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PubMed1993

Action of nerve agents to cholinesterases.

Changes of acetylcholinesterase activity in the blood and different organs of the rat following intoxication with sarin, soman, VX and 2-dimethylamino-ethyl-(dimethylamido)phosphonofluoridate (GV) in doses of approximately 2 x LD50 (i.m.) were obtained from literature data and by experiment. The time course of acetylcholinesterase inhibition in the blood, regions of brain and diaphragm and the occurrence of signs and symptoms of poisoning (none, salivation, disturbed ventilation and fasciculations, convulsions or death) were summarized and compared. When blood enzyme activities were 70-100% normal, no signs were seen; at 60-70%, salivation occurred; at less than 30-55%, disturbed ventilation and fasciculations were seen while at 15-30%, convulsions occurred. Less than 10% was fatal. In experiments with narcotized dogs, the blood acetylcholinesterase activity and its reactivatability with trimedoxime were determined following intoxication (i.m.) with the above mentioned four compounds. It can be concluded that acetylcholinesterase activity in the blood corresponds to that in the target organs and can be considered as an appropriate parameter for biological monitoring of nerve gas exposure. Moreover, determination of reactivatability of blood acetylcholinesterase indicates more information than simple enzyme activity determination.

Acetylcholinesterase↗
PubMed1993

Cell-cell interactions during the migration of an identified commissural growth cone in the embryonic grasshopper.

One of the fascicles of the posterior commissure of the embryonic grasshopper is pioneered by an individually identifiable neuron named Q1. Q1 initially grows along a longitudinal pathway established by another pioneer neuron, MP1, and then crosses to the midline, where it meets and fasciculates with the axon of the contralateral Q1. The Q1 growth cone follows the contralateral Q1 axon to the contralateral longitudinal pathway, where it then fasciculates with axons of the MP1/dMP2 fascicle. In this work, we have identified a small set of early neurons that Q1 could use as guidance cues while negotiating its way along a specific and stereotyped pathway to the midline. Furthermore, we have observed characteristic morphological changes in the Q1 growth cone that could indicate responses to changing adhesivity in the substrates it contacts. We have also quantified the pattern of dye coupling between neurons in this system. Most of the neurons to which Q1 becomes coupled retain a strong, consistent pattern of dye coupling that shows no recognizable variation at times when growth cones are making pathway decisions. However, we have found one clear instance of transient, site-specific dye coupling between the Q1 growth cone and the ipsilateral MP1 soma. The timing and pattern of dye coupling in this system suggest that dye coupling may play a role in synchronizing the initiation of axon outgrowth among a small population of neurons. Although dye coupling may not play a direct role in neuronal pathfinding, it may exert a profound indirect influence on neuronal interactions by regulating the timing of axon outgrowth.

Animals↗
PubMed1995

[Potassium channel dysfunction at the lesion site in multifocal motor neuropathy as revealed by threshold electrotonus].

Multifocal motor neuropathy presents as a treatable muscular atrophy and is characterized by persistent conduction block and fasciculations or myokymia. Although the pathological findings at the lesion site revealed perivascular demyelination with little evidence of remyelination, the mechanism of conduction block is still unknown. We explored the threshold electrotonus, which registers membrane potential changes through threshold variation, at the lesion site. The findings were consistent with focal potassium channel dysfunction, with some evidence of depolarization block. The disrupted blood-nerve barrier and lack of Schwann cell-mediated extracellular potassium regulation may predispose the membrane depolarization, thereby accounting for the conduction block and fasciculations. Sensory nerve fibers are known to have more inward rectifiers, which take up the extracellular potassium, than motor fibers, and this may explain the sparing of these fibers.

Humans↗
PubMed1996

Sek4 and Nuk receptors cooperate in guidance of commissural axons and in palate formation.

Sek4 and Nuk are members of the Eph-related family of receptor protein-tyrosine kinases. These receptors interact with a set of cell surface ligands that have recently been implicated in axon guidance and fasciculation. We now demonstrate that the formation of the corpus callosum and anterior commissure, two major commissural axon tracts that connect the two cerebral hemispheres, is critically dependent on Sek4 and Nuk. While mice deficient in Nuk exhibit defects in pathfinding of anterior commissure axons, sek4 mutants have defects in corpus callosum formation. The phenotype in both axon tracts is markedly more severe in sek4/nuk1 double mutants, indicating that the two receptors act in a partially redundant fashion. sek4/nuk1 double mutants also exhibit specific guidance and fasciculation defects of diencephalic axon tracts. Moreover, while mice singly deficient in either Sek4 or Nuk are viable, most sek4/nuk1 double mutants die immediately after birth primarily due to a cleft palate. These results demonstrate essential and cooperative functions for Sek4 and Nuk in establishing axon pathways in the developing brain, and during the development of facial structures.

