LETTERS TO THE EDITOR Patrick Veyssière, MD Médecine générale Sainte Foy de Peyrollière France Jean-Louis Montastruc, MD, PhD* Service de Pharmacologie Clinique Centre Midi-Pyrénées de Pharmacovigilance de Pharmacoépidémiologie et d’Informations sur le Médicament Centre Hospitalier Universitaire Hôpitaux de Toulouse Toulouse, France *E-mail: montastruc@cict.fr Jean-Louis Montastruc, MD, PhD Laboratoire de Pharmacologie Médicale et Clinique Unité de Pharmacoépidémiologie EA 3696, Université Paul Sabatier Faculté de Médecine Toulouse, France References 1. Imbimbo BP. Pharmacodynamic-tolerability relationships of cholinesterase inhibitors for Alzheimer’s disease. CNS Drugs 2001; 15:375–390. 2. Memantine. Martindale: the complete drug reference, 35th ed. London: The Pharmaceutical Press; 2007. p 329. 3. Mizoguchi K, Yokoo H, Yoshida M, Tanaka T, Tanaka M. Amantadine increases the extracellular dopamine levels in the striatum by re-uptake inhibition and by N-methyl-D-aspartate antagonism. Brain Res 1994;662:255–258. 4. Baptista T, Lopez ME, Teneud L, et al. Amantadine in the treatment of neuroleptic-induced obesity in rats: behavioral, endocrine and neurochemical correlates. Pharmacopsychiatry 1997;30:43– 54. 5. Deberdt W, Winokur A, Cavazzoni PA, et al. Amantadine for weight gain associated with olanzapine treatment. Eur Neuropsychopharmacol 2005;15:13–21. 6. Floris M, Lejeune J, Deberdt W. Effect of amantadine on weight gain during olanzapine treatment. Eur Neuropsychopharmacol 2001;11:181–182. 7. Graham KA, Gu H, Lieberman JA, Harp JB, Perkins DO. Doubleblind, placebo-controlled investigation of amantadine for weight loss in subjects who gained weight with olanzapine. Am J Psychiatry 2005;162:1744 –1746. 8. Review of Ebixa ADRs in Sweden. Reactions 2005;1054:2. 9. Begaud B, Evreux JC, Jouglard J, Lagier G. Imputation of the unexpected or toxic effects of drugs. Actualization of the method used in France. Therapie 1985;40:111–118. 10. Payette H, Coulombe C, Boutier V, Gray-Donald K. Nutrition risk factors for institutionalization in a free-living functionally dependent elderly population. J Clin Epidemiol 2000;53:579 –587. 11. Sullivan DH, Morley JE, Johnson LE, et al. The GAIN (Geriatric Anorexia Nutrition) registry: the impact of appetite and weight on mortality in a long-term care population. J Nutr Health Aging 2002;6:275–281. 1981 Poststroke Partial Seizures Presenting As Hemifacial Spasm Hemifacial spasm (HS) is an intermittent involuntary rhythmic tonic or clonic contraction of facial musculature innervated by the ipsilateral facial nerve. Between the episodes of spasms, the face is either normal or slightly weak on the affected side.1 Although usually there is no identifiable etiology, it is conventionally thought to be a peripheral process due to either compressive lesions of the facial nerve at the root exit zone (e.g., tumor, arteriovenous malformation), or noncompressive lesions (e.g., stroke, multiple sclerosis). It has been hypothesized that an ephaptic transmission results in facial nerve excitation and HS.2 Anticonvulsants and botulism toxin are the mainstay of the treatment.2 Here, we present the case of a patient who presented with right HS following a left cortical stroke but the cause was epileptic and the treatment involved anti-convulsants. A 74-year-old, fully independent, right-handed male with history of atrial fibrillation and left cortical hemorrhagic stroke, presented with an acute right HS and worsening of his right hemiparesis starting the night before. Since his prior stroke 2 years ago he had been left with a mild right hemiparesis and a subtle dysarthria. The patient was taking 81 mg aspirin at the time of this presentation. He was seen in an outside hospital the night before where a computed tomography (CT) scan of his head was obtained and he was loaded with 1 g of phenytoin with no effect on his facial spasm. On initial examination the patient was lying in bed in no distress with almost continuous spasm of the right upper and lower face interrupted only by brief intermissions lasting 1 to 3 seconds. Patient denied any associated pain. His comprehension, naming and repetition were preserved but his speech was dysarthric. When spasms were not present a right facial droop was noted along with a right pronator drift and hemiparesis, with motor strength at 4/5 on the left and 3/5 on the right. Head CT scan and magnetic resonance imaging (MRI) of the brain demonstrated a left frontal cortical based, acute to subacute, intracerebral hemorrhage overlapping with a chronic bleed with several areas of hemosiderin