The American Journal of Medicine
Volume 122, Issue 4 , Page e7, April 2009

Amlodipine-induced Myoclonus

  • Eric L. Wallace, DO

      Affiliations

    • The Department of Internal Medicine, Wake Forest University School of Medicine, Winston-Salem, NC
    • Corresponding Author InformationRequests for reprints should be addressed to Eric Wallace, DO, Department of Medicine, Wake Forest University School of Medicine, Medical Center Boulevard, Winston-Salem, NC 27157
    • ,
  • Kevin Lingle, MD

      Affiliations

    • The Department of Internal Medicine, Wake Forest University School of Medicine, Winston-Salem, NC
    • ,
  • Dwayne Pierce, PharmD

      Affiliations

    • Department of Pharmacology, Wake Forest University School of Medicine, Winston-Salem, NC
    • ,
  • Scott Satko, MD

      Affiliations

    • Nephrology Section, Wake Forest University School of Medicine, Winston-Salem, NC

Article Outline

 

To the Editor:

Myoclonus can occur as a side effect of multiple medications.1 Several calcium channel blockers have been suspected, including diltiazem, nifedipine, and verapamil,1, 2, 3, 4, 5, 6, 7 and myoclonus is believed to occur by altering neuronal calcium use.6 We report what we believe to be the first case of amlodipine-induced myoclonus.

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Case Summary 

A 79-year-old African American man with stage 4 chronic kidney disease and coronary artery disease was admitted with acute on chronic renal failure secondary to volume depletion from diuretics. The patient's home medication on presentation included aspirin, carvedilol, furosemide, simvastatin, spironolactone, and valsartan. His admission blood pressure was 139/58 mm Hg, and serum electrolytes were normal except for increased potassium (6.9 mEq/L; normal = 3.5-5.0 mEq/L), blood urea nitrogen (77 mg/dL; normal = 8-20 mg/dL), and creatinine (4.0 mg/dL; normal = 0.5-1.5 mg/dL). On admission, spironolactone and valsartan were withheld. On days 2 and 3, the patient's systolic blood pressure increased to the 160 to 180 mm Hg range and treatment with amlodipine 2.5 mg daily was begun. On day 4, his blood pressure remained elevated and amlodipine was increased to 10 mg daily. On day 5, the patient developed involuntary, repetitive jerking of both his upper and lower extremities, consistent with myoclonus. Serum potassium at that time remained slightly elevated (5.3 mEq/L), but blood urea nitrogen (39 mg/dL) and creatinine (2.3 mg/dL) had returned to the patient's baseline levels. Amlodipine was withheld secondary to literature reports of calcium channel blocker-induced myoclonus. Within 24 hours of discontinuing the amlodipine and no other intervention, the patient's myoclonic jerking resolved. He continued to have problems with hypertension, and treatment with clonidine 0.1 mg twice per day was added. On day 8, with a blood pressure of 131/56 mm Hg and potassium (5.3 mEq/L) and creatinine (2.2 mg/dL) levels remaining at baseline, the patient was then discharged to a skilled nursing home without any further recurrence of myoclonus.

Our patient exhibited signs and symptoms consistent with myoclonus, as previously reported with other calcium channel blockers.1, 2, 3, 4, 5, 6, 7 Although he was receiving carvedilol, which also has been reported to cause myoclonus,8 we believe that the myoclonus experienced by this patient was secondary to amlodipine therapy on the basis of the temporal association of administration, the response to increasing dosage, and both a Naranjo score of 7 (probable) and “probable likely” by the World Health Organization causality scale.9, 10

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Conclusions 

The overall incidence of myoclonus resulting from calcium channel blockers is rare, and only isolated cases have been reported in which the onset ranges from immediately during an intravenous push6 to as late as after 10 months of therapy.5 Neurologic symptoms usually stop within 24 hours after cessation of the offending drug but have been reported to persist for up to 3 weeks.7 To our knowledge, this is the first reported case of amlodipine causing this side effect, and the occurrence of this adverse reaction increases the likelihood that myoclonus is a side effect inherent to all calcium channel blockers.

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References 

  1. Vadlamudi L, Wijdicks EF. Multifocal myoclonus due to verapamil overdose. Neurology. 2002;58:984
  2. Jeret JS, Somasundaram M, Asaikar S. Diltiazem-induced myoclonus. N Y State J Med. 1992;92:447–448
  3. Pedro-Botet ML, Bonal J, Caralps A. Nifedipine and myoclonic disorders. Nephron. 1989;51:281
  4. Rodger C, Stewart A. Side effects of nifedipine. Br Med J. 1978;1:1619–1620
  5. Hicks CB, Abraham K. Verapamil and myoclonic dystonia. Ann Intern Med. 1985;103:154
  6. Maiteh M, Daoud AS. Myoclonic seizure following intravenous verapamil injection: case report and review of the literature. Ann Trop Paediatr. 2001;21:271–272
  7. Pina MA, Ara JR, Remirez A, Castiella J. Verapamil and acute dystonia. J Clin Pharm Ther. 1998;23:79–80
  8. Fernandez HH, Friedman JH. Carvedilol-induced myoclonus. Mov Disord. 1999;14:703
  9. Edwards IR, Aronson JK. Adverse drug reactions: definitions, diagnosis, and management. Lancet. 2000;356:1255–1259
  10. Naranjo CA, Shear NH, Lanctôt KL. Advances in the diagnosis of adverse drug reactions. J Clin Pharmacol. 1992;32:897–904

 Funding: None.

 Conflict of Interest: None of the authors have any conflicts of interest associated with the work presented in this manuscript.

 Authorship: All authors had access to the data and played a role in writing this manuscript.

PII: S0002-9343(08)01257-6

doi:10.1016/j.amjmed.2008.10.036

The American Journal of Medicine
Volume 122, Issue 4 , Page e7, April 2009

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