In the past few years somewhat new yet often differing points of view have been affirmed refering to Petit Mal epilepsy, with regard to its clinical, eletrencephalographic and evolutive aspects. The classical concept of PM epilepsy as established by Lennox and Gibbs, with its well defined clinical and EEGraphic characteristics is continually being modified with new research work on clinical and EEGraphic aspects. Numerous clinical cases have been published whose evolution clashes with that classically described and likewise numerous are those cases where the EEG shows signs of focal electric activity besides spike and wave dis-rythmia. Cases have been known where surgical exerese on the focus causes temporary desappearance of the spike and wave disrythmia. The present concept now holding sway is that PM epilepsy is a kind of reaction of infantile encephalon to diverse harmful causes. From this it will be seen we are very far from the concept that PM epilepsy is a pure form of idiopathic epilepsy. For these reasons we decided to re-examine those cases observed between 1950 and 1960. With this in mind we chose 141 PM epilepsy cases, from among over 23000 epileptics, all examined under a standard criterion by a small group of senior assistants. All cases suspected of Psm epilepsy were excluded. The analysis of this group of patients was compared to that of another group with GM as well as PM seizures (104 patients); in 52 of these cases, studies were made concerning the evolutive, clinical and EEGra-phic aspects. METHOD: Clinical criterion was used for selection of the cases. The results of the analysis from the clinical and EEGraphic point of view were exhibited in demonstrative graphs. From the clinical point of view we strove to find out positive hereditary elements, organic cerebral injury factor (intellectual deficit, mood and behaviour disturbances, neurologic or somatic signs, as well as other development anomalies), the presence of febrile convulsions before the setting in of clinical PM syndrome and the eventuality of abnormal birth. We listed the patients according to their sex and investigated the statement that there is a prevalence of PM seizures among women. We attempted to analyse the incidence of cases according to the patient's age, as well as the incidence regarding the onset age of the illness. With regard to the EEG we likewise attempted to analyse those elements enabling us to weigh up the lesional factors in the brain (abnormalities in the background activity, disrythmias with focal characteristics or other paroxysmal abnormalities of a lesional type) and the bilateral and synchronous paroxysmal disrythmias classically known as forming part of the Petit Mal epileptic picture. Out the group of patients presenting pure PM seizures (141 cases) we obtained a clinical and EEGraphic sequence in 37, during a period of time ranging from 1 to 13 years. Of the group of patients presenting GM seizures as well as PM (104 patients) we investigated, in a comparative manner, 15 cases in a cliincal and EEGraphic sequence, during a period ranging from 1 to 9 years. RESULTS: The analysis of the clinical and electroencephalographic aspects in the first group of patients (141 cases with PM seizures) has enabled us to point out - a) A greater occurrence of this disease between the ages 6 and 12 - though there were 48 patients between the ages of 11 and 20 and 16 patients above 20 years old; b) in the majority of cases the disease set in between the age of 6 and 10 (47 cases); in some cases however the disease started up under two years of age; in 31 patients the onset was after 11 years of age; c) as far as sex distribution, there was no significant difference; d) barely 1 case proved to be abnormal in the somatic examination congenital cardiopathy) ; e) the occurrence of psychic disturbances among patients was extremely low; f) there were no cases with past history of abnormal birth; g) back-ground activity was with in the limits of normality in the great majority of cases; h) incidence of bilateral and synchronous spike and wave 3 c/s, was fairly high; slower disrythmia of this