Changes in nerve conduction velocity after six weeks of glucoregulation with portable insulin infusion pumps

Pietri, A.; Ehle, Albert L.; Raskin, Philip

doi:10.2337/diabetes.29.8.668

Cited by 61 publications

(27 citation statements)

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“…The earliest detectable slowing of nerve conduction is readily reversible with metabolic intervention, and is attributed to reversible biochemical abnormalities in diabetic peripheral nerve (1)(2)(3)(4)29 Axo-glial Dysjunction (%) Figure 10. Relationship between MNCV and axo-glial dysjunction in nondiabetic controls (d), insulin-replaced diabetics (b), and insulin-deficient diabetics at baseline (c) and at the completion of the study (a (25,26).…”

Section: Discussionmentioning

confidence: 99%

“…Readily reversible defects in nerve metabolism in the diabetic rat directly contribute to reversible conduction slowing resembling that of early human diabetes (1,2). Although similar metabolic disturbances presumably condition the development of symptomatic neuropathy in susceptible diabetic patients, metabolic intervention produces only limited electrophysiologic or clinical response once diabetic neuropathy is clinically established (3,4). The structural and/ or biochemical lesions responsible for poorly reversible neurological deficits in diabetic patients, and the role of antecedent Receivedfor publication 21 May 1985. reversible functional and metabolic abnormalities in their development, remain unclear.…”

Section: Introductionmentioning

confidence: 99%

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Axo-glial dysjunction. A novel structural lesion that accounts for poorly reversible slowing of nerve conduction in the spontaneously diabetic bio-breeding rat.

Sima¹,

Lattimer²,

Yagihashi³

et al. 1986

J. Clin. Invest.

171

117

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Biochemical abnormalities in peripher, nerve are thought to precede and condition the development of diabetic neuropathy, but metabolic intervention in chronic diabetic neuropathy produces only limited acute clinical response. The residual, metabolically unresponsive neurological deficits have never been rigorously defined in terms of either persistent metabolic derangements or irreversible structural defects because (a) human nerve tissue is rarely accessible for anatomical and biochemical study and (b) experimentally diabetic animals do not develop the structural hallmarks of human diabetic neuropathy. Detailed neuroanatomical-functional-biochemical correlation was therefore undertaken in long-term spontaneously diabetic BB-Wistar rats that functionally and structurally model human diabetic neuropathy. Vigorous insulin replacement in chronically diabetic BB rats essentially normalized both the sural nerve fiber caliber spectrum and the decreased sciatic nerve myo-inositol and (Na,K)-ATPase levels generally associated with conduction slowing in diabetic animals; yet, nerve conduction was only partially restored toward normal. Morphometric analysis revealed a striking disappearance of paranodal axo-glial junctional complexes that was not corrected by insulin replacement. Loss of these strategic junctional complexes, which are thought to limit lateral migration of axolemmal Na channels away from nodes of Ranvier, correlates with and can account for the diminished nodal Na permeability and resultant nodal conduction delay characteristic of chronic diabetic neuropathy in this animal model.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Axo-glial dysjunction. A novel structural lesion that accounts for poorly reversible slowing of nerve conduction in the spontaneously diabetic bio-breeding rat.

Sima¹,

Lattimer²,

Yagihashi³

et al. 1986

J. Clin. Invest.

171

117

View full text Add to dashboard Cite

show abstract

“…There have been no comparable studies of autonomic function. The concept of direct metabolic damage to nerves by hyperglycaemia [5] is based on studies of motor nerve conduction velocity [15][16][17][18][19][20][21][22]. Yet it is sensory and autonomic nerve involvement, rather than damage to somatic motor fibres, which is responsible for the common and clinically serious manifestations of diabetic neuropathy [3,6].…”

Section: Discussionmentioning

confidence: 99%

Progression of subclinical polyneuropathy in young patients with Type 1 (insulin-dependent) diabetes: associations with glycaemic control and microangiopathy (microvascular complications)

