Peripheral Nerve Conduction Velocity Research Articles

Axon-glia interactions and the domain organization of myelinated axons requires neurexin IV/Caspr/Paranodin.

Myelinated fibers are organized into distinct domains that are necessary for saltatory conduction. These domains include the nodes of Ranvier and the flanking paranodal regions where glial cells closely appose and form specialized septate-like junctions with axons. These junctions contain a Drosophila Neurexin IV-related protein, Caspr/Paranodin (NCP1). Mice that lack NCP1 exhibit tremor, ataxia, and significant motor paresis. In the absence of NCP1, normal paranodal junctions fail to form, and the organization of the paranodal loops is disrupted. Contactin is undetectable in the paranodes, and K(+) channels are displaced from the juxtaparanodal into the paranodal domains. Loss of NCP1 also results in a severe decrease in peripheral nerve conduction velocity. These results show a critical role for NCP1 in the delineation of specific axonal domains and the axon-glia interactions required for normal saltatory conduction.

Glutathione and alpha-lipoate in diabetic rats: nerve function, blood flow and oxidative state.

Increased oxidative stress is considered to be a causal factor in the development of diabetic complications, among which peripheral neuropathy. The pathophysiology of nerve dysfunction in diabetes has been explained both by reduced endoneurial microcirculation and alterations in endoneurial metabolism. It is unclear whether antioxidants primarily improve nerve blood flow or normalise systemic or endoneurial oxidative metabolism. Therefore, we evaluated the effects of the antioxidants glutathione and alpha-lipoic acid on both nerve microcirculation and the antioxidative capacity and lipid peroxidation in experimentally diabetic rats. Streptozotocin-diabetic rats were treated with different doses of alpha-lipoic acid, reduced glutathione or placebo, and were compared with nondiabetic controls. We measured systemic and endoneurial antioxidants, malondialdehyde and whole blood hydrogen peroxide. Furthermore, we evaluated sciatic and tibial motor and sensory nerve conduction velocity, caudal nerve conduction velocity, and assessed sciatic nerve blood flow and vascular resistance by Laser-Doppler flowmetry. We observed a rise in erythrocyte glutathione by 27 % (P < 0.05), and a trend towards decreased plasma malondialdehyde in alpha-lipoic acid, but not in glutathione-treated animals in comparison with the placebo group. Simultaneously, sciatic nerve blood flow and vascular resistance were improved by daily alpha-lipoic acid administration by 38% (P < 0.05). Peripheral nerve conduction velocity and endoneurial glutathione were not significantly influenced by antioxidant treatment. Only minor beneficial effects of alpha-lipoic acid on nerve blood flow and oxidative state occur at the given doses; these effects were insufficient to improve nerve conduction deficits.

Description of a short-term Taxol ®-induced nociceptive neuropathy in rats

This work describes a new animal model of neuropathic pain produced by the single intraperitoneal administration of Taxol ® (32 mg/kg) to male Sprague–Dawley rats. During the course of the experiment, the clinical status of the rats remained satisfactory and motor function was not altered. A number of classical behavioural tests of nociception as well as histological and electrophysiological investigations were performed. Taxol ® administration produced an important and rapidly developing mechanical hyperalgesia, a thermal hypoalgesia but no mechanical or thermal allodynia. Degenerative changes were observed in the sciatic nerve, the nerve fibres in the paw subcutaneous tissue and in the lumbar spinal cord. When Taxol ® or vehicle (a mix of Cremophor and ethanol) were repeatedly injected once a week for 5 weeks, similar nociceptive disorders were observed in addition to a decrease in peripheral nerve conduction velocity. The selective dysfunction of high-diameter myelinated fibres observed after one single administration of Taxol ® (32 mg/kg) may be attributable to paclitaxel-induced neuropathy, however other mechanisms causing neurochemical dysfunction must also be involved.

Diabetic peripheral neuropathy: evidence for apoptosis and associated mitochondrial dysfunction.

