Access the full text.
Sign up today, get DeepDyve free for 14 days.
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
JAMA – American Medical Association
Published: Apr 9, 1898
Read and print from thousands of top scholarly journals.
Already have an account? Log in
Bookmark this article. You can see your Bookmarks on your DeepDyve Library.
To save an article, log in first, or sign up for a DeepDyve account if you don’t already have one.
Copy and paste the desired citation format or use the link below to download a file formatted for EndNote
Access the full text.
Sign up today, get DeepDyve free for 14 days.
All DeepDyve websites use cookies to improve your online experience. They were placed on your computer when you launched this website. You can change your cookie settings through your browser.