Intraoperative changes in motor nerve conduction latency in carpal tunnel syndrome A prospective study of47 patients with 51 hands treatedfor carpal tunnel syndrome by surgical release of the deep transverse carpal ligament was performed using intraoperative motor nerve conduction latency measured over a standard distance across the carpal tunnel both before and after release of the ligament. The results of intraoperative conduction latencies indicated a dramatic and immediate reduction in the conduction latency across the carpal canal in all but seven patients, two of whom had diabetes . When the results were subjected to statistical analysis , they were significant (P = 0 .00001) . Althoughfurther studies are indicated, these data suggest that a rapidly reversible mechanical or metabolic block, such as ischemia in the segment of the median nerve, may be responsible for the symptoms of carpal tunnel syndrome.
William W. Eversmann, Jr., M.D., Lieutenant Colonel, MC, USA, and Joseph A. Ritsick, M.D., Major, MC, USA, Denver, Colo.
Carpal tunnel syndrome results from a lesion of the median nerve as it lies beneath the flexor retinaculum at the wrist. Release of the deep transverse carpal ligament not only relieves a majority of patients of the symptoms of carpal tunnel syndrome but also may expose an indentation of the median nerve . Discussion of the pathophysiology of carpal tunnel syndrome usually considers two primary causes of the syndrome: one contributing to the pain and paresthesias associated with the condition, and one leading to the pathological changes described by Marie and Foix and more recently Thomas and Fullerton . 1.4 Consequently ischemia has been implicated in the production of many of the symptoms of carpal tunnel syndrome, while direct pressure indicted in the destructive changes observed in both experimental models and post mortem studies . Since the onset of this syndrome often is insidious and ill~defined and therefore detailed study is difficult , an approach to the study of physiologic recovery of the nerve after release of the deep transverse carpal ligament was begun to elucidate the cause of the carpal tunnel syndrome. The purpose of this paper is to describe the intraoperative changes in the motor nerve conducFrom the Hand Surgery, Orthopedic , and Physical Medicine Ser· vices, Fitzsimons Army Medical Center, Denver, Colo. Received for publication Feb . 7, 1977. Revised for publication March 28 . 1977. Reprint requests: William W. Eversmann . Jr., M.D., LTC, MC , USA, Orthopedic Service, Fitzsimons Army Medical Center, Denver, CO 80240.
Vol. 3, No. I, pp. 77-81
tion latency which the authors think are indicative of early recovery of function of the median nerve and may reflect the pathophysiology of the carpal tunnel syndrome.
Materials and methods Forty-seven consecutive patients with 51 hands treated for carpal tunnel syndrome by division of the deep transverse carpal ligament were studied at time of operation by determining the motor nerve conduction velocity before and after release of the ligament. All patients were evaluated before operation, and the operation was supervised by the same surgeon (W. E.) and all intraoperative conduction velocities were performed by the same physician (J . R.) using the same equipment. After the upper extremity had been prepared , two points 4 cm apart were marked on the palmar surface of the thenar eminence. These points were markers for insertion of the recording electrodes . From the mid-point between the two points of the recording electrodes, a point 8 cm proximal on the volar distal forearm was made and another point 2.5 cm more proximal was made for the stimulating electrodes. A neutral ground electrode was placed in the hypothenar muscle and marked for reference . Needle electrodes were used at all sites and all sites were marked so that they could be duplicated after surgical release of the ligament . Having placed the sterile electrodes, a motor conduction latency across the carpal tunnel was recorded. Following January, 1978
THE JOURNAL OF HAND SURGERY
77
78
The Journal of HAND SURGERY
Eversrrumn and Ritsick
Table I Associated disease
No. of patients
Diabetes Hypothyroidism Rheumatoid arthritis Gout Amyotrophic lateral sclerosis Carcinoma prostate , orchiectomy, estrogen treatment
7 2
surgical release of the transverse carpal ligament, the tourniquet was released, hemostasis was secured, and the operative wound was closed. This time interval, usually about JO minutes, allowed the extremity to recover from the effect of the tourniquet ischemia and the nerve to adjust to the normal body temperature from the cooler ambient temperature to which it had been exposed . This delay was necessary to control two variables, namely , tourniquet ischemia and temperature known to affect the conduction time. 5 - 7 Having completed the closure, a second motor conduction latency was performed, placing the electrodes at the previously marked locations. Seven patients underwent internal neurolysis of the median nerve according to the criteria and method of Curtis and Eversmann. 8 These patients had internal neurolysis because prior to operation they had either atrophy of the abductor polJicis brevis muscle, loss of the ability to discriminate two points on sensory examination, loss of light touch sensibility, or constant loss of sensibility in the area of the hand supplied by the median nerve. Most patients had more than a single indication for internal neurolysis, three had muscular atrophy, four had loss of the ability to discriminate two points, one had loss of light touch, and four had constant loss of sensibility in the median sensory area. The technique of internal neurolysis begins with longitUdinal opening of the epineurium and, using two- to six-power loupe magnification , careful teasing apart of the fascicles in those areas where interfascicular scarring is present. Throughout the procedure the deep or dorsal aspect of the median nerve is left undisturbed to preserve whatever microcirculation may be present on the posterior surface of the nerve. The entire dissection of the median nerve is done with magnification to preserve the fascicules and interfascicular plexus of the median nerve. The patients who had internal neurolysis underwent three motor latency determinations---one before the release of the ligament, one after the release of the ligament, and a third after the internal neurolysis.
