[Skip to Content]
Access to paid content on this site is currently suspended due to excessive activity being detected from your IP address Please contact the publisher to request reinstatement.
[Skip to Content Landing]
April 9, 1898


JAMA. 1898;XXX(15):869-870. doi:10.1001/jama.1898.02440670057008

This article is only available in the PDF format. Download the PDF to view the article, as well as its associated figures and tables.


The pathologic etiology of migraine has been long enough the subject of speculation, but we are still in the phase of conjecture or at least theory; our positive acquisitions of knowledge as to the essential pathologic process are so far practically nothing. The notion that it is a vasomotor neurosis has been largely abandoned, and neurologists at the present time are inclined to class it with epilepsy as a fulgurant cortical neurosis, a symptom of cortical instability associated, it may be, with some conditions of morbid metabolism, such as the uric acid or arthritic diatheses. While it may be assumed that it is a derangement to some extent of the function of the sensory cortical elements due to various irritations arising from the digestive organs, the sexual apparatus, the general or spinal sensory tracts, etc., etc., its ultimate cause must be looked for somewhere back of all these in some

First Page Preview View Large
First page PDF preview
First page PDF preview