Peripheral Conduction Velocity Research Articles

New findings about neuropathological outcomes in the PKU mouse throughout lifespan

Phenylketonuria (PKU, OMIM 261600) is a genetic disorder caused by a deficiency of the hepatic enzyme phenylalanine hydroxylase (PAH). If left untreated, PKU leads to systemic phenylalanine (Phe) accumulation, which can result in irreversible brain damage and intellectual disabilities. In the last 60 years, early and strict dietary restriction of phenylalanine (Phe) intake proved to prevent the severe clinical phenotype of untreated PKU. While the specific mechanisms through which phenylalanine causes brain damage are still poorly understood, preclinical models have been deeply explored to characterize the neurotoxic effect of Phe on neurodevelopmental processes. At the same time, that on the aging brain still needs to be explored. In the brain of untreated PAHEnu2(−/−) mouse, we previously reported a reduction of myelin basic protein (MBP) during postnatal development up to 60 PND. Later in the diseased mouse's life, a spontaneous and persistent restoration of MBP was detected. In this present longitudinal study, ranging from 14 to 540 post-natal days (PND) of untreated PAHEnu2(−/−) mice, we further investigated: a) the long-life consistency of two Phe-related brain metabolic alterations, such as large neutral amino acids (LNAA) and biogenic amine neurotransmitters' depletion; b) the outcome of locomotor functions during the same life span; c) the integrity of myelin as assessed ex vivo by central (hippocampus) and peripheral (extensor digitorum longus-sciatic nerve) action potential conduction velocities. In contrast with the results of other studies, brain Leu, Ile, and Val concentrations were not significantly altered in the brain PAHEnu2(−/−) mouse. On the other hand, 3-O-Methyldopa (3-OMD, a biomarker of L-DOPA), serotonin, and its associated metabolites were reduced throughout most of the considered time points, with consistent reductions observed prevalently from 14 to 60 PND. Normal saltatory conduction was restored after 60 PND and remained normal at the last examination at 360 PND, resulting nonetheless in a persistent locomotor impairment throughout a lifetime. These new findings contribute to laying the foundations for the preclinical characterization of aging in PKU, confirming neurotransmitter defects as consistent metabolic traits. LNAAs have a minor role, if any, in brain damage pathogenesis. Transient myelin synthesis failure may impact brain connectivity during postnatal development but not nervous signal conduction.

Trapezius Motor Evoked Potentials From Transcranial Electrical Stimulation and Transcranial Magnetic Stimulation: Reference Data, Characteristic Differences and Intradural Motor Velocities in Horses

Reason for Performing StudySo far, only transcranial motor evoked potentials (MEP) of the extensor carpi radialis and tibialis cranialis have been documented for diagnostic evaluation in horses. These allow for differentiating whether lesions are located in either the thoraco-lumbar region or in the cervical myelum and/or brain. Transcranial trapezius MEPs further enable to distinguish between spinal and supraspinal located lesions. No normative data are available. It is unclear whether transcranial electrical stimulation (TES) and transcranial magnetic stimulation (TMS) are interchangeable modalities.ObjectivesTo provide normative data for trapezius MEP parameters in horses for TES and TMS and to discern direct and indirect conduction routes by neurophysiological models that use anatomical geometric characteristics to relate latency times with peripheral (PCV) and central conduction velocities (CCV).MethodsTranscranial electrical stimulation-induced trapezius MEPs were obtained from twelve horses. TES and TMS-MEPs (subgroup 5 horses) were compared intra-individually. Trapezius MEPs were measured bilaterally twice at 5 intensity steps. Motoneurons were localized using nerve conduction models of the cervical and spinal accessory nerves (SAN). Predicted CCVs were verified by multifidus MEP data from two horses referred for neurophysiological assessment.ResultsMean MEP latencies revealed for TES: 13.5 (11.1–16.0)ms and TMS: 19.7 (12–29.5)ms, comprising ∼100% direct routes and for TMS mixed direct/indirect routes of L:23/50; R:14/50. Left/right latency decreases over 10 > 50 V for TES were: –1.4/–1.8 ms and over 10 > 50% for TMS: –1.7/–3.5 ms. Direct route TMS-TES latency differences were 1.88–4.30 ms. 95% MEP amplitudes ranges for TES were: L:0.26–22 mV; R:0.5–15 mV and TMS: L:0.9 – 9.1 mV; R:1.1–7.9 mV.ConclusionThis is the first study to report normative data characterizing TES and TMS induced- trapezius MEPs in horses. The complex trapezius innervation leaves TES as the only reliable stimulation modality. Differences in latency times along the SAN route permit for estimation of the location of active motoneurons, which is of importance for clinical diagnostic purpose. SAN route lengths and latency times are governed by anatomical locations of motoneurons across C2-C5 segments. TES intensity-dependent reductions of trapezius MEP latencies are similar to limb muscles while MEP amplitudes between sides and between TES and TMS are not different. CCVs may reach 180 m/s.