In addition to the intraoperati ve motor conduction latencies done on all patients, most patients were examined by detailed sensory examination, motor and sensory conduction latencies, and, if necessary, electromyogram before as well as after operation, as indicated by the severity of the carpal tunnel syndrome.
Results Thirty-five women and 12 men comprised the consecuti ve series of patients. Of the 51 hands, 44 underwent simple release of the deep transverse carpal ligament while the remaining seven also had internal neurolysis of the median nerve . Table I indicates the associated medical conditions which may be associated with their carpal tunnel syndrome. The higher-thanusual incidence of diabetes mellitus (I 4%) in this series apparently was due to chance . The preoperative symptoms, including pain, paresthesia, numbness in the median nerve distribution , night symptoms awakening the patient but often relieved by splinting, positive wrist flexion test (Phalen) , and often positive percussion test over the carpal tunnel, were typical for carpal tunnel syndrome. Thenar wasting was not usual but did occur in this series, as did loss of the ability to accurately discriminate two points on sensory testing. The duration of symptoms varied from a few months to as long as 27 years. The preoperative motor and/or sensory conduction latencies of the median nerve across the wrist were usually above the established normal values. These studies were performed using cutaneous electrodes and were not the basis for either diagnosis or selection for operation. The postoperative conduction latencies, which also were performed using cutaneous electrodes, often revealed a transient rise in conduction latency before returning to a normal or near-normal value. Diabetic patients particularly seemed to take longer to return to a normal or near-normal value and most often had a persistently elevated latency-in one patient as high as a 5.6 msec motor latency. The intraoperative conduction latencies all were performed with needle electrodes, all were performed by the same physician using the same equipment, and all were motor conduction latencies, since a satisfactory contact could not be reliably maintained for sensory conduction studies. The results of the intraoperative motor conduction latencies are listed in Table II. Although some of the prerelease conduction latencies were within the normal range (less than 4.5 msec) , four patients showed an even lower conduction latency after release of the deep transverse carpal ligament. Three patients whose initial conduction latencies were in the normal range had an
Vol. 3 No.1
January, 1978
increase in the latency after release of the ligament. When the prerelease and postrelease values were subjected to student's t test, a P value of 0.00001 was determined-a significant result. Discussion
The ability of a nerve to function is dependent on several physiologic mechanisms, of which the sodium pump, axoplasmic transport, and integrity of the cell membrane are representative. 9 To support these mechanisms, the mitochondria along the entire axon generate adenosine triphosphate through oxidative phosphorylation. 1O- 12 The level of high-energy phosphate is critical, since if it should fall below 50% of normal, the fast axoplasmic transport system will fail. 13 The fast axoplasmic transport system is responsible for transport of the proteins, polypeptides, glycoproteins, glycoJipids, and other specific substances, such as catecholamines and acetylcholinesterase, from the endoplasmic reticulum (Nissl bodies) to the membrane along the axon or even the end organ of the axon. 9 According to the concept of Singer, 14 the axon membrane is a lipid bilayer with globular protein within, and, if so, the proteins would confer ion selectivity to the axon membrane.lO Therefore, the protein selectivity and integrity of the membrane as well as the function of the sodium pump and axoplasmic transport systems all are dependent upon a pool of adenosine triphosphate generated by oxidative phosphorylation along the entire axon. Anoxia of a segment of the axon will cause the fast axoplasmic transport system to fail by damming of the labeled transport components just above the anoxic region. l l Furthermore, these anoxic episodes are reversible so long as the duration of the anoxia is limited. 15 In experimental studies, anoxia of 1 hour allowed complete and rapid recovery, while a duration of 1% hours produced a more complete block which recovered more slowly and over a longer period of time. In these as in earlier studies, electrical responses and fast axoplasmic transport both were found to fail within approximately 15 minutes (10 to 30 minutes) of the onset of anoxia .10 This close correlation lends further support to the concept of a common high-energy phosphate pool supplying energy not only to the sodium pump controlling ionic asymmetry across the cell membrane and therefore excitability, but also to fast axoplasmic transport. 9 The improvement in the motor conduction latency observed in this study seems to agree with the experimental as well as the clinical data. In this study a statistically significant (P = 0.00001) reduction in the motor conduction latency occurred in 51 hands of patients
