Clinical, Electrophysiological, and Serological Evaluation of Patients with Cramp-Fasciculation Syndrome

Poyraz, Mürüvvet; Matur, Zeliha; Aysal, Fikret; Tüzün, Erdem; Hanoğlu, Lütfü; Öge, Ali Emre

doi:10.5152/npa.2016.14816

Cited by 10 publications

(5 citation statements)

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“…In patients with a high degree of PNH, the hyperexcitability of motor nerve membranes is continuous, and abnormal discharges can be detected on routine needle EMG. 12 However, patients with relatively mild clinical symptoms exhibit lower frequencies and discontinuous discharge modes and can thus even show normal EMG results. 13 Afterdischarges are continuous discharges after stimulation of action potentials and can promote hyperactivity of motor nerve membranes, thus serving as sensitive markers when hyperexcitability levels are low.…”

Section: Discussionmentioning

confidence: 99%

“…This phenomenon can be explained by the electrophysiological mechanism of PNHS. In patients with a high degree of PNH, the hyperexcitability of motor nerve membranes is continuous, and abnormal discharges can be detected on routine needle EMG 12 . However, patients with relatively mild clinical symptoms exhibit lower frequencies and discontinuous discharge modes and can thus even show normal EMG results 13 .…”

Section: Discussionmentioning

confidence: 99%

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Peripheral nerve hyperexcitability syndrome: A clinical, electrophysiological, and immunological study

Shi

Gao

et al. 2021

Muscle and Nerve

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Introduction Peripheral nerve hyperexcitability syndrome (PNHS) is characterized by muscle fasciculations and spasms. Nerve hyperexcitability and after‐discharges can be observed in electrophysiological studies. Autoimmune mechanisms play a major role in the pathophysiology of primary PNHS. Methods We retrospectively conducted a case–control study recruiting patients with clinical and electrophysiological features of PNHS. Control patients were diagnosed with other neuronal or muscular diseases. Contactin‐associated protein2 (CASPR2) and leucine‐rich glioma‐inactivated1 (LGI1) antibodies were examined. Results A total of 19 primary PNHS patients and 39 control patients were analyzed. The most common symptoms for the case group were fasciculations (11/19) and muscle spasms (13/19). Case group patients were likely to demonstrate electrodiagnostic findings of nerve hyperexcitability (17/19) and after‐discharges in the tibial nerve (19/19). We found high prevalence of CASPR2 (9/19) and LGI1 (6/19) antibodies in the case group. Discussion Primary PNHS patients were likely to show after‐discharges in the tibial nerve. The pathogenesis of PNHS is autoimmune CASPR2 and LGI1 antibodies are possible pathogenic antibodies for primary PNHS.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Peripheral nerve hyperexcitability syndrome: A clinical, electrophysiological, and immunological study

Shi

Gao

et al. 2021

Muscle and Nerve

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“…In this case, pregabalin caused a total remission of the cramps, fasciculations, and rhabdomyolysis attacks, with normalization of baseline CK for his race and body habitus [values oscillated between 400 s to 1000s] (13), however cerebellar dysfunction persisted.. The selection of pregabalin was based in its membrane stabilizing effect and prior sporadic cases reports where pregabalin was effective to treat fasciculation and cramps syndrome and unreported cases seen by authors (14,15,16).…”

Section: Discussionmentioning

confidence: 76%

Genetic Rhabdomyolysis within the Spectrum of the Spinocerebellar Ataxia Type 2 Responsive to Pregabalin

Rossi

Tsakadze

et al. 2021

Preprint

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BackgroundSpinocerebellar Ataxia type 2 is a slowly progressive adult onset ataxia with a broad clinical presentation. Case presentationWe describe a man with Spinocerebellar Ataxia type 2 with chronic, severe, and recurrent rhabdomyolysis, as part of the cerebellar ataxia genetic spectrum. Initially rhabdomyolysis was refractory to multiple medications, but entirely resolved and remained in chronic remission with pregabalin. ConclusionThis is the first report of Spinocerebellar Ataxia type 2 associated with chronic, severe, recurrent rhabdomyolysis as part of its genetic phenotype responsive to pregabalin.

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“…In this case, pregabalin caused a total remission of the cramps, fasciculations, and rhabdomyolysis attacks, with normalization of baseline CK for his race and body habitus [values oscillated between 400s and 1000s] [ 13 ], however cerebellar dysfunction persisted. The selection of pregabalin was based in its membrane stabilizing effect and prior sporadic cases reports where pregabalin was effective to treat fasciculation and cramps syndrome and unreported cases seen by authors [ 14 , 15 ].…”

Section: Discussionmentioning

confidence: 99%

Genetic rhabdomyolysis within the spectrum of the Spinocerebellar Ataxia type 2 responsive to pregabalin

Rossi

Tsakadze

et al. 2021

cerebellum ataxias

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Background Spinocerebellar Ataxia type 2 is a slowly progressive adult onset ataxia with a broad clinical presentation. Case presentation We describe a man with Spinocerebellar Ataxia type 2 with chronic, severe, and recurrent rhabdomyolysis, as part of the cerebellar ataxia genetic spectrum. Initially rhabdomyolysis was refractory to multiple medications, but entirely resolved and remained in chronic remission with pregabalin. Conclusions This is the first report of Spinocerebellar Ataxia type 2 associated with chronic, severe, recurrent rhabdomyolysis as part of its genetic phenotype responsive to pregabalin.

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Clinical, Electrophysiological, and Serological Evaluation of Patients with Cramp-Fasciculation Syndrome

Cited by 10 publications

References 10 publications

Peripheral nerve hyperexcitability syndrome: A clinical, electrophysiological, and immunological study

Peripheral nerve hyperexcitability syndrome: A clinical, electrophysiological, and immunological study

Genetic Rhabdomyolysis within the Spectrum of the Spinocerebellar Ataxia Type 2 Responsive to Pregabalin

Genetic rhabdomyolysis within the spectrum of the Spinocerebellar Ataxia type 2 responsive to pregabalin

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