Atividade elétrica cerebral do rato com lesões da formação reticular mesencefálica

Pereira, Walter C.; Rocha, Tania Leme da; Timo-Iaria, Cesar

doi:10.1590/S0004-282X1970000300001

Resumos

No presente estudo foram utilizados 73 ratos em preparações agudas e crônicas, nas quais lesamos a formação reticular mesencefálica com corrente contínua (3,5 a 4,0 mA durante 5 a 10 segundos). O eletródio ativo era implantado estereotàxicamente segundo as coordenadas de König e Klippel. As lesões eram feitas parcial ou totalmente, uni ou bilateralmente, e em todos os animais procedeu-se ao controle histológico das áreas lesadas, usando-se o método de Weil. O registro da atividade elétrica cortical foi feito com polígrafo Beckman de 4 canais, utilizando-se derivações bipolares curtas (1mm) com eletródios esféricos de platina. As experiências permitiram as seguintes conclusões: 1 — As características eletrofisiológicas dos fusos que ocorrem após lesões da formação reticular mesencefálica são muito semelhantes às dos fusos espontâneos e barbitúricos, inclusive quanto à projeção cortical. Quanto à duração dos potenciais que os constituem, contudo, notamos que a faixa de variação era mais centuada (20 a 80 ms), o que pode ser atribuído à maior complexidade dos potenciais do cérebro isolado, possivelmente pela falta de ação cronadora da formação reticular sobre o sistema sincronizador talâmico. 2 — Os mecanismos envolvidos na gênese dos fusos do sono barbitúrico ou espontâneo e os do cérebro isolado são, pelo menos em parte, dependentes do bloqueio da formação reticular mesencefálica. 3 — A formação reticular mesencefálica ativa preferencialmente o hemisfério cerebral homolateral; o contingente cruzado talvez seja mobilizado somente quando estímulos alertantes intensos atingem o tegmento mesencefálico. 4 — Além da formação reticular mesencefálica deve haver outros mecanismos ativadores corticais, visto que, em preparações agudas de cérebro isolado, observamos: a) surtos de curta duração de atividade dessincronizada; b) oscilações freqüentes do ECoG durante o registro, denotando fases de maior ou menor sincronização do traçado; c) ondas teta nas áreas límbicas (talvez evidenciando alerta) registradas simultâneamente com fusos em áreas neocorticais.

Seventy three rats were prepared for acute and chronic experiments. The midbrain reticular formation was electrolitically destroyed (3,5 — 4,0 mA and 5 — 10 sec) by means of an active electrode estereotactically guided according with the atlas of König an Klippel. The procedure was destined to provoke parcial, total, unilateral and bilateral lesions in different preparations. The ECoG was recorded with a 4-channel Beckman polygraph. Short bipolar leads were used in all experiments. 1. Spindling wich occurred after the operation was similar to spindling found in phisiological sleep and in barbiturate narcosis as well. Similarity was striking as to the electrophysiological properties and cortical projections. However, the duration of the individual potentials dispersed much more than in the above mentioned conditions (20 — 80 msec), wich may be related to the higlher complexity exhibited by the spindles which appear on the ECoG after destruction of the reticular formation of the midbrain, possibly due to lack of reticular timing of the thalamic synchronizing system activity, since spindling was more regular when circumscribed lesions of the midbrain were made. 2. The mechanisms involved in production of spindles during spontaneous and barbiturate sleep and after lesioning of the midbrain reticular formation are at least partially dependent upon reticular blocking. 3. The midbrain reticular formation activates mainly the ipsilateral hemisphere. The crossed component of the activating system is, probably, brought in action only when arousing stimuli are very strong. 4. Besides midbrain reticular formation other cortical activating mechanisms certainly play a role in arousing, since, in acute preparations, simultaneously with neocortical spindling, we frequently recorded: a) short-lasting periods of desynchronization of the ECoG; b) synchronization of the ECoG is not steady but waxes and wanes in time; c) theta waves, wich are associated with limbic arousal, are recorded on the cortical limbic areas.

