Conduction Velocity Of Nerve Fibers Research Articles

Myelin histology: a key tool in nervous system research.

The myelin sheath is a lipoprotein-rich, multilayered structure capable of increasing conduction velocity in central and peripheral myelinated nerve fibers. Due to the complex structure and composition of myelin, various histological techniques have been developed over the centuries to evaluate myelin under normal, pathological or experimental conditions. Today, methods to assess myelin integrity or content are key tools in both clinical diagnosis and neuroscience research. In this review, we provide an updated summary of the composition and structure of the myelin sheath and discuss some histological procedures, from tissue fixation and processing techniques to the most used and practical myelin histological staining methods. Considering the lipoprotein nature of myelin, the main features and technical details of the different available methods that can be used to evaluate the lipid or protein components of myelin are described, as well as the precise ultrastructural techniques.

Serum Uric Acid Levels Are Related to Diabetic Peripheral Neuropathy, Especially for Motor Conduction Velocity of Tibial Nerve in Type 2 Diabetes Mellitus Patients.

Oxidative stress is one of the most critical factors that contribute to the pathogenesis of neuronal damage, including diabetic peripheral neuropathy (DPN). Uric acid is a kind of natural antioxidant that plays a major role in the antioxidant capacity against oxidative stress. Here, we aim to determine the role of serum uric acid (SUA) in the DPN of patients with type 2 diabetes mellitus (T2DM). Patients and Methods. 106 patients with T2DM were recruited and divided into the DPN group and the control group. Clinical parameters, especially for motor nerve fiber conduction velocity and sensory nerve fiber conduction velocity, were collected. Differences between T2DM patients with and without DPN were compared. Correlation and regression analyses were performed to explore the association between SUA and DPN. Compare with 57 patients with DPN, 49 patients without DPN showed lower HbA1c and elevated SUA levels. Additionally, SUA levels are negatively associated with the motor conduction velocity of tibial nerve with or without adjusting for HbA1c. Besides, it is suggested that decreased SUA levels may influence the motor conduction speed of the tibial nerve by multiple linear regression analysis. Moreover, we demonstrated that decreased SUA level is a risk factor for DPN in patients with T2DM by binary logistic regression analysis. Lower SUA is a risk factor for DPN in patients with T2DM. Additionally, decreased SUA may influence the damage of peripheral neuropathy, especially for motor conduction velocity of the tibial nerve.

Motorische Neurografie und Reflexstudien: Wegweiser der klinischen Elektrophysiologie

Würdigung der Publikation: Electrophysiological studies of nerve and reflex activity in normal man I. Identification of certain reflexes in the electromyogram and the conduction velocity of peripheral nerve fibers

Overexpression of Sirtuin 1 protein in neurons prevents and reverses experimental diabetic neuropathy.

In diabetic neuropathy, there is activation of axonal and sensory neuronal degeneration pathways leading to distal axonopathy. The nicotinamide-adenine dinucleotide (NAD+)-dependent deacetylase enzyme, Sirtuin 1 (SIRT1), can prevent activation of these pathways and promote axonal regeneration. In this study, we tested whether increased expression of SIRT1 protein in sensory neurons prevents and reverses experimental diabetic neuropathy induced by a high fat diet (HFD). We generated a transgenic mouse that is inducible and overexpresses SIRT1 protein in neurons (nSIRT1OE Tg). Higher levels of SIRT1 protein were localized to cortical and hippocampal neuronal nuclei in the brain and in nuclei and cytoplasm of small to medium sized neurons in dorsal root ganglia. Wild-type and nSIRT1OE Tg mice were fed with either control diet (6.2% fat) or a HFD (36% fat) for 2 months. HFD-fed wild-type mice developed neuropathy as determined by abnormal motor and sensory nerve conduction velocity, mechanical allodynia, and loss of intraepidermal nerve fibres. In contrast, nSIRT1OE prevented a HFD-induced neuropathy despite the animals remaining hyperglycaemic. To test if nSIRT1OE would reverse HFD-induced neuropathy, nSIRT1OE was activated after mice developed peripheral neuropathy on a HFD. Two months after nSIRT1OE, we observed reversal of neuropathy and an increase in intraepidermal nerve fibre. Cultured adult dorsal root ganglion neurons from nSIRT1OE mice, maintained at high (30 mM) total glucose, showed higher basal and maximal respiratory capacity when compared to adult dorsal root ganglion neurons from wild-type mice. In dorsal root ganglion protein extracts from nSIRT1OE mice, the NAD+-consuming enzyme PARP1 was deactivated and the major deacetylated protein was identified to be an E3 protein ligase, NEDD4-1, a protein required for axonal growth, regeneration and proteostasis in neurodegenerative diseases. Our results indicate that nSIRT1OE prevents and reverses neuropathy. Increased mitochondrial respiratory capacity and NEDD4 activation was associated with increased axonal growth driven by neuronal overexpression of SIRT1. Therapies that regulate NAD+ and thereby target sirtuins may be beneficial in human diabetic sensory polyneuropathy.