The new micropatterned interdigitated electrode for selective assessment of the nociceptive system.

In this neurophysiological study, we aimed at verifying the nociceptive selectivity of the new, micropatterned electrode (150IDE), recently designed to generate an electric field limited to the intraepidermal free nerve endings. Using the new 150IDE, we recorded evoked potentials after stimulation of the face and hand dorsum in 22 healthy participants and in patients with exemplary conditions selectively affecting the nociceptive system. We also measured the peripheral conduction velocity at the upper arm and verified the nociceptive selectivity of 150IDE assessing the effect of a selective block of nociceptive nerve fibres of radial nerve with local anaesthetic infiltration. In healthy participants and in patients, we have also compared the 150IDE-evoked potentials with laser-evoked potentials. In healthy participants, the 150IDE-evoked pinprick sensation and reproducible scalp potentials, with latency similar to laser-evoked potentials. The mean peripheral conduction velocity, estimated at the upper arm, was 12m/s. The selective nociceptive fibre block of the radial nerve abolished the scalp potentials elicited by the 150IDE stimulation. In patients, the 150IDE-evoked potentials reliably detected the selective damage of the nociceptive system. Our neurophysiological study shows that this new 150IDE provides selective information on nociceptive system. 150IDE is a promising new tool for investigating nociceptive system in patients with neuropathic pain.

Tumor necrosis factor alpha in peripheral neuropathy in type 2 diabetes mellitus

ObjectiveTo compare serum levels of tumor necrosis factor alpha (TNF-α) between type 2 diabetes mellitus patients with and without peripheral neuropathy (PN). Also, to study the relation between peripheral nerves conduction velocity and serum level of TNF-α in those patients.Patients and methodsThis study included three groups with 40 patients in each group. Diabetic PN patients (groups I and II) were compared with diabetic patients without PN (group III). Groups I and II differed in the duration of clinical neuropathy with less than 5 years in group I and more than 5 years in group II.All patients were subjected to general and neurological examination, neuropathy symptom score (NSS), neuropathy disability score (NDS), glycosylated hemoglobin (HbA1c), serum level of TNF-α and both sensory and motor nerve conduction study.ResultsThis study showed raised serum levels of TNF-α in diabetic patients with PN, more with increased duration of neuropathy. TNF-α levels showed statistically significant negative correlation with nerve conduction velocity but positive correlations with each of neuropathy disability score, neuropathy symptom score, and glycosylated hemoglobin.ConclusionTNF-α might be involved in the pathogenesis of diabetic PN, and its serum level might be used as a biomarker for the severity of diabetic PN.

Cooling the skin for assessing small-fibre function.

In this clinical and neurophysiological study using a novel cold stimulator, we aim at investigating whether cold-evoked potentials (CEPs) may prove to be a reliable diagnostic tool to assess trigeminal small-fibre function. Using a novel device consisting of micro-Peltier elements, we recorded CEPs after stimulating the supraorbital and perioral regions and the hand dorsum in 15 healthy participants and in 2 patients with exemplary facial neuropathic pain conditions. We measured peripheral conduction velocity at the upper arm and studied the brain generators using source analysis. In healthy participants and patients, we also compared CEPs with laser-evoked potentials. In the healthy participants, cold stimulation evoked reproducible scalp potentials, similar to those elicited by laser pulses, although with a latency of about 30 ms longer. The mean peripheral conduction velocity, estimated at the upper arm, was 12.7 m/seconds. The main waves of the scalp potentials originated from the anterior cingulate gyrus and were preceded by activity in the bilateral opercular regions and bilateral dorsolateral frontal regions. Unlike laser stimulation, cold stimulation evoked scalp potential of similar amplitude across perioral, supraorbital, and hand dorsum stimulation. In patients with facial neuropathic pain, CEP recording showed the selective damage of cold pathways providing complementary information to laser-evoked potential recording. Our clinical and neurophysiological study shows that this new device provides reliable information on trigeminal small fibres mediating cold sensation and might be useful for investigating patients with facial neuropathic pain associated with a distinct damage of cold-mediating fibres.

