Preserved cutaneous silent periods in severe entrapment neuropathies

Noxious digital nerve stimulation during isometric contraction of hand muscles leads to transient suppression of the electromyographic activity, the so-called cutaneous silent period (CSP), which is mostly due to a spinal reflex mediated by A-delta fibers. We investigated two patients with carpal tunnel syndrome (CTS) and two patients with ulnar entrapment at the elbow (UNE), in whom routine sensory conduction studies failed to document afferent fiber continuity across the lesion site. In three patients, motor nerve conduction studies and electromyography failed to demonstrate intact efferent fibers. Noxious stimulation of digit II elicited distinct CSPs in ulnar-innervated hand muscles in both patients with CTS, and stimulation of digit V evoked CSPs in median-innervated hand muscles in both UNE patients. The presence of a CSP can only be explained by preserved A-delta fibers crossing the respective lesion site. Thus, preserved CSPs may serve to document residual nerve continuity in severe entrapment neuropathies when fast-conducting fibers are so compromised that their continuity cannot be detected by standard electrodiagnostic techniques.     

Normative data of F-wave measures in China

ObjectiveTo establish normal ranges of F-wave measures in China as compared to published data in Brazil and Japan.MethodWe studied F waves in 127 healthy Chinese subjects, aged 21–78 years old, stimulating the median, ulnar, tibial and peroneal nerves distally and proximaly.ResultThe F-wave latencies had a linear correlation to the subject height in all nerves tested, showing a steeper (P < 0.05) regression line in Brazil compared to China and Japan for the tibial nerve. The Chinese population also had a higher distally elicited F-wave persistence and faster F wave conduction velocities than previously reported for both ulnar and tibial nerves. These values showed significant difference (P < 0.05) compared to Brazil but not to Japan.ConclusionF-wave latencies show a linear correlation to subject height, although the slope of regression lines varies among countries, reflecting the difference in F-wave persistence and F-wave conduction velocity.SignificanceOur study provides a rational for the use of a latency-height nomogram in clinical studies and underscores the importance of developing country specific normative data.     

Cutaneous silent period changes in Type 2 diabetes mellitus patients with small fiber neuropathy

ObjectiveSmall myelinated (A-δ) and unmyelinated (C) somatic sensory fibers are initially affected and may be the earliest exhibited sign of neuropathy in glucose dysmetabolism. Cutaneous silent period (CSP) is an inhibitory spinal reflex and its afferents consist of A-δ nerve fibers. The aim of this study was to evaluate CSP changes in Type 2 diabetic patients with small fiber neuropathy.MethodsForty-three patients and 41 healthy volunteers were included. CSP latency and duration, as well as CSP latency difference of the upper and lower extremities, were examined.ResultsNerve conduction studies were within normal limits in both groups. Lower extremity CSP latency was longer (122.1 ± 15.5 vs. 96.4 ± 6.4 ms; p < 0.001), CSP duration was shorter (29.5 ± 8.9 vs. 43.1 ± 5.0 ms; p < 0.001), and latency difference was longer (48.1 ± 12.6 vs. 22.7 ± 3.7; p < 0.001) in patients than controls. The difference was more significant in patients with neuropathic pain. No significant difference existed in upper extremity on CSP evaluation.ConclusionThe CSP evaluation together with nerve conduction study, has been demonstrated to be beneficial and performance of latency difference in addition to CSP latency and duration may be a valuable parameter in electrophysiological assessment of diabetic patients with small fiber neuropathy.SignificanceAn additional CSP evaluation may be considered in cases which nerve conduction studies do not provide sufficient information.     

