E-C Coupling Time Research Articles

Measurement of excitation-contraction coupling time in critical illness myopathy

ObjectiveThis study aimed to develop a simple and reliable technique to assess excitation-contraction (E-C) coupling for early diagnosis of critical illness myopathy (CIM). MethodsWe prospectively performed clinical and electrophysiological examinations on patients admitted to intensive care unit (ICU). In addition to full neurological examinations and routine nerve conduction study, motor related potential (MRP) was recorded using an accelerometer attached to the base of hallux after tibial nerve stimulation, and E-C coupling time (ECCT) was measured from the latency difference between soleus compound muscle action potential (CMAP) and MRP. ResultsOf 41 patients evaluated, 25 met the criteria for ICU-acquired weakness, 23 of whom had CIM. The time to the first electrophysiological examination (time to first test) correlated negatively with CMAP and with MRP. Conversely, a positive correlation was observed between the time to first test and ECCT. E-C coupling impairment occurred in most of our patients with CIM by the third day of ICU admission, and prolonged ECCT could be the earliest detectable abnormality. ConclusionsThe ECCT measurement is an easy and reliable technique to detect reduced muscle membrane excitability in the early stage of CIM. SignificanceThe ECCT measured by our method using an accelerometer may be a parameter that predicts the development of CIM.

P-MU003. The impairment of excitation-contraction coupling in ICU-acquired weakness

Introduction . The aim of this study is to elucidate the impairment of excitation-contraction (E-C) coupling in ICU-acquired weakness (ICUAW) using a unique electrophysiologic method in patients received the intensive care in ICU. Methods . We examined 13 patients with ICUAW and 11 normal controls. We performed successive recordings of electrophysiological tests after ICU admission. First, CMAPs of abductor hallucis muscle (AH) and sural SNAPs were recorded using a conventional method. In addition, the tibial nerve was stimulated at the popliteal fossa using a supramaximal rectangular pulse to record CMAPs from soleus muscle (SOL). Simultaneously, movement- related potential (MRP) was recorded using an accelerometer (SV1101; NEC, Tokyo Japan) taped at the base of hallux and calculated E-C coupling time (ECCT) based on the latency differences between soleus CMAP and MRP. Results . We recorded significantly decreased CMAP amplitudes in 6 AHs and 8 SOLs and significantly longer CMAP durations in 2 SOLs. Also, we recorded significantly decreased MRPs in 9 patients and significantly prolonged ECCTs in 10 patients. These abnormal findings were detected even in very short durations of ICU stay such as 2-3 days. The durations of ICU stay seemed to be correlated with involvement of CMAP amplitudes of AH/SOL, MRPs and ECCTs. Ten patients showed decreased SOL-CMAP amplitude concomitant with decreased MRP and/or prolonged ECCT in spite of preservation of SOL-CMAP duration. In addition, CMAP amplitudes of AH/SOL and MRP were significantly smaller in patients than in controls. Furthermore, CMAP durations of AH and ECCTs were significantly longer in patients than in controls. Conclusion . The E-C coupling may be impaired in the very early stages of CIM. Noninvasive measurement of MRP and ECCT is easy to perform, and may be useful to detect the impairment of E-C coupling in the early stages of ICUAW.

Measurement of excitation-contraction coupling time in lower extremities.

The aim of this study was to apply a novel method to measure excitation-contraction coupling time (ECCT) in normal soleus muscles. We performed simultaneous recordings of soleus compound muscle action potential (CMAP) and foot movement-related potential (MRP), and measured ankle plantar flexion torque in 36 healthy subjects. We calculated ECCT and examined the relations between CMAP, MRP, ECCT and ankle plantar flexion torque. Statistical analyses established reference ranges (mean ± SE) for CMAP (13.4 ± 0.9 mV), MRP (5.3 ± 0.4 m/s2), ECCT (5.2 ± 0.1 ms), torque (85.9 ± 6.4 Nm) and torque/body weight (1.4 ± 0.1 Nm/kg). The torque showed a positive linear correlation with CMAP (p = 0.041) and a negative linear correlation with ECCT (p = 0.045). Soleus ECCT can be recorded easily, and is useful to assess the impairment of E-C coupling in muscles of the lower extremities.

