Motor Nerve Conduction Velocity in Diabetes Mellitus

Skillman, Thomas G.; Johnson, Ernest W.; Hamwi, George J.; Driskill, Helen J

doi:10.2337/diab.10.1.46

Cited by 86 publications

(29 citation statements)

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“…In our patients distal slowing was as pronounced in the upper as in the lower extremities, but in the more proximal segments of the nerves slowing was two to three times greater in the lateral popliteal than in the median nerve. This is consistent with the findings of Skillman et al (1961) and of Johnson (1962) and with the more pronounced clinical involvement of the legs than of the arms. That slowing in motor conduction in our patients scattered less than in other series of patients (Mayer, 1963;Eeg-Olofsson and Petersen, 1966) (Calverley and Mulder, 1960).…”

Section: Motor Conduction and Evoked Muscle Actionsupporting

confidence: 92%

Electrophysiological studies in diabetic neuropathy

Lamontagne

Buchthal

1970

Journal of Neurology, Neurosurgery & Psychiatry

175

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SUMMARY In 30 patients with diabetic neuropathy sensory potentials in the median nerve, motor conduction in the lateral popliteal and median nerves, and electromyographic findings in distal and proximal muscles were compared with the severity of symptoms and signs. All patients had abnormalities in at least one of the electrophysiological parameters. The sensory potentials were the most sensitive indicator of subclinical involvement; abnormalities were found in 24 patients, 12 of whom had no sensory symptoms or signs and five of whom had no other clinical or electrophysiological evidence of neuropathy in the upper extremities. This indicates that sensory nerve fibres may be affected before motor. The next most sensitive parameter was the presence offibrillation potentials, found in more than half the distal muscles examined. Slowing in motor conduction in the lateral popliteal nerve was the only electrophysiological change correlated to the severity of the neuropathy, and no other electrophysiological parameter was correlated to the duration or the severity of the neuropathy or the diabetes. An onset of neuropathy before or simultaneously with the manifestations of the diabetes, as well as the frequent occurrence of asymptomatic changes in sensory conduction, support the evidence at hand that the neuropathy develops concomitantly with and as an integral part of the metabolic disturbance rather than as a consequence of the vascular complications of diabetes. Of three patients with clinical signs or symptoms of a diabetic amyotrophy, two had asymptomatic electrophysiological abnormalities in distal nerves and muscles, consistent with widespread involvement of the peripheral nerves. The third patient had electromyographic changes in the medial vastus muscles suggestive of a myopathy. Motor and sensory conduction in distal and proximal nerves were normal.Previous studies of electrophysiological changes in diabetic neuropathy have dealt with fibrillation potentials, polyphasic potentials, or conduction velocity in motor and, in a few instances, mixed and distal sensory nerves

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Section: Motor Conduction and Evoked Muscle Actionsupporting

confidence: 92%

Electrophysiological studies in diabetic neuropathy

Lamontagne

Buchthal

1970

Journal of Neurology, Neurosurgery & Psychiatry

175

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“…Without wishing to imply that the neural lesion of human diabetics is the same as that observed in these studies, we point out that slowing of motor fiber conduction was noted in almost all of the 103 unselected diabetic patients by Mulder, Lambert, Bastron, and Sprague (16) and in sensory nerve fibers in diabetics by Liberson (17). A considerable number of similar observations in man are now available (18)(19)(20)(21)(22). The nature of the factors involved in addition to carbohydrate metabolism could not be ascertained.…”

Section: Resultsmentioning

confidence: 92%

Nerve Conduction Changes in Experimental Diabetes*

Eliasson¹

1964

J. Clin. Invest.

184

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The problem of diabetic neuropathy has not been studied experimentally to the same extent as have other manifestations of diabetes mellitus. One reason may be that neurological symptoms have not been apparent in animals that have been made diabetic. Lukens (2) stated in his review of alloxan diabetes that nervous system lesions had not been observed. Pancreatectomized animals have been prepared in large numbers, but no mention has been made of neurological complications. Minor neurological deficit, particularly of the sensory functions, could easily have been overlooked (3).The data presented below demonstrate a decrease in conduction velocity under in vitro conditions in the peripheral nerves from alloxanized rats but only if these rats also become diabetic. Because of the toxic effects of alloxan, a group of pancreatectomized rats was also prepared and showed essentially the same slowing of conduction. Treatment with insulin of the animals before the experiment or addition of insulin in vitro did not restore conduction velocity to normal values. MethodsSprague-Dawley rats 1 were used. The rats weighed between 300 and 450 g and were over 5 months old. The animals were injected with alloxan monohydrate in citrate buffer in amounts of 40 to 50 mg per kg (4). Litter mates were used as controls. Intravenous injection method was used, and injections were given after 18 hours of starvation. Some of the injected animals did not become diabetic. These animals were used as * Submitted for publication July 22, 1963; accepted August 14, 1964. Presented in part at the meeting of the American Physiological Society in September 1959 and published in abstract form (1). The investigation was supported in part by U. S. Public Health Service research grant no. NB-02141 from the National Institute of Neurological Diseases and Blindness and in part by grant no. 200 from the National Multiple Sclerosis Society. controls of the effect of nondiabetogenic doses of alloxan on nerve conduction. Blood sugar levels were measured at weekly intervals and on the day of the experiment with the glucose oxidase method. The rats were considered to be diabetic when the fasting blood sugar exceeded 200 mg per 100 ml and glucosuria was present. In the experiments with insulin treatment 24-hour urine volumes were collected daily under toluene for 1 week (up to the day preceding the experiment) from both treatment and control groups. Glucosuria is recorded for each group of rats in grams glucose per 24 hours ± SD. The weights of the rats were checked before injection of alloxan and at the time of the experiment. To provide control for loss of body weight, a number of animals were starved on water only, and the conduction velocity of nerves from these animals was tested.Insulin treatment was given according to two different schedules. In one group the insulin treatment was started 3 weeks after the injection of alloxan at a time when the initial hepatic and kidney damage should have disappeared. A dose of 4 U protamine zinc insulin 2 was selected o...

