Figure. Sagittal scan of brain MRI taken in December 2002: the arrow shows the left posterior parietal lesion, hyperintense on T2-weighted imaging, without gadolinium enhancement (A). H-E stain of brain biopsy specimen showing a focal demyelinated area with perivascular inflammatory reaction consisting of mononuclear cells at low (⫻100, B) and higher magnification (⫻250, C). Immunohistochemistry with anti-SV40 antibody showing a crossreactive nuclear positivity in infected oligodendrocytes (D). Rome; and Unità Operativa di Anatomia ed Istologia Patologica (Dr. Vago), Dipartimento di Scienze Cliniche Luigi Sacco Università degli Studi di Milano, Milan, Italy. Received January 16, 2004. Accepted August 3, 2004. Address correspondence and reprint requests to Dr. Simona Di Giambenedetto, Istituto di Clinica delle Malattie Infettive, Università Cattolica del Sacro Cuore, Largo Gemelli 8, 00168 Rome, Italy; e-mail: simonadg72@hotmail.com Copyright © 2004 by AAN Enterprises, Inc. References 1. Berger JR, Concha M. Progressive multifocal leukoencephalopathy: the evolution of a disease once considered rare. J Neurovirol 1995;1:5–18. 2. Antinori A, Cingolani A, Lorenzini P, et al. Clinical epidemiology and survival of progressive multifocal leukoencephalopathy in the era of highly active antiretroviral therapy: data from the Italian Registry Investigative Neuro AIDS (IRINA). J Neurovirol 2003;9(suppl 1):47–53. Myocardial infarction following brief convulsive seizures Peter S. Chin, MD; Kelley R. Branch, MD; and Kyra J. Becker, MD The CNS influences the electrical and mechanical functions of the heart.1 Seizures can produce EKG repolarization abnormalities, arrhythmias, and perhaps myocardial injury.2,3 Acute coronary insufficiency leading to myocardial infarction (MI) has been reported with status epilepticus and occurs rarely in association with electroconvulsive therapy (ECT).4,5 MI has not been reported after self-limited spontaneous convulsions. We present two cases of acute coronary syndrome (ACS) with MI after generalized tonicclonic (GTC) seizure. Case reports. Patient 1. A 69-year-old man with a history of right frontal and occipital infarcts came to the emergency room after two witnessed GTC seizures that began with leftward eye deviation. He denied antecedent chest pain or dyspnea. After a period of postictal somnolence, he reported retrosternal chest pain. EKG showed 2-mm ST-segment depressions in leads V3 to V6. Troponin I peaked at 86 ng/mL. Nuclear stress testing suggested reversible ischemia in the left anterior descending (LAD) artery distribution. MRI of the brain showed no acute abnormali- 3. Miralles P, Berenguer J, Lacruz C, et al. Inflammatory reaction in progressive multifocal leukoencephalopathy after highly active antiretroviral therapy. AIDS 2001;15:1900 –1902. 4. Safdar A, Rubocki RJ, Horvath JA, Narayan KK, Waldron R. Fatal immune restoration disease in human immunodeficiency virus type1infected patients with progressive multifocal leukoencephalopathy: impact of antiretroviral therapy-associated immune reconstitution. Clin Infect Dis 2002;35:1250 –1257. 5. Hoffmann C, Horst HA, Albrecht H, Schlote W. Progressive multifocal leukoencephalopathy with unusual inflammatory response during antiretroviral treatment. J Neurol Neurosurg Psychiatry 2003;74:1142– 1144. 6. Du Pasquier RA, Koralnik IJ. Inflammatory reaction in progressive multifocal leukoencephalopathy: harmful or beneficial? J Neurol 2003; 9(suppl 1):25–31. 7. De Luca A, Cingolani A, Linzalone A, et al. Improved detection of JC virus DNA in cerebrospinal fluid for diagnosis of AIDS-related progressive multifocal leukoencephalopathy. J Clin Microbiol 1996;34:1343– 1346. ties; EEG revealed no epileptiform patterns. He was started on phenytoin for poststroke epilepsy and was lost to follow-up evaluation. Six months later, he had another witnessed GTC seizure complicated by cardiogenic shock; phenytoin level at the time of presentation was 4.3 ␮g/mL. Troponin I peaked at 69 ng/mL. Coronary angiography demonstrated severe three-vessel disease with plaque rupture in the LAD; he underwent uneventful coronary bypass surgery. Patient 2. A 53-year-old man with a history of hypertension, diabetes, and alcoholism was brought to the emergency room after a witnessed GTC withdrawal seizure that occurred in a supermarket. He denied preceding cardiac symptoms and had no history of ischemic heart disease or seizures. On arousal, he reported nausea and epigastric pain. EKG showed 2-mm ST-segment elevations in leads II, III, and aVF. Coronary angiography and intravascular ultrasound revealed moderate stenosis of the LAD and a ruptured plaque in the right coronary artery without thrombus. The patient was treated medically. He ruled in for an ST-elevation MI with a peak troponin I of 223 ng/mL. Noncontrast head CT showed chronic white matter changes. EEG was normal. Discussion. These cases demonstrate that ACS leading to MI can follow brief epileptic convulsions and provoked alcohol withdrawal seizures. Although presumably rare, the occurrence of ACS after a seizure is not surprising in patients with coronary December (2 of 2) 2004 NEUROLOGY 63 2453 artery disease given the physiologic effects of a generalized convulsion on the heart. A GTC seizure