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This article discusses the neurophysiology of myofascial pain syndrome. The local twitch response is a characteristic finding of this condition; it is activated by snapping palpation, pressure, or needle insertion at the trigger point. It is manifested by a burst of activity in the muscle band that contains the activated trigger point. No activity is seen at other muscles bands. Data from experiments with the rabbit indicate that this is a spinal reflex, as it is abolished by transection of the motor nerve innervating the trigger point and infusion of lidocaine. Transection of the spinal cord above the level of the trigger point fails to permanently alter the trigger point response. Needle examination recordings from trigger points show low-voltage spontaneous activity and activity resembling end-plate spikes. This activity is reduced with infusion of phentolamine and local intramuscular infusions of phenoxybenzamine. There are four hypotheses to explain the findings seen at the trigger point. The first is that trigger points are found at the muscle spindle. While this theory may explain the effects of alpha-adrenergic antagonists at the trigger point, it does not fully explain the electromyographic (EMG) findings recorded at the trigger point. The second theory is that trigger points represent hyperactive end-plate regions, as the EMG activity recorded at trigger points resembles that described at the end-plate region. Other theories that either deny the existence of myofascial pain syndrome or believe it represents a focal dystonia are also discussed. [ABSTRACT FROM AUTHOR]

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Failure to demonstrate abnormalities on diagnostic tests in patients felt certain to have a disease is all too common, especially when symptoms are mild to moderate. One strategy used in such cases is to perform multiple tests hoping that one will confirm the clinical suspicion. An example of this strategy is found in carpal tunnel syndrome where multiple tests are often used to confirm the diagnosis. Unfortunately, this approach is often erroneous. Since no diagnostic test can perfectly discriminate between normal and abnormal, critical values are set at levels where most subjects are correctly classified. Using this methodology, approximately 2.5% of patients who are normal will be mistakenly called abnormal. This type I error, is additive when additional independent tests are performed. Since no two tests for a single condition are completely independent, the total error is less than the sum of the individual errors for each test. Even after accounting for interdependency, the total error of combined tests may be unacceptably high. If a single, highly discriminating, test is not available and multiple tests are used, abnormalities in more than a single test are needed to distinguish between normals and abnormals.

One hundred four normal subjects ranging in age from 17 to 77 years and in height from 115 to 203 cm underwent nerve conduction studies of sural, peroneal, tibial, and median nerves. Foot temperature was measured in each patient. A strong inverse correlation was found between height and sural (r = -0.7104), peroneal (r = -0.6842), and tibial (r = -0.5044) conduction velocities. These correlations were significant at the P less than 0.001 level. Median conduction velocity was not correlated with height. Height was correlated with the distal latencies of all nerves studied (sural r = 0.6518, peroneal r = 0.4583, tibial r = 0.7217, median r = 0.5440). These correlations were significant at the P less than 0.001 level. Age was inversely correlated with both tibial (r = -0.4071) and median (r = -0.3464) nerve conduction velocities but not with sural and peroneal conductions. There were no correlations between distal latencies and age. If the variation in conduction velocity accounted for by the linear relationship with height was removed, then age would be inversely correlated to all conduction velocity measurements with the exception of the sural. Temperature is inversely correlated with the sural (r = -0.2233), peroneal (r = -0.2102), and tibial (r = -0.2710) distal latencies. In all instances, the effects of age and temperature were minor determinants when compared with the effects of height. Diagnostic conclusions made from nerve conduction data without correcting for height may be invalid in patients taller and shorter than normal.(ABSTRACT TRUNCATED AT 250 WORDS)

We studied the fate of skeletal muscle obtained from patients with amyotrophic lateral sclerosis (ALS) after transplantation into immunodeficient nude mice. The transplanted muscle consistently survived in the nude mice without immunological rejection. The myofibers in these muscles underwent degeneration, followed by regeneration, maturation, and eventual functional innervation by the mouse motor neurons. The ability to grow diseased human muscle successfully over a prolonged period in nude mice offers an in vivo model to study the etiology of ALS and possibly of other neuromuscular disorders.

Of 50 normal subjects, 23 (46%) had at least one false positive electrodiagnostic test for carpal tunnel syndrome (CTS). There were 30% of the subjects who exhibited an abnormal median to ulnar sensory amplitude ratio of less than 1.1. In 7 subjects 8 extremities (14%) revealed prolonged residual latencies, and 4 extremities in 4 subjects (8%) had a difference of 0.4 msec between the median and ulnar palmar sensory latencies. The results of this study indicate that certain reported criteria for CTS are abnormal in a high percentage of normal subjects, thereby making them of limited value in the diagnosis of CTS. Of all the criteria studied, it appears that the comparison of the median to ulnar sensory latency across the carpal tunnel is of greatest potential value. However, even here a more conservative difference of 0.5 msec between median and ulnar nerves must be used to avoid false positive tests for CTS.