bluuebunny/crossref_metadata_2025_split huggingface dataset:
Aberrant reinnervation following hypoglossal nerve damage
Authors: Wilson John R. , Sumner Austin J. , Eichelman Jutta 
Published: January 2005

AbstractHypoglossal nerve damage is a known complication of carotid endarterectomy, occurring in approximately 5% of endarterectomies. The vast majority of these patients recover without functional disability from this injury even if the tongue remains hemiplegic. We report 2 patients who suffered hypoglossal nerve section during neck surgery. Although they were initially mildly symptomatic, they developed increasingly severe dysarthria and dysphagia beginning 4 months after surgery. EMG revealed abnormal coactivation of the genioglossus and styloglossus muscles on the affected side, suggesting aberrant reinnervation. Aberrant reinnervation is a well‐known complication of facial nerve injury, but has not been previously recognized in hypoglossal nerve injury. Like the face, the tongue is composed of many muscles that must perform complex movements. Normally, injury to one hypoglossal nerve causes little or no disability, but when aberrant reinnervation occurs, the tongue no longer moves in a coordinated manner, and significant dysarthria ensues.
M/RMS: An EMG method for quantifying upper motoneuron and functional weakness
Authors: Haughton John F. , Little James W. , Powers Randall K. , Robinson Lawrence R. , Goldstein Barry 
Published: January 2005

AbstractA new method for quantifying upper motoneuron (UMN) weakness using standard EMG equipment is presented and compared to the twitch occlusion method. Control subjects and patients with stroke, spinal cord injury (SCI), and peripheral nerve injury (PNI) were evaluated. Force, EMG, and twitch force from nerve electrical stimulation were recorded during isometric contractions of the biceps and triceps. Ratios of the elicited CMAP amplitude (M)/voluntary‐root‐mean‐square EMG activity (RMS) and of the voluntary contraction twitch force (T1)/ the resting twitch force (Tmax) were the two measures of UMN weakness studied. Both ratios are linearly correlated with force for controls, log M/RMS (r =s 0.96) and Ti/Tmax (r = 0.86). Log M/RMS ratio was abnormally high (> mean + 2 SD; i.e., >1.09) for weak muscles affected by stroke and incomplete SCI, but was normal in muscles weakened by PNI. An elevated M/RMS ratio, may aid in quantification of deficient supraspinal activation from UMN or functional weakness. © 1994 John Wiley & Sons, Inc.
Utilization of myoblasts from transgenic mice to evaluate the efficacy of myoblast transplantation
Authors: Kinoshita Ikuo , Huard Johnny , Tremblay Jacques P. 
Published: January 2005

AbstractA possible treatment for Duchenne muscular dystrophy is the injection of normal myoblasts into dystrophic muscles to induce the formation of new, healthy, and dystrophin‐positive muscle fibers. To develop this therapy, it is important to identify the muscle fibers formed by the injected myoblasts in the host muscles. In this study, we used myoblasts from transgenic mice which have a gene expressing β‐galactosidase under the control of the promoter of quail fast skeletal muscle troponin I. This transgene is expressed in myotubes and muscle fibers, but not in myoblasts. Twenty‐eight days after myoblast transplantation in nude and in mdx mice, muscle fibers containing of β‐galactosidase were identified by x‐gal staining. In mdx mice, most of the β‐galactosidase‐positive muscle fibers resulting from the myoblast transplantation were also dystrophin positive. This technique could make it possible to follow the success of myoblast transplantation even in mice that are not depleted of dystrophin. © 1994 John Wiley & Sons, Inc.
Fatigue associated EMG behavior of the first dorsal interosseous and adductor pollicis muscles in different groups of subjects
Authors: Zijdewind Inge , Kernell Daniel 
Published: January 2005

AbstractWe have studied the fatigue‐associated behavior of surface EMG in two histochemically different muscles of the hand: first dorsal interosseous (FDI) and adductor pollicis (AP; relatively more type I fibers in AP than in FDI). During a fatigue test evoked by electrical stimulation of the ulnar nerve, the mean amplitudes of compound muscle action potentials (M‐waves) exhibited the same overall pattern for both muscles: a rapid phase of potentiation followed by a gradual decline. However, if the group of subjects was subdivided on the basis of hand length, significant differences emerged in the reactions of AP: in large hands, no fatigue‐associated M‐wave decline was seen, whereas in small hands a distinct decline was observed. A possible explanation for this phenomenon might be the presence of a greater amount of EMG contamination from other muscles in smaller hands. In the supposedly “cleaner” recordings from larger hands, significant differences between FDI and AP were observed with regard to their fatigue‐associated EMG reactions (M‐wave depression in FDI but not in AP). The direction of these differences was in accordance with expectations on the basis of known differences in histochemical fiber type composition. © 1994 John Wiley & Sons, Inc.
The natural history of a “benign” rib lesion in a patient with a demyelinating polyneuropathy and an unusual variant of poems syndrome
Authors: Simmons Zachary , Wald John , Albers James W. , Feldman Eva L. 
Published: January 2005