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“…8 Hypoesthesia and hyperalgesia in diabetic polyneuropathy p e rcentile category. Early investigators did not categorize NC as a percentile abnorm a l i t y, but they did demonstrate that the conduction velocities of diabetic patients without findings of DPN were significantly lower than those of control subjects (22). Both their demonstration and our demonstration of subtle QST, NC dysfunction, and autonomic dysfunction, before the development of overt DPN, undoubtedly have biological, disease, and tre a t m e n t implications.…”

Section: O N C L U S I O N S -mentioning

confidence: 98%

Patterns of quantitative sensation testing of hypoesthesia and hyperalgesia are predictive of diabetic polyneuropathy: a study of three cohorts. Nerve growth factor study group.

et al. 2000

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OBJECTIVE: To test quantitative sensation testing (QST) patterns of hypoesthesia and hyperalgesia as indicators of diabetic polyneuropathy (DPN) and its severity RESEARCH DESIGN AND METHODS: We used Computer-Assisted Sensory Examination IV; characterized the QST results of the foot of each patient in three diabetic cohorts (approximately 1,500 patients) as hyperesthetic (< or = 2.5th percentile), low-normal (2.5th-50th percentiles), high-normal (50th-97.5th percentiles), or hypoesthetic (> or = 97.5th percentile); and tested associations with symptoms, impairments, and test abnormalities. RESULTS: Overall neuropathic impairment was most severe in the pancreas-renal transplant and nerve growth factor cohorts, but it was much less severe in the population-based Rochester Diabetic Neuropathy Study (RDNS) cohort. The frequency distribution of sensory abnormalities mirrored this difference. When the QST spectra of diabetic cohorts were compared with those of the control subject cohort for vibration and cooling sensations, the only abnormality observed was hypoesthesia, which was expressed as an increased number of subjects with values at or above the 97.5th percentile or by an increased percentage of cases with high-normal values. Symptoms and impairments of DPN were significantly more frequent in the subjects with values at or above the 97.5th percentile than in the subjects whose values were between the 50th and 97.5th percentiles. For heat pain (HP) sensation thresholds (intermediate pain severity [HP:5], pain threshold [HP:0.5], and pain-stimulus response slope [HP:5-0.5]), an increased frequency of both hypoalgesia and hyperalgesia was observed (especially in the RDNS cohort). Steeper pain-stimulus response slopes were significantly associated with sensory symptoms, including severity of pain. CONCLUSIONS: 1) Decreased vibratory sensation (hypoesthesia) appears to be characteristic of mild DPN, whereas panmodality hypoesthesia is characteristic of severe DPN. 2) A shift of vibratory and cold detection thresholds (and also of attributes of nerve conduction and a measure of autonomic dysfunction) from low-normal (2.5th-50th percentiles) to high-normal (50th-97.5th percentiles) appears to precede overt expression of DPN and to thereby provide evidence of subclinical abnormality 3) Heat stimulus-induced hyperesthesia (low thresholds) occurs especially in mild DPN, and, because it correlates with DPN symptoms and impairments, it must be attributed to hyperalgesia rather than to supersensitivity Therefore, hypoalgesia or hyperalgesia may be an indicator of early DPN.

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Motor Nerve Conduction Velocity in Diabetes Mellitus

Cited by 86 publications

References 0 publications

Electrophysiological studies in diabetic neuropathy

Electrophysiological studies in diabetic neuropathy

Nerve Conduction Changes in Experimental Diabetes*

Patterns of quantitative sensation testing of hypoesthesia and hyperalgesia are predictive of diabetic polyneuropathy: a study of three cohorts. Nerve growth factor study group.

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