Characterization of the relationship between motor end-plate jitter and the safety factor

Lin, Te-Sheng; Cheng, Kuo‐Sheng

doi:10.1002/(sici)1097-4598(199805)21:5<628::aid-mus9>3.0.co;2-a

Cited by 9 publications

(7 citation statements)

References 25 publications

(47 reference statements)

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“…4). For further assessment of this dissociation, we performed a computer simulation of a stimulated single fiber EMG, using a technique detailed in our earlier report 8…”

Section: Resultsmentioning

confidence: 99%

“…According to the quantal theory, EPP amplitudes depend on the quantal content (number of quanta released at each firing) and the quantal size or MEPP (postsynaptic potential change for each packet release). In this simulation, EPP was calculated using the following equation5, 8: EPP t = m · MEPP(1 − e t /τ ), where EPP t represents EPP amplitude at time t, t is the time after ACh quantal release, m is the quantal content, and τ represents the membrane decay time constant at the end‐plate. It is postulated that m is a binomially distributed variable, which is determined by the number of quanta immediately available for release ( n ) and the probability of release ( p ).…”

Section: Resultsmentioning

confidence: 99%

“…In the normal end‐plate, muscle fibers discharge at the rising phase of the EPP. With a small EPP, muscle fibers fail to discharge8 if τ is normal as in myasthenia gravis. This may not necessarily be the case, however, if τ is abnormally prolonged because the EPP could then eventually reach the threshold, which tends to fluctuate randomly 8.…”

Section: Discussionmentioning

confidence: 99%

“…With a small EPP, muscle fibers fail to discharge8 if τ is normal as in myasthenia gravis. This may not necessarily be the case, however, if τ is abnormally prolonged because the EPP could then eventually reach the threshold, which tends to fluctuate randomly 8. Thus, the discharge probability increases in the face of prolonged interpotential interval variations, resulting in little blocking despite a large jitter.…”

Section: Discussionmentioning

confidence: 99%

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Pathophysiology of weakness in a patient with congenital end‐plate acetylcholinesterase deficiency

et al. 2002

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A Japanese patient with congenital end-plate acetylcholinesterase (AChE) deficiency developed severe proximal and truncal muscle weakness with preservation of distal strength. Electrophysiological studies included a train of stimuli at 3 HZ, which induced a marked decremental response in the deltoid but not in the first dorsal interosseous (FDI) muscle. Single fiber electromyography (EMG) revealed a high blocking rate (23.1 +/- 30.5%, n = 13) with a markedly increased jitter (mean consecutive difference [MCD] 297 +/- 218 micros) in the deltoid, but a low blocking rate (6.2 +/- 7.4%, n = 16) despite an equally increased jitter (MCD 227 +/- 147 micros) in the FDI. In vitro microelectrode study and computer simulation suggested that the combination of a large jitter and a low blocking rate may be ascribed to a reduced end-plate potential (EPP) amplitude with an abnormally prolonged decay time constant (tau). These characteristics may constitute the primary underlying pathophysiologic mechanism in our patient and in similar cases of congenital myasthenic syndrome.

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“…4). For further assessment of this dissociation, we performed a computer simulation of a stimulated single fiber EMG, using a technique detailed in our earlier report 8…”

Section: Resultsmentioning

confidence: 99%

Section: Resultsmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

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Pathophysiology of weakness in a patient with congenital end‐plate acetylcholinesterase deficiency

et al. 2002

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“…It has been shown that variations in jitter are most prominent in end-plates with low safety factors which are activated by slight voluntary contraction. 13 In addition, a clinical study comparing the diagnostic yields of stimulation and voluntary SFEMG clearly demonstrated voluntary SFEMG to be of greater utility in revealing motor end-plate dysfunction. 14 In our study, 3 patients showed pronounced NMT abnormality, and 1 had borderline dysfunction of NMT in SFEMG.…”

Section: Commentsmentioning

confidence: 99%

Abnormal Neuromuscular Transmission in Cluster Headache

Ertaş¹,

Baslo²

2003

Headache

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Safety margin at single neuromuscular junctions

Trontelj¹,

Mihelin²,

Khuraibet³

2002

Muscle Nerve

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Jitter measurement with axonal microstimulation was used to study synaptic function at 115 neuromuscular junctions (NMJs) of normal subjects at various stimulation rates. Jitter was lowest at 0.5 Hz; it increased slightly at 1, 2, and 5 Hz and remained at that level at 10 Hz (a light work load) and 20 Hz (a heavy work load); and it increased further at 50 Hz (an extreme load). This pattern was seen for the majority of the NMJs, suggesting a high safety factor of neuromuscular transmission maintained rather uniformly over a wide range of discharge rates. A proportion of the normal NMJs had relatively large jitter; these tended to show prominent facilitation as the rate was raised from 5 or 10 to 20 Hz. Similar but more dramatic facilitation improving the safety factor was seen at most NMJs in myasthenia, which was studied for comparison. Such facilitation was not found at normal NMJs with low jitter.

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Characterization of the relationship between motor end-plate jitter and the safety factor

Cited by 9 publications

References 25 publications

Pathophysiology of weakness in a patient with congenital end‐plate acetylcholinesterase deficiency

Pathophysiology of weakness in a patient with congenital end‐plate acetylcholinesterase deficiency

Abnormal Neuromuscular Transmission in Cluster Headache

Safety margin at single neuromuscular junctions

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