AbstractPatients with POEMS (polyneuropathy, organomegaly, endocrinopathy, M‐protein, and skin changes) syndrome exhibit great clinical variability and often have osteosclerotic myeloma. We present a patient with an acquired demyelinating polyneuropathy who was eventually diagnosed as having POEMS syndrome. Her long period of observation permitted documentation of the natural history of a plasmacytoma, including its remarkably slow rate of growth and its transformation from a nonsclerotic to a sclerotic bone lesion. Her clinical and laboratory features emphasize the variability of this syndrome. Biopsy of benignappearing bone lesions should be considered in patients with acquired demyelinating polyneuropathies who do not respond to standard treatment modalities. Serial x‐rays may not distinguish benign lesions from plasmacytomas in this treatable condition. © 1994 John Wiley & Sons, Inc.
AAEM case report #28: Monomelic amyotrophy
Authors: Donofrio Peter D. 
Published: January 2005

AbstractMonomelic amyotrophy is a rare form of motor neuron disease usually presenting as painless asymmetric weakness and atrophy in the distal upper extremities of young adults. Only rarely are the legs involved and pyramidal findings are uncommon. Monomelic amyotrophy is most often observed in people of Japanese and Indian heritage and affects men almost exclusively. Most cases are sporadic. Laboratory testing is frequently normal or nonspecific except for electrophysiologic studies which typically demonstrate reduced compound muscle action potential amplitudes, fasciculations, and features consistent with acute and chronic denervation in distal upper extremity muscles. Necropsy in 1 patient identified anterior horn cell shrinkage, necrosis, and gliosis in appropriate spinal cord segments. Symptoms and signs often progress for several years before spontaneously arresting. The differential diagnosis for monomelic amyotrophy is broad, including processes which affect the cervical cord, roots, brachial plexus, and individual or multiple nerves in the upper extremity. © 1994 Peter D. Donofrio, M.D. Published by John Wiley & Sons, Inc.
Effects of exercise on muscle activation and metabolism in multiple sclerosis
Authors: Kent‐Braun Jane A. , Sharma Khema R. , Weiner Michael W. , Miller Robert G. 
Published: January 2005

AbstractWe investigated the role of metabolism in muscle fatigue during voluntary exercise in persons with mild multiple sclerosis (MS). Six MS and 8 healthy control subjects performed intermittent, progressive, isometric contractions of the ankle dorsiflexors, during which we measured maximum voluntary force (MVC), inorganic phosphate (Pi), phosphocreatine (PCr), and pH. During exercise. MVC fell sooner in MS, but by the end of exercise the relative decrease in MVC was similar in both groups. In contrast, at the end of exercise Pi/PCr increased to 1.86 ± 0.22 in controls but to only 0.66 ± 0.04 in MS (P < 0.01); likewise, pH was 6.75±0.04 in controls and unchanged (7.06 ± 0.04) in MS (P <0.01). The smaller metabolic change at the same relative exercise intensity suggests a failure of muscle activation that is present even in mild MS. Neurophsyiologic measures of activation indicated some central activation failure and no neuromuscular junction impairment in MS, and suggested that activation failure beyond the muscle membrane(excitation–contraction coupling) may be important in MS. We conclude that metabolic factors do not play a significant role in the development of muscle fatigue during voluntary exercise in mild MS. © 1994 John Wiley & Sons, Inc.
Magnetically induced muscle contraction is caused by motor nerve stimulation and not by direct muscle activation
Authors: Machetanz Jochen , Bischoff Christian , Pichlmeier Reiner , Riescher Hermann , Meyer Bernd‐Ullrich , Sader Astrio , Conrad Bastian 
Published: January 2005