Atividade elétrica cerebral do rato com lesões da formação reticular mesencefálica

Electrocorticographic study of the rats's bram after lesioning of the midbrain reticular formation

Walter C. Pereira^I; Tania Leme da Rocha^II; Cesar Timo-Iaria^III

^IAssistente da Clinica Neurológica, Faculdade de Medicina da Universidade de São Paulo

^IIAssistente do Departamento de Fisiologia e Farmacologia do Instituto de Ciências Biomédicas da Universidade de São Paulo

^IIIProfessor Adjunto do Departamento de Fisiologia e Farmacologia do Instituto de Ciências Biomédicas da Universidade de São Paulo

RESUMO

No presente estudo foram utilizados 73 ratos em preparações agudas e crônicas, nas quais lesamos a formação reticular mesencefálica com corrente contínua (3,5 a 4,0 mA durante 5 a 10 segundos). O eletródio ativo era implantado estereotàxicamente segundo as coordenadas de König e Klippel. As lesões eram feitas parcial ou totalmente, uni ou bilateralmente, e em todos os animais procedeu-se ao controle histológico das áreas lesadas, usando-se o método de Weil. O registro da atividade elétrica cortical foi feito com polígrafo Beckman de 4 canais, utilizando-se derivações bipolares curtas (1mm) com eletródios esféricos de platina. As experiências permitiram as seguintes conclusões:

1 As características eletrofisiológicas dos fusos que ocorrem após lesões da formação reticular mesencefálica são muito semelhantes às dos fusos espontâneos e barbitúricos, inclusive quanto à projeção cortical. Quanto à duração dos potenciais que os constituem, contudo, notamos que a faixa de variação era mais centuada (20 a 80 ms), o que pode ser atribuído à maior complexidade dos potenciais do cérebro isolado, possivelmente pela falta de ação cronadora da formação reticular sobre o sistema sincronizador talâmico. 2 Os mecanismos envolvidos na gênese dos fusos do sono barbitúrico ou espontâneo e os do cérebro isolado são, pelo menos em parte, dependentes do bloqueio da formação reticular mesencefálica. 3 A formação reticular mesencefálica ativa preferencialmente o hemisfério cerebral homolateral; o contingente cruzado talvez seja mobilizado somente quando estímulos alertantes intensos atingem o tegmento mesencefálico. 4 Além da formação reticular mesencefálica deve haver outros mecanismos ativadores corticais, visto que, em preparações agudas de cérebro isolado, observamos: a) surtos de curta duração de atividade dessincronizada; b) oscilações freqüentes do ECoG durante o registro, denotando fases de maior ou menor sincronização do traçado; c) ondas teta nas áreas límbicas (talvez evidenciando alerta) registradas simultâneamente com fusos em áreas neocorticais.

SUMMARY

Seventy three rats were prepared for acute and chronic experiments. The midbrain reticular formation was electrolitically destroyed (3,5 4,0 mA and 5 10 sec) by means of an active electrode estereotactically guided according with the atlas of König an Klippel. The procedure was destined to provoke parcial, total, unilateral and bilateral lesions in different preparations. The ECoG was recorded with a 4-channel Beckman polygraph. Short bipolar leads were used in all experiments.

1. Spindling wich occurred after the operation was similar to spindling found in phisiological sleep and in barbiturate narcosis as well. Similarity was striking as to the electrophysiological properties and cortical projections. However, the duration of the individual potentials dispersed much more than in the above mentioned conditions (20 80 msec), wich may be related to the higlher complexity exhibited by the spindles which appear on the ECoG after destruction of the reticular formation of the midbrain, possibly due to lack of reticular timing of the thalamic synchronizing system activity, since spindling was more regular when circumscribed lesions of the midbrain were made.

2. The mechanisms involved in production of spindles during spontaneous and barbiturate sleep and after lesioning of the midbrain reticular formation are at least partially dependent upon reticular blocking.

3. The midbrain reticular formation activates mainly the ipsilateral hemisphere. The crossed component of the activating system is, probably, brought in action only when arousing stimuli are very strong.

4. Besides midbrain reticular formation other cortical activating mechanisms certainly play a role in arousing, since, in acute preparations, simultaneously with neocortical spindling, we frequently recorded: a) short-lasting periods of desynchronization of the ECoG; b) synchronization of the ECoG is not steady but waxes and wanes in time; c) theta waves, wich are associated with limbic arousal, are recorded on the cortical limbic areas.

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Clínica Neurológica Faculdade de Medicina da Universidade de São Paulo Caixa Postal 3461 São Paulo, SP Brasil.

