Abstract
Introduction: Myoclonus are paroxysmal muscle contractions of short duration or abrupt loss of muscle tone, called positive and negative myoclonus respectively. A clinical case of generalized positive and negative myoclonus is presented and the aim is to describe the multiple pathophysiological mechanisms and etiologies that trigger it.
Case presentation: A 35-year-old man with type 1 diabetes mellitus complicated by diabetic kidney disease on hemodialysis developed catheter-associated bacteremia due to Staphylococcus aureus and presented positive and negative myoclonus. Uremia, infection, and drugs with pro-myoclonic potential were identified as possible triggers; The incidental finding of an ischemic lesion in the caudate nucleus did not explain the semiology found in the patient. The control and removal of all the pro-myoclonic factors mentioned was carried out, along with pharmacological management with levetiracetam, thus achieving control of the symptoms.
Discussion: Patients with chronic kidney disease are susceptible to the accumulation of guanidine-type toxic products, which have the potential to produce myoclonus. Furthermore, infections, the use of drugs with pro-myoclonic potential and structural lesions such as cortical ischemia are etiologies that should be considered in the differential diagnosis. The greatest impact on symptoms is observed with the control of the triggering factor and if it persists, pharmacological therapy provides good results.
Conclusion: Myoclonus are relatively common movement disorders in chronic kidney disease. Identification of the trigger is crucial for its management along with the use of drugs with anti-myoclonic activity.
References
Caviness JN. Myoclonus. Continuum. 2019;25(4):1055-80. https://doi.org/10.1212/CON.0000000000000750
Caviness JN, Alving LI, Maraganore DM, Black RA, Mcüonnell SK, Rocca WA. The incidence and prevalence of myoclonus in Olmsted County, Minnesota. Mayo Clin Proc. 1999;74(6):565-9. https://doi.org/10.4065/74.6.565
Erro ME, Navarro MC. Myoclonic spasms: Their clinical and neurophysiological charactersitics, aetiology and treatment. Rev Neurol. 2009;48 Suppl. 1.
Hamed SA. Neurologic conditions and disorders of uremic syndrome of chronic kidney disease: presentations, causes, and treatment strategies. Expert Rev Clin Pharmacol. 2019;12(1):61-90. https://doi.org/10.1080/17512433.2019.1555468
Prieto-Pérez L, Montastruc J, García-Ruiz PJ. Myoclonus secondary to gabapentin in a patient with chronic renal failure. Rev Neurol. 2011;52(8):512. https://doi.org/10.33588/rn.5208.2011053
Zhang C, Glenn DG, Bell WL, O'Donovan CA. Gabapentin-induced myoclonus in end-stage renal disease. Epilepsia. 2005;46(1):156-8. https://doi.org/10.1111/j.0013-9580.2005.20804.x
Pranzatelli MR. Serotonin and Human Myoclonus: Rationale for the use of serotonin receptor agonists and antagonists. Arch Neurol. 1994;51(6):605-17. https://doi.org/10.1001/archneur.1994.00540180083018
Asconapé J, Diedrich A, DellaBadia J. Myoclonus associated with the use of gabapentin. Epilepsia. 2000;41(4):479-81. https://doi.org/10.1111/j.1528-1157.2000.tb00192.x
Huppertz HJ, Feuerstein TJ, Schulze-Bonhage A. Myoclonus in epilepsy patients with anticonvulsive add-on therapy with pregabalin. Epilepsia. 2001;42(6):790-2. https://doi.org/10.1046/j.1528-1157.2001.44000.x
Baysal Kirac L, Aydogdu I, Acarer A, Alpaydin S, Bayam FE, Onbasi H, et al. Myoclonic status epilepticus in six patients without epilepsy. Epilepsy Behav Case Rep. 2013;1(1):10-3. https://doi.org/10.1016/j.ebcr.2012.10.003
Pal G, Lin MM, Laureno R. Asterixis: a study of 103 patients. Metab Brain Dis. 2014;29(3):813-24. https://doi.org/10.1007/s11011-014-9514-7
Grill MF, Maganti R. Cephalosporin-induced neurotoxicity: clinical manifestations, potential pathogenic mechanisms, and the role of electroencephalographic monitoring. Ann Pharmacother. 2008;42(12):1843-50. https://doi.org/10.1345/aph.1L307
Brefel-Courbon C, Gardette V, Ory F, Montastruc JL. Drug-induced myoclonus: a French pharmacovigilance database study. Neurophysiol Clin. 2006;36(56):333-6. https://doi.org/10.1016/j.neucli.2006.12.003
Montoya-Giraldo MA, Montoya DV, Atehortúa DA, Buendía JA, Zuluaga AF, Montoya-Giraldo MA, et al. Mioclonías inducidas por salbutamol. Biomédica. 2018;38(3):303-7. https://doi.org/10.7705/biomedica.v38i3.3813
Vista de mioclonías como presentación de neurotoxicidad inducida por opioides [Internet]. [Consultado el 12 de marzo del 2023]. Disponible en: https://revistas.fucsalud.edu.co/index.php/repertorio/article/view/1378/2288
Gungor O, Aydin Z, Inci A, Oguz EG, Arici M. Seizures in patients with kidney diseases: a neglected problem? Nephrol Dial Transplant. 2023;38(2):291-9. https://doi.org/10.1093/ndt/gfab283.
Tater P, Pandey S. Post-stroke movement disorders: clinical spectrum, pathogenesis, and management. Neurol India. 2021;69(2):272. https://doi.org/10.4103/0028-3886.314574
Kim JS. Asterixis after unilateral stroke: Lesion location of 30 patients. Neurology. 2001;56(4):533-6. https://doi.org/10.1212/WNL.56.4.533
Rio J, Montalbán J, Pujadas F, Alvarez?Sabín J, Rovira A, Codina A. Asterixis associated with anatomic cerebral lesions: a study of 45 cases. Acta Neurol Scand. 1995;91(5):377-81. https://doi.org/10.1111/j.1600-0404.1995.tb07024.x
Janssen S, Bloem BR, van de Warrenburg BP. The clinical heterogeneity of drug-induced myoclonus: an illustrated review. J Neurol. 2017;264(8):1559. https://doi.org/10.1007/s00415-016-8357-z
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