AbstractWhen magnetically stimulating peripheral nerves, a local cocontraction of muscle under the coil is observed. We assessed whether this contraction results from: (1) magnetic stimulation of motor nerves, or (2) direct depolarization of the muscle membrane. Wrist extensor muscles of normal subjects were magnetically stimulated with the coil placed directly above the muscle. Neuromuscular transmission was then blocked by atracurium using a technique of local curarization. As a reference, the radial nerve was stimulated electrically. Magnetic and electrical stimuli were applied alternatingly every 10 s. Twitch force of wrist extension was measured isometrically over a period of about 70 min including the phase of complete neuromuscular block. Twitch amplitudes elicited by magnetic and electrical stimuli were equivalent during the whole experiment. These results suggest that muscle cocontraction following magnetic stimulation results from depolarization of terminal motor nerve branches. © 1994 John Wiley & Sons, Inc.
Recording characteristics of the surface EMG electrodes
Authors: Barkhaus Paul E. , Nandedkar Sanjeev D. 
Published: January 2005

AbstractRoutine motor nerve conduction studies are conducted using surface EMG electrodes. Most techniques of estimating the number of motor units (MUs) are based on surface EMG recordings. Therefore, it is important to assess the uptake area of these electrodes. We recorded surface EMG motor unit action potentials (SMUAPs) from the biceps muscle of normal subjects. The SMUAP amplitude fell from 42 μV for the superficially located MUs (i.e., within 10 mm of skin surface) to 11 μV for the deep MUs (i.e., more than 20 mm from the skin surface). We infer that the pickup radius of the surface electrode is less than 20 mm. The implications of the limited uptake area of the surface electrodes to the analysis of compound muscle action potentials, estimation of the number of MUs, and the surface EMG recordings are discussed. © 1994 John Wiley & Sons, Inc.
Passive transfer of seronegative myasthenia gravis to mice
Authors: Burges Judith , Vincent Angela , Molenaar Peter C. , Newsom‐Davis John , Peers Chris , Wray Dennis 
Published: January 2005

AbstractMuscle weakness in myasthenia gravis is due to autoantibody‐induced loss of functional acetylcholine receptors (AChR). About 15% of myasthenia gravis patients, however, do not have detectable anti‐AChR antibodies. To investigate the effect of their plasma immunoglobulins on neuromuscular transmission, mice were injected with plasma (and in some cases purified immunoglobulin G (IgG)) from 7 “seronegative” myasthenia gravis (SMG) patients, and neuromuscular transmission parameters were examined. When injected for 15 days, all patients' plasma caused reductions in miniature endplate potential amplitudes, while endplate potential quantal content was significantly reduced by plasma from 4 of the 7 patients. There were no changes in ACh‐induced depolarization or single channel properties, and 125l‐α‐bungarotoxin binding studies showed no effect on AChR number, except in 1 case. Purified IgG injected for 3 days had similar effects to plasma injected for 15 days. Our findings confirm that SMG is autoantibody mediated and that there are pathogenic IgG antibodies. SMG appears to be a heterogeneous disorder and the target(s) for the antibodies may be diverse. © 1994 John Wiley & Sons, Inc.
Very efficient myoblast allotransplantation in mice under FK506 immunosuppression
Authors: Kinoshita Ikuo , Vilquin Jean‐Thomas , GuéRette BenoǐT , Asselin Isabelle , Roy Raynald , Tremblay Jacques P. 
Published: January 2005

AbstractTransgenic CD1 mice expressing β‐galactosidase were used as myoblast donors. The myoblasts were injected in normal or mdx muscles previously irradiated and injected with notexin. Twenty‐eight days after myoblast transplantation, the percentage of muscle fibers β‐galactosidase‐positive was low in mice not immunosuppressed but was high (80%) in those treated with FK506. In mdx mice, muscle fibers expressing β‐galactosidase were also dystrophin positive. Most of the mice not treated with FK506 produced antibodies against the donor myoblasts. These results indicate that FK506 is a very useful immunosuppressive drug for myoblast transplantation in mice. Irradiation and notexin injection used in our experiments are, however, not feasible in humans. Other manipulations capable of increasing the participation of donor myoblasts to regeneration will therefore have to be identified before new clinical trials are attempted. © 1994 John Wiley & Sons, Inc.
The medial calcaneal nerve: Anatomy and nerve conduction technique
Authors: Park Tracy A. , Del Toro David R. 
Published: January 2005

