The primary role of the Erb's point--axilla segment in median and ulnar motor nerve conduction determinations in alcoholic neuropathy

Motor nerve conduction velocity (MNCV) was explored in the Erb's point-axilla (N-A) nerve segment of median and ulnar nerves, bilaterally, in 10 patients with a history of prolonged heavy drinking but in whom no other predisposing factors to peripheral neuropathy were found. For comparison, MNCV was determined also in the axilla-elbow (A-E), elbow-wrist (E-W) nerve segments, as well as the motor terminal latency (MTL) of the same nerves. A total of 140 nerve segments were tested tested but only 133 results were obtained. Abnormal MNCV or MTL was found in 36 or 27% of all tested nerve segments. From the latter, 38.9% were in the N-A nerve segments. Of N-A nerve segments tested, reduction in MNCV was found in 46.7%. Our results are statistically significant.     

Median and ulnar nerve conduction determinations in the Erb's point--axilla segment in normal subjects.

Twenty-one median and 22 ulnar nerves were tested in 12 patients for motor nerve conduction velocity (MNCV) and motor nerve conduction time (MNCT) in the segments from Erb's point (N) to axilla (A) bilaterally. It was found that on this segment for both nerves, MNCV values equal to or smaller than 51 m/s or conduction times equal to or longer than 4 ms are to be considered abnormal. For comparative studies and for checking the normality of the tested nerves in their entire length, the more distally located segments in the same nerve were also tested. For diagnostic purposes, the differences between right and left MNCV or MNCT values determined in the same person on N-A segments of homologous nerves were analysed. Motor nerve conduction velocity or MNCT determinations on the N-A nerve segment are expected to replace MNCV determinations on the longer N-AE (AE=100 mm above elbow) nerve segment, which is now in use, for diagnosis of the thoracic outlet syndrome.     

Electrophysiological study of neuromuscular function in a population poisoned by lead

A comprehensive electrophysiological examination of the peripheral nervous system was carried out in 12 patients who proved to be toxicated with lead (high lead blood levels, and diminished activity of the delta-aminolevulinate dehydratase, ALA D, in erythrocytes). Maximal motor nerve conduction velocities and terminal latencies were investigated in the median, radial and deep peroneal nerves. Also the amplitude of the evoked muscle response (M wave) was measured in thenar, extensor longus and extensor digitorium brevis muscles. Sensory conduction velocity and amplitude of the nerve compound action potential were measured at the median nerve. Tibialis anterior muscle responses to deep peroneal nerve repetitive stimulation were also explored. Conventional needle electromyogram was performed in the deltoid and tibialis anterior muscles. Slight diminished motor and sensory conduction velocities were found as well as a reduction of the amplitude of the evoked muscle response of the compound sensory action potential. Four out of the 12 patients tested showed either decremental or incremental amplitude of the muscle response with nerve repetitive stimulation. A electromyographical diminished interference pattern was found in all patients tested. Most of the remaining motor unit potentials were fragmented or polyphasic. Just one patient disclosed potentials of enhanced duration and amplitude. No relationship was found between blood lead levels or ALA D erythrocytes concentration and the different electrophysiological tests performed, except between reduced ALA D concentration and diminished amplitudes of the M wave and of the sensory compound action potential, and also between ALA D and diminished radial motor conduction velocity.(ABSTRACT TRUNCATED AT 250 WORDS)     

Distribution,clinical correlates and significance of axonal loss and demyelination in chronic inflammatory demyelinating polyneuropathy