Differentiation between uniform and non-uniform motor nerve conduction slowing

ObjectiveDemyelination may cause a uniform reduction of the conduction velocity of all fibres of a peripheral nerve segment, or may affect only certain nerve fibres in a non-uniform way while sparing others. This study was done to improve the detection of non-uniform conduction slowing by using the high-frequency attenuation (HFA) method.MethodsNerve conduction data from patients with early inflammatory demyelinating neuropathy (non-uniform demyelination, n = 20), hereditary neuropathy (uniform demyelination, n = 9), motor neuron disease (axon loss, n = 20), and from healthy control subjects (n = 20) were analysed.ResultsHFA, compound muscle action potential (CMAP) amplitude decay, and F-wave chronodispersion correlated significantly. Among these variables both HFA and amplitude decay most sensitively identified non-uniform demyelination (35%). In the patients with uniform demyelination, the most frequent finding was a reduced nerve conduction velocity (NCV) (100%). The most specific marker of non-uniform demyelination was HFA. For uniform demyelination it was NCV.ConclusionsThe pattern of correlations between the variables studied confirms that NCV and F-min are indicators of uniform conduction slowing. HFA, amplitude decay, and F-wave chronodispersion indicate non-uniform conduction slowing, for which HFA is both sensitive and specific.SignificanceThe HFA method improves both the diagnostic sensitivity and specificity of nerve conduction studies in patients with non-uniform demyelination.     

Cutaneous silent periods are not affected by the antihistaminic drug cetirizine

ObjectiveNoxious digital nerve stimulation leads to transient suppression of the electromyographic activity in isometrically contracted hand muscles, known as the “cutaneous silent period” (CSP). To date, neurotransmitters potentially involved in mediating this electromyographic (EMG) suppression remain unknown. Anecdotal observation lead to the hypothesis that antihistaminic medication may counteract nociceptive EMG suppression, as CSPs in one male subject who was accustomed to CSP recordings were temporarily lost following ingestion of an antihistaminic drug for acute rhinitis. A second otherwise healthy male subject, who was on long-term cetirizine for allergic rhinitis, presented without clearly defined CSPs when volunteering for normal values.MethodsWe undertook a systematic study in five healthy subjects (including the one with temporarily lost CSPs) who underwent serial CSP testing after ingestion of 10 mg cetirizine. CSPs were elicited in thenar muscles following digit II and digit V stimulation (20 times sensory threshold, 100 sweeps rectified and averaged) before and 90, 180, and 360 min following intake of medication.ResultsCSP onset latency, CSP end latency and CSP duration, as well as the index of suppression did not change significantly following ingestion of 10 mg cetirizine. Repeat study in the subject with no clearly defined CSPs on long-term treatment revealed persistently absent CSPs after a 5-week withdrawal from cetirizine.ConclusionCSPs are not affected by therapeutic doses of the H1 antihistaminic cetirizine.SignificanceOur findings suggest that histamine plays no major role as a neurotransmitter of CSPs.     

Polyneuropathy induced by HIV disease and antiretroviral therapy

ObjectiveTo investigate the underlying mechanisms of polyneuropathy induced by HIV infection or antiretroviral drugs.MethodsWe tested 100 HIV patients (59 with AIDS). Ninety-three patients received antiretroviral drugs. Forty-four were treated with neurotoxic compounds (ddI, ddC, d4T). Nerve conduction velocities and the sympathetic skin response (SSR) in palms and soles were measured in all patients. In skin biopsies (ankle and thigh), the intraepidermal nerve fiber density (IENFD) and the number of epidermal fibers without contact to the basal membrane (fragments) were quantified using PGP9.5 staining.ResultsSeverity of the disease (CD4 + count) correlated to conduction velocities of peroneal (p < 0.01, Spearmans rank correlation), sural (p < 0.01) and median nerves (p < 0.05/p < 0.001, sensory/motor). In contrast, the duration of neurotoxic treatment did not impair conduction velocities (p > 0.3) but correlated to reduced IENFD in the ankle (r = ?0.24, p < 0.05). Despite their reduced IENFD, patients with long neurotoxic treatment had a high number of fragments irrespective of their CD4 + count.ConclusionsNeurotoxic treatment appears to primarily impair thin fiber conduction, whereas HIV neuropathy is linked to large fiber impairment and reduction of fragments of nerve fibers.SignificanceThese findings emphasize the differential pattern of polyneuropathy in HIV patients caused by the infection or induced by antiretroviral treatment.     