Signal Modeling and Simulation of Temporal Dispersion and Conduction Block in Motor Nerves.

Electroneurography is a well-established diagnostic test for supporting the diagnosis of disorders of myelinated peripheral nerves. Neurophysiological quantities are automatically calculated and are used to determine the pathology of the nerve (axonal damage) or its sheath (myelin damage). Specific differential diagnostic criteria are derived from time-domain normative data, which result primarily from a computer simulation in the early 1990s based on animal data, namely rats. However, the rat signals studied differ significantly from those of humans because of anatomical differences. We present a model-based simulation of nerve conduction in healthy and pathological motor nerves. In contrast to earlier simulations, the present model is based on motor unit action potentials extracted from real human measurements facilitating the generation of realistic signals, starting from a conduction velocity distribution. In addition to the modeling of healthy nerves, we model a hereditary peripheral nerve disease as well as an acute and a chronic inflammatory demyelinating condition. Quantitative signal differences based on standard variables in the time-domain are presented. The findings for the demyelinating conditions demonstrate amplitude reductions of 71% and 65% between the distal and proximal responses, which result from an increase in the variance of the nerve fiber conduction velocities. The simulation results closely match those of empirical measurements, indicating that the signal model captures relevant pathological mechanisms. An amplitude reduction of more than 50% in demyelinating conditions is in accordance with routine measurements and shows that temporal dispersion is quite well-modeled compared to previous simulation models. The simulation outcomes can serve as the basis for an improved pathophysiological understanding of peripheral nerve disorders and should aid neurophysiologists to refine their diagnostic armamentarium resulting in a more precise differential diagnosis.

Neural Stem Cell Transplantation Improves Locomotor Function in Spinal Cord Transection Rats Associated with Nerve Regeneration and IGF-1 R Expression

Transplantation of neural stem cells (NSCs) is a potential strategy for the treatment of spinal cord transection (SCT). Here we investigated whether transplanted NSCs would improve motor function of rats with SCT and explored the underlying mechanism. First, the rats were divided into sham, SCT, and NSC groups. Rats in the SCT and NSC groups were all subjected to SCT in T10, and were administered with media and NSC transplantation into the lesion site, respectively. Immunohistochemistry was used to label Nestin-, TUNEL-, and NeuN-positive cells and reveal the expression and location of type I insulin-like growth factor receptor (IGF-1 R). Locomotor function of hind limbs was assessed by Basso, Beattie, Bresnahan (BBB) score and inclined plane test. The conduction velocity and amplitude of spinal nerve fibers were measured by electrophysiology and the anatomical changes were measured using magnetic resonance imaging. Moreover, expression of IGF-1 R was determined by real-time polymerase chain reaction and Western blotting. The results showed that NSCs could survive and differentiate into neurons in vitro and in vivo. SCT-induced deficits were reduced by NSC transplantation, including increase in NeuN-positive cells and decrease in apoptotic cells. Moreover, neurophysiological profiles indicated that the latent period was decreased and the peak-to-peak amplitude of spinal nerve fibers conduction was increased in transplanted rats, while morphological measures indicated that fractional anisotropy and the number of nerve fibers in the site of spinal cord injury were increased after NSC transplantation. In addition, mRNA and protein level of IGF-1 R were increased in the rostral segment in the NSC group, especially in neurons. Therefore, we concluded that NSC transplantation promotes motor function improvement of SCT, which might be associated with activated IGF-1 R, especially in the rostral site. All of the above suggests that this approach has potential for clinical treatment of spinal cord injury.