Background: The distribution of axonal loss and demyelination has rarely been studied in chronic inflammatory demyelinating polyneuropathy (CIDP). Whether electrophysiological parameters may represent clinically relevant biomarkers of disease activity in the disorder remains uncertain. The purpose of this study was (i) to ascertain the distribution of electrophysiological motor abnormalities to optimize the diagnostic utility of nerve conduction studies and (ii) to establish electro‐clinical correlations in an attempt to find the potential parameters that could represent adequate biomarkers of disease activity and prognosis. Methods: The clinical and electrophysiological motor features of 31 prospectively recruited patients with clinically stabilized CIDP were analysed. Results: Axonal loss predominated in the lower limbs, but demyelination was more common in the upper limbs. About 50% of all demyelinating abnormalities were detected in asymptomatic regions. Presence of weakness correlated with abnormal compound muscle action potential (CMAP) and abnormal motor nerve conduction velocity (MNCV). Degree of weakness and functional scores only consistently correlated with CMAP amplitudes. CMAP abnormality correlated with abnormal MNCV, abnormal distal motor latency (DML) and presence of conduction block (CB). However, although CMAP amplitudes also correlated with MNCVs and DMLs in raw values, they did not relate to the degree of CB. Conclusion: Electrodiagnosis of CIDP is optimized by extensive testing of upper limb nerves and of asymptomatic regions. Raw value CMAP amelioration and MNCV normalization may be adequate markers of clinical improvement in CIDP. Similarly, raw value MNCV and DML amelioration, as well as CB reversal may represent adequate prognostic markers.     

Muscle fiber conduction abnormalities in early diabetic polyneuropathy.

OBJECTIVE: Diabetic polyneuropathy (PNP) has been proposed to be a primary disorder of sensory nerves. At an early stage motor nerve conduction velocity (MNCV) and muscle strength remain preserved due to compensatory mechanisms (axonal sprouting, reinnervation). We evaluated the use of invasive muscle fiber conduction velocity (MFCV) measurements as a method to detect muscle fiber denervation atrophy, as an early sign of motor axonal loss in diabetes mellitus (DM). METHODS: Twelve selected male patients (8 type 1, 4 type 2; mean age 35.8 years, SD 10.6), without any sign of micro- or macroangiopathy, were studied by systematic clinical and neurophysiological testing including MFCV estimation. RESULTS: Hand-held dynamometry was normal in all subjects. There were no signs of recent denervation by concentric needle EMG in any of the patients. Sensory nerve conduction velocity (SNCV) was abnormal in 6 subjects, MFCV in 6 subjects (5 had also low SNCV). The ratio of fastest/slowest muscle fibers in MFCV was correlated to SNCV of sural nerve (-.59, p < .05), but not to MNCV. CONCLUSIONS: Half of the clinically asymptomatic DM subjects showed sensory involvement together with MFCV abnormalities, despite normal needle EMG and force. SIGNIFICANCE: MFCV estimation offers a sensitive method in detecting early signs of motor axonal dysfunction in DM.     

F-wave conduction velocity in Guillain-Barré syndrome. Assessment of nerve segment between axilla and spinal cord.

The F-wave conduction velocity (FWCV) in the central segment (axilla to spinal cord) of the median and ulnar nerves was compared to the motor nerve conduction velocity (MNCV) in the more distal segments in nine patients with mild cases of the Guillain-Barré syndrome. In four patients, FWCV was slow despite normal or borderline MNCV. In four others, both FWCV and MNCV were abnormal. One patient showed slow MNCV with normal FWCV. The average FWCV was significantly decreased (40.9 +/- 12.0 meters/sec for median and 42.9 +/- 8.3 meters/sec for ulnar nerves) when compared to the corresponding normal values (64.3 +/- 6.4 meters/sec and 63.1 +/- 5.9 meters/sec). These data support the hypothesis that the central segment of a nerve is predominantly involved in some patients with Guillain-Barré syndrome.     

Triethyltin sulfate-induced neuropathy in rats. Electrophysiologic, morphologic, and biochemical studies.

Adult rats given high orally administered doses of triethyltin (TET) sulfate lost weight, developed hind limb wasting, and became paraplegic or quadriplegic within three weeks of intoxication. A 33% reduction in the motor nerve conduction velocity (MNCV) of the sciatic nerve in the absence of significant demyelination was observed. There was observed, however, intramyelinic edema formation and an increased number of axonal neurofilaments and neurotubules; changes that paralleled the decrease in MNCV during the period of intoxication. Although the animals became asymptomatic and the MNCV normalized within two to three weeks of discontinuing the TET intoxication, the intramyelinic vacuoles and the increased numbers of neurofilaments and neurotubules persisted.     