Peripheral neuropathy caused by severe hypothermia

ObjectiveTo report follow-up data in the evaluation of peripheral neuropathy in a 29-year old female after accidental deep hypothermia (13.7 °C) in 1999.MethodsNerve conduction studies (NCS) and electromyography (EMG) were performed 20 days after the accident and again after 5 months and 1, 3, 5 and 11 years. Macro EMG was performed after 3, 5 and 11 years. To evaluate small fiber function, RR-interval, sympathetic skin response, quantitative sensory testing and skin biopsy for quantification of intra-epidermal nerve fiber density were performed in 2009.ResultsIn the intensive care unit sensory and motor responses were absent except for the tibial nerves, and EMG showed profuse denervation. Improvement of amplitudes and conduction velocities was seen during the first 5 years. Muscular atrophy of hand muscles persisted. Large fibers were involved more extensively than small fibers.ConclusionsA severe axonal sensorimotor polyneuropathy developed in the intensive care unit following severe hypothermia. The mechanism was most likely cold injury to peripheral nerves.SignificanceThe clinical picture and the laboratory findings indicate that even multi-organ dysfunction and, of specific interest in this study, a severe axonal degeneration may come to a good restitution after long time.     

Plasticity of lower limb motor axons after cervical cord injury

ObjectiveTo assess changes in peripheral motor excitability after traumatic spinal cord injury (SCI).MethodsConventional nerve conduction and nerve excitability studies were longitudinally investigated in a patient diagnosed as C6 American Spinal Injury Association (ASIA) C incomplete. Recordings were undertaken from the peroneal nerve to tibialis anterior, and the median nerve to abductor pollicus brevis throughout the period of hospital admission.ResultsRecordings were acutely abnormal in common peroneal axons 6 days after injury. Threshold electrotonus was “fanned in”; during the recovery cycle superexcitability was abolished, and refractoriness at 2.5 ms was increased (patient 152.84%; controls 37.13 ± 3.83%). All parameters recovered briefly after surgical stabilization on day 9, before regressing by day 13. Excitability values recovered by day 68 when the patient was discharged ambulant as ASIA D. Recordings remained relatively unaffected in median axons throughout the admission period.ConclusionsDecentralisation after SCI had significant effects on lower limb axons, not attributable to direct trauma. Conversely, median axons remained spared. Modeling of the lower limb excitability changes suggested that interruption of energy-dependent processes contributed to the peripheral abnormalities, perhaps through involvement of upstream transynaptic processes.SignificanceThese findings may suggest the potential for plasticity of peripheral axonal excitability in response to acute SCI.     

Cutaneous silent periods in patients with Fabry disease

We assessed the cutaneous silent period (CSP) in 24 patients with Fabry disease with small-fiber sensory neuropathy and 12 normal subjects to test the hypothesis that small-diameter afferents are responsible for producing the CSP. Sensory nerve conduction studies and quantitative sensory testing for cold and vibration detection thresholds were also measured. Overall, Fabry patients had impaired thermal, but not vibration, detection thresholds, with greatest impairment in the feet. In the upper extremity, CSP latencies, duration, and suppression of electromyographic activity (EMG) did not differ. In the lower extremity, patients had reduced suppression of EMG during the CSP compared to normal controls. CSP durations exhibited a bimodal distribution in patients, including a subset of seven patients with durations shorter than all controls. This subset had profound loss of thermal sensation in the feet, but this was also true of some patients who had normal CSPs. Patients with shortened CSPs had modestly elevated vibration thresholds and reduced sensory potentials in comparison to patients with normal CSPs. Reduced CSPs in Fabry patients are associated with, but not entirely explained by, the severity of small-fiber neuropathy as measured by quantitative sensory testing. The possibility that large-diameter fibers provide a minor contribution to producing the CSP should be considered.     

