Disease relevance of Neural Conduction

• The close relationship between myo-inositol and the median sensory NCV following transplantation suggests that elevated plasma myo-inositol concentrations may be related to nerve conduction abnormalities in uremic polyneuropathy [1].
• Because of the unusual neurosensory toxicity of oxaliplatin, detailed neurologic examination, needle electromyography (EMG), and nerve conduction studies (NCS) were performed before and the day after oxaliplatin in a subset of 13 patients [2].
• Coexistence of nerve conduction deficit with increased Na(+)-K(+)-ATPase activity in galactose-fed mice. Implications for polyol pathway and diabetic neuropathy [3].
• Autosomal dominant cerebellar ataxia type I. Nerve conduction and evoked potential studies in families with SCA1, SCA2 and SCA3 [4].
• X-linked dominant Charcot-Marie-Tooth disease (CMTX) is a sensorimotor peripheral neuropathy in which males have usually more severe clinical symptoms and decreased nerve conduction velocities than do females [5].

Psychiatry related information on Neural Conduction

• Similarly, galactose-feeding over 4 weeks resulted in an elevation of glycosylated haemoglobin levels with significant (p less than 0.001) reductions of pain threshold and motor nerve conduction velocity [6].
• Reversible acute axonal polyneuropathy associated with Wernicke-Korsakoff syndrome: impaired physiological nerve conduction due to thiamine deficiency [7]?
• Clinical safety was monitored, including assessment of neurologic status at baseline and throughout the study using a comprehensive battery of standardized neurologic tests (eg, Purdue Pegboard Test, Mini-Mental State Examination, nerve conduction studies) and neuropsychological tests [8].
• Electromyography, nerve conduction velocity and latency showed no correlation with aluminium levels or dementia [9].

High impact information on Neural Conduction

• The number of patients with NIDDM who had nerve-conduction abnormalities in the legs and feet increased from 8.3 percent at base line to 16.7 percent after 5 years and to 41.9 percent after 10 years [10].
• The effects of myo-inositol on nerve conduction are now explained by concepts that were largely unappreciated in 1976, including the fundamental role of phosphoinositide metabolism in cell regulation and the importance of the activity of sodium-potassium-ATPase in nerve conduction [11].
• Aldose reductase inhibition improves nerve conduction velocity in diabetic patients [12].
• The group with highest levels had a significantly (P less than 0.01) lower conduction velocity (25.3 +/- 4.9 m per second) than the group with normal or slightly elevated parathyroid hormone, who had only mild depression of nerve conduction (45.1 +/- 1.3 m per second) [13].
• Carpal tunnel syndrome. Importance of sensory nerve conduction studies in diagnosis [14].

Chemical compound and disease context of Neural Conduction

• Acute, subacute and chronic streptozotocin-diabetic rats displayed a reduction of pain threshold (p less than 0.001) associated with slowed motor nerve conduction velocities (p less than 0.001) [6].
• Treatment with aminoguanidine from the induction of diabetes mellitus prevented a 22% decrease in sciatic motor nerve conduction velocity (p less than 0.001), and a 10% deficit in sensory saphenous conduction velocity (p less than 0.01) [15].
• In diabetic neuropathy, a cilostazol-supplemented diet improved both NBF and nerve conduction in a dose- and time-dependent fashion [16].
• In this investigation we studied the effect of glutathione-treatment on the development of diabetic neuropathy in streptozotocin-induced diabetic rats by measuring sensory and motor nerve conduction velocities [17].
• The development of somatic polyneuropathy in the BB/W-rat was significantly attenuated by acarbose treatment with a partial prevention of the characteristic nerve conduction velocity slowing during the first 3 months of diabetes, but no longer at 4 months [18].

Biological context of Neural Conduction

• Serum urea nitrogen, creatinine, hematocrit, nerve conduction velocity, calcium, inorganic phosphorus, serum proteins, and electrolytes have been maintained in acceptable ranges [19].
• Mice engineered to lack GM2/GD2 synthase (GalNAc-T), with resultant deficit of GM2, GD2, and all gangliotetraose gangliosides, were originally described as showing a relatively normal phenotype with only a slight reduction in nerve conduction [20].
• Rapid thyroid hormone-dependent saturation of myelin marker gene expression in Schwann cells and oligodendrocytes of the VIIIth nerve may guarantee nerve conduction and synchronized impulse transmission at the onset of hearing [21].
• Prevention and reversal of defective axonal transport and motor nerve conduction velocity in rats with experimental diabetes by treatment with the aldose reductase inhibitor Sorbinil [22].
• At the functional level, electrophysiology recordings demonstrated a significant reduction of motor nerve conduction velocity in stathmin(-/-) mice [23].