Correlation between distal motor latency and compound muscle action potential in amyotrophic lateral sclerosis

OBJECTIVES: Amyotrophic lateral sclerosis (ALS) is a fatal neurodegenerative disorder, characterized by a selective progressive degeneration of the motor system. Electromyography is essential for the diagnosis of ALS. The measurement of motor conduction of peripheral nerves is of major importance to recognize other possible causes of progressive muscle wasting. However, there are also pathologic changes in nerve conduction studies in ALS patients. METHODS: In this study we analysed the values of distal motor latency (DML), compound muscle action potential (CMAP) and motor nerve conduction velocity (MNCV) in 95 patients with definite ALS. RESULTS: We found slight slowing of MNCV and moderate to strong reduction of CMAP and a prolongation of DML. We found no significant correlation between MNCV and CMAP. DISCUSSION: The main finding of the present work was the negative correlation between DML and CMAP. It is interpreted as a very distal axonal damage as the main reason for prolongation of DML in ALS patients.     

F-wave conduction velocity in the deep peroneal nerve: Charcot-marie-tooth disease and dystrophia myotonica

The F-wave has been used to estimate the motor nerve conduction velocity (MNCV) along the proximal segment (spinal cord to knee) of the axons of the deep peroneal nerve in patients with Charcot-Marie-Tooth disease and those with dystrophia myotonica. A new, modified method has been applied to estimate proximal MNCV in patients in whom F-waves or M-responses cannot be obtained from the small muscles of the foot. Terminal latencies and MNCV along the distal nerve segment (knee to ankle) have also been estimated using conventional techniques. The results have been compared with those obtained for control subjects. Proximal MNCV was severely slowed in every patient with Charcot-Marie-Tooth disease; the degrees of proximal and distal MNCV decreases were related. In patients with dystrophia myotonica, distal and proximal MNCVs were significantly reduced in comparison with control subjects; the MNCV slowing was not related to the degree of muscle atrophy. This is consistent with the hypothesis that the nerves and muscles are independently affected in dystrophia myotonica. It is concluded that the F-wave MNCV technique is as useful as, and may be more sensitive than, the conventional MNCV method.     

Analysis of F-wave in metabolic neuropathies: a comparative study in uremic and diabetic patients

Motor nerve conduction study along the entire length of the ulnar and tibialis posterior nerves was carried out in 30 diabetics compared with 30 uremic patients and 30 control subjects. The conduction in the proximal and the distal nerve segments was evaluated by the determination of the M and F latencies, MNCV (between the stimulus sites), FWCV (between the spinal cord and the stimulus sites), and F-ratio (conduction time ratio of proximal to distal segment). In both groups of patients the lower limbs appear much more involved than the upper, where the ulnar nerve is more commonly affected in uremic than in diabetic patients. In diabetic neuropathy the motor conduction abnormalities are diffuse over the total length of the nerve, but more marked distally in the ulnar nerve.     

Prevalence of subclinical neuropathy in diabetic patients: assessment by study of conduction velocity distribution within motor and sensory nerve fibres

Nerve conduction velocity distribution (CVD) study is a newly-developed electrodiagnostic method for detecting alterations in the composition of nerve fibres according to their conduction velocity. The presence of subclinical neuropathy was evaluated in 138 diabetic patients by CVD study of four motor nerves (external popliteal and ulnar nerves bilaterally) and two sensory nerves (median nerve bilaterally), and the data obtained were compared with standard electrophysiological parameters in the same nerve segments. CVD studies revealed an altered distribution pattern in 106 of 129 evaluable patients for motor nerves (82%) and in 67 of 115 evaluable patients for sensory nerves (58%), while standard examination gave abnormal findings in 92 of 137 patients (67%) and in 33 of 118 patients (11%), respectively. Of the patients adequately evaluated by both techniques, 21 of 129 patients (16%) revealed altered CVD data unaccompanied by slowing of maximum nerve conduction velocity, and 37 patients of 101 (37%) showed similar findings for sensory nerves. Subclinical alterations of motor and sensory nerve CVD were not significantly related to age or to metabolic control expressed as glycated haemoglobin levels; a significantly longer duration of disease was found in patients with motor and mixed subclinical neuropathy with respect to non-neuropathic patients. The CVD study allowed us to detect subclinical abnormalities of motor and sensory nerve fibres; often this is a more sensitive method than the standard electrodiagnostic study. This method can be very useful as a diagnostic tool and in research in the study of the progression of diabetic neuropathy. Received: 21 March 1997 Received in revised form: 8 September 1997 Accepted: 7 October 1997     

Correlation of median forearm conduction velocity with carpal tunnel syndrome severity.