1. AJMONE-MARSON, C. The thalamus: data on its functional anatomy and some aspects of thalamo-cortical integration. Arch. ital. Biol. 103:847-882, 1965.
2. ANDERSEN, P. ANDERSSON, S. A. JUNGE, K. & SVEEN, O. Patterns of spontaneous barbiturate spindle activity within the thalamus. Electroenceph. clin. Neurophysiol. 24:90, 1968.
3. ANDERSEN, P. ANDERSSON, S. A. & LOMO, T. Thalamo-cortical relations during spontaneous barbiturate spindles. Electroenceph. clin. Neurophysiol. 24:90, 1968.
4. AZZARONI, A. & PARMEGGIANI, P. L. Freedback regulation of the hoppocampal teta-rhythm. Helv. physiol. Pharmacol. Acta 25:309-321, 1967.
5. BACH-Y-RITA, G. BAURAND, C. & CHRISTOLOMME, A. A comparison of EEG modifications induced by coagulation of subthalamus, preoptic region and mesencephalic reticular formation. Electroencepha. clin. Neurophysiol. 26:493-502, 1969.
6. BISHOP, G. H,; CLARE, M. H. & LANDAU, W. M. The equivalence of recruiting and augmenting phenomena in the visual cortex of the cat. Electroenceph. clin. Neurophysiol. 13:34-42, 1961.
7. BRADLEY, P. B. EAYRS, J. T. GLASS, A. & HEALTH, R. W. The maturational and metabolic consequences of neonatal thyroidectomy upon the recruiting responses in the rat. Electroenceph. clin. Neurophysiol. 13:577-586, 1961.
8. COBB, W. A. The normal adult EEG. In D. Hill & G. Parr: Electroencephalography: A Symposium on its Various Aspects. MacDonald, London, 1963, ed. 2, pp. 232-249.
9. COBB, W. A. The EEG of lesions in general. In D. Hill & G. Parr: Electroencephalography: A Symposium on its Various Aspects. MacDonald, London, 1963, ed. 2. pp. 295-316.
10. CORDEAU, J. P. & MANCIA, M. Effect of unilateral chronic lesions of the midbrain on the electrocortical activity of the cat. Arch. ital. Biol. 96:374-399, 1958.
11. DEMPSEY, E. W. & MORISON, R. S. The production of rhythmically recurrent cortical potentials after localized thalamic stimulation. Amer. J. Physiol. 135:293-300, 1942.
12. ELDEIBERG, E. WHITE, J. C. & BRAZIER, M. A. B. The hippocampal arousal pattern in rabbits. Exp. Neurol. 1:483-490, 1959.
13. FRENCH, J. D. VERZEANO, M. & MAGOUN, H. W. A neural basis for the anesthetic state. Arch. Neurol. Phychiat. (Chicago) 69:519-529, 1953.
14. GREEN, J. D. & ARDUINI, A. A. Hippocampal electrical activity in arousal. J. Neurophysiol. 17:533-557, 1954.
15. HESS, W. E. Jr. Sleep and sleep disturbances in the electroencephalogram. In K. Akert, C. Bally & J. P. Schade: Sleep Mechanisms. Elsevier, Amsterdam, 1965, pp. 127-139.
16. INGVAR, D. H. Electrical activity of isolated cortex in the unanesthetized cat with intact brain stem. Acta physiol. scand. 33:151-168, 1955.
17. JASPER, H. H. Diffuse projection systems: the integrative action of the thalamic reticular system: Electroenceph. clin. Neurophysiol. 1:405-420, 1949.
18. JOUVET, M. Recherches sur les structures nerveuses et les mécanismes responsables des differentes phases du sommeil physiologique. Arch. ital. Biol. 100: 125, 1962.
19. KAWAMURA, H. NAKAMURA, Y. & TOKIZANE, T. Effect of acute brain stem lesions on the electrical activities of the limbic system and neocortex. Jap. J. Physiol. 11:564-575, 1961.
20. KNOTT, J. R. INGRAM, W. R. & CHILES, W. D. Effects of subcortical lesions on cortical electroencephalogram in cats. Arch. Neurol. Psychiat. (Chicago) 73:203-215, 1955.
