Medidas quantitativas clínicas e eletrencefalográficas de epileptogênese na epilepsia do lobo temporal

Bittencourt, P.R.M. de; Gabardo, A.C.; Marcourakis, T.

doi:10.1590/S0004-282X1994000300003

Resumos

Neste estudo controlado, prospectivo e parcialmente cego foram avaliados dois grupos de 10 portadores de epilepsia do lobo temporal, respectivamente de bom e mau prognóstico. Foram definidas medidas de epileptogênese baseadas nas freqüências de crises e na quantificação de atividade epileptogênica nas derivações eletrencefalográficas de lobo temporal. Os grupos de estudo foram semelhantes a no mínimo um dos grupos de controle em idade, sexo, nível educacional e social, regime terapêutico, idade de início e tempo de evolução da epilepsia. Houve uma diferença global do grupo de epilepsia do lobo temporal com mau prognóstico das outras populações, atingindo significação estatística em epileptogênese clínica, e uma tendência dos dados sugerindo maior epileptogênese eletrencefalográfica na mesma população. Os resultados indicam a utilidade experimental de algumas das medidas introduzidas, mas também seus problemas. Revisão da literatura pertinente é realizada.

epilepsia do lobo temporal; epileptogênese; EEG

In this controlled, prospective and partially blind study two groups of patients with temporal lobe epilepsy were evaluated, respectively with good and bad prognosis. Measurements of epileptogenesis were based on frequency of seizures, and on epiletogenic eletroencephalographic abnormalities obtained from scalp electrodes over the temporal lobes. The results were analised by non-parametric analysis of variance, comparison of groups and analysis of correlation. The results indicated the temporal lobe groups were similar to at least one of the control groups in age, sex, educational and social level, therapeutic regime, age at onset and length of history of epilepsy. The quantitative measurements showed a global difference between the group of temporal lobe with bad and good prognosis, reaching statistical significance in clinical epileptogenesis, and a trend towards greater epileptogenesis on the eletroencephalogram, in the same group of patients. The results indicate the experimental usefulness of some of the original measurements used in the study, but also their problems. A review of the literature is carried out.

temporal lobe epilepsy; epileptogenesis; EEG

Medidas quantitativas clínicas e eletrencefalográficas de epileptogênese na epilepsia do lobo temporal

Quantitative clinical and EEG measures of epileptogenesis in temporal lobe epilepsy

P.R.M. de Bittencourt^I; A.C. Gabardo^II; T. Marcourakis^III

^IUnidades de Neurologia Clínica do Hospital Nossa Senhora das Graças, Curitiba

^IITomografia Computadorizada do Hospital Nossa Senhora das Graças, Curitiba

^IIICentro de Investigações em Neurologia da Faculdade de Medicina da Universidade de São Paulo

RESUMO

Neste estudo controlado, prospectivo e parcialmente cego foram avaliados dois grupos de 10 portadores de epilepsia do lobo temporal, respectivamente de bom e mau prognóstico. Foram definidas medidas de epileptogênese baseadas nas freqüências de crises e na quantificação de atividade epileptogênica nas derivações eletrencefalográficas de lobo temporal. Os grupos de estudo foram semelhantes a no mínimo um dos grupos de controle em idade, sexo, nível educacional e social, regime terapêutico, idade de início e tempo de evolução da epilepsia. Houve uma diferença global do grupo de epilepsia do lobo temporal com mau prognóstico das outras populações, atingindo significação estatística em epileptogênese clínica, e uma tendência dos dados sugerindo maior epileptogênese eletrencefalográfica na mesma população. Os resultados indicam a utilidade experimental de algumas das medidas introduzidas, mas também seus problemas. Revisão da literatura pertinente é realizada.

Palavras-chave: epilepsia do lobo temporal, epileptogênese, EEG.