Animals↗
PubMed1997

Characterization of microwell cultures of dissociated brain tissue for studies of cell-cell interactions.

Microwell cultures of dissociated tissue from prenatal rat hippocampus and cerebral cortex as well as from early postnatal cerebellum were used for quantification of neuronal aggregation, process extension, and fasciculation. It was shown that the cells in culture from these different brain regions developed differently with regard to both architecture and rate of differentiation. The effect of a polyclonal antibody against the neural cell adhesion molecule (NCAM), the excitatory amino acid receptor agonist N-methyl-D-aspartate (NMDA), and the neurotoxin acrylamide on aggregation and fiber formation was investigated. Exposure to the NCAM antibody led to formation of fewer but larger aggregates and stimulated the morphological development of the cultures. Acrylamide affected aggregate formation, leading to smaller but more numerous aggregates, and it inhibited process extension and fasciculation. Treatment with NMDA affected process formation and led to formation of more numerous but smaller aggregates. Some of these effects were strongly tissue-dependent. Thus, large differences were seen regarding the effect of the NCAM antibody on aggregation and process extension in cultures from the different brain areas. The culture systems appear to represent convenient and reliable screening tools to study the influence of putative morphoregulatory substances on cell-cell interactions during early neuronal development.

Animals↗
PubMed1997

[The diagnosis of amyotrophic lateral sclerosis supported by motor evoked potential and brain MRI studies].

A 57-year-old man developed severe muscle weakness and atrophy of the upper extremities within a five-month period. Neurological examination revealed severe weakness and atrophy in the scapular muscles and proximal and distal muscles of the upper extremities. Fasciculations were also observed in the various muscles of the upper extremities. There was neither muscle weakness, atrophy nor fasciculation in either his face, neck muscles or lower extremities. He had no pseudobulbar or bulbar signs. Tendon reflexes were mildly hyperactive in the jaw and lower extremities, and normal in the upper extremities. There were no pathological reflexes, spasticity or sensory disturbances. The needle EMG study revealed denervation potentials in all muscles of the upper extremities examined. The nerve conduction study revealed no findings of the conduction block. Cervical spine X-rays revealed the narrowing of the spinal foramens at the left C3/C4 and bilateral C4/C5, C5/C6, and C6/C7 intervertebral levels. In addition, magnetic resonance imaging (MRI) revealed compressions of the cervical cord at C4/C5 and C5/C6 intervertebral levels. These clinical and neuroradiological findings resembled those of the cervical spondylotic amyotrophy (CSA). However, the motor evoked potential (MEP) study revealed the pyramidal tract dysfunction above the levels of the pyramidal decussation. Furthermore, brain MRI revealed abnormal foci in both internal capsules which were characterized by hyperintense relative to cortical gray matter on T2-weighted images and still hyperintense to white matter on proton-density-weighted images. In addition, T2-weighted images demonstrated a low signal within the motor cortex and hyperintense lesions in the white matter of the precentral gyri. These MRI findings indicated the degeneration of the pyramidal tract and corresponded to those found in the patients with amyotrophic lateral sclerosis (ALS) which have been recently reported. It has been difficult to distinguish ALS from CSA. However, MEP and brain MRI studies were useful for distinguishing these two diseases in this patient. In addition, this patient showed typical MRI findings suggesting the degeneration of the pyramidal tract, although this patient had a relatively short course of illness and did not show obvious physical findings suggesting pyramidal tract dysfunction.

Amyotrophic Lateral Sclerosis↗
PubMed1998

X-linked recessive bulbospinal neuronopathy: clinical and molecular studies in a Taiwanese family.

