126 j The Cerebellum 2003; 2: pp 126 128 j Epilepsia partialis continua possibly caused by cerebellar lesion Tatiana Vander, Mark Medvedovsky and Yuval Herishanu Department of Neurology, Soroka Medical Center, Ben Gurion University of the Negev, Beer Sheva, Israel The cerebellum is known to have inhibitory effects on seizures. Nevertheless, cerebellar dysplastic lesions can be epileptogenic. We report a patient presenting with epilepsia partialis continua (EPC) following a hemorrhagic cerebellar lesion. Possible pathophysiological mechanisms are discussed. Keywords: Epilepsia partialis continua - cerebellum - diaschisis Vander T, Medvedovsky M, Herishanu Y. Epilepsia partialis continua possibly caused by cerebellar lesion Cerebellum 2004; 3: 126-128 Introduction over left frontotemporal region (Figure 1). Simultaneous EMG from Right Abductor pollicis brevis showed rhythmic 1 Hz/sec myoclonic discharge. On back-averaging, the correlation between EEG spikes and EMG discharge was non-consistent. MRI of the brain showed a large hypointense lesion in right cerebellar hemisphere suggestive of post-hemorrhagic gliosis (Figure 2). Ictal PET with (18F) ¯uorodeoxyglucose (18F-FDG) revealed focal hypometabolism in the lesion of right cerebellar lobe. The diagnosis of epilepsia partialis continua was made. She was treated with Carbamazepine 1200 mg/day for one month, followed by Topiramate 400 mg/day for two months and afterward Lamotrigine 400 mg/day during two months. On follow-up, no signi®cant improvement was seen. The question of whether seizures can originate in the cerebellum remains controversial. While several reports have been published, supported by intracranial ictal and interictal EEG recording and PET/SPECT ®ndings and suggesting that cerebellar pathology may produce focal seizures, no case of epilepsia partialis continua (EPC) caused by a cerebellar lesion has been reported in the english literature.1 We describe a patient who developed EPC following a cerebellar hemorrhage. Case Report A 58-year-old woman was admitted to the Department of Neurology because of involuntary rhythmic movements of her right hand and lower lip. Two months prior to this admission, she suffered from right lobar cerebellar hemorrhage and was discharged from the hospital without any neurological de®cit. She was suffering from diabetes mellitus treated with Metformin and from arterial hypertension treated with beta-blockers. On admission she was afebrile, alert and cooperative. The examination of the heart, lung and abdomen was unremarkable. No signs of meningeal irritation or motor or sensory de®cit were found. She presented continuous rhythmic clonic jerks with a frequency of 1-2 Hz of her right lower lip and right hand. The seizures continued during sleep with reduced amplitude and were exacerbated by voluntary movements of the affected parts. The routine laboratory work-up was normal. Repeated EEG recording disclosed intermittent epileptiform discharges Received 20 August 2003; Accepted 10 January 2004 Correspondence: Tatiana Vander, Department of Neurology, Soroka Medical Center, Beer Sheva, 84105 Israel. Tel: ‡972 8 6400595. Fax: ‡972 8 6403660. E-mail: vandertatiana@hotmail.com  2004 Taylor & Francis DOI 10.1080/14734220410026220 Discussion The main differential diagnosis in our patient included EPC, oculomasticatory/limb myorhythmia and resting/ postural tremor. While clinical picture is very similar in all diseases, persistence of the movement during sleep, EEG abnormalities and hypometabolic changes on PET study is suggestive of an epileptic phenomenon. EPC is de®ned clinically as a syndrome of continuous focal jerking of a body part, usually a distal part of a limb, occurring over hours, days or years.2 The cause of EPC is various and includes in¯ammatory lesions, Rasmussen's syndrome, vascular diseases, multisystem diseases, tumors, traumas, perinatal injury, hyperglycemia, Creutzfeldt-Jakob disease,2 multiple sclerosis3 and metabolic disorders.4 EEG in EPC is various from normal record and unspeci®c slowing (Bancaund's type I) to intermittent epileptic discharge and focal electrographic status epilepticus (Bancaund's type II).5 The correlation between EEG changes and EMG discharge may be non-consistent,6 as well as SPECT/PET ®ndings.7 The anatomical and physiological origin of EPC is controversial. It has been argued that EPC is a form of Epilepsia partialis continua and cerebellum j 127 Figure 1 The EEG recording shows focal epileptic discharge over left frontotemporal region with simultaneous EMG recording from Right Abductor pollicis brevis. Figure 2 Flair weighted image discloses large gliotic lesion in right cerebellar hemisphere, corresponding to the previous hemorrhage. focal cortical myoclonus, but subcortical structures have also been involved.2 No reports relating EPC and cerebellar lesions were published. However several reports have described focal seizures, originating from cerebellar