SUMMARY

In this controlled, prospective and partially blind study two groups of patients with temporal lobe epilepsy were evaluated, respectively with good and bad prognosis. Measurements of epileptogenesis were based on frequency of seizures, and on epiletogenic eletroencephalographic abnormalities obtained from scalp electrodes over the temporal lobes. The results were analised by non-parametric analysis of variance, comparison of groups and analysis of correlation. The results indicated the temporal lobe groups were similar to at least one of the control groups in age, sex, educational and social level, therapeutic regime, age at onset and length of history of epilepsy. The quantitative measurements showed a global difference between the group of temporal lobe with bad and good prognosis, reaching statistical significance in clinical epileptogenesis, and a trend towards greater epileptogenesis on the eletroencephalogram, in the same group of patients. The results indicate the experimental usefulness of some of the original measurements used in the study, but also their problems. A review of the literature is carried out.

Key words: temporal lobe epilepsy, epileptogenesis, EEG.

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Agradecimento - Os autores reconhecem o auxílio durante a execução deste estudo dos Drs. P.A. Kowacs, R.R. Seixas e A.F. Seixas, então médicos do Centro Diagnóstico de Curitiba.

Aceite: 12-dezembro-1994.

Estudo apresentado em parte como Tese (PRMB) aprovada em Concurso para Professor Titular de Doenças do Sistema Nervoso na Universidade Federal do Paraná (UFPR) em 1991.

Dr. Paulo Rogério Mudrovitsch de Bittencourt - Unidade de Neurologia Clínica S/C Ltda - Rua Padre Anchieta 155 80410-030 Curitiba PR - Brasil.

