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Predictive factors for myasthenic crisis after transsternal thymectomy have been reported, but little is known about myasthenic crisis after videoscopic thymectomy (MCAVT).We investigated 146 myasthenia gravis patients who underwent videoscopic thymectomy.Patients with MCAVT had a lower forced vital capacity (FVC) (2.1 vs. 3.0 L, P 0.001) than those without. Low-frequency repetitive nerve stimulation showed decremental responses of the orbicularis oculi (47.1% vs. 18.1%, P = 0.001) and nasalis muscles (54.1% vs. 21.4%, P 0.001), which were more pronounced in patients with MCAVT than those without. According to multivariate analysis, FVC (OR 0.144, 95% confidence interval [CI], 0.044-0.479, P = 0.002) and decremental response of orbicularis oculi (odds ratio, 1.029; 95% CI, 1.001-1.058, P = 0.044) were independently associated with MCAVT.FVC and decremental response of orbicularis oculi were associated with MCAVT.

Background and purpose Rhabdomyolysis is a medical emergency characterized by acute skeletal muscle breakdown with a sudden rise and subsequent fall of serum creatine kinase (CK) levels. Rhabdomyolysis events are provoked by exposure to external triggers, possibly in combination with an increased genetic susceptibility. We aimed to describe comprehensively the external triggers and potentially pathogenic genetic variants possibly implicated in increased rhabdomyolysis susceptibility. Methods We performed a retrospective single‐center study, including a total of 1302 patients with an acute CK level exceeding 2000 IU/l. Results Anoxia was the most frequently reported trigger (40%). A subset of 193 patients were clinically suspected of an underlying genetic disorder (recurrent episodes, a positive family history, very high or persistently increased CK levels). In 72 of these patients, an unequivocal genetic defect was identified. A total of 22 genes with pathogenic variants were identified, including 52 different variants. Of those, 11 genes have been previously associated with rhabdomyolysis (ACADVL, ANO5, CPT2, DMD, DYSF, FKRP, HADHA, PGM1, LPIN1, PYGM, RYR1). Eleven genes are probably implicated in increased susceptibility (including AGL, CAPN3, CNBP, DMPK, MAGT1, ACADM, SCN4A, SGCA, SGCG, SMPD1, TANGO2). Conclusion These findings suggest that the spectrum of genetic susceptibility for rhabdomyolysis has not yet been completely clarified. With the increasing availability of next‐generation sequencing in a diagnostic setting, we expect that in more cases a genetic defect will be identified., Rhabdomyolysis events are provoked by exposure to external triggers, possibly in combination with an increased genetic susceptibility. Anoxia was the most frequently reported external trigger (40%). A subset of 193 patients (14.8%) were clinically suspected of an underlying genetic disorder. A total of 22 genes with pathogenic variants were identified, of which 11 have been previously associated with rhabdomyolysis (ACADVL, ANO5, CPT2, DMD, DYSF, FKRP, HADHA, PGM1, LPIN1, PYGM, RYR1). Eleven genes are probably implicated in increased susceptibility (including AGL, CAPN3, CNBP, DMPK, MAGT1, ACADM, SCN4A, SGCA, SGCG, SMPD1, TANGO2).