We hypothesized that diabetic sensory neuropathy is associated with activation of apoptosis and concomitant mitochondrial dysfunction. Studies were performed in excised intact and acutely dissociated dorsal root ganglion (DRG) neurons from control and streptozotocin-induced diabetic rats with decreased peripheral nerve conduction velocities (NCV). Apoptosis was increased in acutely dissociated DRG neurons from 3- to 6-week-old diabetic rats. Basal mitochondrial membrane potential (deltapsi) was significantly more positive in DRG neurons from diabetic rats. Depolarization with glutamate resulted in significantly more positive deltapsi and delayed recovery of deltapsi in neurons from diabetic rats. Restoration of euglycemia for 2 weeks with insulin implants normalized NCV, deltapsi, and apoptosis. Intact and acutely dissociated neurons from diabetic rats demonstrated decreased Bcl-2 levels and translocation of cytochrome C from the mitochondria to the cytoplasm. Neither levels of Bax nor levels of Bcl-XL were altered in diabetic neuropathy. Apoptosis associated with mitochondrial dysfunction may contribute to the pathogenesis of diabetic sensory neuropathy.

Pain-Related somatosensory evoked potentials.

The authors reviewed basic and clinical reports of pain-related somatosensory evoked potentials (SSEP) after high-intensity electrical stimulation [pain SSEP(E)] and painful laser stimulation [pain SSEP(L)]. The conduction velocity of peripheral nerves for both pain SSEP(E) and pain SSEP(L) is approximately 10 to 15 m/second, in a range of Adelta fibers. The generator sources are considered to be the secondary somatosensory cortex and insula, and the limbic system, including the cingulate cortex, amygdala, or hippocampus of the bilateral hemispheres. The latencies and amplitudes are clearly affected by vigilance, attention-distraction, and various kinds of stimulation applied simultaneously with pain. Abnormalities of pain SSEP(L) reflect an impairment of pain-temperature sensation, probably relating to dysfunction of A5 fibers of the peripheral nerve and spinothalamic tract. In contrast, conventional SSEP after nonpainful electrical stimulation reflects an impairment of tactile, vibratory, and deep sensation, probably relating to dysfunction of Aalpha or Abeta fibers of the peripheral nerve and dorsal column. Therefore, combining the study of pain SSEP(L) and conventional SSEP is useful to detect physiologic abnormalities, and sometimes subclinical abnormalities, of patients with peripheral and central nervous system lesions.

Subclinical neurophysiological effects of lead: A review on peripheral, central, and autonomic nervous system effects in lead workers

Background The peripheral nerve conduction velocity (NCV), distribution of nerve conduction velocities (DCV), somatosensory, visual, and brainstem auditory evoked potentials (SEP, VEP, and BAEP, respectively), event-related potential (P300), computerized static posturography with spectral analysis (postural balance), and electrocardiographic R–R interval variability (CVRR) with spectral analysis appear to be promising techniques for assessing subclinical effects of lead on the peripheral, central and autonomic nervous systems. This article presents an overview of research addressing subclinical neurophysiological effects of lead in workers exposed to lead. Methods We reviewed 102 articles to examine the effects and dose–effects relationships of lead on peripheral, central, and autonomic nervous system function together with reversibility of the effects, interaction between lead and other metals, and relative sensitivity and specificity of each technique. Background and methodology were also reviewed. Results and Conclusion Available data suggest that, on a group basis, the reduction in the NCV, together with the effects on the P300 latency, postural balance, and CVRR, occurs at a mean blood lead concentration (BPb) as low as 30–40 μg/dL; the effects on the latencies of the short-latency SEP, VEP, and BAEP, as well as the DCV, start at a BPb as low as 40–50 μg/dL. Further cross-sectional and preferably prospective studies by using each of those methods are needed to establish more precise dose–effects (and response) relationships of lead. Am. J. Ind. Med. 37:193–204, 2000. © 2000 Wiley-Liss, Inc.

Subclinical neurophysiological effects of lead: A review on peripheral, central, and autonomic nervous system effects in lead workers.

The peripheral nerve conduction velocity (NCV), distribution of nerve conduction velocities (DCV), somatosensory, visual, and brainstem auditory evoked potentials (SEP, VEP, and BAEP, respectively), event-related potential (P300), computerized static posturography with spectral analysis (postural balance), and electrocardiographic R-R interval variability (CV(RR)) with spectral analysis appear to be promising techniques for assessing subclinical effects of lead on the peripheral, central and autonomic nervous systems. This article presents an overview of research addressing subclinical neurophysiological effects of lead in workers exposed to lead. We reviewed 102 articles to examine the effects and dose-effects relationships of lead on peripheral, central, and autonomic nervous system function together with reversibility of the effects, interaction between lead and other metals, and relative sensitivity and specificity of each technique. Background and methodology were also reviewed. Available data suggest that, on a group basis, the reduction in the NCV, together with the effects on the P300 latency, postural balance, and CV(RR), occurs at a mean blood lead concentration (BPb) as low as 30-40 microg/dL; the effects on the latencies of the short-latency SEP, VEP, and BAEP, as well as the DCV, start at a BPb as low as 40-50 microg/dL. Further cross-sectional and preferably prospective studies by using each of those methods are needed to establish more precise dose-effects (and response) relationships of lead.

