Motor Nerve Conduction Velocity in Diabetes

Lawrence, Donald G.; Locke, Simeon

doi:10.1001/archneur.1961.00450170021003

Cited by 99 publications

(38 citation statements)

References 13 publications

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“…Decreased nerve conduction velocity is characteristic of diabetic neuropathy, occurring in human diabetic patients [1] and in diabetic laboratory animals [2]. Since the earliest demonstration that aldose reductase inhibitors prevented slowing of motor nerve conduction velocity (MNCV) in rats with experimental diabetes [3], it has become a welldefined end-point for the evaluation of this class of drug.…”

Section: Introductionmentioning

confidence: 99%

Phosphorylation of c-Jun N-terminal kinase (JNK) in sensory neurones of diabetic rats, with possible effects on nerve conduction and neuropathic pain: prevention with an aldose reductase inhibitor

2006

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Aims/hypothesis: This study was designed to determine whether diabetes in rats is associated with phosphorylation of c-Jun N-terminal kinase (JNK) and one of its transcription factors, c-Jun, in sensory neurones innervating the lower limb. We also sought to determine which neuronal phenotypes are affected and to examine the effect of aldose reductase inhibition on JNK and c-Jun phosphorylation. Methods: Diabetes was induced in rats using streptozotocin. Phosphorylation of JNK and c-Jun in lumbar dorsal root ganglia was determined by binding of phospho-specific antibodies using western blots and immunocytochemistry. Neuronal phenotypes were characterised by binding of N52 (an antibody that recognises the heavy neurofilament protein; for large-diameter mechanoceptors) and of calcitonin gene-related peptide and the plant glycoprotein lectin IB4 (for nociceptors). The efficacy of the aldose reductase inhibitor fidarestat was determined by measuring polyol pathway metabolites in sciatic nerve, and functionally by measuring the conduction velocity of motor and sensory nerves. Results: In control rats, activated JNK and c-Jun were primarily associated with mechanoceptors; in diabetes this was increased, but a greater increase was seen in nociceptors. Phosphorylation was prevented in all cells by fidarestat, which normalised polyol pathway metabolites as well as motor nerve and sensory nerve conduction velocity. Conclusions/interpretation: Fidarestat-sensitive phosphorylation of JNK and c-Jun occurs in fast-conduction mechanoceptors-the same class of neurones that registers the changes in sensory nerve conduction velocity-and in nociceptors. This supports the notion that mitogen-activated protein kinase phosphorylation, via the polyol pathway, may convert the direct effects of raised glucose into impaired nerve conduction and neuropathic pain. For proof of this we await the availability of specific JNK antagonists formulated for in vivo use.

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Section: Introductionmentioning

confidence: 99%

Phosphorylation of c-Jun N-terminal kinase (JNK) in sensory neurones of diabetic rats, with possible effects on nerve conduction and neuropathic pain: prevention with an aldose reductase inhibitor

2006

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“…Data on sensory nerve CV in experimental models of diabetes include reduced sensory nerve CV in the dorsal spinal root [1], saphenous nerve [2], tibial nerve [5], sural and tibial nerves [6]. No detailed data on cutaneous nerve conduction velocity in experimental diabetes is available.It is also now generally agreed that peripheral nerve conduction abnormalities occur in diabetic peripheral neuropathy in man [7][8][9][10][11][12]. It is interesting that sensory nerves respond rather differently to treatment compared with motor nerves.…”

mentioning

confidence: 99%

“…It is also now generally agreed that peripheral nerve conduction abnormalities occur in diabetic peripheral neuropathy in man [7][8][9][10][11][12]. It is interesting that sensory nerves respond rather differently to treatment compared with motor nerves.…”

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confidence: 99%

The correlation between sensory nerve conduction velocities and three metabolic indices in rats treated with streptozotocin