Effects of water immersion on short- and long-latency afferent inhibition,short-interval intracortical inhibition,and intracortical facilitation

ObjectiveThe aim of the present study was to investigate the effect of water immersion (WI) on short- and long-latency afferent inhibition (SAI and LAI), short-interval intracortical inhibition (SICI), and intracortical facilitation (ICF).MethodsMotor evoked potentials (MEPs) were measured from the first dorsal interosseous (FDI) muscle of fifteen healthy males before, during, and after a 15-min WI at 30 °C up to the axilla. Both SAI and LAI were evaluated by measuring MEPs in response to transcranial magnetic stimulation (TMS) of the left motor cortex following electrical stimulation of the right median nerve (fixed at about three times the sensory threshold) at interstimulus intervals (ISIs) of 20 ms to assess SAI and 200 ms to assess LAI. The paired-pulse TMS paradigm was used to measure SICI and ICF.ResultsBoth SAI and LAI were reduced during WI, while SICI and ICF were not significantly different before, during, and after WI.ConclusionsWI decreased SAI and LAI by modulating the processing of afferent inputs.SignificanceChanges in somatosensory processing and sensorimotor integration may contribute to the therapeutic benefits of WI for chronic pain or movement disorders.     

Cortical excitability in drug naive juvenile myoclonic epilepsy

PurposeTo evaluate the effect of diurnal variability on cortical excitability using single pulse transcranial magnetic stimulation (TMS), in drug naive patients with juvenile myoclonic epilepsy (JME) and to look for any differences in cortical excitability between males and females.MethodsThirty drug-naive patients with JME and 10 healthy controls were studied. Resting motor threshold (RMT), motor evoked potential (MEP), the duration of central motor conduction time (CMCT) and cortical silent period (CSP) were measured, twice, first early in the morning and again in the afternoon of the same day.ResultsDiurnal variation with higher evening values of CMCT and CSP were observed in the control group. In the study group, diurnal variation in RMT, CMCT and CSP was found with higher values in the morning than in control group. However, only the raised values of CSP [mean, 110.7 ms, morning and 96.44 ms, evening] were of statistical significance [p = 0.005, morning and 0.039, evening] as compared to controls. In the study group, males had higher values of RMT, CMCT and CSP than in females. However, the CMCT in males was lower in the evening study than in females. Further, RMT and morning CMCT was lower in females than in controls. In females, the morning CSP [mean, 100.91 ms, morning versus 87.86 ms, evening] was significantly prolonged [p = 0.017, morning versus 0.221, evening] as compared to controls.ConclusionThe study is suggestive of the existence of impaired supraspinal/intracortical inhibitory circuits which may account for the hyperexcitability of the motor system being prominent in the morning among drug naïve patients with JME. In this study, increased activity of cortical inhibitory networks, as evidenced by prolonged cortical silent period existed among drug naïve JME patients, but was found to be significant only in female patients. This may explain the increased seizure susceptibility in this cohort, at this time of the day and an increased manifestation of JME in females.     

Hand-arm vibration syndrome: Clinical characteristics,conventional electrophysiology and quantitative sensory testing

ObjectiveWorkers exposed to vibrating tools may develop hand-arm vibration syndrome (HAVS). We assessed the somatosensory phenotype using quantitative sensory testing (QST) in comparison to electrophysiology to characterize (1) the most sensitive QST parameter for detecting sensory loss, (2) the correlation of QST and electrophysiology, and (3) the frequency of a carpal tunnel syndrome (CTS) in HAVS.MethodsQST, cold provocation tests, fine motor skills, and median nerve neurography were used. QST included thermal and mechanical detection and pain thresholds.ResultsThirty-two patients were examined (54 ± 11 years, 91% men) at the more affected hand compared to 16 matched controls. Vibration detection threshold was the most sensitive parameter to detect sensory loss that was more pronounced in the sensitivity range of Pacinian (150 Hz, x12) than Meissner’s corpuscles (20 Hz, x3). QST (84% abnormal) was more sensitive to detect neural dysfunction than conventional electrophysiology (37% abnormal). Motor (34%) and sensory neurography (25%) were abnormal in HAVS. CTS frequency was not increased (9.4%).ConclusionFindings are consistent with a mechanically-induced, distally pronounced motor and sensory neuropathy independent of CTS.SignificanceHAVS involves a neuropathy predominantly affecting large fibers with a sensory damage related to resonance frequencies of vibrating tools.     

