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DONALD E. McNEALY, M.D.; FRED PLUM, M.D.

Arch Neurol. 1962;7(1):10-32.

	Since this article does not have an abstract, we have provided the first 150 words of the full text PDF and any section headings.

Introduction

Supratentorial mass lesions may produce neurological dysfunction by 2 mechanisms: Cerebral hemispheric damage from the primary lesion itself and secondary brainstem damage from displacement, tissue compression, swelling, and vascular stasis. Of the 2 processes, the latter often is more immediately threatening to life. Thus, a major factor guiding the choice and timing of treating patients with supratentorial lesions is whether secondary brainstem compression has occurred or is progressing. Previous studies emphasizing late clinical signs and postmortem pathology fail to answer how clinical signs evolve from earliest upper brainstem or third nerve impairment to final medullary collapse.

Seeking this information, we examined serially 52 patients with supratentorial mass lesions and secondary brainstem dysfunction. This paper reports the results: Either of 2 relatively distinct clinical pictures provided the first clear evidence when supratentorial masses were threatening brainstem function. One picture had signs of uncal herniation producing third nerve and lateral midbrain . . . [Full Text PDF of this Article]

Author Affiliations
SEATTLE

From the Division of Neurology, University of Washington School of Medicine.

Footnotes
Received for publication Jan. 25, 1962.

Aided by Grant No. B-1597 from the U.S. Public Health Service.

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