Neurology
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
QUICK SEARCH:   [advanced]


     

This Article
Right arrow Full Text (PDF)
Right arrow Correspondence:
Submit a response
Right arrow Alert me when this article is cited
Right arrow Alert me when Correspondence are posted
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow reprints & permissions
Citing Articles
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Levine, D. N.
Right arrow Articles by Ojemann, R.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Levine, D. N.
Right arrow Articles by Ojemann, R.
NEUROLOGY 1981;31:343
© 1981 American Academy of Neurology

Acute quadriplegia due to bilateral cerebral metastases

David N. Levine, M.D., Peter McL. Black, M.D., Ph.D., George M. Kleinman, M.D. and R. Ojemann, M.D.

From the Neuromedical Service, the Neurosurgical Service, and the Charles Kubik Laboratory of Neuropathology, Massachusetts General Hospital, and the Departments of Neurology, Neurosurgery, and Pathology, Harvard Medical School, Boston, MA.

A 51-year-old man developed severe quadriparesis without sensory loss after a fall on the occiput. When he was treated with corticosteroids, the weakness worsened slightly for 2 days, but he then progressively improved and ultimately walked unassisted. Two months later, postmortem examination disclosed metastatic tumors in the superior portion of each precentral gyrus. The subjacent white matter was edematous. No spinal cord abnormalities were found. The clinical, radiologic, and neuropathologic findings suggest that the quadriplegia resulted from these bilateral cerebral lesions and not from spinal cord dysfunction. The rapid development of cerebral edema, perhaps precipitated by trauma, seemed to account for the acute onset of symptoms in this case.

Address correspondence and reprint requests to Dr. Levine, Neurology Service, Massachusetts General Hospital, Fruit Street, Boston, MA 02114.

Supported in part by Grant No. NS 12103 from the National Institute of Neurological and Communicative Disorders and Stroke.

Accepted for publication May 20, 1980.






HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Copyright © 1981 by AAN Enterprises, Inc.