Motor nerve conduction latency in carpal tunnel syndrome
79
Table II. Intraoperative motor conduction latencies After internal neurolysis
Patient initials Before release J. A. M.H. R. A. L. E. L. E. B. E. T. A. M. B. M. B. V. B. V. B. D. C. D. C. H. E. D. E. T. G. H. G. R. H. M.H. J. H. H. J. R. J. A. J. J. K. L. K. K. K. K. K. B. L. B. L. M.L. L.L. O.M. E. M. L. M. Y. M. M.M. l. M. A. N. G. O. M.R. S. R. A. S. G. S. L. S. N. S. D. S. M. S. D. S. W. K. I.R. W. L. W.
8.0 5.5 6.9 3.7 8.4 5.0 8.2 5.4 6.4 5.0 4.3 9.7 8.6 6.2 3. I 5.2 10.3 8.2 7.8 4.5 5.0 7.1 5.8 8.0 4.7 6.3 5.8 10.1 8.1 4.4 5.2 7.4 5.8 4.0 4.0 7.6 10.8 6.0 7.2 8.3 5.7 4.7 7.1 6.1 3.5 8.3 8.7 10.2 6.4 5.6 8.3
5.2 5.0 5.6 4.2 4.8 4.7 6.6 3.6 5.7 5. I 3.7 7.9 7.1 5.1 3.1 3.4 6.9 5.8 6.0 6.2 5.0 6.7 3.0 5.4 3.3 5.4 3.6 8.3 6.0 3.8 3.3 6.6 4.4 3.2 5.1 5.9 5.8 4.1 5.2 8.6 4.1 4.1 4.6 4.6 3.4 6.5 8.7 8.6 4.7 5.5 4.9
6.7 4.5
5.1
5.9
5.3
4.6 5.4
who underwent release of the carpal tunnel. This improvement occurred within 15 minutes of release of the deep transverse carpal ligament and, when indicated, an internal neurolysis of the median nerve. Such an im-
80
The Journal of HAND SURGERY
Eversmann and Ritsick
mediate reduction in the motor conduction latency indicates that the neurophysiologic conduction defect in these cases of carpal tunnel syndrome was due to an immediately reversible mechanical or metabolic block. Ischemia has been shown experimentally to create such a block,l1 and restoration of function has been rapid following removal of the anoxic block,15 due presumably to restoration of oxidative phosphorylation, replenishment of the high-energy phosphate pool, and reestablishment of the function of the sodium pump and axoplasmic transport systems. Clinically, we usually also see rapid and complete recovery in these patients. During this study most of the patients noted relief of painful symptoms of carpal tunnel syndrome by at least the day after operation and, although a few patients noted slower relief, most of these symptoms had disappeared within 3 to 4 days following operation. The few patients in whom the symptoms of numbness and occasionally abductor pollicis brevis atrophy were relieved over several weeks could be theorized to be those patients with structural changes within the median nerve, such as described by Marie and Foix4 or Thomas and Fullerton. 3 Even these more severely affected patients continued to improve over several months and did achieve at least a near-normal result. The response of the seven hands that underwent internal neurolysis as well as ligament division indicated that in five of the seven hands a continuing reduction of latency occurred between release of the ligament alone and internal neurolysis. Considering all seven hands in this group, more than 50% of the reduction in conduction latency occurred after internal neurolysis. Even though this series is small (only seven hands), the result was statistically significant when subjected to Student's t test analysis (P = 0.0123). Although a total of seven patients is too small a series on which to base a firm statement, it appears that five of the seven patients might well have been predicted to improve significantly with internal neurolysis because there was only a limited improvement after release of the deep transverse carpal ligament. Further clinical correlation is present in patients with diabetes mellitus who have small blood vessel disease associated with diabetic neuropathy of the peripheral nerves. 16.1S The patient with a relative ischemia as a result of diabetic smallvessel disease might be more susceptible to the ischemia of carpal tunnel syndrome. In this study a 14% incidence of associated diabetes mellitus seems to confirm this theory. The clinical response of diabetic patients within this series, although slower, was ultimately as complete in recovery of sensory function in
the median distribution of the hand as that of the nondiabetic patients. Apparently relief of part of the ischemic process to a segment of the median nerve was sufficient to allow clinical recovery of the nerve.
