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Limbic seizures in children
  1. Richard Robinson

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Limbic seizures in childhood differ from those in adults. They are more likely to be caused by cortical dysplasias, related malformations, and tumours. They are more easily, but not invariably, controlled by drugs. Have new imaging and EEG techniques advanced the cause and effect debate about febrile seizures and mesial temporal sclerosis (MTS)? Such considerations make this monograph timely.

Initial chapters on the history of the subject, the evolving definition of what constitutes limbic structures, their functional organisation and the relevance of MTS are clear, instructive, and thought provoking. “Limbus” is a border, in this case the border between the midbrain and the rest of the cerebral hemisphere. In non-primates, primarily concerned with smell, it has decreased in size relative to the elaborating neocortex, but in so doing has acquired multiple connections with association cortices. The hippocampus and perihippocampal cortex are distinguished by several features. Their cell properties are particularly determined by the level of activity—long term potentiation or depression. These enduring properties could subserve memory. Whereas the perihippocampus may code memories by semantic association, the hippocampus assigns them a personal context in time and space. The number of possible associations and ways of filing past events is almost infinite. The original roots in olfactory function may linger as the powerful evocation of memories by smell (Madeleine cakes served Proust for his life's work). It is possible that the flexibility and enhanced activity of certain hippocampal circuits on which its function is contingent make it peculiarly liable to epileptogenesis.

Many patients with catastrophic epilepsy do not have MTS. Seizures themselves do not cause MTS. Fifteen per cent of patients with MTS have dual pathology, 15% have increased neuronal heterotopias, and 15% have bilateral involvement. Degree of cell loss is not related to duration of epilepsy. Mossy fibre sprouting is not seen in children younger than 10, suggesting that this is a secondary progressive lesion. From facts such as these Spencer et al conclude that mesial temporal lobe epilepsy has a probable developmental aetiology. Hippocampal abnormalities pre-exist (and can be demonstrated in unaffected members of familial temporal lobe pedigrees) but convey vulnerability to febrile convulsions and subsequent MTS.

Subsequent chapters treat different aspects of limbic seizures—language disturbances, motor automatisms, impairment of consciousness, autonomic changes, and postural changes. The literature distinguishing frontal lobe from temporal lobe complex partial seizures is summarised. There are chapters on structural and functional imaging.

This book arose out of a colloquium. Of the 26 contributions all but four are from French or Italian centres. The two from America are particularly good and perhaps the standard of the rest might have been higher if the net had been spread wider. Some authors speak from very limited experience. The chapters on treatment are particularly disappointing. That systematic errors in English abound and much information is repeated throughout implies lack of adequately firm editorial grip.

This book will be useful to paediatric epileptologists, but the patchy quality overall precludes a warm recommendation to a wider audience.

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