Neonatal vincristine administration modulates intrinsic neuronal excitability in the rat dorsal root ganglion and spinal dorsal horn during adolescence.

Our recent work has shown that the early-life administration of vincristine (VNC), commonly used to treat pediatric cancers, evokes mechanical pain hypersensitivity in rats that emerges during adolescence and persists into adulthood. However, the underlying mechanisms remain unclear, as nothing is known about how neonatal VNC treatment influences peripheral and central nociceptive processing at the cellular level. Here, we used in vitro intracellular microelectrode and whole-cell patch-clamp recordings to evaluate the consequences of early-life VNC administration on the intrinsic membrane properties of adolescent dorsal root ganglion and spinal superficial dorsal horn neurons. The results demonstrate that VNC treatment increased the prevalence and rate of repetitive firing in both large- and medium-diameter sensory neurons, while reducing repetitive firing in small-diameter neurons, in comparison with vehicle-treated littermate controls. By contrast, passive membrane properties and peripheral conduction velocities were similar between experimental groups across all classes of primary afferents. Within the adolescent superficial dorsal horn, neonatal VNC exposure significantly enhanced the intrinsic membrane excitability of lamina I spinoparabrachial neurons, as evidenced by a decrease in rheobase and elevation of repetitive firing frequency compared with controls. Meanwhile, putative interneurons within lamina I exhibited a reduction in repetitive action potential discharge after early-life chemotherapy. Collectively, these findings suggest that neonatal VNC treatment evokes cell type-specific changes in intrinsic excitability at multiple levels of the ascending pain pathway. Overall, this work lays an essential foundation for the future exploration of the ionic mechanisms that drive chemotherapy-induced chronic pain in children and adolescents.

Change in peripheral nervous conduction velocity in patients with occupational chronic mercury poisoning and related influencing factors

Objective: To investigate the change in peripheral nervous conduction velocity in patients with occupational chronic mercury poisoning and related influencing factors. Methods: From February 2011 to December 2014, urinary mercury examination and neural electromyography were performed for 104 patients with occupational chronic mercury poisoning. The data on age, type of work, working years of mercury exposure, and past medical history were collected, and peripheral nervous conduction velocity and its correlation with age, working years of mercury exposure, and urinary mercury concentration were analyzed. Results: All the 104 patients with occupational chronic mercury poisoning had a mean of 45.37±9.82 years, median (P(25), P(75)) working years of 7 (3, 11) , and a median (P(25), P(75)) urinary mercury concentration of 88.50 (56.25, 163.03) μg/g Cr. The major clinical manifestations of peripheral nerve injuries were numbness of extremities (20.2%) , hypopselaphesia/hypalgesia or hyperpselaphesia/hyperalgesia (9.6%) , and bone/muscle pain in the extremities (6.7%) . Neural electromyography showed an increase in denervation potential (fibrillation potential or positive sharp wave) and a detection rate of abnormal peripheral nervous conduction velocity as high as 65.4%. The patients with an older age and more working years had a higher incidence rate of abnormal sensory conduction velocity of the ulnar nerve. There were significant reductions in motor and sensory conduction velocities of the median nerve, motor and sensory conduction velocities of the ulnar nerve, motor conduction velocity of the common peroneal nerve, and the sensory conduction velocity of the superficial peroneal nerve (P<0.05) , with the increase in urinary mercury concentration. Conclusion: Patients with occupational mercury poisoning have a high rate of abnormal neural electromyographic findings, which can be used as an important method for early identification of chronic peripheral nerve injuries induced by mercury poisoning. The degree of peripheral nerve injuries increases with the increasing time of mercury exposure and urinary mercury concentration.

Developmental window of sensorineural deafness in biotinidase-deficient mice.

