MR intensity measurements of nondenervated muscle in patients following severe forearm trauma.

Fluid increases resulting in higher MRI signal intensities in T(2) -weighted and short tau inversion recovery (STIR) sequences can be used to diagnose nerve injury. By comparing the signal intensities over time, MRI may become a new method for monitoring the healing process. Muscle edema is assessed by comparing the signal intensity of affected muscle with that of nonaffected muscle. However, in severe forearm trauma, the signal of nondenervated muscle may also be increased by wound edema, thus masking the effect of denervation. Hence, the purpose of this study was to investigate the influence of wound edema on muscle signal intensity in 29 consecutive patients examined on a 1.5-T MRI scanner at 1, 3, 6, 9 and 12 months after severe forearm trauma. The long-term course of wound edema and the influence of wound distance were thus investigated using a standardized imaging, calibration and post-processing protocol. The signal intensities of nondenervated intrinsic hand muscles were measured in the affected and contralateral sides. Muscle signal intensities were increased on the trauma side at 1 and 3 months (18% and 7.4%, respectively; p < 0.001) and normalized thereafter. In the contralateral hand, no significant signal changes were seen. No relationship was found between wound distance and the severity of wound edema. This study shows that wound edema influences muscle signal intensity comparisons in patients with forearm trauma. When comparing denervated muscle with nondenervated muscle, an additional scan of the contralateral side is indicated during the first 6 months after trauma to assess the extent of wound edema. After 6 months, the ipsilateral side can be used for muscle signal intensity comparisons.

Median, ulnar, and combined median-ulnar nerve injuries: functional outcome and return to productivity.

BACKGROUND: Forearm and wrist injuries are a common cause of morbidity and are often associated with suboptimal recovery of hand function. This study describes and compares outcome after median, ulnar, or combined median-ulnar nerve injuries. METHODS: Three hundred thirteen wrist and forearm nerve injuries operated on between 1980 and 1997 in a large university hospital were reviewed in relation to complications, return to work, and sensor and motor recovery. Of these 313 patients, 220 (age range, 5-73 years) met the inclusion criteria. RESULTS: Motor recovery, progress of sensory reinnervation, and number of severed structures were related to the type of injury (p < 0.05). Multiple linear regression analysis revealed a relation between the appearance of sensory reinnervation and motor recovery (beta = 0.02; 95% confidence interval, 0.01-0.04; p = 0.01). A probability of 24% of work loss, after a mean follow-up of 17.7 months, was found. Poor sensory and motor recovery were associated with work disability (odds ratio [OR], 2.9; p = 0.002; and OR, 2.9; p = 0.007, respectively). No relationship was found between type of injury and return to work (p = 0.47). Level of injury (OR, 2.6; p = 0.01), type of work (OR, 3.1; p = 0.002), number of complications (p < 0.001), and hand-therapy (OR, 0.24; p = 0.001) were found to influence return to work. CONCLUSION: It may be concluded that peripheral nerve injuries at the forearm level can result in substantial functional loss and have major social consequences. This study identified factors influencing return to work that can be used to optimize postoperative treatment strategy.

Changes in the compound action current amplitudes in relation to the conduction velocity and functional recovery in the reconstructed peripheral nerve.

The average axon diameter in the proximal segment of a transected and reconstructed peripheral nerve will decrease shortly after the transection and increase again when the regenerating axons make contact with their targets. The magnetically recorded nerve compound action current (NCAC) amplitude and the conduction velocity (CV) are directly related to the axon diameters. In this experiment, the peroneal nerve was unilaterally transected and reconstructed in 42 rabbits. After 3, 4.5, 6, 8, 12, 20, and 36 weeks of regeneration time, hind leg motor function recovery, NCAC amplitude, and CV(1st peak) were studied. Our results demonstrate a significant decrease in signal amplitude and CV in the first 8 weeks after reconstruction. These decreases are related (P < 0.05). After 8 weeks of regeneration time, motor function and the CV of the recorded signals start to recover, but the signal amplitudes do not. Based on the correlation of the CV and signal amplitude with axon diameter, they would both be expected to increase with recovering function. As an explanation for this lack of increase of signal amplitude, we suggest that, at the same time as some axons reach their target organs and start to mature, a number of the axons which have not reached a proper target organ will lose their signal-conducting capability. This will cause a decrease in compound signal amplitude, which cancels out the expected increase in NCAC amplitude, due to axonal maturation.

A magnetic evaluation of peripheral nerve regeneration: I. The discrepancy between magnetic and histologic data from the proximal segment.

Histologic techniques can quantify the number of axons in a nerve, but give no information about electrical conductibility. The number of functional myelinated neuronal units in a nerve can be quantified based on a magnetic recording technique. When studying reconstructed peripheral nerves a significant difference between the results found with these two techniques can be observed. A comparison was made between the long-term changes in the number of histologically and magnetoneurophysiologically measured neuronal units proximal to a nerve reconstruction. This study was performed on 6 New Zealand White rabbits, 20 weeks after the peroneal nerve had been reconstructed. The contralateral nerves were used as a control. Histologic examination demonstrates a statistically significant decrease of approximately 5% in the number of myelinated fibers. The magnetoneurophysiological results demonstrate a decrease which is estimated to be caused by the loss of approximately 50% of the functional myelinated neuronal units in the nerve. Therefore we conclude that of the initially available myelinated neuronal units, 5% degenerate completely, 45% are vital but lose their signal conducting capability, and the remaining 50% are vital and continue to conduct signals. Apparently, only this latter group of 50% of the initially available functional neuronal units appears to remain available for functional recovery.