S20-3 The impairment of excitation-contraction coupling in ICU-acquired weakness

Introduction. The aim of this study is to elucidate the impairment of excitation-contraction (E-C) coupling in ICU-acquired weakness (ICUAW) using a unique electrophysiologic method in patients received the intensive care in ICU. Methods. We examined 13 patients with ICUAW and 11 normal controls. We performed successive recordings of electrophysiological tests after ICU admission. First, CMAPs of abductor hallucis muscle (AH) and sural SNAPs were recorded using a conventional method. In addition, the tibial nerve was stimulated at the popliteal fossa using a supramaximal rectangular pulse to record CMAPs from soleus muscle (SOL). Simultaneously, movement- related potential (MRP) was recorded using an accelerometer (SV1101; NEC, Tokyo Japan) taped at the base of hallux and calculated E-C coupling time (ECCT) based on the latency differences between soleus CMAP and MRP. Results. We recorded significantly decreased CMAP amplitudes in 6 AHs and 8 SOLs and significantly longer CMAP durations in 2 SOLs. Also, we recorded significantly decreased MRPs in 9 patients and significantly prolonged ECCTs in 10 patients. These abnormal findings were detected even in very short durations of ICU stay such as 2-3 days. The durations of ICU stay seemed to be correlated with involvement of CMAP amplitudes of AH/SOL, MRPs and ECCTs. Ten patients showed decreased SOL-CMAP amplitude concomitant with decreased MRP and/or prolonged ECCT in spite of preservation of SOL-CMAP duration. In addition, CMAP amplitudes of AH/SOL and MRP were significantly smaller in patients than in controls. Furthermore, CMAP durations of AH and ECCTs were significantly longer in patients than in controls. Conclusion. The E-C coupling may be impaired in the very early stages of CIM. Noninvasive measurement of MRP and ECCT is easy to perform, and may be useful to detect the impairment of E-C coupling in the early stages of ICUAW.

The impairment of excitation-contraction coupling in icu-acquired weakness

The aim of this study is to elucidate the impairment of excitation-contraction (E-C) coupling in ICU-acquired weakness (ICUAW) using a unique electrophysiologic method in patients received the intensive care in ICU. We examined 9 patients with ICUAW and 10 normal controls. We performed successive recordings of electrophysiological tests after ICU admission. First, CMAPs of abductor hallucis muscle (AH) and sural SNAPs were recorded using a conventional method. In addition, the tibial nerve was stimulated at the popliteal fossa using a supramaximal rectangular pulse to record CMAPs from soleus muscle (SOL). Simultaneously, movement-related potential (MRP) was recorded using an accelerometer (SV1101) taped at the base of hallux and calculated E-C coupling time (ECCT) based on the latency differences between soleus CMAP and MRP. MRPs as well as CMAP amplitudes of AH and SOL were significantly smaller in patients than in controls. Also, ECCTs and CMAP durations of AH were significantly longer in patients than in controls. Nine patients were subdivided into 6 patients with critical illness myopathy (CIM) and 3 patients with critical illness polyneuropathy (CIP) based on the sural SNAP abnormality. All CIM patients consistently showed significantly prolonged ECCTs, and 5 CIM patients showed significantly decreased MRPs. These abnormalities occurred within several days after ICU admission. The E-C coupling may be impaired in the very early stages of CIM. Noninvasive measurement of MRP and ECCT is easy to perform, and may be an useful indicator of muscle involvement in the early stages of ICUAW.

Excitation-Contraction Coupling Time is More Sensitive in Evaluating Cardiac Systolic Function.

Background:Pressure overload-induced myocardial hypertrophy is a key step leading to heart failure. Previous cellular and animal studies demonstrated that deteriorated excitation–contraction coupling occurs as early as the compensated stage of hypertrophy before the global decrease in left ventricular ejection fraction (LVEF). This study was to evaluate the cardiac electromechanical coupling time in evaluating cardiac systolic function in the early stage of heart failure.Methods:Twenty-six patients with Stage B heart failure (SBHF) and 31 healthy controls (CONs) were enrolled in this study. M-mode echocardiography was performed to measure LVEF. Tissue Doppler imaging (TDI) combined with electrocardiography (ECG) was used to measure cardiac electromechanical coupling time.Results:There was no significant difference in LVEF between SBHF patients and CONs (64.23 ± 8.91% vs. 64.52 ± 5.90%; P = 0.886). However, all four electromechanical coupling time courses (Qsb: onset of Q wave on ECG to beginning of S wave on TDI, Qst: onset of Q wave on ECG to top of S wave on TDI, Rsb: top of R wave on ECG to beginning of S wave on TDI, and Rst: top of R wave on ECG to top of S wave on TDI) of SBHF patients were significantly longer than those of CONs (Qsb: 119.19 ± 35.68 ms vs. 80.30 ± 14.81 ms, P < 0.001; Qst: 165.42 ± 60.93 ms vs. 129.04 ± 16.97 ms, P = 0.006; Rsb: 82.43 ± 33.66 ms vs. 48.30 ± 15.18 ms, P < 0.001; and Rst: 122.37 ± 36.66 ms vs. 93.25 ± 16.72 ms, P = 0.001), and the Qsb, Rsb, and Rst time showed a significantly higher sensitivity than LVEF (Rst: P =0.032; Rsb: P = 0.003; and Qsb: P = 0.004).Conclusions:The cardiac electromechanical coupling time is more sensitive than LVEF in evaluating cardiac systolic function.

