Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Fasciculation”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 397 records · Page 22Linked to original sources
PubMed1984

Pain-reducing effect of self-taming suxamethonium.

The effect was evaluated of a small "self-taming" dose of suxamethonium (0.1 mg/kg) on fasciculations and postoperative muscle pain following a normal intubating dose of suxamethonium (1.0 mg/kg). Forty outpatients undergoing bronchoscopy were randomly allocated to pretreatment with either sodium chloride or suxamethonium 0.1 mg/kg. The pretreatment dose was followed in 60 s by suxamethonium 1.0 mg/kg. Visual rating and mechanical registration of muscle fasciculations were done separately. Muscle pain was found in 74% and in 26% of the patients following pretreatment with sodium chloride and suxamethonium 0.1 mg/kg, respectively (P less than 0.01). No significant relationship was found between pain and muscle fasciculations. It is concluded that self-taming with suxamethonium has a marked pain-reducing effect; and this technique may be used as an alternative to pretreatment with a non-depolarizing relaxant.

Adult↗
PubMed2002

Diphenhydramine as a protective agent in a rat model of acute, lethal organophosphate poisoning.

OBJECTIVE: To evaluate the effects of diphenhydramine chloride (DPH) on mortality in a rat model of acute, severe organophosphate poisoning (OP). METHODS: Wistar rats (n = 40) were randomized to pretreatment with either normal saline (controls), 5 mg/kg atropine, 3 mg/kg DPH, 15 mg/kg DPH, or 30 mg/kg DPH given as a single intramuscular injection 5 minutes prior to a subcutaneous injection of 25 mg/kg dichlorvos (n = 8 per group). The primary endpoint was 10-minute survival. Survival at 24 hours was a secondary endpoint. Comparison of survival rates between groups was carried out by ANOVA and the Student-Newman-Keuls test. RESULTS: Dichlorvos exposure resulted in profound fasciculations within 2 minutes of injection in all cohorts. In controls, fasciculations were followed by respiratory arrest within 10 minutes (0% survival). The rats receiving atropine pre-treatment exhibited similar fasciculations (nicotinic effects) without subsequent respiratory arrest, resulting in a significant improvement in survival (88%, p < 0.001). The DPH-treated rats exhibited a significant dose-dependent reduction in mortality, with the 3 mg/kg, 15 mg/kg, and 30 mg/kg groups demonstrating 0%, 25%, and 100% survival, respectively. There was no additional mortality between 10 minutes and 24 hours in any group. There was no significant difference in survival between the high-dose DPH and the atropine groups. CONCLUSIONS: Diphenhydramine chloride significantly reduced mortality in rats with acute, severe dichlorvos exposure.

Animals↗
PubMed1993

Clinical syndrome and diagnosis of hyperkalaemic periodic paralysis in quarter horses.

Of the 16 horses studied, 14 belonged to a family previously shown to be susceptible to hyperkalaemic periodic paralysis (HPP), and 8 were shown to have HPP. Diagnosis of HPP by electromyographic detection of myotonic discharges or by oral administration of KCl to induce clinical signs and hyperkalaemia had similar reliability and gave the same result in 80% of cases. KCl had to be administered at doses up to 0.2 g/kg bodyweight to produce signs in some horses. KCl challenge testing was more time consuming than EMG and resulted in one fatality. Overall, electromyography and potassium challenge testing together gave the most accurate diagnosis. Horses were more likely to manifest signs of HPP if they were immature. There was no sex predisposition. The most frequent sign of HPP was muscle fasciculation. Other signs were sweating, muscle spasm, and weakness. Respiratory rate increased greatly during some attacks. Attacks of muscle fasciculation without hyperkalaemia were observed in 2 HPP-affected horses. Affected horses had a greater frequency of spontaneous clinical abnormalities, due mainly to trailering problems, traumatic abrasions and episodes of continuous muscle fasciculation. Hyperkalaemia was confirmed in only one of these instances.