21. KÖNIG, J. F. R. & KLIPPEL, R. A. The Rat Brain: a Stereotaxic Atlas. Williams, Baltimore, 1963.
22. KRIEG, W. J. S. Connections of the cerebral cortex. I. The albino rat: topography of the cortical areas. J. comp. Neurol. 84:221-275, 1946.
23. KRUPP, P. MONNIER, M. & STILLE, S. Topischer Einfluss des caffein auf das Gehirn. Arch. exp. Pathol. Pharmak. 235:381-384, 1959.
24. LOOMIS, A. L. HARVEY, E. N. & HOBART, G. Distribution of disturbance patterns in the human electroencephalogram, with special reference to sleep. J. Neurophysiol. 1:413-430, 1938.
25. MILHORAT, T. H. BALDWIN, M. & HANTMAN, D. A. Experimental epilepsy after rostral reticular excision. J. Neurosurg. 24:595-611, 1966.
26. MORISON, R. S. & DEMPEY, E. W. A study of thalamo-cortical relations. Amer. J. Physiol. 135:281-292, 1942.
27. MORUZZI, G. Synchronizing influences of the brain stem and the inhibitory mechanism underlying the production of sleep by sensory stimulation. Electroenceph. clin. Neurophysiol. (suppl.) 13:231-256, 1960.
28. MORUZZI, G. & MAGOUN, H. W. Brain stem reticular formation and activation of the EEG. Electroenceph. clin. Neurophysiol. 1:455-473, 1949.
29. NEGRĂO, N. Ciclos de sono, fusos de sono natural e anestésico e potenciais de recrutamento no rato. Tese. Faculdade de Medicina da Universidade de Săo Paulo, 1967.
30. OSHIMA, K. MIYAMA, T. & KAWAMURA, H. Studies on EEG of the neo, paleo and archicortices in albino rat. Jap. J. Physiol. 12:601-610, 1962.
31. POLLEN, D. A. PEROT, P. & REID, K. H. Experimental bilateral wave and spike from thalamic stimulation on relation to level of arousal. Electroenceph. clin. Neurophysiol. 15:1017-1028, 1963.
32. PURPURA, D. P. A neurohumoral mechanism of reticulo-cortical activation. Amer. J. Physiol. 186:250-254, 1956.
33. ROSE, J. E. & WOOLSEY, C. N. Organization on mamalian thalamus and its relationships to cerebral cortex. Electroenceph. clin. Neurophysiol. 1:391-404, 1949.
34. ROTH, M. SHAW, J. & GREEN, J. The form, voltage, distribution and physiological significance of the K complex. Electroenceph. clin. Neurophysiol. 8:385-402, 1956.
35. ROTHBALLER, A. B. Studies on the adrenaline-sensitive component of the reticular activating system. Electroenceph. clin. Neurophysiol. 8:603-621, 1956.
36. SCHERRER, H. & HERNÁNDEZ-PEÓN, R. Enhancement of recruiting responses after midbrain transection. Anat. Rec. 121:363, 1955.
37. SHIMAZONO, Y. HORIE, T. HORI, N. CHIKAZAWA, S. OKABE, M. & HAYASHI, M. On the "hippocampal rhythmic waves" in acute and chronic experiments in dogs. Int. J. Neurol. (Montevideo) 5:151-167, 1965.
38. SPENCER, W. A. & BROOKHART, J. M. Electrical patterns of augmenting and recruiting waves in depths of sensorimotor cortex of cat. J. Neurophysiol. 24:26-49, 1961.
39. SPENCER, W. A. & BROOKHART, J. M. A study of spontaneous spindle waves in sensorimotor cortex of the cat. J. Neurophysiol. 24:50-65, 1961.
40. TOKIZANE, T. Sleep mechanism: hypothalamic control of cortical activity. In M. Jouvet: Neurophysiologie des États de Sommeil. Centre National de la Recherche Scientifique, Paris, 1965, pp. 151-185.
41. WALTER, W. G. The Living Brain. Penguin, Middlesex, 1968.
42. WILLIAMS, D. A study of thalamic and cortical rhythms in petit mal. Brain 76:50-69, 1953.