Electrophysiological biomarkers of an organophosphorous pesticide, dichlorvos

The correlations between the relatively low level, chronic dichlorvos (DDVP) treatment and the early electrophysiological changes were investigated in three series of experiments. In the first series, male Wistar rats were orally given daily by gavage 0.98, 1.96 and 3.92 mg/kg of DDVP for 4, 8, or 12 weeks, and recordings were made at the end of each period. In the second one, the male and female rats of three consecutive generations were treated with the same doses, the investigated parameters were recorded at the age of 12 weeks of the male animals. In the third experiment, the doses were administered in different stages of development: during pregnancy, pregnancy+lactation, pregnancy+lactation+postweaning, and the electrophysiological markers were recorded also at the age of 12 weeks of male offspring. The analyzed elecrophysiological parameters were: electrocorticogram, sensoric cortical evoked potentials, conduction velocity and refractory periods of peripheral nerve. The data showed that the relatively low level dichlorvos exposure caused dose-, duration-, generation-, developmental stage-dependent and partly significant alterations in all the investigated electrophysiological parameters. The analyzed functional parameters proved to be sensitive biomarkers of the exposure as they were changed by the lower doses, while the brain cholinesterase activity was considerably inhibited only in the groups given the highest dose.

IGF-I deficient mice show reduced peripheral nerve conduction velocities and decreased axonal diameters and respond to exogenous IGF-I treatment

Although insulin-like growth factor-I (IGF-I) can act as a neurotrophic factor for peripheral neurons in vitro and in vivo following injury, the role IGF-I plays during normal development and functioning of the peripheral nervous system is unclear. Here, we report that transgenic mice with reduced levels (two genotypes: heterozygous Igf1+/- or homozygous insertional mutant Igf1m/m) or totally lacking IGF-I (homozygous Igf1-/-) show a decrease in motor and sensory nerve conduction velocities in vivo. In addition, A-fiber responses in isolated peroneal nerves from Igf1+/- and Igf1-/- mice are impaired. The nerve function impairment is most profound in Igf1-/- mice. Histopathology of the peroneal nerves in Igf1-/- mice demonstrates a shift to smaller axonal diameters but maintains the same total number of myelinated fibers as Igf1+/+ mice. Comparisons of myelin thickness with axonal diameter indicate that there is no significant reduction in peripheral nerve myelination in IGF-I-deficient mice. In addition, in Igf1m/m mice with very low serum levels of IGF-I, replacement therapy with exogenous recombinant hIGF-I restores both motor and sensory nerve conduction velocities. These findings demonstrate not only that IGF-I serves an important role in the growth and development of the peripheral nervous system, but also that systemic IGF-I treatment can enhance nerve function in IGF-I-deficient adult mice.

Higher sensitivity of CA1 synapses to aglycemia in streptozotocin-diabetic rats is age-dependent

We studied conduction velocity in peripheral nerves and the block of synaptic transmission produced by lack of glucose in hippocampal slices from 4- and 12-month-old streptozotocin-induced diabetic rats and their age-matched controls. In sural nerves of young and old diabetic rats, the conduction velocity was reduced by 30–35%. In slices from young diabetics, CA1 synaptic transmission was more sensitive to aglycemia than in control slices. However, all slices from older rats showed comparable increases in CA1 synaptic sensitivity to aglycemia. We conclude that the cerebral adaptation to diabetic hyperglycemia apparent in the hippocampus of young rats is masked in older rats by an age-dependent increase in sensitivity to lack of glucose.

The relationship of peripheral motor nerve conduction velocity to age-associated loss of grip strength.