PO-177 Effect of rational exercise on delaying brain aging and its mechanism analysis

Objective Aging is an inevitable rule in the process of life. When human growth and development mature, with the increase of age, the organs and organs of the body will have functional and morphological degenerative changes. China has now entered an aging society, and the aging related diseases are increasing, and the aging of the brain and related diseases are one of the main reasons for the decline of the quality of life of the elderly. It is particularly important to study methods of delaying brain aging. The development of physical exercise to promote the development of brain health has become a hot spot. Appropriate exercise can effectively improve the normal physiological function of the hippocampus neurons, delay the aging process of the central nervous system, and explore the effect of physical exercise on the brain senescent patients and its mechanism of action is very necessary.
 Methods  Through the retrieval of Chinese knowledge network, Wanfang Data knowledge service platform, VVP cube knowledge discovery system, 100 chain database collection sports related research literature on brain senescence, collating literature information, in-depth integration of literature, analysis of the effect of physical exercise on brain aging and mechanism.
 Results  (1) The brain is the most advanced part of the central nervous system, and the structure and function of the brain are very complex, and each brain region bears the corresponding function, in which the hippocampus is considered to be related to the learning and memory function. The aging of the central nervous system plays a leading role in the aging of the body, and its pathological changes are mainly found in the cerebral cortex and hippocampus. After the growth of the mature period, the myelin development in the brain is damaged, the brain myelin development is damaged, the nerve cells atrophy, the intracellular lipofuscin accumulates, the synaptic connections and the neurotransmitters decrease, and the ability to accept and transmit information is reduced, and the specific expression is reaction retardation, intelligence, learning, memory, analysis, judgment and push. The attenuation of the ability to be reasonable. Brain senescence is often accompanied by changes in brain weight, brain nerve cells, nerve fiber conduction velocity and brain cell dysfunction. It is a complex process, and any single factor can not explain its mechanism. In recent years, with the rapid development and promotion of molecular biology and cell biology, great progress has been made in the study of aging, and some theories about aging are put forward. The mechanism of aging of brain mainly includes the following theories: the free radical damage theory, the theory of genetic mutation, the theory of end grain loss, the theory of mitochondria, and the protein. Qualitative change theory, waste accumulation theory, aging network theory and so on. At present, free radical damage and telomere theory are widely recognized. In recent years, nonenzymatic glycosylation has also made great progress.
 (2) The hippocampus, the marginal system in the nervous system, is an important brain area for learning and memory. It plays a key role in the memory of various new knowledge, and the brain senescence is closely related to it. Aging related memory changes were positively correlated with activity changes in the two brain regions of the prefrontal cortex and hippocampus. In the hippocampus, dentate gyrus is the most serious subregion affected by aging. The hippocampus and prefrontal cortex are highly susceptible to aging. Therefore, the ability of brain control tasks will decrease correspondingly with the increase of age. The cerebral cortex is the high pole center of the human body's functional activities, is the area where neurons are concentrated, and is the material basis of people's thinking activities. The cerebral cortex analyses and synthesizes various stimuli from the internal and external environment of the body, produces sensations, thoughts, and establishes language and governing actions. The cerebral cortex, as part of the brain tissue, also enters the old age with aging.
 (3) Appropriate exercise can improve the state of brain senescence to a certain extent, and even reverse the decrease of the number of peripheral nerve terminal branches caused by aging. The effect of exercise intensity and duration on the hippocampus is very important. The exercise that has protective effects on the hippocampus is usually a small intensity and longer duration of exercise. Long term exercise can reverse the loss of the cholinergic fibers in the senescence process and promote the lateral shoots, and the content of synaptophysin in the hippocampus follows the age of age. Decline, long term exercise can delay the decrease of synaptophysin, promote the increase of neurons and the proliferation of dendrites, clarify the mechanism of motion retarding the aging effect of brain, and postpone brain senescence to promote the compensatory effect of the structure of central nervous system (CNS).
 (4) Exercise is one of the means to interfere with the aging of the brain. It is observed by electrical stimulation that some regions of the cerebral cortex have a close relationship with physical movement. Electrical stimulation of some regions of the cerebral cortex can cause some muscle contraction in certain parts of the cerebral cortex, and exercise can increase the thickness of the cerebral cortex. Increase the nerve cell dendrites of the brain. Exercise can promote the dynamic balance of free radical metabolism, enhance the ability to clear free radicals in the body, enhance the antioxidant capacity of the cerebral cortex, and improve the antioxidant capacity of brain cells.
 (5) Reasonable exercise can promote metabolism, enhance vitality, improve cardiovascular function and enhance immunity. Exercise can also protect animals from premature death, thereby prolonging the survival time of animals. The study of the effect of exercise on the peripheral nervous system shows that long term exercise can delay the morphological changes of the senescence related neuromuscular junction (NMJ) in rodents, promote the release of neurotransmitters in the end of exercise, and even reverse the decline of the age related peripheral nerve terminal branches. Exercise can improve psychomotor dysfunction with age by delaying the decline of age-related dopamine system function. Long-term moderate exercise can reduce the loss of neurons in the anterior horn of the spinal cord in the process of aging, and motor has a protective effect on neurons. Moreover, exercise can improve spatial learning behavior, and clearly shows the positive role of exercise in the prevention and treatment of brain aging. Exercise with different loads has a certain effect on scavenging free radicals in the brain and reducing lipid peroxidation level in the brain, thus delaying brain aging.
 Conclusions  Hippocampus and prefrontal cortex are particularly susceptible in many regions of aging. Appropriate exercise can improve the state of brain senescence to a certain extent, and even reverse the decrease in the number of peripheral nerve terminal branches caused by aging. Looking at the history of the study of the action of the motion to the organism, it can be seen that there are two obvious trends in the study. One is the function of the movement to the system of the circulation system, the immune system of the motion system, and the two is the whole organ and molecule level of the movement. Therefore, only after a comprehensive understanding of the molecular mechanism of the action of the movement on the central nervous system, it is possible to fully and accurately elucidate the mechanism of action, and only in this way can we establish the position of motion in delaying brain aging.