Datas de Publicação

Publicação nesta coleção
22 Abr 2013
Data do Fascículo
Set 1970

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

[1] 1. AJMONE-MARSON, C. The thalamus: data on its functional anatomy and some aspects of thalamo-cortical integration. Arch. ital. Biol. 103:847-882, 1965.

[2] 2. ANDERSEN, P. ANDERSSON, S. A. JUNGE, K. & SVEEN, O. Patterns of spontaneous barbiturate spindle activity within the thalamus. Electroenceph. clin. Neurophysiol. 24:90, 1968.

[3] 3. ANDERSEN, P. ANDERSSON, S. A. & LOMO, T. Thalamo-cortical relations during spontaneous barbiturate spindles. Electroenceph. clin. Neurophysiol. 24:90, 1968.

[4] 4. AZZARONI, A. & PARMEGGIANI, P. L. Freedback regulation of the hoppocampal teta-rhythm. Helv. physiol. Pharmacol. Acta 25:309-321, 1967.

[5] 5. BACH-Y-RITA, G. BAURAND, C. & CHRISTOLOMME, A. A comparison of EEG modifications induced by coagulation of subthalamus, preoptic region and mesencephalic reticular formation. Electroencepha. clin. Neurophysiol. 26:493-502, 1969.

[6] 6. BISHOP, G. H,; CLARE, M. H. & LANDAU, W. M. The equivalence of recruiting and augmenting phenomena in the visual cortex of the cat. Electroenceph. clin. Neurophysiol. 13:34-42, 1961.

[7] 7. BRADLEY, P. B. EAYRS, J. T. GLASS, A. & HEALTH, R. W. The maturational and metabolic consequences of neonatal thyroidectomy upon the recruiting responses in the rat. Electroenceph. clin. Neurophysiol. 13:577-586, 1961.

[8] 8. COBB, W. A. The normal adult EEG. In D. Hill & G. Parr: Electroencephalography: A Symposium on its Various Aspects. MacDonald, London, 1963, ed. 2, pp. 232-249.

[9] 9. COBB, W. A. The EEG of lesions in general. In D. Hill & G. Parr: Electroencephalography: A Symposium on its Various Aspects. MacDonald, London, 1963, ed. 2. pp. 295-316.

[10] 10. CORDEAU, J. P. & MANCIA, M. Effect of unilateral chronic lesions of the midbrain on the electrocortical activity of the cat. Arch. ital. Biol. 96:374-399, 1958.

[11] 11. DEMPSEY, E. W. & MORISON, R. S. The production of rhythmically recurrent cortical potentials after localized thalamic stimulation. Amer. J. Physiol. 135:293-300, 1942.

[12] 12. ELDEIBERG, E. WHITE, J. C. & BRAZIER, M. A. B. The hippocampal arousal pattern in rabbits. Exp. Neurol. 1:483-490, 1959.

[13] 13. FRENCH, J. D. VERZEANO, M. & MAGOUN, H. W. A neural basis for the anesthetic state. Arch. Neurol. Phychiat. (Chicago) 69:519-529, 1953.

[14] 14. GREEN, J. D. & ARDUINI, A. A. Hippocampal electrical activity in arousal. J. Neurophysiol. 17:533-557, 1954.

[15] 15. HESS, W. E. Jr. Sleep and sleep disturbances in the electroencephalogram. In K. Akert, C. Bally & J. P. Schade: Sleep Mechanisms. Elsevier, Amsterdam, 1965, pp. 127-139.

[16] 16. INGVAR, D. H. Electrical activity of isolated cortex in the unanesthetized cat with intact brain stem. Acta physiol. scand. 33:151-168, 1955.

[17] 17. JASPER, H. H. Diffuse projection systems: the integrative action of the thalamic reticular system: Electroenceph. clin. Neurophysiol. 1:405-420, 1949.

[18] 18. JOUVET, M. Recherches sur les structures nerveuses et les mécanismes responsables des differentes phases du sommeil physiologique. Arch. ital. Biol. 100: 125, 1962.

[19] 19. KAWAMURA, H. NAKAMURA, Y. & TOKIZANE, T. Effect of acute brain stem lesions on the electrical activities of the limbic system and neocortex. Jap. J. Physiol. 11:564-575, 1961.

[20] 20. KNOTT, J. R. INGRAM, W. R. & CHILES, W. D. Effects of subcortical lesions on cortical electroencephalogram in cats. Arch. Neurol. Psychiat. (Chicago) 73:203-215, 1955.