Conclusion It is ischemia to which the nerve is most sensitive, and not compression, except as compression induces a segmental ischemia that appears to be the initial defect in causing the carpal tunnel syndrome. With the onset of a segmental ischemia of the median nerve beneath the deep transverse carpal ligament, a series of neurophysiologic responses, all of which compromise the function of the median nerve, are begun. Only with prolonged, uninterrupted, or repeated episodes of ischemia to a segment of the median nerve do the structural changes which have long been associated with compression come to pass. It appears from our studies that, even at this later stage in the destruction of the median nerve, recovery can be affected both electrically and clinically by appropriate procedures that restore the physiologic processes within the axons of the median nerve. REFERENCES I. Staal A: General discussion on pressure neuropathies. In Vinken PJ, Bruyn GW, editors: Handbook of clinical neurology, vol 7, New York, 1970, Elsevier Publishing Co 2. Aguayo AJ: Neuropathy due to pressure and entrapment. In Dyck PJ, et ai, editors: Peripheral neuropathy. Philadelphia, 1975, WB Saunders , Co 3. Thomas PK, Fullerton MM: Nerve fiber size in the carpal tunnel syndrome. J Neurol Neurosurg Psychiatry 26:520, 1963 4. Marie P et Foix: Atrophie isolee de I'eminene thenar d'oringine nervitque. Rev Neurol (Paris) 26:647-649, 1913 5. Fullerton PM: The effect of ischemia on nerve conduction in the carpal tunnel syndrome . J Neurol Neurosurg Psychiatry 26:385, 1963 6 . Gilliatt RW , Wilson TG : A pneumatic-tourniquet test in the carpal tunnel syndrome . Lancet 2:595-597, 1953 7. Gilliatt RW, Wilson TG: Sensory loss in patients with peripheral nerve lesions. J Neurol Neurosurg Psychiatry 17:104-114, 1954 8. Curtis RM, Eversmann WW: Internal neurolysis as an adjunct to the treatment of the carpal-tunnel syndrome. J Bone Joint Surg 55-A:733-740, 1973 9. Dyck PJ, Thomas PK, Lambert EH: Peripheral neuropathy . Philadelphia, 1975, WB Saunders Co 10. Ochs S: Axoplasmic transport-a basis for neural pathology. In Dyck PJ, et aI, editors: Peripheral neuropathy , Philadelphia, 1975, WB Saunders Co , p 213
Vol. 3 No. I January , 1978
II. Ochs S: Local supply of energy to the fast axoplasmic transport mechanism. Proc Nat Acad Science USA 68: 1279-1282, 1971 12. Ochs S: The dependence of fast transport in mammalian nerve fibers on metapolism. Acta Neuropathol [Suppl] 5:86-96, 1971 13. Sabri MI, Ochs S: Characterization of fast and slow transported proteins in dorsal root and sciatic nerve of cat. J Neurobiol 4: 145-165, 1973 14. Singer SJ: A fluid lipid-globular protein mosiac model of membrane structure. Ann NY Acad Sci 194: 16-23, 1972
Motor nerve conduction latency in carpal tunnel syndrome
81
15 . Leone 1, Ochs S: Reversibility of fast axoplasmic transport following differing durations of anoxic block in vitro and in vivo (abstract). Soc Neurosci 3:147, 1973 16. Vinken PJ, Bruyn GW: Handbook of clinical neurology . Vol VII, Amsterdam, 1970, North-Holland, p 553 17 . Cohen MM: Differential diagnosis of toxic neuropathy . In Vinken Pl , and Bruyn GW, editors: Handbook of clinical neurology. Amsterdam, North-Holland, p 552 18. Gilliatt RW, Willison RG: Peripheral nerve conduction in diabetic neuropathy . J Neurol Neurosurg Psychiatry 25:11,1962
INFORMA TION FOR AUTHORS
Most of the provisions of the Copyright Act of 1976 became effective on January 1, 1978. Therefore, all transmittal letters must be accompanied by the following statement, signed by each author: "The undersigned author(s) transfers all copyright ownership of the manuscript entitled (title of article) to the American Society for Surgery of the Hand in the event the work is published. The author(s) warrants that the article is original, is not under consideration by another journal, and has not been previously published." Authors will be consulted, when possible, regarding republication of their material.