tumors.1,8 Mesiwala et al.1 reported a child suffering from subcortical focal epilepsy with secondary generalization, refractory to antiepileptic medications in whom scalp EEG disclosed bilateral electrical anomalies. Ictal and interictal SPECT revealed a focal perfusion abnormality in the cerebellum and intraoperative EEG supported the cerebellar origin of seizure discharges that spread to the cortical surface. Ganglioglioma of the cerebellum was excised together with the cerebellar hemisphere and the patient became free of seizures. These reports suggest that at least in cases of structural lesions, the epileptic activity may indeed begin within the cerebellum. There are extensive cerebrocerebellar connections in the human brain. Projections from the cerebellum extend to the cerebrum through relay centers in the thalamus. Thus it is possible that epileptic activity arising in the cerebellum could spread through the cerebellothalamo- 128 j T Vander et al. cortical projections to the cerebral surface.9 In two elderly patients with a structural cerebellar lesion, suffering from complex partial epilepsy, Umemura and Suzuki10 demonstrated ªcrossed cerebellar hyperperfusionº, a reversed crossed cerebellar diaschisis (CCD). A CCD has been described in patients suffering from stroke, infections, tumors and seizures and is characterized by depression of regional brain perfusion, metabolism and neuronal activity in the cerebellum contralateral to a cortical lesion.11 This phenomenon may be documented by MRI or functional imaging such as PET or SPECT. Proposed mechanism underlying CCD include disconnection of glutamatergic corticopontocerebellar tract.12 Conversely, the unilateral cerebellar lesion may have an in¯uence on the contralateral cerebral hemisphere (crossed cerebello-cerebral diaschisis).13 Cerebellar cortical projections are inhibitory by means of the release of the inhibitory transmitter gamma-aminobutyric acid (GABA) from the Purkinje cells. In this concept, cerebellar lesion may cause disinhibition of contralateral cortical cells and release of epileptic activity via the above pathophysiological mechanism. EPC in our patient appeared in a strong temporal relation with a cerebellar hemorrhage and this fact together with the absence of cortical abnormalities on MRI study support a possible role of cerebellar lesion in induction of seizures. This case provides further evidence that cerebellar pathology probably may induce cortical seizures, if functional connections are retained. References 1. Mesiwala AH, Kuratani JD, Avellino AM, Roberts TS, Sotero MA, Ellenbogen RG. Focal motor seizures with secondary generalization arising in the cerebellum. Case report and review of the literature. J Neurosurg 2002; 97: 190-196. 2. Cockerell OC, Rothwell J, Thompson PD, Marsden CD, Shorvon SD. Clinical and physiological features of epilepsia partialis continua. Cases ascertained in the UK. Brain 1996; 119: 393-407. 3. Hess DC, Sethi KD. Epilepsia partialis continua in multiple sclerosis. Int J Neurosci 1990; 50: 109-111. 4. Veggiotti P, Colamaria V, Dalla Bernardina B, Martelli A, Mangione D, Lanzi G. Epilepsia partialis continua in a case of MELAS: clinical and neurophysiological study. Neurophysiol Clin 1995; 25: 158-166. 5. Pandian JD, Thomas SV, Santoshkumar B, Radhakrishnan K, Sarma PS, Joseph S, Kesavadas C. Epilepsia partialis continua - a clinical and electroencephalography study. Seizure 2002; 11: 437441. 6. Velasco M, Velasco F, Alcala H, Diaz de Leon AE. Wakefulnesssleep modulation of EEG-EMG epileptiform activities: a quantitative study on a child with intractable epilepsia partialis continua. Int J Neurosci 1990; 54: 325-327. 7. Barrington SF, Koutrou manidis M, Agathonikou A, Marsden PK, Binni CD, Polkey CE, Maisey MN, Panayiotopoulos CP. Clinical value of `ictal' FDG-positron emission tomography and the routine use of simultaneous scalp EEG studies in patient with intractable partial epilepsies. Epilepsia 1998; 39: 753-766. 8. Chae JH, Kim S-K, Wang K-C, Kim KJ, Hwang Y-S, Cho B-K. Hemifacial seizures of cerebellar ganglioglioma origin: seizure control by tumor resection. Epilepsia 2002; 42: 1204-1207. 9. Norden A, Blumenfeld H. The role of subcortical structures in human epilepsy. Epilepsy Behavior 2002; 3: 219-231. 10. Umemura A, Suzuki T. Crossed cerebellar hyperperfusion in symptomatic epipepsy - two case reports. Neurol Med Chir 2000; 40: 65-68. 11. Chakravarty A. MR evaluation of crossed and uncrossed cerebral cerebellar diaschisis. Acta Neurol Scand 2003; 108: 60-65. 12. Otte A, Roelcke K, von Ammon et al. Crossed cerebellar diaschisis and brain tumor biochemistry studied with positron emission tomogtaphy, [F18] ¯uorodeoxyglucose and [11C] methionine. J Neurol Science 1998; 156: 33-77. 13. Attig E, Botez MI, Hublet C, Vervonk C, Jacquy J, Capon A. Cerebral crossed diaschisis caused by cerebellar lesion: role of the cerebellum in mental functions. Rev Neurol (Paris) 1991; 147: 200-207.