Biotinidase deficiency is an autosomal recessively inherited disorder that results in the inability to recycle the vitamin, biotin. If untreated, the disorder can result in a range of neurological and cutaneous symptoms, including sensorineural deficits and deafness. To understand early mechanistic abnormalities that may precede more generalized and nonspecific effects of metabolic deficits such as weight loss and acidosis, we have analyzed auditory brainstem responses (ABRs) in biotinidase-deficient knockout (Btd -/- ) mice in the periweaning period with or without dietary biotin supplementation. We find significant increases in the latency of wave V of the ABR elicited by pure tone stimuli at one octave intervals, which precede substantial increases in ABR thresholds. Finer interpeak latency analyses of these changes indicate they are confined to the latter ABR waves associated with the CNS and likely reflect slowed brainstem transmission time. In contrast, peripheral nervous system conduction velocity appears normal. Further, we find that biotin-supplementation after the onset of symptoms reverses the latency shifts, which has significant relevance for early treatment in patients. Finally, ABR latencies in Btd -/- mice fed a biotin-supplemented diet for the first month of life appear refractory to transmission time slowing during a subsequent bout of biotin deficiency. These data suggest a transient vulnerability window for biotin deficiency in the auditory brainstem. Finally, we also observe a developmental vulnerability window involving follicular melanosome production or melanocyte survival. Sensorineural deafness precedes peripheral hearing loss in developmental biotinidase deficiency and is transient if rescued by dietary biotin within a short developmental window.

Mice with a deletion of the major central myelin protein exhibit hypersensitivity to noxious thermal stimuli: involvement of central sensitization

Null mutations in the gene encoding the major myelin protein of the central nervous system, proteolipid protein 1 (PLP1), cause an X-linked form of spastic paraplegia (SPG2) associated with axonal degeneration. While motor symptoms are the best known manifestations of this condition, its somatosensory disturbances have been described but poorly characterized. We carried out a longitudinal study in an animal model of SPG2 — mice carrying a deletion of the Plp1 gene (Plp-null mice). Plp-null mice exhibited severe early-onset thermal hyperalgesia, in the absence of thermal allodynia. We first performed an electrophysiological testing which showed an early decrease in peripheral and spinal conduction velocities in Plp null mice. Such as the abnormal sensitive behaviors, this slowing of nerve conduction was observed before the development of myelin abnormalities at the spinal level, from 3months of age, and without major morphological defects in the sciatic nerve. To understand the link between a decrease in nerve velocity and an increased response to thermal stimuli before the appearance of myelin abnormalities, we focused our attention on the dorsal horn of the spinal cord, the site of integration of somatosensory information. Immunohistochemical studies revealed an early-onset activation of astrocytes and microglia that worsened with age, associated later in age with perturbation of the expression of the sensory neuropeptides calcitonin-gene-related peptide and galanin. Taken together, these results represent complementary data supporting the hypothesis that Plp-null mice suffer from ganglionopathy associated with late onset central demyelination but with few peripheral nerve alterations, induced by the glial-cell-mediated sensitization of the spinal cord. The mechanism suggested here could underlie pain experiments in other leukodystrophies as well as in other non-genetic demyelinating diseases such as multiple sclerosis.

後脛骨神経刺激による末梢伝導速度・脊髄伝導速度・中枢伝導速度の測定と臨床応用

後脛骨神経刺激による末梢伝導速度・脊髄伝導速度・中枢伝導速度の測定と臨床応用

Patterns of contact heat evoked potentials (CHEP) in neuropathy with skin denervation: Correlation of CHEP amplitude with intraepidermal nerve fiber density

