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The Basal Ganglia V Advances in Behavioural Biology Volume 47.
  1. ROGER BARKER

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    The Basal Ganglia V Advances in Behavioural Biology Volume 47. Edited by chihiro ohye, minoru kimura and john s. mckenzie. (Pp 519; $139.50). New York: Plenum Press, 1996. ISBN 0-306-45386-X.

    There are great changes taking place in the field of movement disorders and this book which represents the proceedings from the fifth Triennial Meeting of the International Basal Ganglia Society held in May 1995 comes at an appropriate time. The ground covered in this book is more for the scientist than the neurological practitioner, but as one negotiates the seven sections and 61 chapters a number of important points are raised which are relevant both for the current and future management of basal ganglia related disorders. However these points will be lost to most neurologists and neurosurgeons because the format of the book is rather daunting with every chapter detailing the experimental design and results with usually one concluding fact per chapter. Thus the book is inefficient in its presentation of data for those not directly working in this area, which is important as most investigators who work in this field have contributed to this book and so are almost certainly in receipt of a complimentary copy. However collections of work such as are represented in this book often herald changes in clinical practice, and so it is crucial that some of these points are brought out, perhaps by the use of introductory summary chapters at the start of each section.

    The book opens with a reappraisal of the anatomical connections of the basal ganglia, and makes a number of important observations. Firstly it provides a framework for the modern management of basal ganglia disorders, by providing the anatomical, physiological and pharmacological organisation of these structures. After all it was only through experimental work that the scientific basis and rationale for the newer neurosurgical approaches was defined—for example, posteroventral pallidotomy and subthalamic stimulators in Parkinson’s disease. Of importance to these models of basal ganglia function are chapters which make the point that the segregated input from the cortex to the striatal complex, necessary for the parallel pathway hypothesis of basal ganglia function, is at best a gross simplification, not least because it reduces many basal ganglia structures to the level of simple relay stations. Furthermore the current models of basal ganglia dysfunction in movement disorders often omit a number of important connections, including the input to the subthalamic nucleus (STN) from the primary and supplementary motor cortical areas; the amygdalostriatal projection; a possible thalamic projection to the STN and globus pallidus and the pallidotegmental pathway. This latter projection to the tegmentum, especially the pedunculopontine nucleus (PPN), is significant and consists of axon collaterals from the pallido (and nigro)-thalamic projection and maybe as important as the cortical projection of the basal ganglia in the control of movement, especially locomotion.

    Whilst this first section of the book provides much anatomical data on the shortcomings of our current models of basal ganglia function in health and disease there is a useful discussion in the second section on the pharmacology of the pathways within the basal ganglia. Two major points come out of this section. Firstly the nigral dopaminergic projection activating the striatal dopamine receptors is important not only in synaptic transmission but the long term gene expression of other neurotransmitters. Furthermore the loss of this pathway as occurs in Parkinson’s disease may also lead to the loss of corticostriate and thalamostriate synapses which has implications in the therapy of this condition. Secondly a number of different neurotransmitter receptors have been isolated in the basal ganglia which may also be important in the future as targets for anti-Parkinson’s disease treatment, and includes the A2a adenosine receptor, the metabotropic glutamate receptor, and cannabinoid receptors.

    The advent of surgical interventions clinically in Parkinson’s disease has led to some neurophysiological studies, which form the basis for the third section of the book. These studies coupled to previous experimental observations have revealed that neurons in the striatum respond maximally to movements directed at targets of interest, or at the beginning of a complex movement. This implies that the basal ganglia are involved in the interface of sensory processing (including verbal commands), motor programming, and the desire to move, and in addition may be specifically involved in learning sequence motor tasks and attention. In contrast the PPN which has always been thought to be critical in locomotion has so far only shown changes in neuronal activity relating to voluntary arm movement, at least in nonhuman primates.

    The fourth section of this book deals more with the clinical disorders of the basal ganglia, especially the anatomical and physiological substrates of the tremor, rigidity and akinesia which characterise Parkinson’s disease. No answers are apparent but PET data suggest the tremor is at least mediated by the pallido-thalamo (VIM nucleus) cortical pathway. Rigidity on the other hand is associated with increased activity in the internal segment of the globus pallidus (GPi) and underactivity in frontal motor areas, and there is some correlation between the degree of clinical akinesia and GPi hyperactivity. Furthermore the eye movement abnormalities of basal ganglia disease are coded for in the STN projection to the superior colliculus.

    The last three sections of the book concentrate on models of basal ganglia disorders and raise a number of questions on the mode of cell death in Parkinson’s disease, including discussions on apoptosis; iron-ferritin accumulation (which may be secondary to nigral cell death) and new environmental toxins (for example, tetrahydro-B-carboline TaClo). In addition there is increasing interest in the cognitive aspects of Parkinson’s disease which may precede any motor manifestations, and thus be useful in studies designed to look at very early Parkinson’s disease.

    Overall the book is interesting if somewhat repetitive with a large number of printing errors. The figures are adequate, but not of a very high quality. It is a tome for the student of neuroscience with an interest in basal ganglia related movement disorders, rather than the clinician wanting to catch up on some background neuroscience. This book is therefore more likely to find a home in libraries than the clinician’s bookshelf.

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