OBJECTIVE: Median nerve entrapment neuropathy at the wrist can be accompanied by slowed motor conduction within the forearm. Existing studies conflict regarding a correlation between the severity of the entrapment neuropathy in carpal tunnel syndrome (CTS) and slowing of median motor nerve conduction velocity (MNCV) in the forearm. Here, it was asked if there is a correlation between markers of CTS severity and median forearm MNCV, and if there is an explanation for the preceding conflicting results. METHODS: Median MNCV in the forearm was correlated with neurophysiologic markers of severity of a median neuropathy at the wrist in 91 hands from 64 patients with clinical and electrodiagnostic evidence of CTS. RESULTS: Median MNCV within the forearm segment was negatively correlated with the median nerve distal motor latency (r=-0.64, P<0.001, n=91) and positively correlated with the CMAP amplitude of the abductor pollicis brevis muscle (r=0.45, P<0.001, n=91). These correlations only occurred in patients with a prolonged median distal motor latency. Previous investigations that failed to find such correlations used variable or non-standardized methods or analyzed smaller numbers of patients. CONCLUSIONS: Slowing of median MNCV in the forearm is related to the severity of the entrapment of median motor fibers at the wrist. SIGNIFICANCE: Slowed forearm median MNCV can be a marker of motor nerve injury at the wrist.     

Peripheral neuropathy in multiple sclerosis: a clinical and electrophysiologic study

Peripheral nerve abnormalities are uncommon in multiple sclerosis (MS). When present, they are usually attributed to factors associated with advanced disease, such as malnutrition or cytotoxic drugs. We prospectively evaluated 22 mildly disabled MS patients with sensory complaints for evidence of neuropathy using the Neuropathy Symptom Score (NSS), clinical examination, and electrophysiologic studies of peripheral nerves. Distal latency, F-wave response, and nerve conduction velocity (NCV) and amplitude in the ulnar, median, tibial, peroneal and sural nerves were examined. Neuropathy was recorded if electrophysiologic abnormalities were detected in at least two peripheral nerves in the same patient. The most frequent electrophysiologic abnormalities noted were prolonged F-wave response and low motor amplitude in the peroneal nerve, slow sensory conduction velocities of the ulnar and sural nerves, and prolonged distal latencies in the sensory ulnar and sural nerves. Electrophysiologic abnormalities were found in 33 of 244 nerves examined (14.7%) and occurred in 10 patients (45.5%). Neuropathic symptoms were mild and did not correlate with electrophysiologic abnormalities. Age, disease duration, disease course and neurologic disability as evaluated by the Kurtzke Expanded Disability Status Scale, were not associated with the presence of neuropathy. Our findings indicate a high frequency of sensory-motor neuropathy in a selected group of MS patients.     

Therapeutic Effects of Aldose Reductase Inhibitor on Experimental Diabetic Neuropathy through Synthesis/Secretion of Nerve Growth Factor

We investigated alterations in nerve growth factor (NGF) and ciliary neurotrophic factor (CNTF) contents during treatment with epalrestat, an aldose reductase inhibitor (ARI), on streptozotocin (STZ)-induced diabetic neuropathy in rats. Diabetic rats showed a statistically significant reduction in H-wave-related sensory nerve conduction velocity (HSNCV) and in NGF content in sciatic nerves during the experiment of 8 weeks. No reduction in the CNTF content in sciatic nerves was seen in the diabetic rats. The epalrestat treatment, which started 4 weeks after STZ injection, resulted in a significantly greater NGF content and faster HSNCV than those in untreated diabetic rats. But no statistically significant alterations of motor nerve conduction velocity (MNCV) or CNTF content were seen during the treatment. ARI showed the stimulating effect for NGF synthesis/secretion in rat Schwann cell culturein vitro.These findings suggest that decreased levels of NGF in diabetic sciatic nerves may be involved in the pathogenesis of diabetic neuropathy in these rats and further show that epalrestat treatment can be useful for the treatment of diabetic neuropathy through NGF-induction in Schwann cells and/or inhibition of the polyol pathway.     