Age Factors↗
PubMed1986

Primary amyloidosis with peripheral neuropathy and signs of motor neuron disease.

A 51-year-old man had primary amyloidosis, with typical amyloid neuropathy and signs of motor neuron disease, including widespread fasciculation in limb muscles, tongue atrophy and fasciculation, swallowing and chewing difficulty, symmetric hyperreflexia, and bilateral Hoffmann's signs. Fasciculations, fibrillations, and positive sharp waves were found in electromyography of all muscles tested. Motor nerve conduction velocities were moderately slow. Lambda chains were detected in serum and CSF. Amyloid was found in sural nerve biopsy. This combination of amyloid neuropathy and features of amyotrophic lateral sclerosis is related to the motor neuron disease of plasma cell dyscrasias.

Amyloidosis↗
PubMed2000

Slit inhibition of retinal axon growth and its role in retinal axon pathfinding and innervation patterns in the diencephalon.

We have analyzed the role of the Slit family of repellent axon guidance molecules in the patterning of the axonal projections of retinal ganglion cells (RGCs) within the embryonic rat diencephalon and whether the slits can account for a repellent activity for retinal axons released by hypothalamus and epithalamus. At the time RGC axons extend over the diencephalon, slit1 and slit2 are expressed in hypothalamus and epithalamus but not in the lateral part of dorsal thalamus, a retinal target. slit3 expression is low or undetectable. The Slit receptors robo2, and to a limited extent robo1, are expressed in the RGC layer, as are slit1 and slit2. In collagen gels, axon outgrowth from rat retinal explants is biased away from slit2-transfected 293T cells, and the number and length of axons are decreased on the explant side facing the cells. In addition, in the presence of Slit2, overall axon outgrowth is decreased, and bundles of retinal axons are more tightly fasciculated. This action of Slit2 as a growth inhibitor of retinal axons and the expression patterns of slit1 and slit2 correlate with the fasciculation and innervation patterns of RGC axons within the diencephalon and implicate the Slits as components of the axon repellent activity associated with the hypothalamus and epithalamus. Our findings suggest that in vivo the Slits control RGC axon pathfinding and targeting within the diencephalon by regulating their fasciculation, preventing them or their branches from invading nontarget tissues, and steering them toward their most distal target, the superior colliculus.

Animals↗
PubMed1992

Potential of memantine, D-tubocurarine, and atropine in preventing acute toxic myopathy induced by organophosphate nerve agents: soman, sarin, tabun and VX.

Male Sprague-Dawley rats when administered sc a sublethal dose of organophosphorus cholinesterase inhibitors such as the nerve agents, soman (100 micrograms/kg, sc), sarin (110 micrograms/kg, sc), tabun (200 micrograms/kg, sc), or VX (12 micrograms/kg, sc), developed seizures and severe muscle fasciculations within 15-20 min, lasting for 4-6 hr. Marked inhibition of acetylcholinesterase (AChE) and necrotic lesions in skeletal muscles such as soleus, extensor digitorum longus, and diaphragm were evident between 1-24 hr following injection. Pretreatment with memantine HCl (MEM, 18 mg/kg, sc) together with atropine sulfate (ATS, 16 mg/kg, sc), 60 min and 15 min, respectively, prior to nerve agents attenuated AChE inhibition, prevented myonecrosis, and muscle fasciculations as well as other signs of cholinergic toxicity. Pretreatment combining d-tubocurarine (d-TC, 0.075 mg/kg, sc) and ATS (16 mg/kg, sc) prevented the myonecrosis and fasciculation without protecting AChE against inhibition by these nerve agents. Neither MEM, d-TC, nor ATS in the concentration given interfered with the normal behavior of the rats. The role of d-TC and ATS interaction with presynaptic receptors regulating ACh release and MEM's role in modulating neural hyperactivity as protective mechanisms are discussed.

Acetylcholinesterase↗
PubMed1990

The avian tectobulbar tract: development, explant culture, and effects of antibodies on the pattern of neurite outgrowth.