1. Bancaud J. Historical introduction to concepts and classification of frontal lobe seizures. Epilepsia 1988, 29: 204.
2. Binnie CD. The use of inter-ictal EEG in the study of antiepileptic drugs. In Buser PA, Cobb WA, Okuma T. Kyoto Symposia. Amsterdam: Elsevier 1982, p 504-512.
3. Binnie CD, Debets RMC, Engelsman M, Meijer JWA, Meinardi H, Overweg J, Peck AW, van Wieringen A, Yuen WC. Double-blind crossover trial of lamotrigine (Lamictal) as add-on therapy in intractable epilepsy. Epilepsy Res 1989, 4: 222-229.
4. Bittencourt PRM. Epilepsy in Latin America. In Laidlaw J, Richens A, Oxley J. A textbook of Epilepsy. Ed 3. Edinburgh: Churchill Livingstone, 1988, p 518-528.
5. Bittencourt PRM. May barbiturates be epiletogenic? In Lüders H. Second International Cleveland Clinic Epilepsy Symposium - Epilepsy Surgery: pathophysiology, clinical symptomatology, medical treatment, patient selection and surgical techniques, 1990, Cleveland: Cleveland Clinic Foundation, 1990, p 19.
6. Bittencourt PRM, Antoniuk SA, Costa JC, Fonseca LC, Gorz AM, Marcourakis T, Gonçalves e Silva GE. Carbamazepine and phenytoin in epilepsies refractory to barbiturates: efficacy, tolerability and mental function. Epilepsy Res 1993, 16: 147-155.
7. Bittencourt PRM, Dhillon S. Benzodiazepines: clinical aspects. In Richens A, Marks V. Therapeutic drug monitoring. Edinburgh: Churchill Livingstone, 1981, p 255-271.
8. Bittencourt PRM, Mazer S, Marcourakis T, Ferreira ZS, Reinhard AMG. Rational polytherapy for epilepsy. Epilepsia (na prensa).
9. Bittencourt PRM, Richens A. Case report: anticonvulsant-induced status epilepticus in Lennox-Gastaut syndrome. Epilepsia 1981, 22: 129-134.
10. Bittencourt PRM, Turner M. Latin American aspects. In Dam M, Gram L. Comprehensive epileptology. New York: Raven Press, 1990, p 807-820.
11. Browne TR, Mattson RH, Penry JK, Smith DB, Treiman DM, Wilder B J, Ben-Menachem E, Napoliello MJ, Sherry KM, Szabo GK. Vigabatrin for refractory complex partial seizures: multicenter single-blind study with long-term follow-up. Neurology 1987, 37: 184-189.
12. Commission on Antiepileptic Drugs of the International League Against Epilepsy. Guidelines for clinical evaluation of antiepileptic drugs. Epilepsia 1989, 30: 400-408.
13. Commission on Classification and Terminology of the International League Against Epilepsy. Proposal for classification of epilepsies and epileptic syndromes. Epilepsia 1985, 26: 268-278.
14. Commission on Classification and Terminology of the International League Against Epilepsy. Proposal for revised classification of epilepsies syndromes. Epilepsia 1989, 30: 389-399.
15. Commission on Classification and Terminology of the International League Against Epilepsy. Proposal for revised clinical and eletroencephalographic classification of epileptic seizures. Epilepsia 1981, 22: 489-501.
16. Dam M, Ekberg R, Loyning Y, Waltimo O, Jakobsen K. A double-blind study comparing oxcarbazepine and carbamazepine in patients with newly diagnosed previously untreated epilepsy. Epilepsy Res 1989, 3: 70-76.
17. Dean C, Penry JK. Valproate monotherapy in 30 patients with partial seizures. Epilepsia 1987, 28: 605.
18. Delgado-Escueta AV, Chauvel P, Halgren E, Bancaud J. A NATO international advanced research workshop on frontal lobe seizures and epilepsies. Epilepsia 1988, 29: 204-221.
19. Dingledine R. NMDA receptors: what do they do? Trends Neurosci 1986, 9: 47-49.
20. Dreifuss FE. Monitorização intensiva. J Liga Bras Epilep 1990, 3: 58-59.
21. Foster AC, Fagg GE. Taking apart NMDA receptors. Nature 1987, 329: 395-397.
22. Gibson JP, Yarrington JT, Loudy DE, Gerbig CG, Hurst GH, Newberne JW. Chronic toxicity studies with vigabatrin, a GABA-transaminase inhibitor. Toxicol Pathol 1990, 18: 225-238.
23. Gorz AM, Silvado CES, Bittencourt PRM. Barbiturate-refractory epilepsy: safe schedule for therapeutic substitution. Arq Neuropsiquiatr 1986, 44: 225-231.
24. Jawad S, Richens A, Goodwin G, Yuen WC. Controlled trial of lamotrigine (Lamictal) for refratory partial seizures. Epilepsia 1989, 30: 356-363.
25. Kowacs PA, Oliveira TV, Mazer S, Ferreira ZS, Marcourakis T, Bittencourt PRM. Vigabatrin: dose and time-related effects on epilepsy? Epilepsia 1991, 32 (Suppl 1): 12.
26. Loiseau P, Duche B. Carbamazepine: clinical use. In Levy RH, Dreifuss FE, Mattson RH, Meldrun BS, Penry JK. Antiepileptic drugs. New York: Raven Press, 1989, p 533-554.
27. Löscher W, Stephens DN. Chronic treatment with diazepan or the inverse benzodiazepine receptor agonist FG 7142 causes differential changes in the effects of GABA receptor stimulation. Epilepsy Res 1988, 2: 253-259.
28. Mac Donald RL, Meldrum BS. Principles of antiepileptic drug action. In Levy RH, Dreifuss FE, Mattson RH, Meldrum BS, Penry JK. Antiepileptic drugs. New York: Raven Press, 1989, 59-83.
29. Meldrum BS, Porter RJ. Current problems in epilepsy: new anticonvulsant drugs. London: John Libbey, 1986, p 341.
30. Morselli PL, Bossi L, Munari C. Should EEG recording be included in clinical trials on the new antiepileptic drugs? In Buser PA, Cobb WA, Okuma T. Kyoto Symposia. Amsterdam: Elsevier, 1982, p 482-486.
31. Mumford JP, Dam M. Meta-analisys of European placebo-controlled studies of vigabatrin in drug resistant epilepsy. Br J Clin Pharmacol 1989, 27: 1019-1079.
32. Porter RJ, White G. Objectives and strategy in the search for novel antiepileptic drugs: evaluation in man. In Meldrum BS, Porter RJ. New anticonvulsant drugs. London: John Libbey, 1985, p 46-61.
33. Ragazzo PC, Luccas FJC. Avaliação crítica do EEG no diagnóstico das epilepsias. In Marino R Jr. Epilepsias. São Paulo: Sarvier, 1983, p 31-47.
34. Richens A. Potential antiepileptic drug: vigabatrin. In Levy RH, Dreifuss FE, Mattson RH, Meldrum BS, Penry JK. Antiepileptic drugs. New York: Raven Press, 1989, p 937-946.
35. Riva D. Semiologia das crises epilépticas. In Marino R Jr. Epilepsias. São Paulo: Sarvier, 1983, p 9-16.
36. Rowan AJ, French JA. The role of the eletroencephalogram in the diagnosis and management of epilepsy. In Pedley TA, Meldrum BS. Recent advances in epilepsy. Edinburgh: Churchill Livingstone, 1988, Vol 4, p 63-92.
37. Rowan AJ, Meijer JWA, Beer-Pawlikowski N, Van der Geest P, Meinardi H. Valproate-ethsuximide combination therapy for refractory absence seizures. Arch Neurol 1983, 40: 797-802.
38. Sakamoto AC. Estudo clínico e prognóstico das crises epilépticas que iniciam na infância numa população brasileira. Tese de Doutorado: Faculdade de Medicina de Ribeirão Preto, Universidade de São Paulo. Ribeirão Preto, 1985.
39. Savic I, Widen L, Elander SS. Reversal of benzodiazepine tolerance in epilepsy patients. Epilepsia 1991, 32 (Suppl 1): 10.
40. Schaul N. Pathogenesis and significance of abnormal nonepileptiform rhythms in the EEG. J Clin Neurophysiol 1990, 7: 229-248.
41. Serikawa T, Kogishi K, Yamada J, Ohno Y, Ujihara H, Sasa M, Takaori S. Long-term effects of continual intake of phenobarbital on spontaneously epileptic rat epilepsy. Epilepsia 1991, 319: 9-14.
42. Wilder BJ, Rangel RJ. Phenytoin: clinical use. In Levy RH, Dreifuss FE, Mattson RH, Meldrum BS, Penry JK. Antiepileptic drugs. New York: Raven Press, 1989, p 233-239.