William W. Eversmann, Jr., M.D., Lieutenant Colonel, MC, USA, and Joseph A. Ritsick, M.D., Major, MC, USA, Denver, Colo.
Carpal tunnel syndrome results from a lesion of the median nerve as it lies beneath the flexor retinaculum at the wrist. Release of the deep transverse carpal ligament not only relieves a majority of patients of the symptoms of carpal tunnel syndrome but also may expose an indentation of the median nerve . Discussion of the pathophysiology of carpal tunnel syndrome usually considers two primary causes of the syndrome: one contributing to the pain and paresthesias associated with the condition, and one leading to the pathological changes described by Marie and Foix and more recently Thomas and Fullerton . 1.4 Consequently ischemia has been implicated in the production of many of the symptoms of carpal tunnel syndrome, while direct pressure indicted in the destructive changes observed in both experimental models and post mortem studies . Since the onset of this syndrome often is insidious and ill~defined and therefore detailed study is difficult , an approach to the study of physiologic recovery of the nerve after release of the deep transverse carpal ligament was begun to elucidate the cause of the carpal tunnel syndrome. The purpose of this paper is to describe the intraoperative changes in the motor nerve conducFrom the Hand Surgery, Orthopedic , and Physical Medicine Ser· vices, Fitzsimons Army Medical Center, Denver, Colo. Received for publication Feb . 7, 1977. Revised for publication March 28 . 1977. Reprint requests: William W. Eversmann . Jr., M.D., LTC, MC , USA, Orthopedic Service, Fitzsimons Army Medical Center, Denver, CO 80240.
Vol. 3, No. I, pp. 77-81
tion latency which the authors think are indicative of early recovery of function of the median nerve and may reflect the pathophysiology of the carpal tunnel syndrome.
Materials and methods Forty-seven consecutive patients with 51 hands treated for carpal tunnel syndrome by division of the deep transverse carpal ligament were studied at time of operation by determining the motor nerve conduction velocity before and after release of the ligament. All patients were evaluated before operation, and the operation was supervised by the same surgeon (W. E.) and all intraoperative conduction velocities were performed by the same physician (J . R.) using the same equipment. After the upper extremity had been prepared , two points 4 cm apart were marked on the palmar surface of the thenar eminence. These points were markers for insertion of the recording electrodes . From the mid-point between the two points of the recording electrodes, a point 8 cm proximal on the volar distal forearm was made and another point 2.5 cm more proximal was made for the stimulating electrodes. A neutral ground electrode was placed in the hypothenar muscle and marked for reference . Needle electrodes were used at all sites and all sites were marked so that they could be duplicated after surgical release of the ligament . Having placed the sterile electrodes, a motor conduction latency across the carpal tunnel was recorded. Following January, 1978
THE JOURNAL OF HAND SURGERY
77
78
The Journal of HAND SURGERY
Eversrrumn and Ritsick
Table I Associated disease
No. of patients
Diabetes Hypothyroidism Rheumatoid arthritis Gout Amyotrophic lateral sclerosis Carcinoma prostate , orchiectomy, estrogen treatment
7 2
surgical release of the transverse carpal ligament, the tourniquet was released, hemostasis was secured, and the operative wound was closed. This time interval, usually about JO minutes, allowed the extremity to recover from the effect of the tourniquet ischemia and the nerve to adjust to the normal body temperature from the cooler ambient temperature to which it had been exposed . This delay was necessary to control two variables, namely , tourniquet ischemia and temperature known to affect the conduction time. 5 - 7 Having completed the closure, a second motor conduction latency was performed, placing the electrodes at the previously marked locations. Seven patients underwent internal neurolysis of the median nerve according to the criteria and method of Curtis and Eversmann. 8 These patients had internal neurolysis because prior to operation they had either atrophy of the abductor polJicis brevis muscle, loss of the ability to discriminate two points on sensory examination, loss of light touch sensibility, or constant loss of sensibility in the area of the hand supplied by the median nerve. Most patients had more than a single indication for internal neurolysis, three had muscular atrophy, four had loss of the ability to discriminate two points, one had loss of light touch, and four had constant loss of sensibility in the median sensory area. The technique of internal neurolysis begins with longitUdinal opening of the epineurium and, using two- to six-power loupe magnification , careful teasing apart of the fascicles in those areas where interfascicular scarring is present. Throughout the procedure the deep or dorsal aspect of the median nerve is left undisturbed to preserve whatever microcirculation may be present on the posterior surface of the nerve. The entire dissection of the median nerve is done with magnification to preserve the fascicules and interfascicular plexus of the median nerve. The patients who had internal neurolysis underwent three motor latency determinations---one before the release of the ligament, one after the release of the ligament, and a third after the internal neurolysis.