S12-2. Excitation-contraction coupling in myasthenia gravis: Up to date

Although defective neuromuscular transmission is known to be a cause of muscle weakness in myasthenia gravis (MG), previous studies have shown the possible roles of other processes, the failure of which may also cause muscle weakness in MG. Especially, excitation-contraction (E-C) coupling may be defective in patients with MG. Some investigators have applied the post-tetanic potentiation and/or the staircase phenomenon to elucidate the impairment of E-C coupling in MG. Recently, we reported a new method to assess E-C coupling of masseter and abductor pollicis brevis muscles using an accelerometer. In this method, compound muscle action potentials (CMAP) in the belly-tendon fashion and movement-related potentials (MRP) of jaw and finger movements were simultaneously recorded following nerve stimulation. The E-C coupling time (ECCT) was obtained from the difference in onset latencies between CMAP and MRP. The impairment of E-C coupling was assessed by prolonged ECCT and/or low MRP amplitude. In this lecture, I will discuss our data in MG, (1) correlation of bite force with ECCT of the masseter, (2) correlation between anti-ryanodine receptor antibody and ECCT, (3) early effect of tacrolimus in improving ECCT, (4) impairment of post-tetanic potentiation of muscle twitch, (5) effect of local cooling on E-C coupling.

S45-2 Measurement of excitation-contraction coupling time of masseter in mandibular movement

S45-2 Measurement of excitation-contraction coupling time of masseter in mandibular movement

Correlation of bite force with excitation–contraction coupling time of the masseter in myasthenia gravis

The aim of this study was to elucidate the relationship between the impairment of excitation-contraction (E-C) coupling of masseter and the bite force in patients with myasthenia gravis (MG). In 20 patients with MG, masseteric compound muscle action potential (CMAP) and mandibular movement-related potentials (MRP) were recorded simultaneously after stimulating the trigeminal motor nerve with a needle electrode. The E-C coupling time (ECCT) was calculated by the latency difference between CMAP and MRP. Bite force was measured using a pressure-sensitive sheet. Serial assessments of % decrement in masseteric repetitive nerve stimulation (RNS), ECCT, and bite force were performed before and after corticosteroid therapy alone or in various combinations with FK506, cyclosporin A, intravenous immunoglobulin and immunoabsorption. Percent amplitude decrement in RNS and ECCT decreased significantly accompanying an increase in bite force after treatment. Simple regression analysis demonstrated a linear correlation among % decrement, ECCT and bite force. However, ECCT shortening accompanying bite force recovery without reduction in % decrement was observed in 4 patients. Masseteric E-C coupling is impaired in some MG patients, and functional recovery of E-C coupling contributes at least in part to the increase in bite force after treatment. Impaired E-C coupling contributes to muscle weakness in patients with MG.

22. Hemoglobin concentration changes induced by transcranial magnetic stimulation (TMS) over the primary motor area

The aim of this study was to elucidate the correlation between excitation–contraction coupling time (ECCT) of the masseter and the bite force in myasthenia gravis (MG). Compound muscle action potentials (CMAPs) of the masseter and movement-related potentials (MRPs) using an accelerometer placed on the chin were simultaneously recorded after trigeminal nerve stimulation by a monopolar needle electrode inserted into the mandibular notch. The ECCT was defined as the difference in onset latencies between CMAP and MRP. The repetitive nerve stimulation test (RNS) was also performed in the same masseter before the ECCT recording. The bite force was measured using a pressure-sensitive sheet immediately after the ECCT recording. Successive examinations of RNS/ECCT and the bite force measurements were performed in 18 patients with MG. We calculated percent difference of the bite force to estimate the inter-trial differences of the bite force in each subject. The ECCT was significantly correlated with the percent difference of the bite force (p = 0.02). On the other hand, the percent difference of the bite force did not show any significant relationship with either the decrement in RNS or CMAP amplitude of the masseter. Our results suggest that dysfunction of E–C coupling may contribute to the muscle weakness in MG.