AbstractWe report a new technique for studying conduction in the medial calcaneal nerve (MCN). Dissection of 14 cadaver feet revealed the optimal G1 site to be one third of the way from the apex of the heel to a point midway between the navicular tuberosity and the prominence of the medical malleous. Seventy‐two feet (36 healthy volunteers) were studied using surface stimulation of the tibial nerve 10 cm proximal to the G1 surface electrode. Averaging technique was not required. Reference values (mean ± 2 SD) were determined for MCN onset latency (2.0 ± 0.3 ms), peak latency (2.5 ± 0.3 ms), onset conduction velocity (61 ± 11 m/s), peak conduction velocity (40 ± 5 m/s), baseline‐to‐peak amplitude (18 ± 6 μV), and maximum intrasubject side‐to‐side differences in these values (0.3 ms, 0.3 ms, 15 m/s, 5 m/s, and 17 μV, respectively). This study provides an easily performed, reproducible method for electrophysiologic evaluation of the MCN.© 1995 John Wiley & Sons, Inc.
Extensor digitorum brevis reflex in normals and patients with radiculopathies
Authors: Dillingham Timothy R. , Marin Raul , Belandres Praxedes V. , Chang Audrey 
Published: January 2005

AbstractThis prospective study evaluated the extensor digitorum brevis deep tendon reflex (EDBR) in a normal population and in patients with L‐5 and S‐1 radiculopathies. There were 88 subjects: 53 normals, 17 L‐5, and 18 S‐1 radiculopathy subjects. The clinical EDBR revealed a 91% specificity, with 18% sensitivity for L‐5, and 11% for S‐1. The electrodiagnostic EDBR yielded increased sensitivities of 35% for L‐5 (P = 0.07) and 39% for S‐1 (P = 0.04), with 87% specificity. H‐reflexes showed 50% sensitivity for the S‐1 group (P = 0.0006) and 91% specificity. EDBR latencies were significantly related to age and leg length (r2 = 0.46, P < 0.0001). Age alone explained 26% (P < 0.0001) of the EDBR variability and leg length 20% (P < 0.0001). EDBR clinical and electrodiagnostic reflexes have low sensitivities, high specificities, and do not discriminate L‐5 from S‐1 root involvement.© 1995 John Wiley &Sons, Inc.
Immunopathogenesis and treatment of the guillain‐barré syndrome—part I
Authors: Hartung Hans‐Peter , Toyka Klaus V. , Pollard John D. , Harvey Graham K. 
Published: January 2005

AbstractThe etiology of the Guillain‐Barré syndrome (GBS) still remains elusive. Recent years have witnessed important advances in the delineation of the mechanisms that may operate to produce nerve damage. Evidence gathered from cell biology, immunology, and immunopathology studies in patients with GBS and animals with experimental autoimmune neuritis (EAN) indicate that GBS results from aberrant immune responses against components of peripheral nerve. Autoreactive T lymphocytes specific for the myelin antigens PO and P2 and circulating antibodies to these antigens and various glycoproteins and glycolipids have been indentified but their pathogenic role remains unclear. The multiplicity of these factors and the involvement of several antigen nonspecific proinflammatory mechanisms suggest that a complex interaction of immune pathways results in nerve damage. Data on disturbed humoral immunity with particular emphasis on glycolipid antibodies and on activation of autoreactive T lymphocytes and macrophages will be reviewed. Possible mechanisms underlying initiation of peripheral nerve‐directed immune responses will be discussed with particular emphasis on the recently highlighted association with Campylobacter jejuni infection.© 1995 John Wiley &Sons, Inc.
Interaction of glucocorticoids and activity patterns affect muscle function
Authors: Dodd Stephen L. , Powers Scott K. , Vrabas Ioannis S. , Eason Jane M. 
Published: January 2005

AbstractThe purpose of this study was to determine the effects of glucocorticoids on muscle mass and contractile properties of muscles of similar fiber composition but differing in activity patterns. Rats were divided into two groups and administered prednisolone (5 mg/kg per day) (P;N = 9) or served as controls (C; N = 10) for 10 days. Contractile properties were then determined in the left gastrocnemius‐plantaris‐soleus (GPS) muscle complex and a strip of costal diaphragm (D). An index of fatigue was also determined in both muscle preparations. Whole‐body, GPS, and D weights decreased (P < 0.05) in the P animals (22%, 17%, and 15%, respectively) when compared to C. Specific tension (Po) increased (P < 0.05) in the GPS complex (21%) and decreased in the D (26%). Maximal shortening velocity (Vmax) was not different (P > 0.05) between groups in either the GPS or the D. While the index of fatigue was not different (P > 0.05) between groups in the D, there was a 30% increase (P < 0.05) in the rate of fatigue in the GPS. These data indicate that, although glucocorticoids cause decreased muscle mass in both D and GPS, a change in muscle architecture may prevent a decrease in force‐generating ability in some limb muscles. However, a glucocorticoids do not increase D fatigability as seen in the GPS.© 1995 John Wiley &Sons, Inc.
Charcot–marie–tooth neuropathies: From clinical description to molecular genetics
Authors: Ionasescu Victor V. 
Published: January 2005