A magnetic evaluation of peripheral nerve regeneration: II. The signal amplitude in the distal segment in relation to functional recovery.

Motor and sensory function in a healthy nerve is strongly related to the number of neuronal units connecting to the distal target organs. In the regenerating nerve the amplitudes of magnetically recorded nerve compound action currents (NCACs) seem to relate to the number of functional neuronal units with larger diameters regenerating across the lesion. The goal of this experiment was to compare the signal amplitudes recorded from the distal segment of a reconstructed nerve to functional recovery. To this end, the peroneal nerves of 30 rabbits were unilaterally transected and reconstructed. After 6, 8, 12, 20, and 36 weeks of regeneration time the functional recovery was studied based on the toe-spread test, and the nerve regeneration based on the magnetically recorded NCACs. The results demonstrate that the signal amplitudes recorded magnetically from the reconstructed nerves increase in the first 12 weeks from 0% to 21% of the amplitudes recorded from the control nerves and from 21% to 25% in the following 23 weeks. The functional recovery increases from absent to good between the 8th and the 20th week after the reconstruction. A statistically significant relation was demonstrated between the signal amplitude and the functional recovery (P < 0.001). It is concluded that the magnetic recording technique can be used to evaluate the quality of a peripheral nerve reconstruction and seems to be able to predict, shortly after the reconstruction, the eventual functional recovery.

Loss of viable neuronal units in the proximal stump as possible cause for poor function recovery following nerve reconstructions.

Function recovery after nerve reconstructions is often poor. Could this be caused by a loss of viable neuronal units proximal to the nerve reconstruction? The number of neuronal units (i.e., a motor or sensory neuron, including its axon and axonal branches) in the proximal segments of reconstructed peripheral nerves were studied using a novel magnetic recording technique. In five rabbits a common personal nerve was transected and microsurgically reconstructed. After 8 weeks regeneration time the nerve compound action signals were recorded magnetically from the reconstructed as well as from the healthy contralateral peroneal nerve and from peroneal nerves of five unoperated control animals. The amplitudes of the recorded signals were compared and the diameter distribution histograms were calculated. These calculations were based on the conduction distance between the stimulator and the sensor and the conduction velocities of 30 different axon diameter classes ranging from 3 to 18 microns. Our results indicate that there is a reduction of approximately 50% in the number of viable neuronal units at 10 mm proximal to a simple nerve reconstruction after 8 weeks regeneration time. The number of neuronal units innervating a hand is strongly correlated with clinical function in a healthy hand. The reduction in viable neuronal units after a reconstruction, demonstrated in our experiments, corresponds with a frequently clinically observed decrease in function after nerve reconstructions. Therefore, we suggest that the number of viable neuronal units may be a good indicator of final functional recovery.

A comparison of electric and magnetic compound action signals as quantitative assays of peripheral nerve regeneration.

The evaluation of peripheral nerve regeneration is of great interest in clinical as well as in experimental situations. However, there are few techniques that give early and quantitative information on the status of the regeneration process. If quantitative assays would be available, different surgical techniques and medications could be evaluated more accurately in relation to axonal ingrowth and functional recovery. The purpose of this study was to investigate the merits of nerve compound action signals (NCASs) recorded electrically and signals recorded with a novel magnetic recording technique. We compared the two techniques in the rabbit peroneal nerve, 2, 4, 6, and 8 weeks after a nerve reconstruction. Our conclusions are that the signals recorded with the magnetic sensor are far more reproducible and less prone to stimulus artifact than the electrically recorded signals. Furthermore, the magnetic recording shows that the number of axons that have regenerated increases with time. Previously, this could only be determined with histological studies. Other ingrowth parameters that can be quantified are the average ingrowth distance, and the variation between axons in ingrowth velocity.

Paradox of enhanced contractility in postischemic rat hearts with depressed function.

Depressed function of postischemic hearts may be related to incomplete recovery of coronary perfusion. To circumvent this factor we studied the properties of papillary muscles under controlled extracellular conditions. First, recovery of function was measured in postischemic rat hearts. Next, a muscle was dissected and superfused in a bath. After 40 min of ischemia, recovery of cardiac output was generally zero. Muscles from this group were relaxed or showed small contractures. After 20-30 min of ischemia recovery of coronary flow and cardiac output was 50-100%, and the isolated muscles showed the following properties (compared with Langendorff-perfused controls): 1) increased force at normal or low [Ca2+]; 2) action potential and postextrasystolic potentiation were unchanged, which indicates that Ca2+ influx per beat was unchanged; 3) the decay of potentiation was slowed, indicating a reduced rate of Ca2+ extrusion via Na(+)-Ca2+ exchange. This implies intracellular Ca2+ accumulation and explains the increased force. Postischemic enhancement of contractility (isovolumic pressure) was demonstrated also in whole heart preparations. We conclude that mild injury by preceding ischemia leads to enhanced contractility (Ca2+ accumulation), advanced injury to local contractures, and finally to a general contracture (Ca2+ overload). Recovery of heart function and coronary flow probably depends on the number and size of local contractures.