can be considered a brief physiologic cardiac stress test. Within minutes of a convulsion, plasma norepinephrine and epinephrine levels can reach 12 and 40 times normal.6 Concomitant increases in heart rate, blood pressure, and myocardial contractility, along with augmented cardiac afterload from tonic muscle contraction, collectively increase myocardial oxygen demand. Simultaneously, ictal apnea may lead to hypoxia. The resultant mismatch between myocardial metabolic demands and oxygen delivery could produce myocardial ischemia in patients with a fixed coronary artery stenosis. The physiologic stress associated with isolated seizures may also be severe enough to produce subendocardial ischemia in the absence of coronary flow impairment.7 Alternatively, increased coronary flow and shear stress could rupture vulnerable coronary atherosclerotic plaque, leading to MI. Neither of the reported patients had previous cardiac symptoms; however, the functional and angiographic evidence of coronary atherosclerosis suggests a coronary etiology in both patients. In Patient 1, either supply-demand oxygen mismatch caused by a fixed coronary stenosis or coronary plaque rupture may have caused MI; because coronary angiography was not performed, the actual mechanism of injury remains unknown. Plaque rupture appears to have been the cause of the transmural MI in Patient 2 based on the angiographic findings. Sympathetically mediated neurogenic cardiac damage may also produce EKG changes and troponin elevations.1 Although the mechanism of infarction remains uncertain in these cases, the potential for seizure-related myocardial injury needs to be recognized given the increased prevalence of epilepsy and coronary artery disease with age. Ictal cardiac damage can occur in patients with seizure at risk for coronary artery disease. Although postictal somnolence and endotracheal intubation can delay the diagnosis of seizure-related 2454 NEUROLOGY 63 December (2 of 2) 2004 myocardial ischemia, timely recognition of this complication can facilitate appropriate cardiac evaluation and intervention. Prospective studies of cardiac complications after isolated seizures may provide greater understanding of the various mechanisms of myocardial injury. From the Departments of Neurology (Drs. Chin and Becker) and Neurological Surgery (Dr. Becker), and Division of Cardiology (Dr. Branch), University of Washington and Harborview Medical Centers, Seattle, WA; and the Robert Wood Johnson/VA Clinical Scholars Program, Departments of Medicine and Neurology (Dr. Chin), University of California, Los Angeles and the VA Greater Los Angeles Healthcare System, CA. Received March 8, 2004. Accepted in final form August 9, 2004. Address correspondence and reprint requests to Dr. Kyra J. Becker, Box 359775, Harborview Medical Center, 325 Ninth Avenue, Seattle, WA 98104; e-mail: kjb@u.washington.edu Copyright © 2004 by AAN Enterprises, Inc. References 1. Samuels MA. Neurally induced cardiac damage. Definition of the problem. Neurol Clin 1993;11:273–292. 2. Nei M, Ho RT, Sperling MR. EKG abnormalities during partial seizures in refractory epilepsy. Epilepsia 2000;41:542–548. 3. Dixit S, Castle M, Velu RP, Swisher L, Hodge C, Jaffe AS. Cardiac involvement in patients with acute neurologic disease: confirmation with cardiac troponin I. Arch Intern Med 2000;160:3153–3158. 4. Sechi G, Dessi-Fulgheri P, Glorioso N, Volta G, Rosati G. Myocardial infarction complicating status epilepticus. Epilepsia 1985;26:572–576. 5. Hussar AE, Pachter M. Myocardial infarction and fatal coronary insufficiency during electroconvulsive therapy. JAMA 1968;204:1004 –1007. 6. Simon RP, Aminoff MJ, Benowitz NL. Changes in plasma catecholamines after tonic-clonic seizures. Neurology 1984;34:255–257. 7. Tigaran S, Molgaard H, McClelland R, Dam M, Jaffe AS. Evidence of cardiac ischemia during seizures in drug refractory epilepsy patients. Neurology 2003;60:492– 495. Myocardial infarction following brief convulsive seizures Peter S. Chin, Kelley R. Branch and Kyra J. Becker Neurology 2004;63;2453-2454 DOI 10.1212/01.WNL.0000148608.92290.EB This information is current as of December 28, 2004 Updated Information & Services including high resolution figures, can be found at: http://www.neurology.org/content/63/12/2453.full.html References This article cites 7 articles, 2 of which you can access for free at: http://www.neurology.org/content/63/12/2453.full.html##ref-list-1 Citations This article has been cited by 2 HighWire-hosted articles: http://www.neurology.org/content/63/12/2453.full.html##otherarticles Subspecialty Collections This article, along with others on similar topics, appears in the following collection(s): All Epilepsy/Seizures http://www.neurology.org//cgi/collection/all_epilepsy_seizures Cardiac http://www.neurology.org//cgi/collection/cardiac Permissions & Licensing Information about reproducing this article in parts (figures,tables) or in its entirety can be found online at: http://www.neurology.org/misc/about.xhtml#permissions Reprints Information about ordering reprints can be found online: http://www.neurology.org/misc/addir.xhtml#reprintsus Neurology ® is the official journal of the American Academy of Neurology. 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