Anatomy of epileptogenesis

Anatomy of epileptogenesis

268 Electroencephalography and clinical Neurophysiolog2v, 1989, 7 3 : 2 6 8 - 2 6 9 Elsevier Scientific Publishers Ireland, Ltd. Book Reviews edited...

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268

Electroencephalography and clinical Neurophysiolog2v, 1989, 7 3 : 2 6 8 - 2 6 9 Elsevier Scientific Publishers Ireland, Ltd.

Book Reviews edited by John R. Hughes and P.M. Rossini Anatomy of epileptogenesis. - B.S. Meldrum, J.A. Ferrendelli and H.G. Wieser (Eds.) (Libbey and Co., London, 1988, 187 p., U.S. $49.95)

in the preface the editors point out to the reader that the neuroanatomical basis of epileptic activity has been studied for 100 years and the present volume represents a simple account of the present status of that problem. The book is divided into 12 different chapters, written by 19 different contributors. The senior editor begins with a clear historical introduction, leading the reader from Hughlings Jackson through Penfield to Hayashi and back to Montreal via the centrencephalic and cortico-reticular theories and finally ending with depth studies. One major point is the uncertainty deriving from the fact that similar seizures may be associated with foci-in different cortical areas. In the next chapter Binnie et al. discuss the techniques of investigation, stressing immunocytochemical and labeled amino acid studies. The authors call attention to the supposition of the epileptogehic focus as hyperexcitable to be possibly incorrect, an important point made frequently by Engel. One of the major emphases in this chapter is, however, on the striking similarity between the major glutaminergic pathways and the patterns of metabolic activation during focal seizures. Ch. 3 is also by the senior editor on models. This account is written clearly with an emphasis on the initiation and spread of seizure activity by decreasing stability through decreased potassium conductance or increasing calcium conductance, decreasing G A B A inhibition and enhancing excitation, especially through N M D A receptors. Sound-induced seizures have likely interested all of us and Millan summarizes the current understanding of these seizures pointing out the importance of the inferior collicuhis (IC). Other auditory nuclei seem not to play as important a role. Data argue for an increase in the excitatory aspartergic transmission within the 1C of the susceptible rats. The importance of the brain-stem and diencephalon is then handled by Miller and Ferrendelli who emphasize the anterior thalamic nuclei and mammillary system in pentylenetetrazol seizures, revitalizing some old concepts of the centrencephalic system. Limbic and kindled seizures by Handforth and Ackermann are clarified by useful summaries that spell out the typical spread of seizure activity from the hippocampus, amygdala and olfactory cortex. The striato-nigral inhibitory pathways also are properly emphasized. Chemically induced seizures (Patel) concentrate on kainateAnitiating seizure activity arising in the hippocampus, spreading to the entorhinal and pyriform cortex and pilocarpine-initiating activity arising in the nucleus accumhens and spreading to the amygdala, hippocampus and cortex. The latter model draws our attention also to the basal ganglia, often disregarded in these discussions. Naquet then clearly

presents the similarities between photic epilepsy in m a n and in the very well known Papio papio, emphasizing both the occipital and fronto-rolandic (FR) cortex. One remaining problem seems unresolved, viz., the pathways from the occipital to the F R cortex. Wieser provides another excellent justification for his 'selective amygdalo-hippocampectomy' and next Spencer discusses seizure spread, leaving the impression that nearly all possibilities are likely. The usual chapter on PET scan comes from the U C L A group, who provides a complete account of citing the conclusions that can be drawn from these studies, One of the most interesting of the negative conclusions is that no diffuse or localized dysfunction has been identified by PET during absence seizures. The final chapter (Wolf) on classifying epilepsy according to anatomy has one major point: the situation is ' m o r e complex than often believed.' This book has accomplished its goal, as stated by the editors. The reviewer was impressed by the clarity of each chapter and the up-to-date status of each discussion. Therefore, neurophysiologists and EEGers interested in the anatomy of epileptogenesis will not be disappointed by this excellent book. John R. Hughes Unwersitv of lllinois Medical Center, Chicago, IL 60612 (U.S.A.)

Elements of petit real epilepsy. - M.S. Mysiobodsky and A.F. Mirsky (EAs.) (Peter Lang Publ., New York, 1988, 419 p., U.S. $81.95)

Petit mal or absence seizures have intrigued all of us, especially since they likely represent, aside from sleep, 'the only safe round-trip excursion into unconsciousness.' In the preface the 2 editors make clear that this book should be of value to both clinicians and neuroscientists and they are correct. The contents include 12 different chapters, 5 of which are handled by one or both of the editors. Porter begins the discussion with medications in general, anti-absence in particular, and surveys this field in a most complete fashion. The reader may be surprised of this choice as the first chapter on this topic, but the non-clinician will receive a brief clinical orientation. Genetics is next, reviewed exhaustively by the authors, Anderson and Hauser. Consistent with one major point made throughout this book, the data indicate greater complexities than generally are appreciated and the reader will not find simple summaries on the genetic question. However, the literature is well reviewed. Next, the senior editor discusses 'petit real status as a paradigm of the

0013-4649/89/$03.50 ,i~ 1989 Elsevier Scientific Publishers Ireland, Ltd.