ObjectiveContact heat evoked potentials (CHEPs) provide an objective approach to investigate cerebral responses to thermal stimuli mediated by Aδ fibers. Skin denervation is often associated with reduced thermal sensibilities. We aimed to investigate the influences of skin denervation on CHEPs in neuropathic patients. MethodsCHEPs were recorded at the vertex area by applying contact heat stimuli of 51°C on the distal leg of neuropathic patients with sensory symptoms and pathological evidence of skin denervation in the distal leg. Patterns and parameters of CHEPs in the neuropathic group were compared with those in the control group of age- and gender-matched subjects. ResultsThere were 25 neuropathic patients with reduced intraepidermal fiber (IENF) density (1.46±1.70fibers/mm, range: 0–5.32). In the control group, well-defined averaged tracings of CHEPs with an initial negative peak (N-wave) followed by a positive peak (P-wave) were consistently recorded in all 25 subjects. The peripheral conduction velocities of CHEPs were 9.92±4.06m/s (range: 6.06–16.60), in the range of Aδ fibers. The group of neuropathic patients had markedly reduced N–P amplitudes (p<0.0001) and prolonged N-wave latencies (p=0.049) compared to the control group. IENF density was the only neuropathic parameter correlated with N–P amplitude on multiple linear regression analysis (p=0.010) compared to large-fiber parameters. ConclusionsIn neuropathic patients with pathological evidence of skin denervation, there were reduced amplitude and prolonged latencies in CHEPs mediated by Aδ fibers. The reduction of CHEP amplitude corresponded to the degree of skin denervation. SignificanceCHEP offers electrophysiological evidence of thermal responses and provides an objective, non-invasive approach to assess the physiological counterparts of skin denervation in neuropathic patients.

Pain Processing Is Faster than Tactile Processing in the Human Brain

Pain signals threat and drives the individual into a behavioral response that significantly depends on a short stimulus-response latency. Paradoxically, the peripheral and spinal conduction velocities of pain are much slower than of tactile information. However, cerebral processing times and reaction times of touch and pain have not yet been fully assessed. Here we show that reaction times to selective nociceptive cutaneous laser stimuli are substantially faster than expected from the peripheral conduction velocities. Furthermore, by using magnetoencephalography, we found that latencies between earliest stimulus-evoked cortical responses and reaction times are approximately 60 ms shorter for nociceptive than for tactile stimuli. These findings reveal that cerebral processing of pain is substantially faster than processing of tactile information and relatively compensates for the slow peripheral and spinal conduction velocities of pain. Our observation shows how the cerebral organization of pain processing enhances motor responses to potentially harmful stimuli and thereby subserves the particular behavioral demands of pain.

Glial Cell Line-Derived Neurotrophic Factor Expression in Skin Alters the Mechanical Sensitivity of Cutaneous Nociceptors

Neurons classified as nociceptors are dependent on nerve growth factor (NGF) during embryonic development, but a large subpopulation lose this dependence during embryonic and postnatal times and become responsive to the transforming growth factor beta family member, glial cell line-derived growth factor (GDNF). To elucidate the functional properties of GDNF-dependent nociceptors and distinguish them from nociceptors that retain NGF dependence, the cellular and physiologic properties of sensory neurons of wild-type and transgenic mice that overexpress GDNF in the skin (GDNF-OE) were analyzed using a skin, nerve, dorsal root ganglion, and spinal cord preparation, immunolabeling, and reverse transcriptase-PCR assays. Although an increase in peripheral conduction velocity of C-fibers in GDNF-OE mice was measured, other electrophysiological properties, including resting membrane potential and somal action potentials, were unchanged. We also show that isolectin B4 (IB4)-positive neurons, many of which are responsive to GDNF, exhibited significantly lower thresholds to mechanical stimulation relative to wild-type neurons. However, no change was observed in heat thresholds for the same population of cells. The increase in mechanical sensitivity was found to correlate with significant increases in acid-sensing ion channels 2A and 2B and transient receptor potential channel A1, which are thought to contribute to detection of mechanical stimuli. These data indicate that enhanced expression of GDNF in the skin can change mechanical sensitivity of IB4-positive nociceptive afferents and that this may occur through enhanced expression of specific types of channel proteins.

Peripheral axon caliber and conduction velocity are decreased after burn injury in mice

Peripheral neuropathies are reported to arise as a result of the systemic inflammatory response produced by a full-thickness cutaneous burn injury. This study was designed to characterize the magnitude and time course of functional and morphological changes in peripheral axons that arise after a full-thickness dermal burn injury in an animal model. A 20% body surface area (20% BSA) full-thickness dermal burn was applied to the back of C57BL6 female mice. Longitudinal H- and M-wave recordings were used to determine the conduction velocities (CV) of large myelinated motor and sensory axons in the tibial nerve of sham control and burn-injured mice. Motor CVs were significantly reduced from 6 h to 28 days after the burn, and sensory CVs were significantly reduced from 7 to 14 days after the burn. Morphological evaluation also showed that the mean caliber of large axons in tibial nerves and L5 ventral and dorsal roots in burned mice was significantly decreased. The results demonstrate that both functional and morphological deficits may be produced in peripheral nerve axons at sites well removed from a full-thickness dermal burn injury. The neural deficits may contribute to changes in neuromuscular transmission and the development of limb and respiratory muscle weakness that also accompany burn injury.