The tectobulbar tract is the first long-distance projecting fiber pathway to appear during the development of the avian optic tectum (dorsal half of the mesencephalon). Immunologically stained wholemounts of the E3 mesencephalon reveal that the early tectobulbar axons course in a dorsal-to-ventral direction and abruptly turn in a caudal direction shortly before reaching the ventral midline. During subsequent development, more tectobulbar axons are generated that form a parallel array of thick fascicles coursing ventrally within the mesencephalon. At this later stage of development, the tectobulbar tract bifurcates into an ipsilateral and contralateral pathway, both growing in a caudal direction near the mesencephalic ventral midline. Bifurcation and change in direction of growth is accompanied by a complete loss of the fasciculated growth pattern. Each tectobulbar axon is thus divided into a proximal fasciculated and a distal unfasciculated segment. Tectobulbar fascicles occupy the most superficial surface layer of the mesencephalon at early stages and are displaced deeper into the tissue beginning at embryonic day 5. In both of these locations, tectobulbar axons express molecules involved in axon-axon and axon-substrate interactions like the G4 antigen, neural cell adhesion molecule (N-CAM), neurofascin, and T61 antigen as revealed by immunohistochemistry and immunoblotting. Stripes of the mesencephalon explanted onto a basal lamina substratum show vigorous outgrowth of neurites. These processes grow in fascicles at a growth rate of 40 microns/h. Staining of the neurites with specific antibodies, as well as the position of the retrogradely labeled cell bodies, is in agreement with these processes being tectobulbar axons. This in vitro explant system was used to investigate the expression and possible functional involvement of N-CAM, neurofascin, G4 protein, and T61 antigen in the growth of these axons. The presence of antigen-binding fragments of polyclonal anti-G4 antibodies completely blocks fasciculation of the neurites but has no influence on their rate of elongation. Antibodies against N-CAM and neurofascin have no detectable effects. The number and length of the in vitro growing axons are reduced by the monoclonal T61 antibody. This effect is reversible. The elucidation of the exact course in vivo and the accessibility to the axons growing in vitro make the tectobulbar tract an excellent model system for the investigation of the role of these and other proteins in axonal growth and guidance during the development of the CNS.

Animals↗
PubMed1986

Neurite outgrowth patterns in cerebellar microexplant cultures are affected by antibodies to the cell surface glycoprotein L1.

To probe for the role of the L1 cell surface glycoprotein during neurite outgrowth and fasciculation in the early postnatal mouse cerebellar cortex, a microexplant culture system was used. Fasciculation of neurites was reduced in the presence of antigen-binding fragments (Fab) of poly- and monoclonal L1 antibodies, as compared to untreated controls. In addition, speed of neurite outgrowth was enhanced in the presence of antibodies. Migration of cell bodies of small neurons was also significantly increased. Very similar effects on these outgrowth parameters were observed with Fab fragments from poly- and monoclonal neural cell adhesion molecule (N-CAM) antibodies. Antibodies from preimmune sera had no effect. These findings suggest that L1 antigen not only plays a role in adhesion of isolated neural cell bodies and migration of granule cell neurons in the early postnatal mouse cerebellar cortex (Lindner et al., 1983; Rathjen and Schachner, 1984), but also in neurite outgrowth and fasciculation.

Animals↗
PubMed1987

A comparison of d-tubocurarine pretreatment and no pretreatment in obstetric patients.