神经型布氏杆菌病周围神经损害的临床与电生理研究

目的研究神经型布氏杆菌病周围神经损害的临床特征,探讨电生理对其的诊断价值。方法对32例神经型布氏杆菌病周围神经损害患者(病例组)和32名性别及年龄与病例组匹配的正常对照组进行神经电生理检查,并对所得检查结果进行统计学分析。结果病例组与对照组在运动末梢潜伏期(distal motor latency,DML)、复合肌肉动作电位(compound motor active potentials,CMAP)波幅、运动神经传导速度(motor nerve conduction velocity,MCV)、感觉神经动作电位潜伏期(sensory nerve action potential latency,SL)、感觉神经动作电位(sensory nerve action potential,SNAP)波幅及感觉神经传导速度(sensory nerve conduction velocity,SCV)方面的比较,差异均有统计学意义(P0.05)。电生理检查提示上下肢周围神经损害,感觉神经及运动神经均受累,其中感觉神经占55.47%,运动神经占16.80%,上肢以正中神经(64条)最多见,下肢以腓肠神经(16条)最多见。四肢运动神经256条中43条传导速度减慢,占16.80%,四肢感觉神经256条中142条传导速度减慢,占55.47%,SCV较MCV改变明显,上肢病变重于下肢。结论神经电生理检查为神经型布氏杆菌病周围神经损害的临床诊断提供了客观依据。     

Sensory nerve conduction in demyelinating and axonal Guillain-Barré syndromes

Guillain-Barré syndrome is divided into acute inflammatory demyelinating polyneuropathy (AIDP) and acute motor axonal neuropathy (AMAN) based on motor nerve conduction studies. We investigated whether sensory nerve conduction studies contribute to the electrodiagnosis of AIDP and AMAN. In consecutive 59 patients with AIDP (n = 26) or AMAN (n = 33), results of sensory nerve conduction studies in the median, ulnar and sural nerves were reviewed. Sensory nerve conduction abnormalities were found for 85% of AIDP patients and for only 6% of AMAN patients. In AIDP patients, the abnormalities were present in 85% of patients in the median nerves, 85% in the ulnar nerves and 38% in the sural nerves. AMAN is very rarely associated with sensory nerve involvement. Abnormal sensory nerve conduction is supportive of AIDP and is more frequently found for the median and ulnar nerves than sural nerves.     

Neuropathy in the spontaneously hypertensive rat: An electrophysiological and histological study

Introduction: Hypertension is identified as a risk factor for development of polyneuropathy. In this study we examined nerve conduction and morphological alteration of peripheral nerves in spontaneously hypertensive rats (SHR). Methods: Motor nerve conduction velocity (MNCV) in the sciatic–tibial nerve and sensory nerve conduction velocity (SNCV) in the sural nerve were measured. Pathological investigations included spinal cord, dorsal root ganglion, and hindlimb nerves in SHR and Wistar–Kyoto rats (WKY) aged 4–64 weeks. Results: Blood pressure was significantly higher in SHR than WKY animals at 4 weeks and elevated further with aging. MNCV and SNCV were significantly slower in SHR compared with WKY after age 24 weeks. Prominent morphological changes in SHR nerves included axonal atrophy and myelin splitting. SHR also had endoneurial microangiopathy with reduplication of basement membrane. Conclusions: SHR showed slowed nerve conduction velocity and pathological abnormalities of hindlimb nerves. Sustained severe hypertension may cause axonal atrophy and endoneurial microangiopathy. Muscle Nerve 54 : 756–762, 2016     

Peripheral neuropathy response to erythropoietin in type 2 diabetic patients with mild to moderate renal failure

This study assessed the added effect of 6 months of erythropoietin (EPO) administration in patients suffering from diabetic neuropathy with mild to moderate chronic kidney disease (CKD) managed with gabapentin. Twenty diabetic patients with mild to moderate CKD were included; 12 in gabapentin and 8 in EPO+gabapentin group. The subjects underwent nerve conduction studies (NCS) at the initiation of the investigation and after 6-month treatment. NCS were made in deep and superficial peroneal, tibial, and sural nerves. After 6 months, in both the groups, proximal motor latency (PML) nonsignificantly improved in deep peroneal and tibial nerves; conversely, dorsal motor latency (DML) got slightly impaired in these two nerves. A nonsignificant disruption and improvement was observed in deep peroneal and tibial motor nerve conduction velocity (MNCV), respectively, in gabapentin group. Although the F-wave of tibial and deep peroneal nerves remained stable in gabapentin group, a nonsignificant improvement was observed in EPO+gabapentin group. H-reflex of tibial nerve and all the evaluated parameters of sural and superficial peroneal nerves remained constant in all patients. Thus, it can be concluded that 6-month administration of EPO+gabapentin, or gabapentin alone in mild to moderate CKD patients with diabetic neuropathy could not improve nerve performance.     