Age-associated loss of muscle strength is attributed to decreasing muscle mass. Both strength and mass are dependent on peripheral innervation. However, the association between nerve function and age-associated strength loss has not been studied directly. The median nerve contribution to grip strength was estimated using nerve conduction velocity (NCV). Grip strength and NCV were measured in 197 male participants of the Baltimore Longitudinal Study of Aging (age 59.0 +/- 13.9 years). Multiple regression and path analyses were used separately to examine the association between median NCV and grip strength. Grip strength showed a negative quadratic relationship with increasing age (r2 = 0.32, p < 0.001) with a major change in slope occurring after 64.7 years of age. Median NCV (r2 = 0.14, p < 0.001) declined linearly with age. Median NCV significantly contributed to grip strength (p < 0.001) while controlling for forearm muscle mass (forearm circumference), self-reported 24-hour caloric expenditures, and age. The median nerve has an independent contribution to age-associated levels of muscle strength. The level of the effect was smaller than what could be attributed to forearm muscle mass or age.

Laminin α2-chain gene mutations in two siblings presenting with limb-girdle muscular dystrophy

We report two siblings, an 11-year-old boy and his 7-year-old sister, referred to us with a diagnosis of muscular dystrophy. The boy presented at 22 months with delay in walking. A very high serum creatine kinase (CK) level and a dystrophic muscle biopsy lead to a diagnosis of Duchenne muscular dystrophy prior to the identification of the dystrophin gene. Two years later his sister presented with similar problems. A diagnosis of limb-girdle muscular dystrophy was made when they were shown to have inherited different X-chromosomes and normal expression of dystrophin and all sarcoglycans. Their conditions remained static. Recently a slowing of the peripheral motor nerve conduction velocities and T2-weighted brain magnetic resonance imaging showed increased signal of the white matter, both of which are features of merosin-deficient congenital muscular dystrophy. Immunolabelling using a C-terminal laminin α2 chain antibody showed a reduction in expression, while labelling with another antibody that recognises a 300-kDa fragment showed a very significant reduction. Mutational analysis of the LAMA2 gene showed two mutations: one was a G→C point mutation at position −1 of intron 28 acceptor splicing site. This mutation induced activation of a cryptic splice at nucleotide 4429 of exon 29 and partial skipping of this exon, with conservation of the open reading frame. The other was a nonsense mutation due to a C_T transition at position 5525 of the cDNA sequence (exon 37), resulting in a stop codon. These data confirm that mutations of the LAMA2 gene that do not completely disrupt the production of the protein can give rise to phenotypes considerably milder than classical merosin-deficient congenital muscular dystrophy. Partial laminin α2 deficiency should be considered in the differential diagnosis of limb-girdle muscular dystrophy.

Computer simulation of post-spike facilitation in spike-triggered averages of rectified EMG.

When the spikes of a motor cortical cell are used to compile a spike-triggered average (STA) of rectified electromyographic (EMG) activity, a post-spike facilitation (PSF) is sometimes seen. This is generally thought to be indicative of direct corticomotoneuronal (CM) connections. However, it has been claimed that a PSF could be caused by synchronization between CM and non-CM cells. This study investigates the generation of PSF using a computer model. A population of cortical cells was simulated, some of which made CM connections to a pool of 103 motoneurons. Motoneurons were simulated using a biophysically realistic model. A subpopulation of the cortical cells was synchronized together. After a motoneuron discharge, a motor unit action potential was generated; these were summed to produce an EMG output. Realistic values were used for the corticospinal and peripheral nerve conduction velocity distribution, for slowing of impulse conduction in CM terminal axons, and for the amount of cortical synchrony. STA of the rectified EMG from all cortical neurons showed PSF; however, these were qualitatively different for CM versus non-CM cells. Using an epoch analysis to determine reliability in a quantitative manner, it was shown that the onset latency of PSF did not distinguish the two classes of cells after 10,000 spikes because of high noise in the averages. The time of the PSF peak and the peak width at half-maximum (PWHM) could separate CM from synchrony effects. However, only PWHM was robust against changes in motor unit action-potential shape and duration and against changes in the width of cortical synchrony. The amplitude of PSF from a CM cell could be doubled by the presence of synchrony. It is proposed that, if a PSF has PWHM < 7 ms, this reliably indicates that the trigger is a CM cell projecting to the muscle whose EMG is averaged. In an analysis of experimental data where macaque motor cortical cells facilitated hand and forearm muscle EMG, 74% of PSFs fulfilled this criterion. The PWHM criterion could be applied to other STA studies in which it is important to exclude the effects of synchrony.