[21] 21. KÖNIG, J. F. R. & KLIPPEL, R. A. The Rat Brain: a Stereotaxic Atlas. Williams, Baltimore, 1963.

[22] 22. KRIEG, W. J. S. Connections of the cerebral cortex. I. The albino rat: topography of the cortical areas. J. comp. Neurol. 84:221-275, 1946.

[23] 23. KRUPP, P. MONNIER, M. & STILLE, S. Topischer Einfluss des caffein auf das Gehirn. Arch. exp. Pathol. Pharmak. 235:381-384, 1959.

[24] 24. LOOMIS, A. L. HARVEY, E. N. & HOBART, G. Distribution of disturbance patterns in the human electroencephalogram, with special reference to sleep. J. Neurophysiol. 1:413-430, 1938.

[25] 25. MILHORAT, T. H. BALDWIN, M. & HANTMAN, D. A. Experimental epilepsy after rostral reticular excision. J. Neurosurg. 24:595-611, 1966.

[26] 26. MORISON, R. S. & DEMPEY, E. W. A study of thalamo-cortical relations. Amer. J. Physiol. 135:281-292, 1942.

[27] 27. MORUZZI, G. Synchronizing influences of the brain stem and the inhibitory mechanism underlying the production of sleep by sensory stimulation. Electroenceph. clin. Neurophysiol. (suppl.) 13:231-256, 1960.

[28] 28. MORUZZI, G. & MAGOUN, H. W. Brain stem reticular formation and activation of the EEG. Electroenceph. clin. Neurophysiol. 1:455-473, 1949.

[29] 29. NEGRĂO, N. Ciclos de sono, fusos de sono natural e anestésico e potenciais de recrutamento no rato. Tese. Faculdade de Medicina da Universidade de Săo Paulo, 1967.

[30] 30. OSHIMA, K. MIYAMA, T. & KAWAMURA, H. Studies on EEG of the neo, paleo and archicortices in albino rat. Jap. J. Physiol. 12:601-610, 1962.

[31] 31. POLLEN, D. A. PEROT, P. & REID, K. H. Experimental bilateral wave and spike from thalamic stimulation on relation to level of arousal. Electroenceph. clin. Neurophysiol. 15:1017-1028, 1963.

[32] 32. PURPURA, D. P. A neurohumoral mechanism of reticulo-cortical activation. Amer. J. Physiol. 186:250-254, 1956.

[33] 33. ROSE, J. E. & WOOLSEY, C. N. Organization on mamalian thalamus and its relationships to cerebral cortex. Electroenceph. clin. Neurophysiol. 1:391-404, 1949.

[34] 34. ROTH, M. SHAW, J. & GREEN, J. The form, voltage, distribution and physiological significance of the K complex. Electroenceph. clin. Neurophysiol. 8:385-402, 1956.

[35] 35. ROTHBALLER, A. B. Studies on the adrenaline-sensitive component of the reticular activating system. Electroenceph. clin. Neurophysiol. 8:603-621, 1956.

[36] 36. SCHERRER, H. & HERNÁNDEZ-PEÓN, R. Enhancement of recruiting responses after midbrain transection. Anat. Rec. 121:363, 1955.

[37] 37. SHIMAZONO, Y. HORIE, T. HORI, N. CHIKAZAWA, S. OKABE, M. & HAYASHI, M. On the "hippocampal rhythmic waves" in acute and chronic experiments in dogs. Int. J. Neurol. (Montevideo) 5:151-167, 1965.

[38] 38. SPENCER, W. A. & BROOKHART, J. M. Electrical patterns of augmenting and recruiting waves in depths of sensorimotor cortex of cat. J. Neurophysiol. 24:26-49, 1961.

[39] 39. SPENCER, W. A. & BROOKHART, J. M. A study of spontaneous spindle waves in sensorimotor cortex of the cat. J. Neurophysiol. 24:50-65, 1961.

[40] 40. TOKIZANE, T. Sleep mechanism: hypothalamic control of cortical activity. In M. Jouvet: Neurophysiologie des États de Sommeil. Centre National de la Recherche Scientifique, Paris, 1965, pp. 151-185.

[41] 41. WALTER, W. G. The Living Brain. Penguin, Middlesex, 1968.

[42] 42. WILLIAMS, D. A study of thalamic and cortical rhythms in petit mal. Brain 76:50-69, 1953.