type was present in 4 cases only; i) larval disrythmias by spikes or multiple-spikes and slow ware occurred quite often and appeared both in the mioclonic form of PM as well as in the other forms of the disease; j) diffuse and irregular slow sharp waves, were found in 7 patients and sharp focal waves in 4; these alterations would always seem to appear associated with bilateral and synchronous disrythmias. The analysis of these same elements in the second group (104 patients with PM plus GM seizures) has enabled us to note the following details: a) later age of onset; b) in 5 cases there was child-birth asphyxia; c) higher incidence of cases presenting bilateral and synchronous disrythmias with a frequency below 3 c/s. The development aspects of our patients was not uninteresting. Out of 37 patients with pure PM seizures we noted: a) that the age of onset did not on the whole favour or unfavour the evolution; b) the great majority of cases developed favorably: 18 patients have no more seizures, 11 still present a very minimum number of seizures; 6 later had GM seizures associated; one patient showed a rather serious impairment of his seizures; c) in cases of favorable development,' synchronous disrythmias by spike and wave 3 c/s disappeared, which was not what happened in the group of cases showing unfavorable development; d) total disappearance of disrythmias was only noted in those cases of favorable development; e) there were cases, both among the favorable and unfavorable development groups, where the initial disrythmias perceptibly modified with time and became diffuse sharp waves; f) background activity was normal in the great majority of cases; g) some of our patients developed with clinical fits even over the age of 30. Out of 15 patients with GM plus PM seizures and on whom development studies were made, we noted that the results differed very little from those of the previous group. We should like to point out, however, that disappearance of the spike and wave 3 c/s disrythmias did not occur, even in those cases presenting favorable clinical development. COMMENTS: After discussing the most interesting facts stated in the analysis of their cases and co-relating them to litterature data found, with particular reference to the works presented at the Congress of Brussels by Jung, Bickford, Droogleever-Fortuyn, Gibbs and Walker, the AA have come to the following conclusions: 1) there are clinical and electroence-phalographic indications that the syndrome "Petit Mal Epilepsy" is a clinical manifestation of diverse brain affections; 2) the starting up of the Petit Mal syndrome occurred at an age below 11 years in the majority of cases; however, there are others where the onset occurred after this age and in some cases even above the age of 20; 3) the persistence of Petit Mal clinical syndrome with electroencephalographic manifestations of the complex spike and wave 3 c/s. type can occur in many patients after the age of 15 and up to the age of 40, which fact is in complete disaccord with the classical idea of Petit Mal epilepsy good prognosis after puberty.

Os autores fizeram revisão do estudo clínico e eletrencefalográfico de 1.000 pacientes com manifestações clínicas do tipo epiléptico, selecionados entre 4.700 casos estudados. Em todos os casos foi obtida anamnese detalhada sobre o tipo de crise, os antecedentes pessoais (em particular antecedentes obstétricos, traumas ou moléstias outras afetando o encéfalo) e heredo-familiares, assim como a idade de início de suas perturbações. Cumpre assinalar que a primeira convulsão foi considerada como início da moléstia, mesmo quando entre ela e as demais tivesse havido um intervalo de anos. Paralelamente, em todos os casos foram feitos exames clínico, neurológico e psiquiátrico, e, em grande número deles, exames de liqüido cefalorraqueano e radiográfico do crânio (craniograma simples, pneumencefalograma e arteriograma). As manifestações clínicas, classificadas segundo o critério de Penfield e colaboradores, foram comparadas com os resultados obtidos pela eletren-cefalografia (simples ou ativada) e finalmente projetadas em gráficos e quadros. Estes foram catalogados separadamente segundo os grupos de idade de 11 a 20 anos, de 21 a 35 anos, e de 36 e mais. Os resultados clínicos e eletrencefalográficos, assim como a comparação entre uns e outros, permitem destacar os seguintes fatos: 1. No total dos pacientes o eletrencefalograma mostrou alterações de tipo lesional em 36,8%, alterações de tipo endógeno em 32,5% e não evidenciou alterações de tipo epiléptico em 30,7%. 