Young

MacIntyre

Martyn³

et al. 1986

Diabetologia

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Summary. The progression of subclinical polyneuropathy over 2.5 years has been studied in a representative group of 75 young patients with Type I (insulin-dependent) diabetes (initial age 16-19years). The relationships between changes in nerve function, glycaemic control and concurrently developing microvascular complications (retinopathy, microproteinuria) were investigated. Deterioration of motor, sensory and autonomic nerve function, retinopathy and microproteinuria was related to poor glycaemic control. In addition, there was an association between developing neural and microvascular complications which was not diminished when their common relationship to hyperglycaemia was taken into account. These findings suggest that, although poor glycaemic control is an essential permissive factor in the early development of diabetic polyneuropathy, other influences, shared with microvascular complications, must also be important.

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“…reported following short-term insulin treatment in early diabetes [12,28,29] and in patients with clinical or symptomatic neuropathy treated with continuous subcutaneous insulin infusion [30][31][32][33][34]. These rapidly reversible changes may have a different pathogenesis with metabolic dysfunction without development of persisting morphological changes [2].…”

Section: Referencesmentioning

confidence: 99%

The effect of 8 years of strict glycaemic control on peripheral nerve function in IDDM patients: the Oslo Study

Amthor

Dahl-J�rgensen²,

Berg³

et al. 1994

Diabetologia

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SummaryWe have investigated the effect of long-term strict glycaemic control on peripheral and autonomic nerve function in 45 IDDM patients (age 18-42 years, diabetes duration 7-23 years) without clinical signs of neuropathy or other neurological disease. They were randomly assigned to treatment either with continuous insulin infusion, multiple injections (4-6 times daily), or conventional treatment (twice daily) for 4 years and followed prospectively for 8 years. Motor and sensory nerve conduction velocities were measured at the start and after 8 years. Autonomic nerve function tests were performed only once, after 8 years. A significant reduction of nerve conduction velocity was observed during 8 years in patients with mean HbA1 more than 10% (n = 12, group mean 10.9%, range 10.1-13.2%) compared to patients with HbAI less than 10% (n = 33, group mean 9.0 %, range 7.5-9.9 %). Change of motor nerve conduction velocity in the peroneal nerve was: -4.8 + 4.9 (SD) vs -2.2 + 5.3 m/s (p < 0.01). Change of motor nerve conduction velocity in the posterior tibial nerve was: -6.8 + 5.7 vs-3.9 +_ 5.1 m/s (p < 0.05). No significant changes were observed in the ulnar nerve. Change of sensoric nerve conduction velocity in the sural nerve was: -8.9 + 8.0 vs -4.6 + 5.3 m/s (p < 0.05). Multiple regression analysis showed that a change in HbA1 of 1% resulted in a 1.3 m/s change in nerve conduction velocity during 8 years. A significantly lowered heart-rate variation during deep breathing (p < 0.05) and heart-rate response to standing (p < 0.01) was found in patients with HbA1 more than 10 % compared to patients with HbA1 less than 10 %. This study confirms that the long-term lowering of blood glucose retards the deterioration in nerve conduction velocity observed in the diabetic nerve. [Diabetologia (1994) 37: 579-584]

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Changes in nerve conduction velocity after six weeks of glucoregulation with portable insulin infusion pumps

Cited by 61 publications

References 0 publications

Axo-glial dysjunction. A novel structural lesion that accounts for poorly reversible slowing of nerve conduction in the spontaneously diabetic bio-breeding rat.

Axo-glial dysjunction. A novel structural lesion that accounts for poorly reversible slowing of nerve conduction in the spontaneously diabetic bio-breeding rat.

Progression of subclinical polyneuropathy in young patients with Type 1 (insulin-dependent) diabetes: associations with glycaemic control and microangiopathy (microvascular complications)

The effect of 8 years of strict glycaemic control on peripheral nerve function in IDDM patients: the Oslo Study

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