ФУНКЦИОНАЛЬНАЯ ДИАГНОСТИКА И ИГЛОРЕФЛЕКСОТЕРАПИЯ У ПАЦИЕНТОВ С ОСТЕОХОНДРОЗОМ ШЕЙНОГО ОТДЕЛА ПОЗВОНОЧНИКА

We developed an algorithm for spinal diagnostics to optimize the diagnosis and treatment of patients with cervical osteochondrosis. This algorithm includes physical and neurological examination of a patient, radiological methods, multi-layer spiral CT (MRI) of cervical spine, densitometry and electroneuromyography (ENMG) and is used in practical work of neurosurgical unit of Irkutsk Scientific Center of Surgery and Traumatology. We managed 40patients with cervical osteochondrosis in period I–III localized in CIII–CIV, CIV–CV, CV–CVI, CVI–CVII segments and with severe muscular tonic syndrome (cervicalgia, cervical cranialgia, cervicobrachialgia). Patients with osteochondrosis in period I–II had medium decreased conduction of peripheral nerve motor fibers on both sides of spine, which indicates the lesion of some motor fibers. In patients with osteochondrosis in period III in case of protrusion and herniation of intervertebral discs the ENMG values corresponded to the increase in neurility and conduction velocity of motor nerve and muscle fibers in diseased segment.Conservative treatment was conducted up to the Standard approved by the Ministry of Health of the Russian Federation and was supplemented with acupuncture (9–10 sessions) based on the changes in ENMG values. Performed treatment caused significant decrease in pain syndrome, reduction of neurological manifestations and, as a consequence, positive dynamics of ENMG values. Proposed algorithm for management of patients with osteochondrosis allowed to diagnose the localization of diseased functional spinal unit, to reveal problem peripheral nerves and, as a result, to choose adequate treatment tactics and to estimate its effectiveness.

