National Demonstration Project On Epilepsy In Brazil [projeto Demonstrativo Em Epilepsia No Brazil]

Epilepsy is the most prevalent non-communicable serious neurological condition worldwide. Unfortunately, the majority of people with epilepsy in low-income countries do not receive appropriate treatment. Stigmatisation is the rule. In this setting, the World Health Organization, the International League against Epilepsy and the International Bureau for Epilepsy launched the Global Campaign against Epilepsy in 1997. This entered its second phase in 2001 and as part of it has set up demonstration projects in the People's Republic of China, Zimbabwe, Senegal and, more recently, in Brazil. The objective of the demonstration projects is to show, through methodological evaluation, that it is possible to establish a model of treatment for people with epilepsy in primary health care settings. The Brazilian demonstration project has targeted regions in Campinas and São Jose do Rio Preto, both in Sao Paulo State. A task force has been established to assess strategies to expand this project nationwide.611153156Sander, J.W., Shorvon, S.D., Epidemiology of the epilepsies (1996) J Neurol Neurosurg Psychiatry, 61, pp. 433-443Temkin, O., (1994) The Falling Sickness: A History of Epilepsy from the Greeks to the Beginnings of Modern Neurology. 2.Ed., , Baltimore: John Hopkins Univ PressKale, R., Global campaign against epilepsy: The treatment gap (2002) Epilepsia, 43 (SUPPL. 6), pp. 31-33Nashef, L., Fish, D.R., Sander, J.W., Shorvon, S.D., Incidence of sudden unexpected death in an adult outpatient cohort with epilepsy at a tertiary referral centre (1995) J Neurol Neurosurg Psychiatry, 58, pp. 462-464Sander, J.W., Global Campaign against epilepsy: Overview of the demonstration projects (2002) Epilepsia, 43 (SUPPL. 6), pp. 34-36Kobayashi, E., Li, L.M., Sander, J.W., Report of Brazilian Demonstration Project, , http://www.aspe.hc.unicamp.br/pt/pdf/Report_Demo_Project_Brazil_Workshop.pdf, 17-8-200

Ictal ECG changes in temporal lobe epilepsy Alterações eletrocardiográficas ictais em epilepsia do lobo temporal

Changes in cardiac rhythm may occur during epileptic seizures and this has been suggested as a possible mechanism for sudden unexpected death amongst patients with chronic epilepsy (SUDEP). We have studied ECG changes during 61 complex partial seizures of temporal lobe origin in 20 patients. Tachycardia was observed in 24/61 (39%) and bradycardia in 3/61 (5%). The mean and median tachycardia rate was 139 and 140 beats/min (range 120-180). The longest R-R interval observed was 9 seconds. No difference was found in regard to the lateralisation of seizures and cardiac arrhytmia. One of the patients with bradycardia was fitted with a demand cardiac pacemaker, which appeared to decrease the number of his falls. In conclusion, ictal cardiac changes which may be seen in temporal lobe epilepsy (TLE) are sinus tachycardia and occasionally sinus bradycardia. Patients presenting vague complains suggestive of either TLE or cardiac dysrhythmia, simultaneous monitoring with EEG/ECG is required, and if the episodes are frequent, video-EEG should be considered. Further studies on this subject are warranted as this may shed some light on possible mechanisms for SUDEP.Alterações no ritmo cardíaco podem ocorrer durante crises epilépticas. Estas alterações têm sido sugeridas como possível mecanismo para explicar morte súbita em pacientes com epilepsia crônica. Analisamos o eltrocardiograma (ECG) em 61 crises parciais complexas do lobo temporal de 20 pacientes. Taquicardia foi observada em 24/61 (39%) e bradicardia em 3/61 (5%). A média e a mediana da taquicardia foram 139 e 140 batimentos por minuto (variando de 120-180). O intervalo R-R mais longo foi 9 segundos. Não houve diferença em relação a lateralisação das crises e alteração do ritmo cardíaco. Um paciente com bradicardia recebeu marcapasso de demanda, com diminuição importante das suas quedas durante as crises. Em conclusão, as alterações cardíacas ictais em crises do lobo temporal mais comuns são taquicardia sinusal e menos frequentemente bradicardia. Em pacientes com queixas vagas que sugerem tanto epilepsia e arritmia cardíaca, monitorização simultânea com EEG/ECG é recomendada e se as crises forem frequentes, vídeo-EEG deve ser considerado. Estudos nesta área são necessários para esclarecimento de possíveis mecanismos da morte súbita em pacientes com epilepsia

Myoclonic epilepsy of late onset in trisomy 21 Epilepsia mioclônica de início tardio na trissomia 21

We report the case of a patient with trisomy 21 (T21) with late onset epilepsy. The electro-clinical features were of myoclonic jerks on awakening and generalised tonic clonic seizures, with generalised spike and wave on EEG, and a progressive dementia. As familial Alzheimer's dementia and progressive myoclonic epilepsy (Unverricht-Lundborg type) are both linked to the chromosome 21, this case may represent a distinct progressive myoclonic epilepsy related to T21.Pacientes com trissomia do cromossoma 21 (T21), com o passar dos anos, são propensos a desenvolver crises epilépticas parciais concomitantes ao aparecimento de degeneração cerebral do tipo Alzheimer. Pacientes com T21 e demência parecem ter risco maior de apresentarem crises epilépticas que outros pacientes com degeneração cerebral do tipo Alzheimer. O caso relatado é de um paciente com T21 com epilepsia de início tardio. A história clínica consiste de crises mioclônicas ao despertar, ocasionais crises generalizadas tônico-clônicas, demência e ponta onda generalisada no EEG. Demência do tipo Alzheimer familial é ligada ao cromossoma 21, bem como epilepsia mioclônica progressiva (tipo Unverricht-Lundborg). Isto sugere que este caso possa representar um tipo distinto de epilepsia mioclônica progressiva, ligado ao cromossoma 21

Forced normalization at the interface between epilepsy and psychiatry

In 1953, Landolt described a group of patients with poorly controlled epilepsy who had psychotic episodes associated with remission of their seizures and disappearance of epileptiform activity on their EEGs. He called this phenomenon “forced normalization.” Since then, neurologists and psychiatrists have been intrigued by this phenomenon, and although it has been also reported by others, its existence continues to be the source of much debate. In this article, we review the clinical characteristics and potential pathogenic mechanisms of forced normalization and illustrate the complexities inherent in reaching this diagnosis, as well as its differential diagnosis in two representative cases