude returns to baseline or above in 9/16 nerves in the recovery period after the 1st compression (20 g) while 16/16 achieved amplitudes >30% of baseline. After the 2nd (80 g) compression, only 4/16 nerves returned to baseline amplitude and 10/16 reached amplitudes greater than 30% of baseline. After the 3rd compression, during which the tension was adjusted to make the CMAP disappear, 0/14 nerves achieved an amplitude >30% of baseline during the recovery period. Thus, the ability to recover is better after compressions that cause smaller declines in CMAP amplitude. Despite the minor changes seen in velocity, only 44% of nerves recovered to equal or better velocity after the 1st compression at 20 g, 29% after the 2nd compression at 80 g and 0% after the final compression.
In order to determine if the degree of CMAP amplitude reduction during low level compression predicted the degree of CMAP reduction with higher level compression, a Spearman rank correlations is performed. The degree of reduction in the CMAP amplitude during the 1st compression to 20 g is positively and significantly correlated with the CMAP amplitude during the 2nd compression to 80 g (Spearman R = 0.5, p < .05) However, there is no significant relation between the reduction in amplitude during the 1st compression and the CMAP amplitude during recovery from 80 g compression (Spearman R = 0.275, p > .05). There is also no significant correlation between the CMAP amplitude reduction during the 1st compression and CMAP amplitude reduction during the final recovery. The degree of reduction in velocity during the 1st compression is positively correlated (Spearman R = 0.77, p < .01) with the degree of velocity reduction during the 2nd compression but not with velocity during the recovery period. On the other hand, there are positive but statistically insignificant correlations between the changes in velocity during the 1st compression to 20 g and the amplitude reductions during the 2nd compression to 80 g.
Trains of spontaneous EMG activity are more commonly recorded when the CMAP amplitude is significantly reduced from baseline. The normalized CMAP amplitude when there was no spontaneous EMG activity was 0.657 while the mean amplitude was 0.36 when spontaneous EMG activity was seen (t = -2.65, p < .01, N = 3897). The CMAP duration was also shorter when spontaneous EMG was recorded (0.989 vs 0.82 p < .01 t = -2.65, N = 3897) than when it was not. There was no effect of the rate of CMAP change on the appearance of spontaneous EMG activity.