Prolongation of F-wave minimal latency: a sensitive predictor of polyneuropathy

Introduction: To evaluate the sensitivity of F-wave minimal latencies, we compared F-waves with motor and sensory nerve conduction studies (MNCS and SNCS) in patients with peripheral neuropathy. Methods: A retrospective chart review conducted in 484 patients confirmed the clinical evidence of a polyneuropathy, and studies of F-wave minimal latencies as well as MNCS and SNCS in each patient. Results: Overall rate of abnormality reached 469/484 (96.9%) for F-wave minimal latencies as compared to 374/484 (77%) for nerve conduction studies (?p < 0.0001). Nerve-specific abnormalities of F-waves showed 290/354 (82%), 140/171 (82%), 367/398 (92%) and 357/376 (95%) for median, ulnar, peroneal and tibial nerves, respectively. Corresponding values for MNCS consisted of 108/354 (31%), 29/171 (17%), 258/398 (65%) and 189/376 (50%) (all p < 0.0001). In contrast, SNCS revealed abnormalities in 120/333 (36%), 60/159 (38%) and 266/474 (56%) of median, ulnar and sural nerves. Conclusion: F-wave minimal latencies serve as the best predictor of polyneuropathy followed by SNCS and then MNCS.     

The acute effects of glycemic control on nerve conduction in human diabetics.

OBJECTIVE: To investigate acute changes in nerve conduction associated with glycemic control. In diabetes, nerve dysfunction can result from reversible metabolic factors associated with hyperglycemia, as well as structural changes. METHODS: Multiple nerve conduction parameters including F-wave latencies were measured in 47 diabetic patients with prominent hyperglycemia before and after intensive insulin treatment. RESULTS: Four weeks after the start of treatment, there was a significant improvement in minimal F-wave latencies of the median (P<0.001) and tibial (P<0.001) nerves, and in distal latencies (P=0.01) and sensory nerve conduction velocities (P<0.001) of the median nerves. Amplitudes of motor and sensory responses did not change significantly. These findings were similar for patients with type 1 (n=8) and those with type 2 (n=39) diabetes. Patients with poorer glycemic control or milder neuropathy tended to show greater changes after treatment. CONCLUSIONS: Glycemic control quickly alters the speed of nerve conduction. F-wave latencies and conduction times across the carpal tunnel are very sensitive parameters. SIGNIFICANCE: Serial nerve conduction studies can detect reversible slowing of nerve conduction presumably caused by metabolic factors, such as decreased Na+/K+-ATPase activity, the altered polyol pathway, and tissue acidosis.     

