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Michael Weller, MD
National Institutes of Health Clinical Neuroscience Branch Bldg 10, Room 3N256 Bethesda, MD 20892

Johannes Kornhuber, MD
Department of Psychiatry University of Würzburg Füchsleinstrasse 15 8700 Würzburg, Germany

Arch Neurol. 1992;49(9):900-901.

	Since this article does not have an abstract, we have provided the first 150 words of the full text PDF and any section headings.

To the Editor.

—We have read with great interest the excellent and comprehensive article by Greenamyre and O'Brien¹ on the potential role of N-methyl-D-aspartate (NMDA) antagonists in the treatment of Parkinson's disease. We would like to extend and enrich this discussion by a brief look at the putative biological basis of schizophrenia and the neuroleptic malignant syndrome (NMS).

In contrast to Parkinson's disease, which is associated or even caused by defective nigrostriatal dopaminergic transmission, schizophrenia is probably characterized by excessive dopaminergic transmission. On the other hand, the dangerous complication of neuroleptic drug treatment, NMS, shares with Parkinson's disease the extrapyramidal symptoms and it has even been reported following discontinuation of antiparkinsonian medication.² Greenamyre and O'Brien state appropriately that "dopamine receptor agonists and glutamate receptor antagonists have similar actions at both the biochemical and behavioral levels."¹ Interactions between dopaminergic and glutamatergic neuronal networks have been . . . [Full Text PDF of this Article]

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