Journals / Journal of Neurological Sciences (Turkish) / 2013 / Cilt: 30 - Sayı: 1

Epilepsili Hastalarda Periferik Sinir Aksonal Eksitabilitesi

Peripheral Nerve Axonal Excitability in Epileptic Patients

Pages
108–115
Publication Date
2022-10-19
DOI
—
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AI Summary & Key Takeaways

AI Insight
⚡ TL;DR(Too Long; Didn't Read)

The study involved 17 patients newly diagnosed withpartial epilepsy and 22 patients with primary generalized epilepsy who were not currentlyprescribed anticonvulsant therapy, and 15 control subjects.Results: Rheobase of motor fibres and stimulus strength at 0.1 ms and 1ms of motor fibres oftotal patients with epilepsy were higher than values of controls.Conclusions: Our results suggested a decreased axonal excitability and a possible decreasedNa+ conductances in peripheral nerves in patients with epilepsy.

📌 3 Key Takeaways

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Objective & Hypothesis:Introduction: Sodium (Na+) channels have an important role for action potential formation inboth central nervous system (CNS) and peripheral nervous system (PNS).
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Key Findings & Data:The study involved 17 patients newly diagnosed withpartial epilepsy and 22 patients with primary generalized epilepsy who were not currentlyprescribed anticonvulsant therapy, and 15 control subjects.Results: Rheobase of motor fibres and stimulus strength at 0.1 ms and 1ms of motor fibres oftotal patients with epilepsy were higher than values of controls.Conclusions: Our results suggested a decreased axonal excitability and a possible decreasedNa+ conductances in peripheral nerves in patients with epilepsy.
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Conclusion & Impact:While there ishyperexcitability of central neurons, reduced peripheral nerve excitability may be in questionin epilepsy.
🔬Design:Research Article
📍Scope:Comprehensive Sample
⚙️Variables:Domain Parameters

Abstract

Introduction: Sodium (Na+) channels have an important role for action potential formation inboth central nervous system (CNS) and peripheral nervous system (PNS). The persistent Na+ current play a role in repetitive firing of action potentials caused by prolonged depolarization,thus could play a role in epilepsy. Nerve excitability measurements are made to investigatebiophysical properties and disturbances of impulse conduction in peripheral axons in humansubjects.Methods: In this study, it was aimed to study strength duration properties of motor andsensory axons to evaluate whether there is a change in the current through persistent Na+ channels of sensory and motor axons in peripheral nerves of epileptic patients because of thepresence of similiar channels in PNS. The study involved 17 patients newly diagnosed withpartial epilepsy and 22 patients with primary generalized epilepsy who were not currentlyprescribed anticonvulsant therapy, and 15 control subjects.Results: Rheobase of motor fibres and stimulus strength at 0.1 ms and 1ms of motor fibres oftotal patients with epilepsy were higher than values of controls.Conclusions: Our results suggested a decreased axonal excitability and a possible decreasedNa+ conductances in peripheral nerves in patients with epilepsy. While there ishyperexcitability of central neurons, reduced peripheral nerve excitability may be in questionin epilepsy.

Özet

Giriş: Sodyum (Na ) kanalları hem santral sinir sistemi hem de periferik sinir sisteminde(PSS) aksiyon potansiyeli oluşumunda önemli bir role sahiptir. Persistan Na+ akımı, uzamışdepolarizasyonun neden olduğu aksiyon potansiyellerinin repetetif ateşlenmesinde rol oynarki bu epilepsiye neden olabilir. Sinir eksitabilite ölçümleri, insanların periferik aksonlarındaimpuls iletiminin biyofiziksel özellikleri ve bozukluklarını incelemek için yapılmaktadır.Metod: Bu çalışmada, PSS'de de benzer kanallar olmasından yola çıkılarak epilepsilihastaların periferik sinir duysal ve motor aksonlarında persistan Na+ akımında değişiklik olupolmadığını değerlendirmek için motor ve duysal aksonların güç-süre özelliklerini çalışmakamaçlanmıştır. Çalışmaya antikonvülzan tedavi almayan, yeni tanı almış parsiyel epilepsili 17hasta ile primer jeneralize epilepsili 22 hasta ve 15 kontrol olgu alındı.Sonuçlar: Epilepsili olgularda motor liflerin reobazı ve 0.1 ms ve 1ms'deki stimulus gücükontrol grubuna göre yüksek bulundu.Karar: Sonuçlarımız, epilepsili olguların periferik sinirlerinde aksonal eksitabilitede azalmave dolayısıyla Na+ iletiminde olası azalmaya işaret etmektedir. Epilepside santral nöronlardahipereksitabilite varken, periferik sinir eksitabilitesinde azalma söz konusu olabilir.