We describe clinical, biochemical, and molecular studies on a Taiwanese family with X-linked recessive bulbospinal neuronopathy. There were three probands and five female carriers among the 23 members examined. The clinical manifestations included progressive muscle weakness, diffuse fasciculation, postural tremor, muscle cramps, dysarthria, dysphagia, diabetes, and gynecomastia. Phenotypic expression varied among the affected subjects. Two carriers also had postural tremor and perioral fasciculation. Endocrine tests were normal except for a mild increase in serum testosterone and/or growth hormone in one patient and one carrier. Type IV hyperlipoproteinemia was observed in two patients, one carrier, and one healthy offspring. Molecular genetic studies confirmed elongation of the CAG triplet repeat in exon 1 of the gene for the androgen receptor. Sequence analysis showed that there were 42 to 43 CAG repeats in the three probands and 42 to 45 in the five carriers. The mutant allele had a tendency to increase by one or two repeats from one generation to the next. The length of CAG repeats at which the mutant allele became unstable was shorter in our family than in previous reports. The normal allele was also unstable and had a tendency to shrink by one of five repeats during transmission. These findings suggest that the number of CAG triplet repeats is variable in both the mutant and normal alleles.

Adolescent↗
PubMed1996

Isaacs' syndrome associated with chronic inflammatory demyelinating polyneuropathy.

We report the first case of Isaacs' syndrome in which an inflammatory demyelinating neuropathy was documented histologically. For 9 months, the patient developed slowly progressive weakness, muscle spasms and stiffness, fasciculations, and myokymia in the arms, which were unmodified by sleep. Nerve conduction studies showed multifocal motor conduction block, abnormal dispersion phenomenon, and abnormal sensory and mixed nerve conduction. Needle electromyogram showed continuous motor unit potentials at rest with bursts of rapid-firing discharges which were unaffected by spinal anesthesia but diminished by peripheral nerve block and completely abolished by local curarization. Sural nerve biopsy demonstrated an inflammatory demyelinating neuropathy. Muscle cramping, twitching, and stiffness responded to phenytoin. The patient's weakness gradually responded to prednisone and azathioprine. Over a 17-year period, the patient had three relapses which were well controlled with prednisone and azathioprine. At this time, the patient is symptom-free without any medication.

Demyelinating Diseases↗
PubMed1979

Diazepam prevents some adverse effects of succinylcholine.

Neuromuscular, circulatory, and adverse effects of intravenous succinylcholine (SCh), mg/kg, were compared in 3 groups of 40 patients each. Group I served as control; group II received diazepam, 0.05 mg/kg, 5 min before SCh; and group III was given d-tubocurarine (d-Tc), 0.05 mg/kg, for pretreatment. Diazepam pretreatment prevented muscle fasciculations, increases in serum potassium (K+) and creatinine phosphokinase (CPK) levels, increased heart rate and arterial pressure, and postoperative myalgia associated with SCh administration. The neuromuscular blocking action of SCh was not affected. Pretreatment with d-Tc did not abolish increases in serum K+ and CPK levels, was associated with a higher incidence of postoperative myalgia, and decreased the onset and magnitude of SCh-induced muscle paralysis. Our data demonstrate that diazepam, a predominant centrally acting muscle relaxant, is more effective than d-Tc in preventing the adverse effects of SCh, a peripherally acting muscle relaxant.

Adolescent↗
PubMed1996

Diisopropylphosphorofluoridate-induced muscle hyperactivity associated with enhanced lipid peroxidation in vivo.

Acute exposure to acetylcholinesterase (AChE) inhibitors such as organophosphates and carbamates induces functional changes at the neuromuscular junctions, leading to fasciculations that ultimately cause muscle fiber necrosis. There is recent evidence that oxygen free radical formation may be a factor in the toxicity of these insecticides. One of the targets of free radical-induced injury is lipid peroxidation. The role of lipid peroxidation in diisopropylphosphorofluoridate (DFP)-induced muscle necrosis was investigated by quantifying two products resulting from the oxidation of lipids in muscle tissue-the thiobarbituric acid-malondialdehyde complex (TBA-MDA) and F2-isoprostanes, the latter being a novel and extremely accurate marker of lipid peroxidation in vivo. When compared with control animals, significant increases in MDA of 96% and in F2-isoprostanes of 56% were found in the diaphragms of rats treated with 2.0 mg/kg DFP after 60 min (P < 0.01). In rats pretreated with the neuromuscular blocking agent d-tubocurarine or the lazaroid U-78517F, an antioxidant, no DFP-induced increases in either MDA or F2-isoprostanes were observed. It is suggested that the AChE inhibitor-induced cholinergic hyperactivity initiates that accumulation of free radicals leading to lipid peroxidation, which may be the initiator of the AChE inhibitor-induced cell injury.