Datas de Publicação

Publicação nesta coleção
19 Jan 2011
Data do Fascículo
Set 1994

This work is licensed under a Creative Commons Attribution-NonCommercial 4.0 International License.

[1] 1. Bancaud J. Historical introduction to concepts and classification of frontal lobe seizures. Epilepsia 1988, 29: 204.

[2] 2. Binnie CD. The use of inter-ictal EEG in the study of antiepileptic drugs. In Buser PA, Cobb WA, Okuma T. Kyoto Symposia. Amsterdam: Elsevier 1982, p 504-512.

[3] 3. Binnie CD, Debets RMC, Engelsman M, Meijer JWA, Meinardi H, Overweg J, Peck AW, van Wieringen A, Yuen WC. Double-blind crossover trial of lamotrigine (Lamictal) as add-on therapy in intractable epilepsy. Epilepsy Res 1989, 4: 222-229.

[4] 4. Bittencourt PRM. Epilepsy in Latin America. In Laidlaw J, Richens A, Oxley J. A textbook of Epilepsy. Ed 3. Edinburgh: Churchill Livingstone, 1988, p 518-528.

[5] 5. Bittencourt PRM. May barbiturates be epiletogenic? In Lüders H. Second International Cleveland Clinic Epilepsy Symposium - Epilepsy Surgery: pathophysiology, clinical symptomatology, medical treatment, patient selection and surgical techniques, 1990, Cleveland: Cleveland Clinic Foundation, 1990, p 19.