The effect of pretreatment with d-tubocurarine on the incidences of succinylcholine-induced fasciculations and post-operative muscle pain, and the time to onset of and 50% recovery from neuromuscular blockade were studied in 75 obstetric patients. Thirty women with term pregnancies undergoing general anesthesia for elective cesarean section or cesarean section indicated by cephalopelvic disproportion were randomly assigned to two groups. Group C-1 patients received 0.05 mg/kg of d-tubocurarine followed by 1.5 mg/kg of succinylcholine, and group C-2 patients received 1.5 mg/kg of succinylcholine, and group C-2 patients received 1 ml of normal saline followed by 1 mg/kg of succinylcholine. An investigator, unaware of the relaxant regimen used, judged severity of fasciculations and postoperative muscle pain and measured times to onset of and 50% recovery from neuromuscular blockade. This same study design was followed in a group of 30 women undergoing tubal ligation 1 day after vaginal delivery (groups T-1 and T-2). The incidence of both fasciculations and postoperative muscle pain was low and was not significantly different between pretreated and nonpretreated groups. Time to 100% twitch depression was also not significantly different between pretreated and nonpretreated groups. Time to 50% recovery from neuromuscular blockade was significantly longer in both nonpretreated groups (C-2 and T-2). An additional group of 15 patients undergoing general anesthesia for cesarean section using 0.7 mg/kg of succinylcholine without d-tubocurarine pretreatment was studied (group C-3). This smaller dose of succinylcholine produced onset and 50% recovery times similar to the group pretreated with d-tubocurarine (group C-1).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1994

Motor unit hyperactivity states (a correlative clinico-electromyographical study).

The systematic overview of spontaneous motor unit or muscle fiber activity is presented. In Part 1 the precise clinical description of fasciculations, myokymia and cramps/spasms was made using a dynamic holistic approach. The differences are often a matter of excitation quantity. Correlations with electrophysiological findings were elaborated on the grounds of literature data and personal experience. Electrophysiological correlations with clinically visible fasciculations resulted in the finding that the same clinical phenomenon may have many entirely different electrophysiological correlates. The special forms of repetitive discharges were described additionally: positive giant potentials of quadriceps muscles appearing in healthy muscular individuals and grouped potential discharges of very chronic nerve ending involvement. The electrophysiological features and genesis of many motor unit hyperexcitability signs were discussed, while topic differentiation possibilities and symptomatic treatment were recommended for some. The spontaneous activity in different nosological entities was presented in Part 2. Again the literature data on diseases with conspicuous fasciculations, myokymia and cramps with additional personal experiences (pesticide intoxication, Isaacs syndrome, hereditary autosomal cramp disease, chronic syndrome due to parathyroid insufficiency, chronic tetanus and others) were presented. A description was also given of personal observations in strictly localized forms: single nerve or root lesions and in M. Romberg patient. Symptomatic and causal treatment was suggested for some of them. Clinically similar signs may have entirely different causes responding specifically to carbamazepine, D3, PAM, or surgical decompression. The electromyographic finding may remain clinically silent even in myotonia.

Electromyography↗
PubMed1996

The behavior of optic axons on substrate gradients of retinal basal lamina proteins and merosin.

To study the behavior of optic axons to continuously changing concentrations of their substrate, explants from embryonic retina were placed across gradients of retinal basal lamina proteins and merosin. The following growth patterns of axons in response to the substrate gradients were found: (1) Axons that grew up gradients, i.e., from low to high substrate concentrations, became longer and less fasciculated with increasing concentration of the substrate. On shallow basal lamina gradients, the axons also showed a directional response that resulted in guidance to higher substrate concentrations. (2) Axons that grew down gradients, i.e., from high to low substrate concentrations, became shorter and more fasciculated with decreasing concentrations of the substrate. On gradients of merosin, a significant alteration in the axonal growth direction toward higher substrate concentrations was detected. Axons heading down gradients never U turned to higher substrate concentrations. (3) Axons confronted with discontinuous substrates were confined to the borders of the substrate exclusively, whereas axons confronted with substrate gradients were able to cross into the territory beyond the substrate. (4) The growth patterns of axons on substrate gradients of basal lamina proteins and merosin were similar but not identical, indicating that axons may respond to substrate gradients dependent on its chemical composition. The present results show that substrate gradients can regulate length and fasciculation of neurites and have a limited capability to direct axons to higher substrate concentrations.

Animals↗
PubMed1996

Variation of serum potassium and creatinine phosphokinase levels in suxamethonium-induced muscle relaxation.