Animals↗
PubMedDate not supplied

Poliomyelitis-like illness after acute asthma (Hopkins syndrome): a histological study of biopsied muscle in a case.

A case of Hopkins syndrome is presented. The patient was a 4-year-old boy who developed weakness of the right leg 2-3 days after a mild asthmatic attack. Needle electromyography revealed fasciculation discharges in the right gastrocnemius muscle. A histological study of the biopsied right quadriceps femoris muscle revealed scattered atrophic fibers, indicating lesions in the anterior horn cells of the spinal cord. This is the first reported case of Hopkins syndrome including muscle pathology.

Asthma↗
PubMed2004

Repetitive nerve stimulation for the evaluation of peripheral nerve hyperexcitability.

OBJECTIVE: To examine the utility of repetitive nerve stimulation (RNS) in the evaluation of peripheral nerve hyperexcitability (PNH). BACKGROUND: PNH describes a group of disorders characterized by muscle cramps, twitching and stiffness. When severe, PNH may be characterized by the presence of continuous muscle fiber activity on routine needle electromyography (EMG). In milder forms of the disease, nerve hyperexcitability may be evidenced by the presence of after-discharges or cramp potentials following RNS. METHODS: Fifty-four patients were prospectively recruited and classified into one of three groups-PNH, other neuromuscular disease and controls. We recorded and quantified the after-discharges and cramp potentials following RNS at 1, 5, 10 and 30 Hz. RESULTS: The proportion of nerves with after-discharges and/or cramp potentials was significantly greater in the PNH group than the control group at both 5 Hz (p=0.03) and 10 Hz (p=0.01), as well as in the neuromuscular disease group compared to controls at 5 Hz (p=0.02). There was also a significant concordance between complaints of muscle cramps and fasciculations and the finding of after-discharges and/or cramp potentials at both 5 Hz (p=0.005) and 10 Hz (p=0.004). At a stimulation frequency of 10 Hz, the sensitivity of RNS for the diagnosis of PNH (primary or secondary) was 79% and the specificity was 88%. CONCLUSION: Our findings suggest that RNS at or below a stimulation frequency of 10 Hz (when positive) is a useful test for the diagnosis of PNH, whether it is primary or secondary.

Adult↗
PubMed2004

Comparative effects of huperzine A, donepezil and rivastigmine on cortical acetylcholine level and acetylcholinesterase activity in rats.

The cholinesterase inhibitors huperzine A, donepezil and rivastigmine were compared for their effects on extracellular acetylcholine concentration and acetylcholinesterase activity in the rat cortex. After i.p. injection, huperzine A (0.25-0.75 micromol/kg), donepezil (2-6 micromol/kg) and rivastigmine (0.75-1.5 micromol/kg) dose-dependently elevated the concentration of acetylcholine. The duration of huperzine A was longest. The time courses of cortical acetylcholinesterase inhibition with middle doses of these agents mirrored the increases of acetylcholine at the same doses. However, acetylcholinesterase inhibition was disproportionately greater after middle dose of rivastigmine than doses of huperzine A and donepezil that increased acetylcholine to a similar extent. Muscle fasciculation appeared only after donepezil with a dose-dependent incidence and intensity. In molar terms, huperzine A was 8- and 2-fold more potent than donepezil and rivastigmine, respectively, in increasing cortical acetylcholine levels, with a longer-lasting effect.

Acetylcholine↗
PubMed1998

A variant form of feline Borna disease.

Borna disease virus (BDV) is a neurotropic agent with capacity to infect and cause encephalomyelitis in a wide range of animals, including horses, sheep, cattle and cats. Recent interest in BDV as a potential human pathogen has been stimulated by reports of BDV-specific antibodies and nucleic acid in patients with neuropsychiatric diseases. The pathogenesis of Borna disease (BD) in naturally infected animals is believed to be immune-mediated, mainly through the action of cytotoxic T cells. In this paper, a case of feline BD with atypical clinical and histopathological features is reported. Clinically, the cat showed muscle fasciculation and proprioceptive defects. Despite absence of encephalitis, numerous neurons were infected with BDV as shown by in-situ hybridization. This indicates that BDV infection may lead to various disease patterns, depending on differences in viral pathogenicity, or on as yet unidentified host-specific factors.