deposition on gradient echo (Fig. 1). Upon admission his phenytoin was continued (for seizure prophylaxis after intracerebral bleed) at 100 mg three times a day, with no effect on his HS. Video-EEG monitoring revealed continuous cycles of rhythmic ictal pattern lasting for 90 to 350 seconds interrupted only for 1 to 3 seconds during which the EEG showed a relatively suppressed background. The ictal activities started in the left central or central-frontal-temporal head regions. A high voltage rhythmic muscle activity was present on the right side. Clinically, these discharges were associated with his facial spasms with brief periods of quiescence in between (Fig. 2). These findings were suggestive of simple partial status epilepticus with the primary focus at the site of his hemorrhagic stroke. Patient’s HS was completely controlled after the free phenytoin level was increased from 1.4 to 1.9 mg/mL. Four days later his phenytoin was replaced with levetiracetam at Published online 26 July 2007 in Wiley InterScience (www. interscience.wiley.com). DOI: 10.1002/mds.21660 Movement Disorders, Vol. 22, No. 13, 2007 1982 LETTERS TO THE EDITOR 500 mg twice a day. His HS remained well controlled during the rest of his hospital course and he was discharged to a subacute rehabilitation facility after one week. A second EEG, performed before discharge, did not show any epileptiform discharges. There are other reports of HS following stroke. Ambrosetto and Forlani, as well as Kawakami et al., report such patients, but both cases involved pontine strokes, compressing the facial nerve due to edema.3,4 Schiess et al., present a case of right HS, in a patient with left ponto-medullary stroke.5 Arunabh et al., cite a caudate stroke inducing HS,6 but neither one of these cases had seizures. Forss et al., report a patient with history of partial seizures who developed left HS as reflex epilepsy provoked by stimulation of the left lower gums.7 A review of 1,500 patients with stroke showed a 3.7% incidence of poststroke movement disorders starting from one day to 10 months after stroke. Chorea was the most common condition among this group while there were no cases of HS.8 Our patient’s neuroimaging demonstrates a discrete cortical based hemorrhage in the left precentral gyrus correlating to the FIG. 2. EEG demonstrating the end of a seizure episode and facial spasm followed by a 3 second period of quiescence before the onset of a new cycle. A high voltage sharp discharge in the left central-frontal head area (max C3 and F7) is followed by a build up of rhythmic low voltage fast activity on the left. The muscle artifact on the right was always present during these events. This pattern repeated itself constantly (seizures lasting 90 –350 second) and coincided with clinical episodes of right hemifacial spasm during which the patient remained awake and alert (simple partial seizures). representation of the face. Presence of focal spikes in the left cortex on EEG, and response to antiepileptic medication, demonstrate that HS can, among other etiologies, present as a manifestation of simple partial seizures and status epilepticus following stroke. Allen Towfigh, MD Navid Mostofi, MD Gholam K. Motamedi, MD* Department of Neurology Georgetown University Hospital Washington, DC *E-mail: motamedi@georgetown.edu References FIG. 1. A: Computed tomography demonstrating hemorrhage in the left frontal cortex. B: Gradient Echo (first row) and T2 weighted (second row) MRI images demonstrating subacute hemorrhage in the left frontal cortex. Movement Disorders, Vol. 22, No. 13, 2007 1. Evidente VG, Adler CH. Hemifacial spasm and other craniofacial movement disorders. Mayo Clin Proc 1998;73:67-71. 2. Wang A, Jankovic J Hemifacial spasm: clinical findings and treatment. Muscle Nerve 1998;21:1740-1747. 3. Ambrosetto P, Forlani S. Lacunar pontine infarction presenting as isolated facial spasm. Stroke 1988;19:784-785. 4. Kawakami M, Sato T, Tochigi S, Ito T. Lacunar pontine infarction with hemifacial spasm as the initial symptom. Stroke 1990;21: 1236. 5. Scheiss RJ, Biller J, Toole JF. Position-dependent Hemifacial Spasm. Surg Neurol 1982;17:423-425. 6. Jain AS, Maheshwari MC. Blepharospasm hemifacial spasm and tremors possibly due to isolated caudate nucleus lesions. J Assoc Physicians India 1992;40:687-689. 7. Forss N, Makela JP, Keranen T, Hari R. Trigeminally triggered epileptic hemifacial convulsions. NeuroReport 1995;6:918-920. 8. Alarcon F, Zijlmans JC, Duenas G, Cevallos N. Post-stroke movement disorders: report of 56 patients. J Neurol Neurosurg Psychiatry 2004;75:1568-1574.