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Neuro‐regulational therapy for neuropsychiatric diseases using Ca ++ antagonists
Author(s) -
Taya Koji,
Watanabe Yasuo
Publication year - 1998
Publication title -
human psychopharmacology: clinical and experimental
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.461
H-Index - 78
eISSN - 1099-1077
pISSN - 0885-6222
DOI - 10.1002/(sici)1099-1077(199808)13:6<389::aid-hup22>3.0.co;2-k
Subject(s) - medicine , dementia , disease , antagonist , migraine , amyotrophic lateral sclerosis , pathological , stroke (engine) , neuroscience , traumatic brain injury , vascular dementia , anesthesia , psychology , psychiatry , receptor , mechanical engineering , engineering
It is possible to discuss the role that Ca ++ antagonists might provide as a therapeutic means of treating various types of cerebral dysfunction, by maintaining a dynamic homeostasis of Ca ++ in brain neurons. In this paper, we will review the results of Ca ++ antagonist treatments of subarachnoid haemorrhage (SAH), traumatic subarachnoid haemorrhage, stroke, migraine, dementia, psychiatric disorders, substance abusers, Menière's disease, and amyotrophic lateral sclerosis, and discuss the future of Ca ++ antagonists and problems in their development. Ca ++ antagonists have been established as a standard therapy for SAH in the USA, but their efficacy for traumatic SAH has not been confirmed because of the pathological variability of this disease. The data on strokes have not always indicated improved outcomes. Dementia may be a disease for which Ca ++ antagonists should be indicated. Many clinical studies have also suggested some effectiveness of Ca ++ antagonists, but the number of patients examined was too small to draw any firm conclusions. Thus, the development of Ca ++ antagonists to treat cerebral dysfunction is not as greatly advanced as would be expected. This is probably due to the fact that most of the currently used Ca ++ antagonists were selected on the basis of their cardiovascular effects, but not their effects on the central nervous system. © 1998 John Wiley & Sons, Ltd.