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Query: UMLS:C0015672 (fatigue)
 51,768 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Post-poliomyelitis syndrome refers to new symptoms that may occur years after recovery from poliomyelitis. The most common of these symptoms are new weakness, fatigue, and pain. This article describes electrodiagnostic studies--conventional electromyography (EMG), single fiber electromyography (SFEMG), and macroelectromyography (macro-EMG)--that have provided information on the post-polio motor unit and on the possible etiology of some post-polio syndrome symptoms. Muscular fatigue, and indirectly, general fatigue, may be due to neuromuscular junction transmission defects in some post-polio individuals, as suggested by reduction of the compound motor action potentials on repetitive stimulation, and increased jitter and blocking on SFEMG. Progressive weakness and atrophy in post-polio syndrome is probably due to a distal degeneration of post-polio motor units with resultant irreversible muscle fiber denervation. Electrodiagnostic evidence of ongoing denervation includes fibrillation and fasciculation potentials on conventional EMG, increased jitter and blocking on SFEMG, and smaller macro-EMG amplitudes in newly weakened post-polio muscles. However, even though electrodiagnostic studies have provided insight into the possible causes of some post-polio syndrome symptoms, no specific electrodiagnostic test for the syndrome is currently available.
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PMID:Electrophysiology and electrodiagnosis of the post-polio motor unit. 178 51

A cross sectional survey on the prevalence of acute pyrethroid poisoning in cotton farmers was conducted in 1987 and 1988. A total of 3113 pyrethroid spraymen (2230 men (71.6%) and 883 women (28.4%] were interviewed after spraying and followed up for 72 hours. Adverse effects of pyrethroid exposure were found in 834 of them (26.8%) manifested as abnormal facial sensations, dizziness, headache, fatigue, nausea, or loss of appetite. Only 10 subjects, who developed significant systemic symptoms and had signs of listlessness or muscular fasciculation, were diagnosed as having mild occupational acute pyrethroid poisoning with a prevalence of 0.31% in subjects exposed to pure pyrethroids and 0.38% in subjects exposed to pyrethroid organophosphate mixtures. Measurements of pyrethroid concentrations in the air of the breathing zone, in skin pads, and in urine samples showed that dermal contamination is the main route of exposure to pyrethroids in cotton growers. Preventive measures are recommended.
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PMID:An epidemiological study on occupational acute pyrethroid poisoning in cotton farmers. 199 11

We saw 166 patients with motor neuron disease over a ten-year period, 116 with amyotrophic lateral sclerosis-111 sporadic and 5 familial-and 50 with progressive muscular atrophy. The age at onset varied widely, with the youngest mean onset occurring in the familial group. The most common presenting symptoms were leg or arm weakness and difficulty speaking or swallowing; fewer patients reported cramping, fasciculation, or fatigue. Mean survival time was less in familial cases, women, older patients, and in those with difficulty speaking and swallowing. A total of 50% of all patients were alive after four years; 13% were alive after ten years. Previous reports on the natural history of motor neuron disease may be overly pessimistic in suggesting that survival time rarely exceeds two years.
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PMID:Motor neuron disease in the Rocky Mountain region. 338 45

Acoustic myography is the recording of sounds produced by contracting muscle. These sounds become louder with increasing force of contraction. We have compared muscle sounds with surface EMG to monitor the dissociation of electrical from mechanical events (presumably, the loss of excitation-contraction coupling) which occur with motor unit fatigue. Acoustic signals were amplified using a standard phonocardiograph, recorded on FM magnetic tape, and digitally analyzed. Muscles were examined at rest, with intermittent contractions, and with sustained contractions. We found that with fatigue, the acoustic amplitude decayed, but the surface EMG amplitude did not. With decreased effort, however, the acoustic and the surface EMG amplitudes declined simultaneously. By simultaneously recording acoustic signals and needle EMG, individual motor units were resolved acoustically in two muscles with decreased numbers of motor units and increased motor unit size. Fasciculations also produced acoustic signals, although no acoustic signal has yet been found that correlates with fibrillations. Analysis of acoustic signals from muscle provides a noninvasive method for monitoring motor unit fatigue in vivo. It may also be useful in distinguishing muscle fatigue from decreased volition.
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PMID:Acoustic myography: a noninvasive monitor of motor unit fatigue. 405 63

The defect of neuromuscular transmission is one of the important signs in ALS. The amplitude of a single motor unit potential from patients with ALS often decrease during tonic voluntary contraction. This phenomenon is closely correlated with fatigue seen in the patient. Overfunctioning of Ach release in the nerve terminal might cause the failure of neuromuscular transmission in ALS. Fasciculations is an another characteristic sign and considered mainly to be peripheral axons in origin. It is postulated that the dysfunction of potassium channel in ALS axons makes the hyperexcitability of the axon membrane, causing fasciculations. Magnetic cortical stimulation sometimes evokes the same potentials as fasciculations, implying the hyperexcitability might be present also in spinal motoneurons or even in pyramidal neurons in ALS. All of these findings lead to the hypothesis that hyperexcitability or overactivity of central and peripheral motoneurons is an essential feature in ALS.
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PMID:[Abnormal hyperexcitability in ALS]. 1037 5