Anatomical context of Neural Conduction

• Normal myelin structure and nerve conduction in the PNS, with N-CAM overexpression at sites normally expressing MAG, suggested compensatory mechanisms [24].
• Autosomal dominant of Charcot-Marie-Tooth disease (CMT), whose gene is type 1B (CMT1B), has slow nerve conduction with demyelinated Schwann cells [25].
• These MDR3 transgenic mice have a slowed motor nerve conduction and dysmyelination of their peripheral nerves [26].
• At the end of the study protocol, motor nerve conduction velocity, sciatic nerve tissue Na(+)-K(+)-ATPase activity, and myo-inositol content were determined [27].
• The distribution of nerve conduction abnormalities is consistent with previous histological studies showing that inflammation and primary demyelination are restricted to the CNS in PLP-EAE, but are present in the CNS and in the spinal roots of the PNS in MBP-EAE [28].

Associations of Neural Conduction with chemical compounds

• Effects of insulin and dietary myoinositol on impaired peripheral motor nerve conduction velocity in acute streptozotocin diabetes [29].
• In accordance with this construct, N-nitro-L-arginine methyl ester, a competitive inhibitor of nitric oxide synthase reversed the increased nerve conduction velocity afforded by aldose reductase inhibitor treatment in the acutely diabetic rat without affecting the attendant correction of nerve sorbitol and myo-inositol [30].
• This phenomenon has been explicitly linked to the impairment of nerve conduction in the acutely diabetic streptozocin-treated rat [31].
• Ponalrestat treatment completely prevented the characteristic nerve conduction slowing and structural abnormalities of the node of Ranvier for 4 mo despite only partial preservation of axonal integrity [32].
• Short-term prevention (4 mo) with acetyl-L-carnitine had no effects on nerve polyols, but corrected the Na+/K+ -ATPase defect and was associated with 63% prevention of the nerve conduction defect and complete prevention of structural changes [33].

Gene context of Neural Conduction

• PMP22 duplication caused mainly demyelinating phenotypes with slowed motor nerve conduction velocity (MCV) and demyelinating histopathology, while axonal features were variably present [34].
• The electrophysiological studies showed that motor nerve conduction velocities in CMTX females, but not males, were heterogeneous between nerves compared with Charcot-Marie-Tooth type 1A (CMT1A) patients and controls [35].
• OBJECTIVES: To expand our understanding of the characteristics of nerve conduction velocity (NCV) in patients with different MPZ mutations, the authors collected and analysed the NCV values from patients with MPZ mutations [36].
• Aqp4 knockout mice demonstrated impaired hearing, but normal neural conduction time [37].
• Mice homozygously deficient for the peripheral myelin protein 22 gene (Pmp22-/-) exhibited increased motor latencies, reduced nerve conduction velocities, and polyphasia of the M-response, which are the typical electrophysiological signs of dysmyelination [38].

Analytical, diagnostic and therapeutic context of Neural Conduction

• The small, but statistically significant, improvement in nerve conduction after treatment of diabetic patients with the aldose reductase inhibitor, sorbinil, suggests that increased polyol (sorbitol) pathway activity may contribute to diabetic nerve conduction slowing [39].
• However, during euglycaemic clamping (plasma glucose approximately 5 mmol/l) in five non-diabetic men (19-38 years of age) infused solely with somatostatin [Study 2], a comparable decrement in nerve conduction velocity was found (1.7 +/- 1.3 m/s, 2p-value: 0.043) [40].
• Vitamin B12 levels and nerve conduction velocities in patients undergoing maintenance hemodialysis [41].
• With the exception of elevated serum lactic acid, the general blood screen, EMG, nerve conduction velocity tests, and ECG were normal [42].
• ARIs, which normalize nerve myo-inositol and nerve conduction slowing, are currently the focus of clinical trials [43].

References