In addition to the intraoperati ve motor conduction latencies done on all patients, most patients were examined by detailed sensory examination, motor and sensory conduction latencies, and, if necessary, electromyogram before as well as after operation, as indicated by the severity of the carpal tunnel syndrome.
Results Thirty-five women and 12 men comprised the consecuti ve series of patients. Of the 51 hands, 44 underwent simple release of the deep transverse carpal ligament while the remaining seven also had internal neurolysis of the median nerve . Table I indicates the associated medical conditions which may be associated with their carpal tunnel syndrome. The higher-thanusual incidence of diabetes mellitus (I 4%) in this series apparently was due to chance . The preoperative symptoms, including pain, paresthesia, numbness in the median nerve distribution , night symptoms awakening the patient but often relieved by splinting, positive wrist flexion test (Phalen) , and often positive percussion test over the carpal tunnel, were typical for carpal tunnel syndrome. Thenar wasting was not usual but did occur in this series, as did loss of the ability to accurately discriminate two points on sensory testing. The duration of symptoms varied from a few months to as long as 27 years. The preoperative motor and/or sensory conduction latencies of the median nerve across the wrist were usually above the established normal values. These studies were performed using cutaneous electrodes and were not the basis for either diagnosis or selection for operation. The postoperative conduction latencies, which also were performed using cutaneous electrodes, often revealed a transient rise in conduction latency before returning to a normal or near-normal value. Diabetic patients particularly seemed to take longer to return to a normal or near-normal value and most often had a persistently elevated latency-in one patient as high as a 5.6 msec motor latency. The intraoperative conduction latencies all were performed with needle electrodes, all were performed by the same physician using the same equipment, and all were motor conduction latencies, since a satisfactory contact could not be reliably maintained for sensory conduction studies. The results of the intraoperative motor conduction latencies are listed in Table II. Although some of the prerelease conduction latencies were within the normal range (less than 4.5 msec) , four patients showed an even lower conduction latency after release of the deep transverse carpal ligament. Three patients whose initial conduction latencies were in the normal range had an
Vol. 3 No.1
January, 1978
increase in the latency after release of the ligament. When the prerelease and postrelease values were subjected to student's t test, a P value of 0.00001 was determined-a significant result. Discussion
The ability of a nerve to function is dependent on several physiologic mechanisms, of which the sodium pump, axoplasmic transport, and integrity of the cell membrane are representative. 9 To support these mechanisms, the mitochondria along the entire axon generate adenosine triphosphate through oxidative phosphorylation. 1O- 12 The level of high-energy phosphate is critical, since if it should fall below 50% of normal, the fast axoplasmic transport system will fail. 13 The fast axoplasmic transport system is responsible for transport of the proteins, polypeptides, glycoproteins, glycoJipids, and other specific substances, such as catecholamines and acetylcholinesterase, from the endoplasmic reticulum (Nissl bodies) to the membrane along the axon or even the end organ of the axon. 9 According to the concept of Singer, 14 the axon membrane is a lipid bilayer with globular protein within, and, if so, the proteins would confer ion selectivity to the axon membrane.lO Therefore, the protein selectivity and integrity of the membrane as well as the function of the sodium pump and axoplasmic transport systems all are dependent upon a pool of adenosine triphosphate generated by oxidative phosphorylation along the entire axon. Anoxia of a segment of the axon will cause the fast axoplasmic transport system to fail by damming of the labeled transport components just above the anoxic region. l l Furthermore, these anoxic episodes are reversible so long as the duration of the anoxia is limited. 15 In experimental studies, anoxia of 1 hour allowed complete and rapid recovery, while a duration of 1% hours produced a more complete block which recovered more slowly and over a longer period of time. In these as in earlier studies, electrical responses and fast axoplasmic transport both were found to fail within approximately 15 minutes (10 to 30 minutes) of the onset of anoxia .10 This close correlation lends further support to the concept of a common high-energy phosphate pool supplying energy not only to the sodium pump controlling ionic asymmetry across the cell membrane and therefore excitability, but also to fast axoplasmic transport. 9 The improvement in the motor conduction latency observed in this study seems to agree with the experimental as well as the clinical data. In this study a statistically significant (P = 0.00001) reduction in the motor conduction latency occurred in 51 hands of patients
Motor nerve conduction latency in carpal tunnel syndrome
79
Table II. Intraoperative motor conduction latencies After internal neurolysis
Patient initials Before release J. A. M.H. R. A. L. E. L. E. B. E. T. A. M. B. M. B. V. B. V. B. D. C. D. C. H. E. D. E. T. G. H. G. R. H. M.H. J. H. H. J. R. J. A. J. J. K. L. K. K. K. K. K. B. L. B. L. M.L. L.L. O.M. E. M. L. M. Y. M. M.M. l. M. A. N. G. O. M.R. S. R. A. S. G. S. L. S. N. S. D. S. M. S. D. S. W. K. I.R. W. L. W.