A comparative magnetoencephalographic study of cortical activations evoked by noxious and innocuous somatosensory stimulations

We recorded somatosensory-evoked magnetic fields and potentials produced by painful intra-epidermal stimulation (ES) and non-painful transcutaneous electrical stimulation (TS) applied to the left hand in 12 healthy volunteers to compare cortical responses to noxious and innocuous somatosensory stimulations. Our results revealed that cortical processing following noxious and innocuous stimulations was strikingly similar except that the former was delayed approximately 60 ms relative to the latter, which was well explained by a difference in peripheral conduction velocity mediating noxious (Aδ fiber) and innocuous (Aβ fiber) inputs. The first cortical activity evoked by both ES and TS was in the primary somatosensory cortex (SI) in the hemisphere contralateral to the stimulated side. The following activities were in the bilateral secondary somatosensory cortex (SII), insular cortex, cingulate cortex, anterior medial temporal area and ipsilateral SI. The source locations did not differ between the two stimulus modalities except that the dipole for insular activity following ES was located more anterior to that following TS. Both ES and TS evoked vertex potentials consisting of a negativity followed by a positivity at a latency of 202 and 304 ms, and 134 and 243 ms, respectively. The time course of the vertex potential corresponded to that of the activity of the medial temporal area. Our results suggested that cortical processing was similar between noxious and innocuous stimulation in SI and SII, but different in insular cortex. Our data also implied that activities in the amygdala/hippocampal formation represented common effects of noxious and tactile stimulations.

Pain-related magnetic fields evoked by intra-epidermal electrical stimulation in humans

Objectives: We recently developed a new method for the preferential stimulation of Aδ fibers in humans. The aim of the present study was to examine whether this method can serve as an appropriate stimulus in a magnetoencephalographic study. Methods: We recorded somatosensory-evoked magnetic fields (SEFs) following intra-epidermal electrical stimulation applied to the hand and elbow. Superficial parts of the skin were electrically stimulated through a needle electrode whose tip was inserted in the epidermis. Results: In all 13 subjects, the equivalent current dipole was estimated in the secondary somatosensory cortices (SII). In 5 out of 13 subjects, simultaneous activation of the primary somatosensory cortex (SI) in the hemisphere contralateral to the stimulation was identified. The mean peak latencies of magnetic fields corresponding to contralateral SI, SII and ipsilateral SII activation following hand stimulation were 162, 158 and 171 ms, respectively. The respective latency following elbow stimulation was 137, 139 and 157 ms, respectively. Estimated peripheral conduction velocity was 15.6 m/s. Conclusions: All the results were consistent with previous findings in pain SEF studies. We concluded that our novel intra-epidermal electrical stimulation is useful for pain SEF studies since it does not need special equipment and is easy to control.

Exhausting fatigue influences F-wave and peripheral conduction velocity, following lumbar radiculopathy

Purpose : The purpose of the study was to determine whether mechanical nerve root compression could indirectly contribute to early muscle fatigue because of impaired activation. Method : The patients' two legs and the control group's dominant leg were subjected to exhausting foot dorsiflexion against 2 kg weight. Electrophysiological parameters were measured under three conditions: before, upon completion of, and five minutes after the exhausting effort (i.e. causing unbearable fatigue). The study was performed in a warm room (24°C), in the EMG laboratory of a rehabilitation centre using standard equipment. Eighteen patients participated in the study (12 males and six females, mean age 47.8 - 12.0 years). They suffered from lumbar radiculopathy and unilateral complaints at the L4, L5 innervation territory. There were 22 matched controls (18 males and 4 females, mean age 44.4 - 9.9 years) that were healthy subjects. The patients' two legs and the dominant leg of the control participants were tested. The peroneal nerve was stimulated supra-maximally, behind the fibular head. Recording the activity of the anterior tibial muscle served to calculate F-wave latency, the conduction velocity of the nerve and muscle complex (NMCV), the compound muscle action potential (CMAP) amplitude and the exhaustion time. Results : Following the exhausting fatigue, the symptomatic, asymptomatic, and control legs exhibited a significant decrease in NMCV and reduced CMAP amplitude ( p < 0.05). In each condition (rest, effort, recovery), the patients' two leg types exhibited similar NMCV (symptomatic vs asymptomatic), yet each of these two types was significantly slower than the controls' NMCV. A significant prolongation of F-wave latency after an exhausting effort was found in the symptomatic legs. Conclusions : Our results suggest that a continuous exhausting effort impairs F-wave latency and NMCV, presumably by decreasing the proportion of fast conducting nerve fibres. Peroneal nerve root compression can contribute to early fatigue of the respective muscles.