Sensory afferent inhibition within and between limbs in humans

ObjectiveTo examine the distribution and inter-limb interaction of short-latency afferent inhibition (SAI) in the arm and leg.MethodsMotor evoked potentials (MEPs) in distal and proximal arm, shoulder and leg muscles induced with ranscranial magnetic stimulation (TMS) were conditioned by painless electrical stimuli applied to the index finger (D2) and great toe (T1) at interstimulus intervals (ISIs) of 15, 25–35, 80 ms (D2) and 35, 45, 55, 65 and 100 ms (T1) in 27 healthy human subjects. TMS was delivered over primary motor cortex (M1) arm and leg areas. Electrical stimulus intensities were varied between 1 and 3 times the sensory perception thresholds. We also tested effects of posterior cutaneous brachial nerve (PCBN) stimulation on MEPs in arm muscles at ISIs of 18 and 28 ms.ResultsD2 but not PCBN electrical conditioning reduced MEP amplitudes in upper limb muscles at ISIs of 25 and 35 ms. SAI was more pronounced in distal as compared to proximal arm muscles. Also, SAI following D2 stimulation increased with higher conditioning intensities. D2 stimulation did not change lower limb muscles MEPs. In ontrast, T1 stimulation did not induce SAI in any muscles but caused MEP facilitation in a foot muscle at an ISI of 55 ms and in upper limb muscles at ISIs of 35 and 55 ms. Short interval intracortical inhibition (SICI) and intracortical facilitation (ICF) were not affected by electrical T1 conditioning.ConclusionD2 stimulation causes segmental SAI in upper limb muscles with a distal to proximal attenuation without affecting leg muscles. In contrast, toe stimulation facilitates motor output both in foot and upper arm muscles.SignificanceOur data suggest that cutaneo-motor pathways in arms and legs are functionally organized in a different way with cutaneo-motor interactions induced by toe stimulation probably relayed at a thalamic level. Abnormal cutaneo-motor interactions following electrical toe stimulation may serve as an electrophysiological marker of thalamic dysfunction, e.g. in neurodegenerative diseases.     

Local injection versus surgery in carpal tunnel syndrome: Neurophysiologic outcomes of a randomized clinical trial

ObjectiveThe aim of our study was to characterize the neurophysiologic outcomes in a randomized clinical trial comparing local corticosteroid injection and decompressive surgery in idiopathic carpal tunnel syndrome.MethodsClinical and neurophysiologic assessments were done at baseline and 12 months after treatment. Four parameters were evaluated in the nerve conduction study (NCS): distal motor latency, motor amplitude, sensory conduction velocity and sensory amplitude. Statistic signification was established by the Student’s t test, independent and paired samples, and Mann–Whitney test. Repeated measures analysis of variance was used by the three domains of symptoms. Correlations between the changes showed in clinical parameters and those evidenced by electromyography were calculated by the Pearson’s test.ResultsBoth groups of therapy were comparable at baseline. In 95 wrists, a second NCS was done 12 months post-treatment. Although clinical outcome improved in a similar way in both groups, we found statistically significant improvement in three (distal motor latency, sensory conduction velocity and sensory amplitude) of four neurophysiologic parameters only in the surgery group, when compared to baseline values.ConclusionsAlthough local corticosteroid injection and decompressive surgery are clinically effective in reducing symptoms of carpal tunnel syndrome, only surgery results in an improvement of the neurophysiologic parameters, at 12-months follow-up.SignificanceOnly decompressive surgery allows resolution of neurophysiologic changes. The symptoms of the syndrome are resolved with corticosteroid injections.     

Electrophysiological Characteristics of the Pediatric Femoral Nerve and Their Use in Clinical Diagnosis

ObjectiveTo explore the electrophysiological characteristics of the pediatric femoral nerve at different ages.MethodsSurface electrodes were used to detect femoral nerve conduction in 163 healthy children aged 0-14 years recruited to this study and divided into six age groups. Based on the range of normal values obtained, the diagnosis of 22 patients with suspected femoral nerve injury was confirmed.ResultsWe obtained normal values for pediatric femoral nerve motor and sensory conduction in all age groups, including proximal and distal compound muscle action potential latencies, proximal compound muscle action potential amplitude and duration, motor conduction velocity, F-wave latency, and sensory conduction velocity. We measured proximal compound muscle action potential in all children in all age groups. The manifestation of femoral nerve injury in the 22 patients was primarily a clear decrease or absence of compound muscle action potential amplitude or a lengthened latency. Electromyographs revealed that 104 muscle parts were involved in the nerve function, in which 59 parts were found to be abnormal (56.73%).ConclusionsThe development of pediatric femoral nerve mainly began after 1 years old and continued to 14 years old. The proximal latency and compound muscle action potential amplitude of the pediatric femoral nerve have clinical value. Detection of the femoral nerve is important in the diagnosis of lower limb monoplegia, especially for acute flaccid paralysis associated with nonpolio enterovirus infection.     