Julu

1988

Diabetologia

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Summary.The fastest conduction velocities of the myelinated (A) and unmyelinated (C) sensory nerve fibres were measured in the saphenous nerves of rats made diabetic up to 5 weeks previously by injection of streptozotocin. The conduction velocity of the fastest A-alpha fibres in treated rats fell by 25% compared to control rats. The effect on the slow A-delta fibres was small but C-fibres were not affected. Levels of glycosylated haemoglobin, random plasma glucose, and the net changes in body weights were also measured. There were significant changes in these three metabolic indices among diabetic rats (t7 <0.001) and the three indices were inter-related. There was a good correlation between A-fibre conduction velocity and levels of glycosylated haemoglobin but no significant relationship between C-fibre conduction velocity and this metabolic index. A-fibre conduction velocity was statistically more correlated with levels of glycosylated haemoglobin than the other two metabolic indices (p < 0.01).Key words: Diabetes, streptozotocin, A-fibres, C-fibres, conduction velocity, glycosylated haemoglobin, random plasma glucose, body weight.It is now well established that peripheral nerve conduction velocity (CV) is slowed in experimental diabetes mellitus [1][2][3][4]. Of the various animal models used, motor nerve CV has been studied most. Data on sensory nerve CV in experimental models of diabetes include reduced sensory nerve CV in the dorsal spinal root [1], saphenous nerve [2], tibial nerve [5], sural and tibial nerves [6]. No detailed data on cutaneous nerve conduction velocity in experimental diabetes is available.It is also now generally agreed that peripheral nerve conduction abnormalities occur in diabetic peripheral neuropathy in man [7][8][9][10][11][12]. It is interesting that sensory nerves respond rather differently to treatment compared with motor nerves. For example, vibratory threshold did not improve with short-term insulin therapy and yet motor nerve CV increased [13]; sensory action potential showed no improvement with insulin treatment while motor nerve CV increased [14]; sensory nerve CV did not improve with diet treatment in Type 2 (non-insulin-dependent) diabetic patients but motor nerve CV improved and correlated well with fasting plasma glucose concentrations [15]. Improvement in both sensory nerve CV and sensory action potential only began after intensive insulin treatment for a long period [16]. This unique response of sensory nerves to the treatment of diabetes, and the fact that the symptoms of diabetic neuropathy are mainly sensory [17], calls for a more detailed study of the sensory nerves especially in experimental models of diabetes where the different classes of fibres can be sampled easily.This study was undertaken to provide some more data on cutaneous nerve CVs in streptozotocin-diabetes and to correlate these with three metabolic indices in order to throw light on the possible mechanism(s) leading to conduction abnormalities. Materials and methods Experimental animalsThirty femal...

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“…If motor nerve fibres are impaired, the action of neuromuscular blocking drugs is exaggerated. 6,7 In patients with diabetes mellitus, demyelination is apparent in the motor nerve endings, 13,14 and recovery from vecuronium-induced neuromuscular block is delayed. 6 The current investigation demonstrates that the duration of neuromuscular block associated with vecuronium is prolonged in hypercholesterolemic patients.…”

Section: Discussionmentioning

confidence: 99%

Recovery from vecuronium is delayed in patients with hypercholesterolemia

Saitoh¹

2006

Can J Anesth/J Can Anesth

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Purpose:To examine the effects of hypercholesterolemia with respect to onset time and recovery from vecuronium-induced neuromuscular block. Methods:A randomized controlled trial was undertaken in 20 adult patients with hypercholesterolemia (hypercholesterolemia group) and 20 healthy patients with normal serum cholesterolemia (control group). Following induction of anesthesia, vecuronium 0.1 mg·kg -1 iv was administered. Onset of neuromuscular block and recovery times in the two groups were compared using supramaximal stimulation of the ulnar nerve. Results:The supramaximal stimulating current in the hypercholesterolemia group was similar to that of the control group (38.1 ± 15.5 vs 31.3 ± 7.6 mA, P = 0.087). Onset of vecuronium-induced neuromuscular block (time to loss of response to T1) in the hypercholesterolemia group was similar to that observed in the control group (243 ± 84 vs 249 ± 56 sec, P = 0.792). Times from vecuronium administration to the return of T1 were also similar in the two groups (29.8 ± 9.7 vs 25.3 ± 6.8 min, P = 0.099). However, mean times for return of T2, T3, and T4 in the hypercholesterolemia group were longer than in the control group (44.5 ± 14.4 vs 34.0 ± 8.4 min for T2, P = 0.018). During recovery from neuromuscular block, T1/control and train-of-four ratio in the hypercholesterolemia group were less than in the control group, 90-120 min and 70-120 min after vecuronium, respectively (P < 0.05). Conclusion: Recovery from vecuronium-induced neuromuscular block is delayed in patients with hypercholesterolemia. (38,1 ± 15,5 vs 31,3 ± 7,6 mA, P = 0,087) (29,8 ± 9,7 vs 25,3 ± 6,8 min, P = 0,099). (44,5 ± 14,4vs 34,0 ± 8,4 min pour T2, P = 0,018 Objectif . Le début du bloc (moment de la perte de réponse à T1) a été similaire dans le groupe d'hypercholestérolémie et le groupe témoin (243 ± 84 vs 249 ± 56 s, P = 0,792). Le temps écoulé entre l'administration du vécuronium et le retour de la réaction à T1 a été aussi comparable entre les groupes Les temps moyens de retour des réactions à T2, T3 et T4 ont été plus longs dans le groupe d'hypercholestérolémie

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Motor Nerve Conduction Velocity in Diabetes

Cited by 99 publications

References 13 publications

Phosphorylation of c-Jun N-terminal kinase (JNK) in sensory neurones of diabetic rats, with possible effects on nerve conduction and neuropathic pain: prevention with an aldose reductase inhibitor

Phosphorylation of c-Jun N-terminal kinase (JNK) in sensory neurones of diabetic rats, with possible effects on nerve conduction and neuropathic pain: prevention with an aldose reductase inhibitor

The correlation between sensory nerve conduction velocities and three metabolic indices in rats treated with streptozotocin

Recovery from vecuronium is delayed in patients with hypercholesterolemia

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