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Acute occlusions occurring in the peripheral vascular tree produce neurovascular phenomena which have been successfully treated for several years in our clinic by administration of antispasmodic drugs, by block of the corresponding sympathetic ganglionated chain or by embolectomy.1This knowledge has not been generally applied to cerebral circulation, mainly because the nervous control of the cerebral vessels has been authoritatively questioned. While the vessels of the cerebral cortex react to mechanical, thermal, chemical and electric stimuli,2and while pial arteries have been seen to go into spasm on being stretched3or on increase of blood pressure,4little evidence has been forthcoming from these sources that any nervous control is clinically significant. In fact, the consensus as summarized by Forbes and Cobb in a symposium on cerebral circulation5stressed that cerebral circulation is remarkably stable, that fright, anger or other emotions do not change the vascular
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Newell C. Gilbert (1948) studied this question.
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