AbstractNinety‐five families with Charcot‐Marie‐Tooth (CMT) neuropathies were studied clinically, electrophysiologically (MNCVs and EMGs), and by molecular genetics. Fifty‐four families (56.8%) were type 1A mapped at 17p11.2‐p12 and DNA duplication was present in 50 (92.6% of CMT1A families). One family with type 1B (1.1%) mapped at 1q22‐q23 showed a point mutation of the myelin Po gene. Eighteen families (18.9%) were type CMT2 based on electrophysiological studies. Molecular genetics was not yet conclusive. Twenty CMT families were with X‐linked dominant inheritance (CMTX1) (21.1%) mapped at Xq13.1 and connexin 32 (CX32) point mutations were present in 15 families (75%) (five nonsense mutations, eight missense mutations, two deletions). Two CMT families (2.1%) with X‐linked recessive inheritance showed no point mutations of CX32 and their mapping was different from CMTX1, respectively at Xp22.2 for CMTX2 and at Xq26 for CMTX3.© 1995 John Wiley &Sons, Inc.
Phrenic nerve conduction study in normal subjects
Authors: Chen Robert , Collins Stephen , Remtulla Hussein , Parkes Anthony , Bolton Charles F. 
Published: January 2005

AbstractPhrenic nerve conduction studies were performed in 50 phrenic nerves from 25 normal subjects using a technique modified from previously described methods. The normal ranges for latency, amplitude, negative peak area, and duration were established. The latency correlates with age and the amplitude increases with chest circumference. With our method, the amplitude increases and the duration decreases with lung volume. We found good right‐left agreement and reproducibility. Therefore, the unaffected side can be used as a reference in unilateral phrenic nerve lesions and previous studies can be used for comparison in serial studies. We recommend that phrenic nerve conduction studies be used routinely to diagnose and monitor patients with respiratory involvement from neuromuscular diseases.© 1995 John Wiley &Sons, Inc.
Progression of neuropathy in peripheral arterial disease
Authors: England John D. , Ferguson Michele A. , Hiatt William R. , Regensteiner Judith G. 
Published: January 2005

AbstractAtherosclerotic peripheral arterial disease (PAD) can cause muscle denervation, but whether it is associated with more severe peripheral nerve disease is not clear. Equally unclear is the effect of exercise training on the neuromuscular aspects of this disease. We performed serial electrophysiologic studies (nerve conduction studies and quantitative electromyography) and muscle strength assessment on 16 patients with moderately severe PAD. Seven of the patients were assigned to a natural history (control) group and 9 to and exercise training group. Over study periods ranging from 3 to 23 months, 6 to 7 patients in the control group and 8 of 9 patients in the exercise training group showed progression of multifocal neuropathic disease in their ischemic legs. For equivalent lengths of time, the degree of neuropathic progression was not significantly different between the control and exercise training group. There was a significant decline in muscle strength for the control group but not for the exercise training group. These results demonstrate that PAD can be associated with the development of a multifocal predominantly motor neuropathy, which is most likely ischemic in etiology. Furthermore, exercise training does not pose an additional risk for the development of neuropathy in patients with moderately severe PAD. © 1995 John Wiley & Sons, Inc.
Failure of anti‐GM1 IgG OR IgM to induce conduction block following intraneural transfer
Authors: Harvey Graham K. , Toyka Klaus V. , Zielasek JÜRgen , Kiefer Reinhart , Simonis Claudia , Hartung Hans‐Peter 
Published: January 2005

AbstractIn order to confirm the reported pathogenicity of human antibodies to monosialoganglioside GM1, immunoglobulin fractions with high anti‐GM1 IgG or IgM titers were prepared from patients with Guillain‐Barré syndrome and multifocal motor neuropathy respectively. These fractions were injected intraneurally into rat tibial nerves with fresh human complement. Neither the anti‐GM1 IgG nor the anti‐GM1 IgM fraction induced significant focal conduction block or slowing compared to a pooled fraction prepared from 5 normal individuals. In contrast, rabbit experimental allergic neuritis serum included as a positive control was highly active. Transverse sections of injected nerve failed to show evidence of demyelination. Staining for human immunoglobulin in cryostat sections showed the presence of injected anti‐GM1 antibody bound to nodes of Ranvier up to 6 days following intraneural transfer. These data fail to confirm previous reports of conduction block from intraneural transfer of anti‐GM1 serum and suggest that such electrophysiological effects may be the result of factors other than or in addition to anti‐GM1 antibodies. © 1995 John Wiley & Sons, Inc.