[6] 6. Bittencourt PRM, Antoniuk SA, Costa JC, Fonseca LC, Gorz AM, Marcourakis T, Gonçalves e Silva GE. Carbamazepine and phenytoin in epilepsies refractory to barbiturates: efficacy, tolerability and mental function. Epilepsy Res 1993, 16: 147-155.

[7] 7. Bittencourt PRM, Dhillon S. Benzodiazepines: clinical aspects. In Richens A, Marks V. Therapeutic drug monitoring. Edinburgh: Churchill Livingstone, 1981, p 255-271.

[8] 8. Bittencourt PRM, Mazer S, Marcourakis T, Ferreira ZS, Reinhard AMG. Rational polytherapy for epilepsy. Epilepsia (na prensa).

[9] 9. Bittencourt PRM, Richens A. Case report: anticonvulsant-induced status epilepticus in Lennox-Gastaut syndrome. Epilepsia 1981, 22: 129-134.

[10] 10. Bittencourt PRM, Turner M. Latin American aspects. In Dam M, Gram L. Comprehensive epileptology. New York: Raven Press, 1990, p 807-820.

[11] 11. Browne TR, Mattson RH, Penry JK, Smith DB, Treiman DM, Wilder B J, Ben-Menachem E, Napoliello MJ, Sherry KM, Szabo GK. Vigabatrin for refractory complex partial seizures: multicenter single-blind study with long-term follow-up. Neurology 1987, 37: 184-189.

[12] 12. Commission on Antiepileptic Drugs of the International League Against Epilepsy. Guidelines for clinical evaluation of antiepileptic drugs. Epilepsia 1989, 30: 400-408.

[13] 13. Commission on Classification and Terminology of the International League Against Epilepsy. Proposal for classification of epilepsies and epileptic syndromes. Epilepsia 1985, 26: 268-278.

[14] 14. Commission on Classification and Terminology of the International League Against Epilepsy. Proposal for revised classification of epilepsies syndromes. Epilepsia 1989, 30: 389-399.

[15] 15. Commission on Classification and Terminology of the International League Against Epilepsy. Proposal for revised clinical and eletroencephalographic classification of epileptic seizures. Epilepsia 1981, 22: 489-501.

[16] 16. Dam M, Ekberg R, Loyning Y, Waltimo O, Jakobsen K. A double-blind study comparing oxcarbazepine and carbamazepine in patients with newly diagnosed previously untreated epilepsy. Epilepsy Res 1989, 3: 70-76.

[17] 17. Dean C, Penry JK. Valproate monotherapy in 30 patients with partial seizures. Epilepsia 1987, 28: 605.

[18] 18. Delgado-Escueta AV, Chauvel P, Halgren E, Bancaud J. A NATO international advanced research workshop on frontal lobe seizures and epilepsies. Epilepsia 1988, 29: 204-221.

[19] 19. Dingledine R. NMDA receptors: what do they do? Trends Neurosci 1986, 9: 47-49.

[20] 20. Dreifuss FE. Monitorização intensiva. J Liga Bras Epilep 1990, 3: 58-59.

[21] 21. Foster AC, Fagg GE. Taking apart NMDA receptors. Nature 1987, 329: 395-397.

[22] 22. Gibson JP, Yarrington JT, Loudy DE, Gerbig CG, Hurst GH, Newberne JW. Chronic toxicity studies with vigabatrin, a GABA-transaminase inhibitor. Toxicol Pathol 1990, 18: 225-238.

[23] 23. Gorz AM, Silvado CES, Bittencourt PRM. Barbiturate-refractory epilepsy: safe schedule for therapeutic substitution. Arq Neuropsiquiatr 1986, 44: 225-231.

[24] 24. Jawad S, Richens A, Goodwin G, Yuen WC. Controlled trial of lamotrigine (Lamictal) for refratory partial seizures. Epilepsia 1989, 30: 356-363.

[25] 25. Kowacs PA, Oliveira TV, Mazer S, Ferreira ZS, Marcourakis T, Bittencourt PRM. Vigabatrin: dose and time-related effects on epilepsy? Epilepsia 1991, 32 (Suppl 1): 12.