2. Os pacientes portadores de alterações do tipo lesional assim se distribuíram segundo os grupos de idade: 39,8% no primeiro grupo (11 a 20 anos), 36,7% no segundo (21 a 35 anos) e 32,30% no terceiro (36 e mais). 3. Êstes mesmos pacientes assim se distribuíram segundo a idade do início da moléstia: 53,9% no grupo de 0 a 10 anos, 31% no grupo de 11 a 20 anos, 29,1% no grupo de 21 a 35 anos e 31,8% no grupo de mais de 36 anos. 4. Os pacientes portadores de alterações do tipo endógeno assim se distribuíram segundo os grupos de idade: 42,25% no primeiro grupo, 33,75% no segundo e 16% no terceiro. 5. Tais pacientes assim se distribuíram segundo a idade do início da moléstia: 30,2% no grupo de 0 a 10 anos, 41,5% no grupo de 11 a 20 anos, 31,9% no grupo de 21 a 35 anos e 8,5% no grupo de 36 anos e mais. 6. Os pacientes em que o EEG nada revelou assim se distribuíram segundo os grupos de idade: 17,94% no primeiro grupo, 29,50% no segundo e 51,70% no terceiro. 7. Esses pacientes, segundo a idade do início da moléstia, assim se distribuíram: 15,9% no grupo de 0 a 10 anos, 27,5% no grupo de 11 a 20 anos, 39% no grupo de 21 a 35 anos, e, finalmente, 59,7% no grupo de 36 anos e mais. 8. O tipo de distúrbio eletrencefalográfico, assim como a topografia das alterações focais, quando presentes, coincidem, em elevada percentagem de casos, com o tipo das manifestações clínicas dos pacientes. 9. As crises de tipo bravais-jacksoniano, em discordância com os demais tipos de crises focais, apresentou elevada proporção de casos com EEG negativo (36 em 91 casos). As crises de epilepsia temporal mostraram 10 casos negativos num total de 132, e as demais crises motoras late-ralizadas evidenciaram somente 18 num total de 125 casos. 10. A crise do tipo GM foi a que mais apresentou EEG negativo (236 num total de 572 casos). A crise de tipo PM confirmou integralmente o diagnóstico de fator endógeno predominante (43 sobre 44 casos). 11. As crises de tipo temporal apresentaram, em grande proporção de casos, distúrbios de tipo lesional no EEG (118 num total de 132 casos) e, em particular, tais distúrbios lesionáis foram de tipo focal nos lobos temporais (86 num total de 118 casos). 12. As demais crises motoras lateralizadas evidenciaram igualmente, em elevada proporção, distúrbios de tipo lesional no EEG (88 num total de 127 casos). 13. A presença de epilepsia em parentes até o terceiro grau mostrou coincidir com a maior proporção de casos de epilepsia endógena (90 num total de 219 pacientes). 14. Em reverso, os sinais neuro-psiquiátricos de afecção orgânica cerebral coincidiram, em elevada proporção, com a presença de distúrbios de tipo lesional nos traçados eletrencefalográficos (93 num total de 120 pacientes) . 15. A ativação pelo sono barbitúrico tem sido feita nos casos em que o exame simples ou ativado pela hiperpnéia nada revelara ou com finalidade de melhor identificar distúrbios frustros. Num total de 202 casos em que foi empregada, conseguiu positivar elementos em 65. Entre os casos em que a ativação pelo sono foi positiva sobressaem os de crise temporal, nos quais foi elucidativa em 37, e negativa somente em 9. 16. A ativação pelo metrazol, usada de rotina mais recentemente, foi feita em 55 pacientes, com o mesmo critério. Ela conseguiu positivar o diagnóstico em 37. 17. E' de salientar que, dos 307 pacientes em que o EEG não evidenciou característicos de tipo epiléptico, percentualmente o maior número estava entre os de idade superior a 35 anos. Isto faz pensar na possível existência de outros fatores correlativos (intoxicações crônicas, anóxia por artériosclérose cerebral, hipoglicemia, etc.), que não os lesionáis cerebrais, na gênese de seus distúrbios paroxísticos.