Distribution of Conduction Velocity (DCV) from measured F-Wave Latency for detection of cervical spondylotic radiculopathy and myelopathy (CRM)

In the previous work of our extended group at Dhaka, Distribution of Conduction Velocity (DCV) of motor nerve fibres in a peripheral nerve trunk was established as an approximate mirror image of Distribution of F-Latency (DFL), for which consecutive 30 to 40 F-latencies were used through multiple stimulation of a peripheral nerve trunk. Using patterns of DFL a considerable amount of experience has been built up in the detection of Cervical Spondylotic Radiculopathy and Myelopathy (CRM). In the present work we have obtained DCV directly from the Conduction Velocity (CV) values obtained from each of the F-latencies. Because of the inverse relationship between latency and velocity, a small variation to the mirror image should be present, particularly when discrete bin widths are used to obtain the frequency distribution. Therefore, one challenge was to choose an appropriate bin width while obtaining DCV directly so that the patterns can be related to those of DFL easily for the detection of CRM. To obtain DFL our extended group at Dhaka had used a bin width of 2 ms which gave good results. To choose a corresponding bin width for DCV four recognized measures of central tendency: Average of the range, Median, Mode and Mean (weighted average) were used and the resulting patterns of DCV were compared to that of DFL to determine the percentage of matches with respect to the detection of CRM. It was observed that Median gave the best DCV with 89% matches followed closely by Mode giving 83% match. The other two gave much lower values, 67% and 50%. Therefore, median value gave the best match which could be used to obtain DCV from the CV values directly, for the determination of CRM.Bangladesh Journal of Medical Physics Vol.7 No.1 2014 56-65

Motor nerve impairment in diabetic patients with symmetrical distal sensory polyneuropathy: A single nerve fiber conduction velocity study

In this study we investigated the clinical utility of single fiber conduction velocity (SF-CV) testing in the evaluation of motor nerve function in diabetic patients with signs and symptoms of symmetrical distal sensory polyneuropathy (DSP). SF-CV findings were compared with conventional nerve conduction studies (NCS). Twenty-eight consecutive type 2 diabetic patients with clinically diagnosed DSP were studied. SF-CV testing of the tibial nerve was abnormal in 16 (57.1%) patients. Twelve patients with normal conventional motor NCS had abnormal findings by tibial SF-CV. SF-CV testing of the tibial nerve was significantly superior to all other motor NCS. SF-CV testing of the tibial nerve often demonstrates motor nerve impairment in diabetic patients with sensory DSP when conventional NCS are normal.

Use of Distribution of F-Latency (DFL) in the Detection of Cervical Spondylotic Neuropathy