8.0 5.5 6.9 3.7 8.4 5.0 8.2 5.4 6.4 5.0 4.3 9.7 8.6 6.2 3. I 5.2 10.3 8.2 7.8 4.5 5.0 7.1 5.8 8.0 4.7 6.3 5.8 10.1 8.1 4.4 5.2 7.4 5.8 4.0 4.0 7.6 10.8 6.0 7.2 8.3 5.7 4.7 7.1 6.1 3.5 8.3 8.7 10.2 6.4 5.6 8.3
5.2 5.0 5.6 4.2 4.8 4.7 6.6 3.6 5.7 5. I 3.7 7.9 7.1 5.1 3.1 3.4 6.9 5.8 6.0 6.2 5.0 6.7 3.0 5.4 3.3 5.4 3.6 8.3 6.0 3.8 3.3 6.6 4.4 3.2 5.1 5.9 5.8 4.1 5.2 8.6 4.1 4.1 4.6 4.6 3.4 6.5 8.7 8.6 4.7 5.5 4.9
6.7 4.5
5.1
5.9
5.3
4.6 5.4
who underwent release of the carpal tunnel. This improvement occurred within 15 minutes of release of the deep transverse carpal ligament and, when indicated, an internal neurolysis of the median nerve. Such an im-
80
The Journal of HAND SURGERY
Eversmann and Ritsick
mediate reduction in the motor conduction latency indicates that the neurophysiologic conduction defect in these cases of carpal tunnel syndrome was due to an immediately reversible mechanical or metabolic block. Ischemia has been shown experimentally to create such a block,l1 and restoration of function has been rapid following removal of the anoxic block,15 due presumably to restoration of oxidative phosphorylation, replenishment of the high-energy phosphate pool, and reestablishment of the function of the sodium pump and axoplasmic transport systems. Clinically, we usually also see rapid and complete recovery in these patients. During this study most of the patients noted relief of painful symptoms of carpal tunnel syndrome by at least the day after operation and, although a few patients noted slower relief, most of these symptoms had disappeared within 3 to 4 days following operation. The few patients in whom the symptoms of numbness and occasionally abductor pollicis brevis atrophy were relieved over several weeks could be theorized to be those patients with structural changes within the median nerve, such as described by Marie and Foix4 or Thomas and Fullerton. 3 Even these more severely affected patients continued to improve over several months and did achieve at least a near-normal result. The response of the seven hands that underwent internal neurolysis as well as ligament division indicated that in five of the seven hands a continuing reduction of latency occurred between release of the ligament alone and internal neurolysis. Considering all seven hands in this group, more than 50% of the reduction in conduction latency occurred after internal neurolysis. Even though this series is small (only seven hands), the result was statistically significant when subjected to Student's t test analysis (P = 0.0123). Although a total of seven patients is too small a series on which to base a firm statement, it appears that five of the seven patients might well have been predicted to improve significantly with internal neurolysis because there was only a limited improvement after release of the deep transverse carpal ligament. Further clinical correlation is present in patients with diabetes mellitus who have small blood vessel disease associated with diabetic neuropathy of the peripheral nerves. 16.1S The patient with a relative ischemia as a result of diabetic smallvessel disease might be more susceptible to the ischemia of carpal tunnel syndrome. In this study a 14% incidence of associated diabetes mellitus seems to confirm this theory. The clinical response of diabetic patients within this series, although slower, was ultimately as complete in recovery of sensory function in
the median distribution of the hand as that of the nondiabetic patients. Apparently relief of part of the ischemic process to a segment of the median nerve was sufficient to allow clinical recovery of the nerve.