[26] 26. Loiseau P, Duche B. Carbamazepine: clinical use. In Levy RH, Dreifuss FE, Mattson RH, Meldrun BS, Penry JK. Antiepileptic drugs. New York: Raven Press, 1989, p 533-554.

[27] 27. Löscher W, Stephens DN. Chronic treatment with diazepan or the inverse benzodiazepine receptor agonist FG 7142 causes differential changes in the effects of GABA receptor stimulation. Epilepsy Res 1988, 2: 253-259.

[28] 28. Mac Donald RL, Meldrum BS. Principles of antiepileptic drug action. In Levy RH, Dreifuss FE, Mattson RH, Meldrum BS, Penry JK. Antiepileptic drugs. New York: Raven Press, 1989, 59-83.

[29] 29. Meldrum BS, Porter RJ. Current problems in epilepsy: new anticonvulsant drugs. London: John Libbey, 1986, p 341.

[30] 30. Morselli PL, Bossi L, Munari C. Should EEG recording be included in clinical trials on the new antiepileptic drugs? In Buser PA, Cobb WA, Okuma T. Kyoto Symposia. Amsterdam: Elsevier, 1982, p 482-486.

[31] 31. Mumford JP, Dam M. Meta-analisys of European placebo-controlled studies of vigabatrin in drug resistant epilepsy. Br J Clin Pharmacol 1989, 27: 1019-1079.

[32] 32. Porter RJ, White G. Objectives and strategy in the search for novel antiepileptic drugs: evaluation in man. In Meldrum BS, Porter RJ. New anticonvulsant drugs. London: John Libbey, 1985, p 46-61.

[33] 33. Ragazzo PC, Luccas FJC. Avaliação crítica do EEG no diagnóstico das epilepsias. In Marino R Jr. Epilepsias. São Paulo: Sarvier, 1983, p 31-47.

[34] 34. Richens A. Potential antiepileptic drug: vigabatrin. In Levy RH, Dreifuss FE, Mattson RH, Meldrum BS, Penry JK. Antiepileptic drugs. New York: Raven Press, 1989, p 937-946.

[35] 35. Riva D. Semiologia das crises epilépticas. In Marino R Jr. Epilepsias. São Paulo: Sarvier, 1983, p 9-16.

[36] 36. Rowan AJ, French JA. The role of the eletroencephalogram in the diagnosis and management of epilepsy. In Pedley TA, Meldrum BS. Recent advances in epilepsy. Edinburgh: Churchill Livingstone, 1988, Vol 4, p 63-92.

[37] 37. Rowan AJ, Meijer JWA, Beer-Pawlikowski N, Van der Geest P, Meinardi H. Valproate-ethsuximide combination therapy for refractory absence seizures. Arch Neurol 1983, 40: 797-802.

[38] 38. Sakamoto AC. Estudo clínico e prognóstico das crises epilépticas que iniciam na infância numa população brasileira. Tese de Doutorado: Faculdade de Medicina de Ribeirão Preto, Universidade de São Paulo. Ribeirão Preto, 1985.

[39] 39. Savic I, Widen L, Elander SS. Reversal of benzodiazepine tolerance in epilepsy patients. Epilepsia 1991, 32 (Suppl 1): 10.

[40] 40. Schaul N. Pathogenesis and significance of abnormal nonepileptiform rhythms in the EEG. J Clin Neurophysiol 1990, 7: 229-248.

[41] 41. Serikawa T, Kogishi K, Yamada J, Ohno Y, Ujihara H, Sasa M, Takaori S. Long-term effects of continual intake of phenobarbital on spontaneously epileptic rat epilepsy. Epilepsia 1991, 319: 9-14.

[42] 42. Wilder BJ, Rangel RJ. Phenytoin: clinical use. In Levy RH, Dreifuss FE, Mattson RH, Meldrum BS, Penry JK. Antiepileptic drugs. New York: Raven Press, 1989, p 233-239.