era1 times per day and she was then weaned off ketamine. At this time the patient was on phenytoin and phenobarbital and remained in a coma. "here were no adverse effects that could be ascribed to the use of ketamine. During the following 3 months the patient developed intermittent seizures and has profound short-term memory and global cognitive deficits. A cranial MRI study at this time showed a moderate degree of diffuse cerebral atrophy, Discussion. This patient had SE that was refractory to treatment with phenobarbital phenytoin, continuous midazolam infusion, propofol, IV valproate, or IV lidocaine infusion. Pentobarbital coma induced for 4 weeks was not sufficient to control her SE. SE refractory t o all currently recommended medications is a relatively rare but challenging neurologic problem. A recent review of the management of SE did not list ketamine as a therapeutic agent.4 In our patient, IV ketamine immediately controlled both clinical and electrographic seizures (see figure), although gradually higher doses of ketamine were required to maintain the response. Animal data suggest that ketamine may possess anticonvulsant properties, possibly by binding to the phencyclidine recognition site of the NMDA receptor.5 NMDA receptor blockade may be a protective response to the deleterious effects of excessive excitatory amino acid.6 Accordingly, ketamine may have both a n anticonvulsant and a neuroprotective effect in SE. Ketamine has a half-life of 2 to 3 hours and is extensively and hepatically metabolized via cytochrome P45O-mediated oxidative pathways to the active metabolite norketamine, which is pharmacologically active. Pharmacokinetic interactions with concomitant antiepileptic medication is not well defined, although there does appear to be significant interaction. The patient's age and the effect of a co-administered enzyme-inducing anticonvulsant medication may underlie her requirement for a n increasing dosage of ketamine to maintain the anticonvulsant effect. Ketamine may prove to be a useful adjuvant in the treatment of refractory SE. The pharmacologic characteristics and potential neuroprotective properties of ketamine may make it particularly attractive in the therapy of refractory SE, although confirmation of our observation of efficacy is required. From the Department of Neurology (Drs. Sheth and Gidal) and the School of Pharmacy (Dr. GidalJ, University of Wisconsin, Madison, WI. Receiued May 11, 1998. Accepted in final form July 11, 1998. Address correspondence and reprint requests to Dr. Raj D. Sheth, Department of Neurology, 600 Highland Auenue, H6l574 CSC, Madison, WI 6 3 792-5132. Copyright 0 1998 by the American Academy of Neurology References 1. Treiman DM. Status epilepticus. Baillieres Clin Neurol 1996;5:821839. 2. Stecker MM, Kramer TH, Raps EC, OlMeeghan R, Dulaney E, Skaar DJ. Treatment of refractory status epilepticus with propofol: clinical and pharmacokinetic findings. Epilepsia 1998;39:18-26. 3. Lothman E. The biochemical basis and pathophysiology of status epilepticus. Neurology 1990;4O(suppl 2):13-23. 4. Loweinstein DH, Alldredge BK. Status epilepticus. N Engl d Med 1998 338:970-976. 5. Lodge D, Johnson KM. Noncompetitive excitatory amino acid receptor antagonists. Trends Pharmacol Sci 1990;11:81-86. 6. Schmitt B, Netser R, Fanconi S, Baumann P, Boltshauser E. Drug refractory epilepsy in brain damage; effect of dextromethorphan on EEG in four patients. J Neurol Neurosurg Psychiatry 1994;57:333-339. Multifocal brain MRI hypointensities secondary to embolic metal fragments from a mechanical heart valve prosthesis: A possible source of epileptic seizures Markus Naumann, MD; Erich Hofmann, MD; and Klaus V. Toyka, MD Recently, Wingerchuk e t a1.I described a patient with brain MRI lesions secondary to embolic metal fragments from a Bjork-Shiley heart valve prosthesis. "he incidence and possible clinical symptoms of such lesions are unknown. We present another patient showing similar lesions on MRI who, in addition, had epileptic seizures. This raises the question of whether metal deposits may be associated with focal neurologic symptoms. Case report. A 66-year-old man had a n aortic valve prosthesis (Starr-Edwards) in 1969 to treat aortic valve stenosis. Twenty years later, this valve was replaced by a St. Jude prosthesis be- Figure. Proton-density (A, C) and T2weighted (B, D) MR images (spin echo 2,420130,100).Bilateral lacunar infarctions in the caudate heads (B). Punctate susceptibility artifacts in both hemispheres (basal ganglia, medullary layer, subcortex) typical for metallic emboli. 1766 NEUROLOGY 51 December 1998 cause of continuously deteriorating pulmonary artery hypertension. Macroscopically, no fracture of the removed Starr-Edwards valve and no thrombotic material were seen. In 1989, a first generalized tonic-clonic seizure occurred during sleep, and anticonvulsant therapy with phenobarbital was initiated at a n outside hospital. In addition, complex-partial seizures occurred that were described by the patient as isolated, recurrent short episodes of a dreamy state with ascending nausea, occasionally associated with visual disturbances. Approximately 10 to 20 complex-focal seizures occurred per month, with a duration of about 10 seconds. In 1997, the patient was admitted to our department for the first time for better seizure control. On admission, neurologic examination, laboratory tests, and CSF were normal, and no cardiac output failure was present. Repeated EEG studies showed intermittent right-sided frontotemporal slow wave bursts. On cranial MRI, several punctate hypointensities were seen randomly distributed over both hemispheres (figure, A through D).No other pathology could be found in the temporal lobes even on specifically angulated high-resolution coronal series. The lesions were especially prominent in the proton-density images of the T2-weighted spin echo series. They showed a peripheral hyperintensity mainly at the