Evaluation of lip sensory disturbance using somatosensory evoked magnetic fields

ObjectiveTo evaluate lip sensory dysfunction in patients with inferior alveolar nerve injury by lip-stimulated somatosensory evoked fields (SEFs).MethodsSEFs were recorded following electrical lip stimulation in 6 patients with unilateral lip sensory disturbance and 10 healthy volunteers. Lip stimulation was applied non-invasively to each side of the lip with the same intensity using pin electrodes.ResultsAll healthy volunteers showed the earliest response clearly and consistently at around 25 ms (P25m) and at least one of the following components, P45m, P60m, or P80m, over the contralateral hemisphere. The ranges of the peak latencies were 23–33, 42–50, 56–67, and 72–98 ms for right-side stimulation and 23–34, 46–49, 52–68, and 71–90 ms for left-side stimulation. Affected-side stimulation did not evoke P25m component in any patients, but invoked traceable responses in 5 patients whose latencies were 57, 89, 65, 53, and 54 ms. Unaffected-side stimulation induced P25m in 2 patients at 27 and 25 ms, but not in the other 4 patients.ConclusionThe P25m component of lip SEFs can be an effective parameter to indicate lip sensory abnormality.SignificanceLip sensory dysfunction can be objectively evaluated using magnetoencephalography.     

Ultrasound-guided needle positioning in sensory nerve conduction study of the sural nerve

ObjectivesTo evaluate the usefulness of ultrasound imaging to improve the positioning of the recording needle for nerve conduction studies (NCS) of the sural nerve.MethodsOrthodromic NCS of the sural nerve was performed in 44 consecutive patients evaluated for polyneuropathy. Ultrasound-guided needle positioning (USNP) was compared to conventional “blind” needle positioning (BNP), electrically guided needle positioning (EGNP), and to recordings with surface electrodes (SFN).ResultsThe mean distance between the needle tip and the nerve was 1.1 mm with USNP compared to 5.1 mm with BNP (p < 0.0001). The mean amplitude of the sensory nerve action potential (SNAP) was 21 μV with USNP and 11 μV with BNP (p < 0.0001). Compared to BNP, nerve–needle distances and SNAP amplitudes did not improve with EGNP. SNAP amplitudes recorded with SFN were significantly smaller than with BNP, EGNP and USNP.ConclusionUltrasound increases the precision of needle positioning markedly, compared to conventional methods. The amplitude of the recorded SNAP is usually clearly greater using USNP. In addition, USNP is faster, less painful and less dependent on the patient.SignificanceUSNP is superior to BNP, EGNP, and SFN in accurate measurement of SNAP amplitude. It has a potential use in the routine near-nerve needle sensory NCS of pure sensory nerves.     

A new technique for dorsal sural nerve conduction study with surface strip electrodes

ObjectiveTo obtain higher amplitude of dorsal sural sensory nerve action potentials (SNAPs), we used a new method for dorsal sural nerve conduction study with surface strip electrodes (SSEs).MethodsDorsal sural SNAPs were recorded orthodromically. The recording electrodes were placed behind the lateral malleolus. SSEs were attached to the laterodorsal aspect of the foot for stimulation of the dorsal sural nerve (DSN). We also used a conventional method with a standard bipolar stimulator and compared the findings.ResultsDorsal sural SNAPs were recordable bilaterally from 49 healthy volunteers. Mean peak-to-peak amplitude for SNAPs was 12.9 ± 6.3 μV, and mean nerve conduction velocity was 44.8 ± 5.5 m/s. The mean amplitude of SNAPs obtained by our method was 118.6% higher than that of SNAPs obtained by the conventional method (12.9 μV vs. 5.9 μV; P < 0.001).ConclusionsThe highest amplitude of dorsal sural SNAPs was constantly obtained by SSEs since SNAPs arising from whole digital branches of the DSN could be elicited by placement of SSEs.SignificanceWhen the DSN supplies more cutaneous branches to the lateral half of the foot, SSEs gives higher amplitude of dorsal sural SNAPs than that of the standard innervation type.