The authors made the review of a thousand of patients with clinical syndrome of epilepsy, in whom clinical and EEG studies were obtained. These one thousand cases were selected among 4,700 cases of epileptic patients with EEG diagnosis. From all cases, detailed history of the type of seizure, of past history (particularly obstetrical history, traumatic lesions and other cerebral lesions), of familial history, and of the beginning of convulsive seizures, have been obtained. In every case the onset of the disease was considered as the first convulsive seizure, even when between the first and the next there was a large period of time. In every case clinical, neurological and psychiatric examinations were obtained. In many of the cases spinal fluid and radiological (craniogram, pneumoencepbalogram and arteriogram) examinations were performed. The clinical manifestations were classified according to Penfield and col. These clinical features were compared with the EEG records (in 202 cases with barbiturate sleep and in 55 cases with metrazol), and projected in graphs and tables. In these the patients were classified according to age in three different groups (from 11 to 20 years of age, from 21 to 35, and with more than 36 years of age). From this study, the authors call the attention to the following data: 1. The EEG showed changes of lesional type in 36.8 per cent of the cases, of endogenous type in 32.5 per cent and did not show epileptic changes in 30.7 per cent. 2. Patients with lesional type of EEG could be classified according to age in the following manner: 39.8 per cent in the first group (from 11 to 20 years of age), 36.75 per cent in the second group (from 21 to 35 years of age) and 32.30 per cent in the third group (with more than 36 years of age). 3. The same patients could be classified according to age of the first seizure: 53.9 per cent in the group from zero to 19 years, 31 per cent in the group from 11 to 20 years, 29.1 per cent in the group from 21 to 35 years, and 31.8 per cent in the group with more than 36 years. 4. Patients with endogenous changes in the EEG were classified according with the age in the following manner: 42.25 per cent in the first group, 33.75 per cent in the second group, and 16 per cent in the third group. 5. These patients were distributed according to age of the first seizure: 30.20 per cent in the group from zero to 10 years, 41.50 per cent in the group from 11 to 20 years, 31.9 in the group from 21 to 35 years, and 8.5 per cent in the group with more than 36 years. 6. The patients with non epileptic changes in the EEG could be classified: 17.94 per cent in the first group, 29.5 per cent in the second and 51.7 per cent in the third. 7. These patients were classified according to the first seizure in: 15.9 per cent in the group from zero to 10 years of age, 27.5 per cent in the group from 11 to 20 years of age, 39 per cent in the group from 21 to 35 years of age and 59.7 per cent in the group with more than 36 years of age. 8. The EEG changes and the topography of these changes, when they were present, were coincident with the clinical syndrome in high percentage. 9. Bravais-Jacksonian seizures had negative EEG in high percentage of cases (36 in 91), in discordance with the other types of focal seizures. Temporal seizures were negative in 10 among 132 cases, and the other motor seizures with lateralization were negative in 18 among 125 cases. 10. GM seizures were the type with higher incidence of negative EEG (236 among 572 cases). PM seizures indicated the diagnosis of endogenous lesion (43 in 44 cases). 11. Temporal seizures presented lesional type of changes in the EEG in high percentage of cases (118 among 132 cases). These lesional type of changes were of focal type in temporal lobes in 86 among 118 cases. 12. The other types of motor seizures with lateralization showed high incidence of lesional changes in the EEG (88 among 127 cases). 13. The incidence of epilepsy among relatives was higher in lhe group of endogenous epilepsy (90 in 219 cases). 14. The neuro-psychiatric signs of cerebral organic diseases were coincident with lesional type of changes in the EEG in high incidence (103 among 130 patients). 15. The barbituric sleep was used when the routine EEG or the EEG with hyperventilation did not show evident changes. In this way it was possible to bring out positive findings in 65 among 202 cases. The barbituric sleep was helpful in 65 cases of temporal seizures and negative in 9. 16. The metrazol was used in 65 patients, with the same criteria. It was helpful in 46. 17. The majority of the 307 patients with EEG showing no epileptic patterns was older than 35 years. This probably indicates the existence of other co-factors (as chronic intoxications, anoxia due to cerebral arteriosclerosis, hypoglycemia, etc.), when cerebral lesions are not present, in the genesis of paroxistic disturbances.