MRI and electrophysiological abnormalities in a case of canine globoid cell leucodystrophy

A six-month-old West Highland white terrier with progressive, multifocal neurological disease was diagnosed with canine globoid cell leucodystrophy (GCL). Magnetic resonance imaging (MRI) of the brain was performed, as well as electrophysiological testing (including brainstem auditory evoked response, peripheral nerve conduction velocity, repetitive stimulation, F wave analysis and electromyography). MRI findings were consistent with diffuse, symmetrical white matter disease. Electrodiagnostic testing revealed evidence of peripheral neuropathy and an abnormal brainstem auditory evoked response. These observations were consistent with the pathological changes in central and peripheral white matter described for canine GCL, and resembled what has been described in human patients. It is believed that the tests may raise the suspicion of GCL in dogs and may aid in monitoring disease progression.

A molecular, cytogenetic, and clinical evaluation of mosaic tandem duplication 17p and Charcot-Marie-Tooth type 1A neuropathy.

An 8 year old girl with partial duplication of the short arm of chromosome 17 had a mosaic 46,XX,der(17)?del(17)(p12)dup(17) (p11.2p12).ish dup(17)(p11.2p13.3)(D17S 379x2, p53x2, D17S122x2, D17S29+) karyotype. The extent of mosaicism...

Effects of Styrene on Peripheral Nerve Conduction Velocities in Rats

Effects of Styrene on Peripheral Nerve Conduction Velocities in Rats: Tadashi Yamamoto, et al. Department of Preventive Medicine and Environmental Health, Osaka City University Medical School—The effects of styrene on the peripheral nerves were studied by measuring conduction velocities of the tail nerve in 24 male Wistar rats which had been exposed to 0 (control), 200 and 2,000 ppm of styrene (8 rats for each concentration) for 32 wk (8 h/dx5 d/wk), from the age of 8 wk, and in the same number of rats which received the same treatment since they were 4 wk of age. Motor nerve conduction velocity (MCV), distal latency (DL) and sensory nerve conduction velocity (SCV) were determined at 2‐wk intervals from the age of 8 wk to 16 wk after the end of exposure. Body weight in the 2,000 ppm (start at 4 and 8 wk of age) and 200 ppm (start at 4 wk of age) exposure groups were significantly lower than in the control group. MCV and DL in the all exposure groups were not significantly different from the control group. SCV in the 2,000 ppm (start at 4 and 8 wk of age) and 200 ppm (start at 8 wk of age) exposure groups were significantly lower than in the control group during the styrene exposure. After discontinuation of exposure, SCV remained small in the 2,000 ppm group (start at 4 wk) compared with that in the controls, but showed recovery in the other exposure groups. The effects on the decrease in SCV were greater in the distal than in the proximal area.

Quantification of the hindlimb extensor thrust response in rats.

This report describes a procedure for measuring the extensor thrust response (ETR) and summarizes the results of initial validation experiments using adult Long-Evans rats. The ETR can be quickly elicited and the force measured by pressing against the hindlimb footpads with a small rectangular plate or bar attached to a digital force gauge. Output of the force gauge is analyzed and displayed with commercially available hardware and software. The first experiment compared the acute effects of i.p. injection of chlorpromazine (CPZ; 1, 4, or 7 mg/kg) or amphetamine (AMP; 0.3, 1, or 3 mg/kg) on the ETR and forelimb/hindlimb grip strength (FL/HL-GS) in male and female rats. CPZ decreased both ETR and FL/HL-GS values. Both 1 and 3 mg/kg AMP increased grip strength values but decreased ETR values. A second experiment compared the evolution of changes in ETR, FL/HL-GS, and peripheral neurophysiological measures during 8 weeks of daily oral dosing of 10 mg/kg acrylamide (ACR) monomer. ACR-treated rats exhibited a progressive decrease in ETR beginning after 3 weeks of dosing, whereas a reduction of HL-GS was observed beginning much later, after 7 weeks of dosing. The deficit in ETR progressed in the absence of any changes in spontaneous or evoked electrophysiological abnormalities in neuromuscular function, but was accompanied by a decrease in peripheral nerve conduction velocity. Taken together, the results indicate that the ETR can be used to characterize functional effects in both single dose and repeated dose experiments. The data also indicate that the ETR does not merely duplicate the information provided by FL/HL-GS, and suggest a hypothesis that the ETR may be sensitive to neurotoxicant-induced changes in somatosensory function.

Effects of hypothermia and sternal retractors on median nerve somatosensory evoked potentials.