Amino Acid Sequence↗
PubMed1998

Diagnosis of amyotrophic lateral sclerosis.

This review of the differential diagnosis of amyotrophic lateral sclerosis focuses on two themes. The first is practical, how to establish the diagnosis based primarily on clinical findings buttressed by electrodiagnosis. The main considerations are multifocal motor neuropathy and cervical spondylotic myelopathy. The second theme is the relationship of motor neuron disease to other conditions, including benign fasciculation (Denny-Brown, Foley syndrome), paraneoplastic syndromes, lymphoproliferative disease, radiation damage, monomelic amyotrophy (Hirayama syndrome), as well as an association with parkinsonism, dementia and multisystem disorders of the central nervous system.

Amyotrophic Lateral Sclerosis↗
PubMed2002

Multifocal motor neuropathy and asymptomatic Hashimoto's thyroiditis: first report of an association.

Motor neuropathy with multifocal conduction blocks represents a recently identified autoimmune disorder of the peripheral nerve myelin. Association of motor neuropathies or neuronopathies with thyroid disorders, such as hyperthyroidism, hypothyroidism or thyroid neoplasms has been rarely described. We studied a 61-year-old man with a 2-year-history of slowly progressive weakness of the left limbs with atrophy and fasciculations. Nerve conduction velocity studies revealed multifocal motor conduction blocks. Serum IgM titer of antibodies against GM1 was elevated (1:1280; n.v. up to 1:640). Thyroid studies were compatible with Hashimoto's thyroiditis. Therapy with high dose intravenous immunoglobulins was followed by a prompt clinical recovery. Then the disease assumed an intravenous immunoglobulins dependent course with a full clinical, but transient, recovery. This is the first observation of an association of multifocal motor neuropathy with high titers of GM1 and Hashimoto's thyroiditis and reinforces the multifocal motor neuropathy autoimmune origin as well as the repeated clinical recoveries after intravenous immunoglobulins. This case also suggests to deeply investigate the thyroid function in patients with multifocal motor neuropathy.

Demyelinating Diseases↗
PubMed2000

[Spontaneous electromyographic activity. Practical importance].

Spontaneous activities are a major semeiologic sign in electromyography. The present article deals with the different aspects recorded in practice in normal and pathological cases. There are two types of spontaneous activities, those related to motor unit hyperactivity (fasciculations and myokymia) and those related to the hyperactivity of one or more muscle fibers: fibrillations, positive sharp waves, myotonic discharges and complex repetitive discharges. In the first case the lesion is located in the axone and in the second in the membrane of the muscle fibers; All theories related to the cells' abnormalities share a common feature: spontaneous activities result from abnormal firing of the membrane action potential of muscular fibers. This functional abnormality may results from different types of lesions within the cells' membrane and determines the aspects of spontaneous activities. Impaired function of muscular cells' membranes can be produced by denervation or lesion of the membrane structure itself. The latter can be multiple and linked with the membrane proteins (such as laminine or dystrophin as in AIDS diseases) or with ion channel disturbances. Multiple membrane cell alterations may produce the same kind of spontaneous activity; for instance, myotonic discharges have the same morphology in Thomsen and Steinert's disease despite their different mechanisms and fibrillations seen in denervations and myopathies. The practical consequences are discussed and a new classification of these spontaneous activities is proposed.

Action Potentials↗
PubMed1994

Influence of dose on suxamethonium-induced muscle damage.

We have examined postoperative muscle pain and early increases in serum concentrations of myoglobin after administration of suxamethonium to see if these changes were dependent on the dose of drug. Thirty ASA I and II adult patients undergoing day-case surgery received a standard anaesthetic technique, including one of three doses of suxamethonium: 0.5, 1.5 or 3.0 mg kg-1. The incidence of postoperative myalgia and the severity of fasciculations were greater after suxamethonium 1.5 mg kg-1 than after a dose of 0.5 or 3.0 mg kg-1. Serum concentrations of myoglobin increased in a dose-dependent manner. Intubating conditions were significantly better with suxamethonium 1.5 or 3.0 mg kg-1 than with 0.5 mg kg-1. Changes in serum concentrations of calcium and potassium were small and similar in the three groups. We conclude that a dose of 3.0 mg kg-1 of suxamethonium provided a better combination of intubating conditions and minimal postoperative myalgia than the two lower doses.

Adult↗