Nitrosative stress and peripheral diabetic neuropathy in leptin-deficient (ob/ob) mice

Nitrosative stress contributes to nerve conduction slowing, thermal hypoalgesia, and impaired nitrergic innervation in animal models of Type 1 diabetes. The role for reactive nitrogen species in Type 2 diabetes-associated neuropathy remains unexplored. This study evaluated the role for nitrosative stress in functional and structural neuropathic changes in ob/ob mice, a model of Type 2 diabetes with mild hyperglycemia and obesity. Two structurally diverse peroxynitrite decomposition catalysts, Fe(III) tetrakis-2-(N-triethylene glycol monomethyl ether)-pyridyl porphyrin (FP15) and Fe(III) tetra-mesitylporphyrin octasulfonate (FeTMPS), were administered to control and 8-week-old ob/ob mice for 3 weeks at the doses of 5 mg kg(-1) day(-1) (FP15) and 5 and 10 mg kg(-1) day(-1) (FeTMPS). The 11-week-old ob/ob mice developed motor nerve conduction velocity (MNCV) and hind-limb digital sensory nerve conduction velocity (SNCV) deficits, thermal hypoalgesia, tactile allodynia, and a remarkable ( approximately 78%) loss of intraepidermal nerve fibers. They also had increased nitrotyrosine and poly(ADP-ribose) immunofluorescence in the sciatic nerve, spinal cord, and dorsal root ganglion neurons. Treatment with two structurally diverse peroxynitrite decomposition catalysts was associated with restoration of normal MNCV and SNCV, and alleviation of thermal hypoalgesia. Tactile response thresholds increased in response to peroxynitrite decomposition catalyst treatment, but still remained approximately 2.7- to 3.2-fold lower compared with non-diabetic controls. Intraepidermal nerve fiber loss was not alleviated by either FP15 or FeTMPS. Nitrotyrosine and poly(ADP-ribose) immunofluorescence in sciatic nerve, spinal cord, and dorsal root ganglia of peroxynitrite decomposition catalyst-treated ob/ob mice were essentially normal. In conclusion, nitrosative stress plays an important role in functional abnormalities associated with large motor, large sensory, and small sensory fiber neuropathy, but not in small sensory nerve fiber degeneration, in this animal model. Peroxynitrite decomposition catalysts alleviate Type 2 diabetes-associated sensory nerve dysfunction, likely by mechanism(s) not involving arrest of degenerative changes or enhanced regeneration of small sensory nerve fibers.     

Physiological and immunohistochemical characterization of cisplatin-induced neuropathy in mice

We investigated the neuropathic effects of cisplatin in two groups of mice treated with 5 or 10 mg/kg/week of cisplatin for 7 or 8 weeks. Peripheral nerve functions were evaluated by sweat imprints, and electrophysiological, rotarod, and nociceptive tests. Protein gene product 9.5 (PGP), calcitonin gene-related peptide (CGRP), and vasoactive intestinal peptide (VIP) were immunohistochemically localized in footpads. Tibial nerves were analyzed morphometrically. Functional deficits developed progressively with higher cumulative doses, more markedly in mice treated with high than in those with low doses. From cumulative doses of 10 mg/kg, significant declines in sensory nerve conduction velocity and sudomotor responses were found, whereas motor and nociceptive functions were involved later. There were no morphometrical changes in tibial nerves. A marked decrease of CGRP- and VIP-immunoreactive nerves occurred in samples from treated mice, whereas PGP-labeled profiles decreased mildly at late stages. Impairment of the content of neuropeptides with neurosecretor role was detectable earlier than functional abnormalities. Immunohistochemical analysis of skin biopsies offers a useful diagnostic tool for peripheral neuropathies.