Os autores, trabalhando com um eletrencefalógrafo Grass, de 6 inscritores, trazem os seus primeiros resultados em casos de tumores intracranianos cirurgicamente verificados (além de 2 já publicados anteriormente). São eles em número de 9. No primeiro, um abscesso profundamente situado no lobo frontal era traduzido por ondas delta e figuras de reverso, no eletrencefalograma do lobo frontal correspondente, ao lado de alterações difusas no restante do hemisfério cerebral, melhoradas em EEG feito ulteriormente, em perfeita concordância com o edema cerebral e o quadro clínico de hipertensão intracraniana inicial. No segundo, ondas extremamente lentas» difusas por todo um hemisfério, com figuras de reverso pré-fronto-parietais e ondas teta, indicavam um glioma difuso e grandemente lesivo para o parênquima nervoso. No terceiro, disritmias paroxísticas frontais predominantes se correlacionavam com antiga epilepsia devida a grande meningioma da foice naquela localização. O caso 4 mostrava ondas lentas difusas por todo um hemisfério cerebral, de predominância pré-frontal, com figuras de reverso bem assisaladas, coincidindo com carcinoma metastático de grande volume, de localização subfrontal. O caso 5 mostrava alterações eletrencefalográficas localizadas, parietoccipitais, à esquerda, coincidentes com meningioma angioblástico parasagital parietoccipital. O sexto se refere a um tumor enorme e consistente, com aspecto de papiloma, que, do prolongamento temporal de ventrículo lateral, comprimia as formações cerebrais suprajacentes, cujo EEG evidenciava alterações focais nítidas frontais e temporais, com ondas e figuras de reverso bem caracterizadas. O caso 7, pelo contrário, evidenciava alterações eletrencefalográficas difusas por todo um hemisfério e repercutindo sôbre a área frontal do hemisfério oposto, indicando lesão cerebral pré-central, concordando inteiramente com a clínica, com a ventrigulografia e com o aspecto do cérebro na craniotomia fronto-partietal, cujo exame histopatológico revelou tecido cerebral próximo a glioma maligno. Finalmente, as observações 8 a 9, com EEG normal, são respectivamente de um adenoma da hipófise e de um neurinoma do acústico, tumores que não afetam direta ou indiretamente os hemisférios cerebrais. O material eletrencefalográfico apresenta alterações focais do tipo de ondas lentas, ondas extremamente lentas com figuras de reversão de fases, ondas teta ou disritmias epilépticas de início e predominância localizadas, nos casos de tumores bem delimitados, ou alterações difusas por todo um hemisfério com predominância em determinadas áreas e repercussão para áreas simétricas do hemisfério oposto, nos casos de tumores difusos e infiltrativos. Tais elementos mostram que o EEG, além do diagnóstico e localização dos tumores intracranianos, pode também fornecer elementos sobre o próprio tipo do tumor. Com tais resultados, os AA. consideram a eletrencefalografia um método de alto valor na semiologia dos tumores intracranianos.

The authors bring their first results of the electroencephalographic studies on localisation of brain tumors surgically verified. They worked with the Grass apparatus of 6 ink-writers. They present 9 cases. The first one is a deep left frontal abscess with the EEG showing delta waves and reverse figures on the left frontal lobe and generalised disturbances on the same side hemisphere in relation with the brain edema. The second case showed very slow waves in all the hesmisphere, with reverse figures and theta waves on pre-fronto-parietal area where was located a diffuse glioma. The third case was a convulsive with paroxystic dysrhythmia predominantly on both frontal pole and operated upon a falx meningioma at the anterior third. The fourth case showed slow waves through all the hemisphere, predominantly on frontal region, due to a very large subfrontal and fossa media metastatic tumor. The fifth case showed electroencephalographic modifications on the left parieto-occipital area due to meningioma at same localisation. The sixth case with delta waves and reverse figures on the frontal and temporal regions was due to a calcified spongioblastoma polare localised anterior to the ventricular carrefour and going so far as the plan of the sphenoid ridge. The seventh case showed diffuse left EEG disturbance with right frontal repercussion, indicating precentral lesion; at the operation, a biopsy indicated tissue near glioma. In this case the EEG was according the clinical, ventriculographic and macroscopic surgical findings. The eighth and ninth cases showed normal EEG and are cases of pituitary adenoma and acoustic neurinoma. The EEG graphics present focal alterations, as delta waves, very slow waves with reverse figures, theta waves and convulsive disrhythmias localised in cases of well limited tumors. In cases of infiltrative tumors, the modifications were diffuse and with repercussion for symetric regions of the other hemisphere. The EEG, outside of the localisation, can give elements for the type of the tumors, limited or infiltrative. The AA. believe in the value of the EEG as an element in the diagnosis of the brain tumors.