rostra1 and dorsal margin, i.e., perpendicular to the direction of the phase encoding gradient, thus fulfilling the criteria for susceptibility artifacts from metal emboli.2 Discussion. The susceptibility artifacts in the brain of our patient resemble the lesions reported by Wingerchuk et al.] and most likely reflect shedded metal material from the original StarrEdwards valve prosthesis. Although in the report by Wingerchuk et al. a fracture-prone, but not obviously broken, Bjork-Shiley valve was associated with brain metal emboli, brain metal artifacts were observed in our patient after implantation of a StarrEdwards prosthesis that looked macroscopically normal when removed. Thus, metal emboli from unbroken mechanical heart valve prostheses are possible. It remains unclear whether some of these metal fragments are the cause of the epilepsy in our patient. Because we did not find any other structural abnormalities, this appears likely. In our patient, punctate susceptibility artifacts were seen in both hemispheres, especially in the basal ganglia, the medullary layer, and the right frontal subcortex. The lesions in the basal ganglia and the medullary layer most likely do not contribute to epileptic seizures, and a causal association between the right frontal subcortical lesion and complex-focal seizures is conceivable. This localization would also be in accordance with the intermittent right-sided frontotemporal slow wave bursts seen on EEG. Further support could be adduced by depth electrode recordings; these were not obtained because the patient became seizure free with carbamazepine. Metal emboli may be more common after cardiac valve implantation than previously estimated but may not be detected because patients cannot be studied with MRI with these valves in place. ized, throbbing, and continuous, with focally worse pain in the temporal or, less often, in the occipital regions.’ We report a patient with a histopathologically confirmed giant cell arteritis whose clinical manifestations mimicked those of cluster headache. Case report. A 74-year-old man without previous personal or familial history of headache was evaluated in our hospital because of a 2-month history that consisted initially of one to two attacks per day and progressed to three to four attacks per day, of severe, boring pain in the left supraorbital area that lasted 15 to 20 minutes. The pain episodes were associated with ipsilateral ptosis, lacrimation, and rhinorrhea, but not with ipsilateral sweating. The patient had no pain between these episodes. Although the headaches did not occur at the same time each day, one of the episodes usually occurred during nocturnal sleep, awaking the patient. He also complained of jaw claudication with chewing and pain in the scapulohumeral joints, although chewing did not precipitate the headache episodes. Neurologic examination, including temporal artery palpation, was normal. The patient was a heavy smoker and had antecedents of chronic obstructive airway disease, cor pulmonale, and a peripheral artery embolism that required left leg amputation. Blood analyses showed, as the most outstanding features, a mild leukocytosis (12,700 white blood celldmm”) and increased erythrocyte sedimentation rate (83 mm in 1hour). Brain CT was normal. Histopathologic study of the left temporal artery confirmed the diagnosis of giant cell arteritis (figure). Following initiation of treatment with prednisone 60 mglday, the patient became asymptomatic. Prednisone dose was tapered gradually in 3 months. Aft,er 6 months of follow-up, the patient remains asymptomatic, and erythrocyte sedimentation rate decreased to 11 mm in 1 hour. From the Departments of Neurology (Drs. Naumann and Toyka) and Neuroradiology (Dr. Hofmann), Bayerische Julius-Maximilians-UniversitatWiirzburg, Germany. Received April 22, 1998.Accepted in final form July 21, 1998. Address correspondence and reprint requests to Priv. -Doz. Dr. Markus Naumann, Neurologische Klinik der Bayerischen Julius-MaximiliansUniversitiit Wiirzburg, Josef-Schneider-Stra/3e 11, 97080 Wiirzburg, Germany. Copyright 0 1998 by the American Academy of Neurology References 1. Wingerchuk DM, Krecke KN, Fulgham JR. Multifocal brain MRI artifacts secondary to embolic metal fragments. Neurology 1997;4914511453. 2. Joseph PM,Atlas SW. Artifacts. In: Atlas SW, ed. Magnetic resonance imaging of the brain and spine. New York Raven Press, 1991:lll-113. Giant cell arteritis presenting as cluster headache F.J. Jimt?nez-Jim’nez,MD, PhD; E. Garcia-ALbea,MD, PhD; M . Zurdo, MD; P.Martinez-Onsurbe,MD; and A. Ruiz de Villaespesa,MD New onset of headache in an elderly patient is a common presenting symptom of giant cell arteritis. Headache is usually general- Figure. Temporal artery shows thickening of the intima, lymphocytic infiltration of the media with multinucleated giant cells, and partial destruction of the internal elastic lamina (H-E, original magnification X80 (A) and X160 (B) before 42.3% reduction). December 1998 NEUROLOGY 51 1767 Multifocal brain MRI hypointensities secondary to embolic metal fragments from a mechanical heart valve prosthesis: A possible source of epileptic seizures Markus Naumann, Erich Hofmann and Klaus V. Toyka Neurology 1998;51;1766-1767 DOI 10.1212/WNL.51.6.1766 This information is current as of December 1, 1998 Updated Information & Services including high resolution figures, can be found at: http://www.neurology.org/content/51/6/1766.full.html References This article cites 1 articles, 1 of which you can access for free at: http://www.neurology.org/content/51/6/1766.full.html##ref-list-1 Citations This article has been cited by 2 HighWire-hosted articles: http://www.neurology.org/content/51/6/1766.full.html##otherarticles 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. Published continuously since 1951, it is now a weekly with 48 issues per year. Copyright . All rights reserved. Print ISSN: 0028-3878. Online ISSN: 1526-632X.