Distribution of F-latencies (DFL) is a new nerve conduction parameter introduced by our laboratory to give a distribution of the conduction velocity (DCV) of motor nerve fibres in a peripheral nerve trunk simply as its mirror image. Earlier work revealed an association between Cervical Spondylotic (CS) neuropathy and DFL patterns obtained from the thenar muscle at the base of the thumb by artificially stimulating the median nerve. DFL froom normal subjects had a single peaked pattern, while that from subjects with CS had double or triple peaks, or a broad peak. The broad peak was suggested to be an indicator of early CS, even when the symptoms are not fully apparent. This led to some hypotheses based on physics, physiology and statistics, in order to explain such patterns. In order to verify these hypotheses, experiments need to be carried out carefully, and the present work is a step towards that goal. In this work DFL of the median nerve was obtained from 15 subjects, 6 normal, and 9 with diagnosed cervical spondylosis. The latter were subjected to further X-ray and MRI investigations, performed blindly at regular clinics. All of the 9 subjects were identified with either compression of nerve roots (radiculopathy), or spinal cord compression due to the bulging of the inter-vertebral discs (myelopathy). This shows with confidence that double or triple peaks of DFL indeed relates to CS, and broad peaks indicate their early stage. The same concept may be extended to other peripheral nerves, both in the hands and legs. Thus DFL may become an important screening test for neuropathy, as a first choice, offering a low cost and widely available test compared to the only other alternative, MRI, for such diagnosis. DOI: http://dx.doi.org/10.3329/bjmp.v4i1.14676 Bangladesh Journal of Medical Physics Vol.4 No.1 2011 37-42

Characteristics of Lower Urinary Tract Dysfunction and Bladder Afferent Nerve Properties in Type 2 Diabetic Goto-Kakizaki Rats

We investigated longitudinal changes in lower urinary tract function, especially sensory function, in the type 2 diabetes mellitus model of Goto-Kakizaki rats. We used 16 Wistar and 16 Goto-Kakizaki rats. Body weight, blood glucose, 24-hour voiding frequency-volume data and cardiovascular system data were measured every 3 weeks starting at age 5 weeks until age 14 weeks and then every 6 weeks until age 44 weeks. At ages 10 and 46 weeks conscious cystometry was done, pelvic afferent nerve fiber conduction velocity was measured using urethane anesthesia and isolated detrusor smooth muscle function was determined. Goto-Kakizaki rats showed lower body weight, higher blood glucose and mean voided volume, and less voiding frequency than Wistar rats throughout the observation period. In 46-week-old Goto-Kakizaki rats lower peak micturition pressure, larger bladder capacity and higher bladder compliance were noted on cystometry, while slower conduction velocity and a lesser proportion of Aδ fibers were observed on conduction velocity measurement. Goto-Kakizaki rats showed a lower contractile response to carbachol but not to electrical field stimulation or high K(+) in isolated detrusor smooth muscle. These differences between the 2 groups of rats at age 46 weeks were not noted at age 10 weeks. Cardiovascular system results did not differ between the 2 groups. The results of this longitudinal study in Goto-Kakizaki rats indicate that type 2 diabetes induces bladder sensory dysfunction, manifesting as slower bladder afferent conduction velocity, larger bladder capacity and greater hypocontractility to acetylcholine.

Methylglyoxal Activates Nociceptors through Transient Receptor Potential Channel A1 (TRPA1): A POSSIBLE MECHANISM OF METABOLIC NEUROPATHIES

Neuropathic pain can develop as an agonizing sequela of diabetes mellitus and chronic uremia. A chemical link between both conditions of altered metabolism is the highly reactive compound methylglyoxal (MG), which accumulates in all cells, in particular neurons, and leaks into plasma as an index of the severity of the disorder. The electrophilic structure of this cytotoxic ketoaldehyde suggests TRPA1, a receptor channel deeply involved in inflammatory and neuropathic pain, as a molecular target. We demonstrate that extracellularly applied MG accesses specific intracellular binding sites of TRPA1, activating inward currents and calcium influx in transfected cells and sensory neurons, slowing conduction velocity in unmyelinated peripheral nerve fibers, and stimulating release of proinflammatory neuropeptides from and action potential firing in cutaneous nociceptors. Using a model peptide of the N terminus of human TRPA1, we demonstrate the formation of disulfide bonds based on MG-induced modification of cysteines as a novel mechanism. In conclusion, MG is proposed to be a candidate metabolite that causes neuropathic pain in metabolic disorders and thus is a promising target for medicinal chemistry.