In amyotrophic lateral sclerosis (ALS), muscles with preserved strength can have fasciculation potentials (FPs) as the only abnormality. The FPs in strong muscles are predominantly simple and stable, and can often be recruited by a slight voluntary contraction. In weak and atrophic muscles, the FPs are generally complex and unstable, tend to have a slower firing rate and are not recruited by voluntary contraction. Macro-electromyography studies suggest that these FPs are part of a more complex motor unit, as opposed to simple FPs which can represent all the motor unit. FPs driven by transcranial magnetic stimulation (TMS) were observed in 13 ALS patients. TMS-driven fasciculations had a simple morphology and were stable. Complex potentials were never cortically driven. These observations strengthen the conviction that fasciculations in ALS can have different origins. Simple, stable FPs arise proximally and are probably related to excitotoxicity phenomena, while complex, unstable FPs are most likely to originate in distal axonal sprouts that are associated with the reinnervation process. Some ALS patients with fatigue and mild weakness can have profuse fasciculations at an early phase in the evolution of the disease. Patients with denervation localized in one region and diffuse FPs should be strongly suspected of having ALS. With this strategy it should be possible to shorten the diagnosis time.
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PMID:Pathophysiological significance of fasciculations in the early diagnosis of ALS. 1146 25

Conduction block is an important functional consequence of demyelination whereby nervous transmission is abolished. Its mechanism has been discussed with respect to the loss of insulation due to disruption of myelin. Recent development of threshold tracking techniques, which enabled noninvasive assessment of axonal membrane potentials and ion channels, has provided evidence that axonal excitability changes significantly and contributes to conduction failure. This view, based upon axo-glial interaction, clarifies the mechanism of muscle fatigue and fasciculation associated with peripheral demyelination and possibly explains selective motor involvement in multifocal motor neuropathy.
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PMID:Physiology of conduction block in multifocal motor neuropathy and other demyelinating neuropathies. 1263 14

The goal of this study is to define the clinical features, pathogenesis and key investigation findings of fasciculation anxiety syndrome in clinicians (FASICS). Twenty consecutive clinicians presenting with fasciculations were prospectively assessed with serial clinical and neurophysiological evaluations. Clinicians with fasciculations formed three groups: 70 % of clinicians experienced symptomatic fasciculations and anxiety about the possibility of amyotrophic lateral sclerosis (ALS), termed FASICS; a further 15 % of clinicians experienced fasciculations associated with cramps and consistent with cramp-fasciculation syndrome (CFS). The final 15 % of clinicians presented with fasciculations associated with sensory symptoms or muscle weakness and were diagnosed with neuropathy (10 %) and ALS (5 %). In FASICS, fasciculations most often involved the lower limbs, without evidence of muscle weakness on clinical examination. Exercise, stress, fatigue and caffeine consumption were identified as common exacerbating factors. Neurophysiological studies confirmed normal nerve conduction studies and the presence of simple fasciculations, without acute denervation or neurogenic motor unit changes. Antibodies to voltage-gated potassium channels were assayed in each clinician and were not detected, and systemic autoantibodies were detected only in clinicians with features of CFS. FASICS is a disorder common among physicians presenting for evaluation of fasciculations. The present study delineates the diagnostic features of FASICS and contrasts the clinical presentation with other causes of fasciculations in clinicians.
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PMID:Fasciculation anxiety syndrome in clinicians. 2340 May

Motor neuron hyperexcitability (MNH) indicates a disorder characterized by an ectopic motor nerve discharge on electromyogram (EMG). Here, we present a series of three cases of subacute MNH with mercury poisoning. The first case showed hyperhidrosis, insomnia, generalied myokymia, cramps, tremor, weight loss, and myokymic and neuromyotonic discharges, followed by encephalopathy with confusion, hallucinations, and memory decrease. The second case was similar to the former but without encephalopathic features. The third case showed widespread fasciculation, fatigue, insomnia, weight loss, and autonomic dysfunction, including constipation, micturition difficulty, and impotence, with multiple fibrillation, unstable fasciculation, widened motor neuron potential, and an incremental response at high-rate stimulation in repetitive nerve stimulation. Based on the symptoms, the three cases were diagnosed as Morvan's syndrome, Isaacs' syndrome, and Lambert-Eaton myasthenic syndrome with ALS-like syndrome, respectively. Mercury poisoning in the three cases was confirmed by analysis of blood and urine samples. All cases recovered several months after chelation therapy and were in good condition at follow-up. Very few cases of MNH linked with mercury exposure have been reported in the literature. The mechanism of mercury-induced MNH may be associated with ion channel dysfunction.
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PMID:Subacute motor neuron hyperexcitability with mercury poisoning: a case series and literature review. 2522 23

Cramp-fasciculation syndrome (CFS) is a rare muscle hyperexcitability syndrome that presents with muscle cramps, fasciculations, and stiffness, as well as pain, fatigue, anxiety, hyperreflexia, and paresthesias. Although familial cases have been reported, a genetic etiology has not yet been identified. We performed whole-exome sequencing followed by validation and cosegregation analyses on a father-son pair with CFS. Both subjects manifested other hypersensitivity-hyperexcitability symptoms, including asthma, gastroesophageal reflux, migraine, restless legs syndrome, tremor, cold hyperalgesia, and cardiac conduction defects. Most symptoms improved with carbamazepine, consistent with an underlying cation channelopathy. We identified a variant in the transient receptor potential ankyrin A1 channel (TRPA1) gene that selectively cosegregated with CFS and the other hypersensitivity-hyperexcitability symptoms. This variant (c.2755C>T) resulted in a premature stop codon at amino acid 919 (p.Arg919*) in the outer pore of the channel. TRPA1 is a widely distributed, promiscuous plasmalemmal cation channel that is strongly implicated in the pathophysiology of the specific hypersensitivity-hyperexcitability symptoms observed in these subjects. Thus, we have identified a novel TRPA1 variant that is associated with CFS as part of a generalized hypersensitivity-hyperexcitability disorder. These findings clarify the diverse functional roles of TRPA1, and underscore the importance of this channel as a potential therapeutic target.
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PMID:A novel TRPA1 variant is associated with carbamazepine-responsive cramp-fasciculation syndrome. 2843 34


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