Conclusion It is ischemia to which the nerve is most sensitive, and not compression, except as compression induces a segmental ischemia that appears to be the initial defect in causing the carpal tunnel syndrome. With the onset of a segmental ischemia of the median nerve beneath the deep transverse carpal ligament, a series of neurophysiologic responses, all of which compromise the function of the median nerve, are begun. Only with prolonged, uninterrupted, or repeated episodes of ischemia to a segment of the median nerve do the structural changes which have long been associated with compression come to pass. It appears from our studies that, even at this later stage in the destruction of the median nerve, recovery can be affected both electrically and clinically by appropriate procedures that restore the physiologic processes within the axons of the median nerve. REFERENCES I. Staal A: General discussion on pressure neuropathies. In Vinken PJ, Bruyn GW, editors: Handbook of clinical neurology, vol 7, New York, 1970, Elsevier Publishing Co 2. Aguayo AJ: Neuropathy due to pressure and entrapment. In Dyck PJ, et ai, editors: Peripheral neuropathy. Philadelphia, 1975, WB Saunders , Co 3. Thomas PK, Fullerton MM: Nerve fiber size in the carpal tunnel syndrome. J Neurol Neurosurg Psychiatry 26:520, 1963 4. Marie P et Foix: Atrophie isolee de I'eminene thenar d'oringine nervitque. Rev Neurol (Paris) 26:647-649, 1913 5. Fullerton PM: The effect of ischemia on nerve conduction in the carpal tunnel syndrome . J Neurol Neurosurg Psychiatry 26:385, 1963 6 . Gilliatt RW , Wilson TG : A pneumatic-tourniquet test in the carpal tunnel syndrome . Lancet 2:595-597, 1953 7. Gilliatt RW, Wilson TG: Sensory loss in patients with peripheral nerve lesions. J Neurol Neurosurg Psychiatry 17:104-114, 1954 8. Curtis RM, Eversmann WW: Internal neurolysis as an adjunct to the treatment of the carpal-tunnel syndrome. J Bone Joint Surg 55-A:733-740, 1973 9. Dyck PJ, Thomas PK, Lambert EH: Peripheral neuropathy . Philadelphia, 1975, WB Saunders Co 10. Ochs S: Axoplasmic transport-a basis for neural pathology. In Dyck PJ, et aI, editors: Peripheral neuropathy , Philadelphia, 1975, WB Saunders Co , p 213
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II. Ochs S: Local supply of energy to the fast axoplasmic transport mechanism. Proc Nat Acad Science USA 68: 1279-1282, 1971 12. Ochs S: The dependence of fast transport in mammalian nerve fibers on metapolism. Acta Neuropathol [Suppl] 5:86-96, 1971 13. Sabri MI, Ochs S: Characterization of fast and slow transported proteins in dorsal root and sciatic nerve of cat. J Neurobiol 4: 145-165, 1973 14. Singer SJ: A fluid lipid-globular protein mosiac model of membrane structure. Ann NY Acad Sci 194: 16-23, 1972
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15 . Leone 1, Ochs S: Reversibility of fast axoplasmic transport following differing durations of anoxic block in vitro and in vivo (abstract). Soc Neurosci 3:147, 1973 16. Vinken PJ, Bruyn GW: Handbook of clinical neurology . Vol VII, Amsterdam, 1970, North-Holland, p 553 17 . Cohen MM: Differential diagnosis of toxic neuropathy . In Vinken Pl , and Bruyn GW, editors: Handbook of clinical neurology. Amsterdam, North-Holland, p 552 18. Gilliatt RW, Willison RG: Peripheral nerve conduction in diabetic neuropathy . J Neurol Neurosurg Psychiatry 25:11,1962
INFORMA TION FOR AUTHORS
Most of the provisions of the Copyright Act of 1976 became effective on January 1, 1978. Therefore, all transmittal letters must be accompanied by the following statement, signed by each author: "The undersigned author(s) transfers all copyright ownership of the manuscript entitled (title of article) to the American Society for Surgery of the Hand in the event the work is published. The author(s) warrants that the article is original, is not under consideration by another journal, and has not been previously published." Authors will be consulted, when possible, regarding republication of their material.