Possible detection of cervical spondylotic neuropathy using Distribution of F-latency (DFL), a new neurophysiological parameter

BackgroundWe have previously reported a new nerve conduction measurement parameter which we named the Distribution of F-latency (DFL) and showed that this was an approximate mirror of the Distribution of Conduction Velocity (DCV) of motor nerve fibers. This work was performed using measurements on the 20 median nerves from 10 volunteers. The DFL showed a number of different patterns including single peaks, broad peaks and double peaks, the latter observed on subjects with Cervical Spondylosis (CS). It was thought that a retrospective analysis of these data could be worthwhile in determining whether Cervical Spondylotic neuropathy could be detected using the DFL.FindingsThe DFL from the 8 median nerves of 4 normal subjects had single peaks, which has been assumed to represent a normal pattern. The DFL from one side of 5 subjects diagnosed with or suspected to have CS had double peaks. Broad peaks were observed in 7 nerves of which 5 were from subjects who had double peaks in the DFL on the contra lateral side.ConclusionsBased on these findings, double peaks in the DFL appear to be associated with CS neuropathy. These findings further suggest that broad peaks in the DFL could indicate the early stages of the disease. Differential compression of nerve branches at the spinal roots are being explored as possible causes. This study does not preclude other pathologies contributing to double or broad peaks, but does suggest that the DFL could form a screening tool for CS neuropathy.

Comparison of Conduction Velocities of Nerve Fibers to Smaller and Larger Muscles in Rats

ABSTRACTThe aim of this study was to compare conduction velocities of motor fibers to smaller and larger muscles and to investigate the advantages and disadvantages of recordings from the gastrocnemius muscle with surface electrodes over the recordings from small foot muscles (interosseous muscles) with needle electrodes in rats. Surface and needle recordings are suitable in measuring the motor conduction velocity of the sciatic (tibial) nerve. It should be noted that the motor velocity measured from the gastrocnemius muscle is higher than the motor velocity elicited from small foot muscles. Surface recordings provide information on the amplitude and duration of M responses.

Morphological evaluation of the human pyramidal tract: Tapering of axons

It is generally accepted that nerve fiber conduction velocity is directly proportional to the fiber diameter under the condition, based on a supposition, that the transverse area of axons is normally maintained constant. Using an ideal preparation method for the purpose of axonal discrimination, we examined 43 human spinal cords after making transverse sections at the cervical, thoracic, lumbar and sacral levels and found a tapering of the axons in the lateral pyramidal tract, as the cross-sectional area of the pyramidal axons showed a definite decrease from the cervical to the sacral levels. Our results contradict the supposition that the transverse area of axons is normally maintained constant, which has for a long time been believed to be true without any evidence for it.

Nociception-related somatosensory evoked potentials in awake dogs recorded after intra epidermal electrical stimulation

At present, the specific neurophysiologic methodology of recording pain-related evoked potentials is considered a most promising approach to objectively quantify pain in man. This study was designed to characterise and evaluate the use of somatosensory evoked potentials to study nociception in a canine model. To this aim, somatosensory evoked potentials were evoked by intra-epidermal electrical stimulation and recorded from the scalp in 8 beagle dogs. Characteristics determined were: (1) the conduction velocities of the peripheral nerve fibres involved, (2) the stimulus intensity response characteristics and (3) the evaluation of possible disturbance of the signals by muscular activity from the hind paw withdrawal reflex (EMG artefact). The results showed (1) the conduction velocities to be in the A-delta fibre range (i.e. fibres involved in nociception), (2) an increase in amplitude and a decrease in latency of the evoked potential following increasing stimulus intensities and (3) the absence of EMG artefact in the signals. These data indicate that the evoked potentials recorded, are related to nociception and thus are suited to quantitatively characterise the perception of noxious stimuli making this model useful for pain- and analgesia-related research.