The therapeutic effect of Lipo PGE 1 on diabetic neuropathy-changes in endothelin and various angiopathic factors

A high blood concentration of endothelin (ET)-1 may participate in the onset and progress of diabetic microangiopathy, resulting in neuropathy. We examined the therapeutic effects of prostaglandin E1 (PGE1), which possesses both a peripheral vasodilating action and inhibition of platelet aggregation, on diabetic microangiopathy. Increases in both skin temperature and peripheral never conduction velocity in diabetic patients were recorded four weeks after Lipo PGE1 administration. A quantitative decrease in urinary albumin concentration was also observed, suggesting its efficacy of action was on diabetic nephropathy. Lipo PGE1 administration reduced the elevated circulating plasma ET-1 levels in the diabetic patients. As an increase in ET-1 concentrations is thought to correlate with the onset and progress of diabetic microangiopathy, the reduction of plasma ET-1 concentration by Lipo PGE 1 administration may be one reason for the improvement in diabetic neuropathy and nephropathy.

The Progression of Uremic Polyneuropathy in Patients on Hemodialysis and Hemofiltration: A Two-Year Study.

Uremic polyneuropathy is one of the major complications of long-term end-stage renal disease. In the present study, we performed an electrophysiologic evaluation in 17 patients having a mean age of 49 ± 11 years. The patients were divided into two groups according to dialysis method. Group A included 9 patients who were undergoing conventional hemodialysis (mean age, 44.2 ± 12.5 years; mean duration on dialysis, 21.7 ± 4.3 months); group B included 8 patients undergoing hemofiltration (mean age, 55.2 ± 5.2 years; mean duration on treatment, 27 ± 7.6 months). Measurements of the distal latency time of the sensory fibers (median, ulnar, and sural nerves), and measurements of the distal latency time and peripheral conduction velocity of the motor fibers (median and peroneal nerves) were performed. In addition, we recorded somatosensory evoked potentials after peripheral stimulation of the median and peroneal nerves. The electrophysiologic evaluations were repeated two times at intervals of 12 months. In group A, a statistically significant worsening of motor and sensory conductance in the upper and lower limbs was observed; in group B, a statistically significant improvement was found. These findings suggest that hemofiltration has a more beneficial effect on motor and sensory conductivity than does conventional hemodialysis.

Peripheral And Central Conduction Abnormalities In Diabetes Mellitus

Objectives: To investigate peripheral and central somatosensory conduction in diabetic patients. Methods: We recorded sensory nerve action potentials and 5‐channel somatosensory evoked potentials (SEPs) with non‐cephalic reference after median nerve stimulation in 55 diabetic patients and 41 age/height matched normal subjects. We determined onset latencies of the spinal N13‐P13 and the cortical N20‐P20 components, and obtained the central conduction time (CCT). Results: Onset latencies of all SEP components were prolonged in diabetic patients. The mean onset CCT in the diabetic group was 6.3 ± 0.5ms (mean ± SD), being significantly longer than that in the control group (6.1 ± 0.2 ms). The peripheral sensory conduction velocity was also decreased in the diabetic group, but there was no significant correlation between peripheral conduction slowing and the onset CCT prolongation. Conclusions: Diabetes affects conductive function in the central as well as peripheral somatosensory pathways. The CCT abnormality does not coincide with lowering of the peripheral sensory conduction. The present results do not favor the hypothesis that a central‐peripheral distal axonopathy plays an important role in development of diabetic polyneuropathy.