Popular depolarising muscle relaxant, suxamethonium (succinylcholine chloride), produces fasciculation in group of muscles and 'after pain'. Mode of its action is neuromuscular blockage. It also may be associated with muscle fibre injury and altered membrane permeability. These may cause rise of serum K+ and creatinine phosphokinase (CPK) levels. But use of diazepam either during or as pretreatment may reduce the fasciculation, 'after pain' and rise of K+ and CPK levels. Present study was undertaken to show whether any correlation of the degree of fasciculation and postsuxamethonium myalgia is present or not and whether diazepam has any role in reducing muscle injury and in turn reducing the levels of serum K+ and CPK.

Adult↗
PubMed1977

[Electromyographic rest-activity. Unusual forms of spontaneous discharge in healthy and sick skeletal muscle].

The forms of spontaneous activity termed as "benign fibrillation potentials" and "benign positive sharp waves" differ from the denervation potentials of the same wave form in the discharge pattern. Fibrillation potentials and positive sharp waves due to a denervation process show a characteristic rhythmical discharge sequence. "Benign fibrillation potentials" and "benign positive sharp waves", on the other hand, display a big difference in the duration of the time intervals between successive waves. It is important to be aware of the frequent occurrence of these benign fibrillations in normal muscles, in order to avoid erroneously diagnosing a denervation process. As in the case of malign fasciculations, "proximal fasciculations" generally occur in lesions of the proximal segment of the lower motoneuron, and have the same diagnostic significance. Unlike malign fasciculations, however, they do not originate in the region of the terminal nerve branches, but at the site of the lesion in question. Local reduction in the stimulus threshold and in the accommodation ensure that a spontaneous impulse will occur. "Low frequency bizarre discharges" and "periods of grouped and serial-discharges" occur mainly in the late phase of a neuromuscular disease and are found especially after traumatic lesions or lesions due to entrapment. We are able to demonstrate that the "low-frequency bizarre discharges" are of myogenic origin, whereas the "periods of grouped and serial-discharges" more than likely originate in the course of the peripheral motoneuron from an active focus.

Action Potentials↗
PubMed1979

Amyotrophic lateral sclerosis. Impairment of neuromuscular transmission.

Neuromuscular transmission was studied in the ulnar-hypothenar group in 55 patients with amyotrophic lateral sclerosis. A decremental response was found in 67.0%. The decrement was larger and present more often in muscles showing atrophy. In addition, muscles with frequent fasciculations showed a larger decrement than the ones with rare fasciculation. A temperature effect similar to that in myasthenia gravis was observed, with a reduction of the decrement following local cooling of the muscles. Administration of edrophonium chloride improved the synaptic defect. Posttetanic exhaustion was observed as well. It is thought that the defect of neuromuscular transmission is due to a decreased trophic function of the neuron followed by morphological changes at the endplate.

Adolescent↗
PubMed1989

Electrocardiographic abnormalities in childhood spinal muscular atrophy.

Tremors of the isoelectric line in routine electrocardiograms have been described in patients with spinal muscular atrophy and have been interpreted as fasciculations of denervated muscles. In order to evaluate this phenomenon, 13 patients with spinal muscular atrophy have been studied (average age: 37.3 months). A first electrocardiogram was recorded routinely; a second tracing was then recorded with double sensitivity and double speed. In addition, all patients were evaluated clinically and had M-mode and cross-sectional echocardiography. Regular and constant spikes on the isoelectric electrocardiographic line were recorded in 12 patients (93.4%); their frequency ranged from 39 to 48 cycles/sec (average: 42.08 +/- 2.64). Contrary to previous reports, we found an "abnormal" electrocardiogram in all our patients with severe spinal muscular atrophy. The only patient with a normal electrocardiogram had a mild and clinically stable form of spinal muscular atrophy. We did not find any significant structural cardiac abnormality by clinical and echocardiographic evaluation. We conclude that continuous tremor on the isoelectric line of electrocardiogram represents a characteristic of spinal muscular atrophy in these patients. It is a result of muscle fasciculations and does not imply any abnormality of the heart.