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Cite This Article

YERDELEN, D., KOC, F. (2022). Epilepsili Hastalarda Periferik Sinir Aksonal Eksitabilitesi. Journal of Neurological Sciences (Turkish), Cilt: 30 - Sayı: 1, 108–115. https://ajindex.com/articles/565120

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References (17)

  1. Brigant JL, Mallart A. Presynaptic currents in mouse motor endings. J. Physiol. (Lond) 1982; 333:619–636
  2. Burke D, Kiernan MC, Bostock H. Excitability of human axons. Clin. Neurophysiol. 2001;112: 1575-1585
  3. Bostock H, Cikurel, K, Burke D. Threshold tracking techniques in the study of human peripheral nerve. Muscle Nerve. 1998; 21:137– 158
  4. Catterall WA, Goldin AL, Waxman SG. International Union of Pharmacology. XLVII. Nomenclature and structure–f unction relationships of voltage gated sodium channels. Pharmacol. Rev. 2005; 57: 397–409
  5. Commission on Classif ication and Terminology of the International League Against Epilepsy. Proposal f or revised classif ication of epilepsies and epileptic syndromes. Epilepsia 1989;30: 389-99
  6. Kanai K, Kuwabara S, Arai K, et al. Muscle cramp in Machado–Joseph disease: altered motor axonal excitability properties and mexiletine treatment. Brain. 2003;126:965– 973
  7. Kiernan MC, Bostock H. Eff ects of membrane polarization and ischemia on the excitability of human motor axons. Brain. 2000;123:2542– 2551
  8. Kiernan MC, Burke D, Andersen KV, et al. Multiple measures of axonal excitability: a new approach in clinical testing. Muscle Nerve. 2000; 23:399–409
  9. Kiernan MC, Hart IK, Bostock H. Excitability properies of motor axons in patients with spontaneous motor unit activity. J. Neurol. Neurosurg. Psychiatry. 2001; 70:56- 64
  10. Kiernan MC, Lin CS, Andersen KV, et al. Clinical evaluation of excitability measures in sensory nerve. Muscle Nerve. 2001; 24:883- 892
  11. Kiernan MC, Krishnan A V, Lin CS, et al. Mutation in the Na+ channel subunit SCN1B produces paradoxical changes in peripheral nerve excitability. Brain. 2005; 128:1841-1846
  12. Krishnan A V, Kiernan MC. Altered nerve excitability properties in established diabetic neuropathy. Brain. 2005; 128: 1178–1187
  13. Kuwabara S, Cappelen-Smith C, Lin CS, et al. Excitability properties of median and peroneal motor axons. Muscle Nerve. 2000; 23:1365– 1373
  14. Meldrum BS, Rogawski MA. Molecular targets f or antiepileptic drug development. Neurotherapeutics. 2007; 4:18-61
  15. Misawa S, Kuwabara S, Ogawara K, et al. Strength–duration properties and glycemic control in human diabetic motor nerves. Clin. Neurophysiol. 2005; 116: 254–258
  16. Mogyoros I, Kiernan MC, Burke D, et al. Excitability changes in human sensory and motor axons during hyperventilation and ischaemia. Brain. 1997; 120: 317–325
  17. Mogyoros I, Kiernan MC, Burke D, et al. Strength–dur