Establishment of a method of contact heat evoked potential and its application in carpal tunnel syndrome

To establish a method to evoke cerebral potentials by stimulating nociceptive fibers, estimate the conduction velocities of nerve fibers mediating these responses, and assess the value of the potentials in carpal tunnel syndrome. One hundred patients with carpal tunnel syndrome and 20 sex-, and aged-matched healthy persons underwent stimulation of contact heat delivered via a circular thermode to excite selectively nociceptors with a rapid rising time at 70 degrees C/s to elicit pain and contact heat evoked potential (CHEP). Thermal stimuli were sent at two intensity levels (49.5 degrees C and 54.5 degrees C) to three body sites: thenar eminence, dorsum of hand, and proximal volar forearm The CHEPs were recorded from Cz and Pz. The relation between the stimulus intensity and pain rating was observed, and the main components of the evoked potential were recorded. The nerve conduction velocity was calculated from the latency difference of the CHEP and center to center distance of distal and proximal stimulus arrays. The pain intensity ratings were 3.2 +/- 0.3 and 4.4 +/- 0.5 when the thenar eminence was stimulated at the temperature of 49.5 degrees C and 54.5 degrees C respectively; and the ratings were 6.3 +/- 0.8 and 7.2 +/- 0.5 on the dorsum of hand and proximal volar forearm at the temperature of 54.5 degrees C respectively. Three components, Cz/N550, Cz/P750, and Pz/P1000, were found in the evoked potentials. The latency of the CHEP was significantly correlated with the arm length, and not significantly correlated with sex, age, and side difference of the arm. The conduction velocities of the Adelta and C fibers of the carpal tunnel syndrome patients were 12.0 m/s +/- 5.6 m/s and 0.6 m/s +/- 0.1 m/s respectively, both lowered, being 93.8% and 99.5% of those of the healthy persons (12.9 m/s +/- 7.5 m/s and 1.7 m/s +/- 0.4m/s respectively). Elicited reliably, CHEP is mediated by Adelta and C fibers. The conduction velocity of C fibers in the patients with carpal tunnel syndrome is decreased.

The recruitment order of electrically activated motor neurons investigated with a novel collision technique

ObjectiveThe development of a novel collision technique for assessment of the activation order of electrically activated nerve fibers, which is an important question in functional electrical therapy or for interpretation of results of motor unit number estimates. MethodsCompound muscle action potentials were recorded with the belly-tendon configuration from the abductor digiti minimi. A novel modified Hopf’s collision technique was applied on ten healthy male subjects to determine the distributions of conduction velocities (DCV) of all ulnar nerve fibers and of the fibers activated by electrical stimuli eliciting 20%, 50%, and 80% of the maximal muscle response. ResultsThe maximum nerve conduction velocity was (means±SE) 64.1±0.85m/s. The median conduction velocity of estimated DCV was 58.9±0.97m/s (stimulus at 20%), 58.0±0.98m/s (50%), 57.2±0.91m/s (80%), and 56.5±0.84m/s (whole nerve) (all different between each other, P<0.001). ConclusionsThe proposed collision technique allows the assessment of nerve conduction velocity distributions at maximal and sub-maximal stimulation levels and provided evidence for an inverse activation order of nerve fibers with electrical stimulation. SignificanceThe excessive fatigue seen with nerve electrical stimulation can be explained by a preferential activation of large diameter nerve fibers. The motor units first activated with electrical stimulation are likely not representative of the motor unit pool in the muscle, which poses limitations in the reliability of some of the proposed methods for motor unit counting.

A Note on the Local Current Associated with the Rising Phase of a Propagating Impulse in Nonmyelinated Nerve Fibers

To extend our recent paper dealing with the cable properties and the conduction velocity of nonmyelinated nerve fibers (Bull. Math. Biol. 64, 1069; 2002), the behavior of the local current associated with the rising phase of a propagating action potential is discussed. It is shown that the process of charging the membrane capacity by means of the local current plays a crucial role in determining the velocity of nerve conduction. The symmetry of the local current with respect to the boundary between the resting and active regions of the nerve fiber is emphasized. It is noted that there are several simple quantitative rules governing the intensities of the capacitive, resistive and total membrane currents observed during the rising phase of an action potential.