Adolescent↗
PubMed1994

Amyotrophic lateral sclerosis: hypothetical pathogenesis.

A hypothetical pathogenesis for a typical case of amyotrophic lateral sclerosis (ALS) follows from opinions of Rowland and results of neuroscientists at Baylor. ALS might typically result from an autoimmune disorder that causes IgG to enhance release of acetylcholine (ACh) from axon terminals. Motor neuron overactivity associated with fasciculation might result from enhanced release of ACh which is taken up by nicotinic ACh receptors. Increased levels of intracellular calcium ions might result from motor neuron overactivity associated with fasciculation. Neuronal cell degeneration and death might result from increased levels of intracellular calcium ions.

Acetylcholine↗
PubMedDate not supplied

Midazolam pretreatment does not ameliorate myoglobinemia or the clinical side effects of succinylcholine.

STUDY OBJECTIVE: To determine whether the levels of serum myoglobin and the occurrence of fasciculations and postoperative symptoms following a single dose of succinylcholine are modified by the prior administration of midazolam. DESIGN: Randomized, double-blind, placebo-controlled study. SETTING: Outpatient surgical service of a university hospital. PATIENTS: 69 ASA physical status I and II healthy, adult female outpatients undergoing laparoscopy (for diagnosis or tubal ligation) with general anesthesia that included succinylcholine. INTERVENTIONS: Patients received pretreatment of either a saline placebo (Group 1, n = 31) or intravenous midazolam 0.03 mg/kg (Group 2, n = 38) 5 minutes before succinylcholine. MEASUREMENTS AND MAIN RESULTS: Serum myoglobin prior to pretreatment and at 5 (t5) and 30 (t30) minutes after succinylcholine was determined by radioimmunoassay. Pain was assessed by telephone interview 24 to 36 hours postoperatively. Baseline myoglobin levels ranged from 14 to 69 ng/ml; the 5- and 30-minute samples varied widely (range, 16 to 900 ng/ml). The rise was 3 or more SDs above the baseline mean in 23% and 42% of Group 1 at t5 and t30, respectively, and in 21% and 35% of Group 2 at t5 and t30, respectively. The differences between groups were not significant. The frequency of fasciculations (77% in Group 1, 87% in Group 2), postoperative sore throat (64% in Group 1, 57% in Group 2), and myalgias (44% in Group 1, 51% in Group 2) also was not significantly different between groups. CONCLUSIONS: Midazolam had no effect on myoglobin level or postoperative symptoms following succinylcholine.

Adult↗
PubMed2006

Predictors of delay in the diagnosis and clinical trial entry of amyotrophic lateral sclerosis patients: a population-based study.

BACKGROUND: The El Escorial and the revised Airlie House diagnostic criteria for amyotrophic lateral sclerosis (ALS) were introduced to select patients for clinical trials. Heterogeneity of clinical presentation at onset and delay in diagnosis may decrease the likelihood for trial entry. OBJECTIVE: Identify risk factors for delay in the diagnosis and trial exclusion. METHODS: ALS incident cases were identified with El Escorial (EEC) and Airlie House criteria (AHC) through a population-based registry established in Puglia, Southern Italy, in the years 1998-99. RESULTS: 130 ALS incident cases were diagnosed with a median interval between onset of symptoms and diagnosis of 9.3 months and not different across both EEC and AHC categories. Twenty percent of cases were not eligible for clinical trials according to the AHC. About 5% of subjects in this series died with only lower motor neuron signs. Predictors for delay in the diagnosis were age between 65 and 75 years and spinal onset while fasciculations and cramps as first symptoms were predictors of exclusion from trials. CONCLUSIONS: In this population-based series, diagnostic delay was longer in subjects with spinal onset and age between 65 and 75 and fasciculation as first symptoms. About 80% of incident cases were trial eligible with AHC criteria. However, a significant number of subjects with ALS, characterized by a limited spread of signs, were not trial eligible while alive.

Adult↗