Somatosensory evoked potentials (SEPs) are altered by hypothermia, which is often used during cardiopulmonary bypass (CPB). However, the effect of hypothermia on SHP amplitudes is unclear. Also, the sternal retractors used during open heart surgery are reported to cause brachial plexus distension and SEP changes. Median nerve SEPs under hypothermic CPB were studied in 29 elective patients scheduled for open heart surgery. In 23 patients who underwent left internal mammary artery (IMA) dissection, the effects of sternal retractors on cortical SEP before the initiation of CPB were investigated. A latency shift of all SEP components was detected when nasopharyngeal temperature decreased from 35.7(SD 0.4) degrees C to 27.8(SD 0.25) degrees C. The mean cortical N20 latency was increased by 39% (P < 0.0001), cervical N13 by 33% (P < 0.0001), and peripheral N9 by 27% (P < 0.0001). The latency changes were reversible when normothermia was restored. The effect of hypothermia on SEP amplitudes was more complex. The mean amplitude of N20 decreased from 2.7 microV to 2.2 microV (P < 0.05) and the amplitude of N13 from 2.5 microV to 2.0 microV (P < 0.0001). In contrast, the N9 component showed an increase from 1.4 microV to 2.1 microV (P < 0.0001) during hypothermia. The sternal retractors did not cause significant cortical SEP amplitude changes during IMA dissection or sternotomy. Also, the latency changes were small, although significant (P < 0.05). Despite the moderate amplitude changes produced by hypothermia, SEPs can be successfully monitored during hypothermia. Theoretically, the different behaviour of amplitude in peripheral and cranial components of SEP during hypothermia is interesting. Hypothermia has a more profound effect on synaptic transmission, represented by the cortical N20 latency, than on the peripheral nerve conduction velocity. Intraoperative monitoring of temperature is essential whenever SEPs are recorded. The sternal retractors were not responsible for the intraoperative SEP changes.

Effects of dietary supplementation with arachidonic acid rich oils on nerve conduction and blood flow in streptozotocin-diabetic rats

Diabetes mellitus is associated with defective essential fatty acid desaturation. In experimental models this contributes to characteristic reductions in peripheral nerve conduction velocity (NCV) and blood flow, which may be corrected by dietary supplementation with γ-linolenic acid (GLA) rich oils to bypass the Δ-6 desaturation deficit. There is debate about the mechanism of this improvement, including whether it depends on synthesis of series 1 prostanoids derived from di-homo GLA or series 2 prostanoids from arachidonic acid (ARA). The aim was to assess the efficacy of two ARA-rich (∼ 39% content) oils in correcting neurovascular dysfunction in streptozotocin-induced diabetic rats. After 6 weeks of untreated diabetes, rats were treated for a further 2 weeks with 1% dietary oil supplements before assessment of sciatic motor NCV and endoneurial blood flow. NCV was 19% reduced in diabetic rats and this was largely (∼ 86%) corrected by both oil treatments. A 48% deficit in endoneurial nutritive blood flow with diabetes was ∼ 70% reversed by the two oils, vascular conductance being in the non-diabetic range. Thus, nerve conduction and perfusion deficits in diabetic rats are corrected by ARA-rich oil treatment. The magnitudes of these changes were similar to expectations based on previous studies of GLA-rich oils, therefore it is likely that the neurovascular effect of increased synthesis of series 2 prostanoids makes a major contribution to the beneficial action of n-6 essential fatty acids in experimental diabetic neuropathy.

Genetic mediation of the correlation between peripheral nerve conduction velocity and IQ.

Variation in peripheral nerve conduction velocity (PNCV) and intelligence was studied in 18-year-old Dutch twins. It has been suggested that both brain nerve conduction velocity and PNCV are positively correlated with intelligence (Reed, 1984) and that heritable differences in nerve conduction velocity may explain part of the well-established heritability of intelligence. The relationship among IQ, obtained with the Wechsler Adult Intelligence Scale, and median nerve PNCV was examined in 159 twin pairs. Genetic analyses showed a heritability of 81% for IQ and 66% for onset PNCV. The small but significant phenotypic correlation between IQ and onset PNCV (.15) was entirely mediated by common genetic factors. Analyses of differences scores for PNCV of this study and PNCV from the same subjects collected at age 16 suggest that there might still be development in PNCV in this age interval. This maturation is highly controlled by genetic factors. It is suggested that variation in IQ that is associated with nerve conduction velocity becomes apparent only after the developmental processes in peripheral nerves are completed. This is in line with the suggestion of increasing heritability of IQ in adulthood.