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Experimental Studies

CHARLES L. GOODELL, M.D.; JOHN MEALEY, JR., M.D.

Arch Neurol. 1963;8(4):429-437.

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

Trotter,¹ in 1914, first emphasized the traumatic etiology of Virchow's pachymeningitis hemorrhagica interna.² Following Putnam and Cushing's study³ in 1925, this lesion has generally been called chronic subdural hematoma. Since then many theories of pathogenesis have been proposed to account for the latent interval between head injury and onset of symptoms. Putnam and Cushing believed that recurrent hemorrhage caused progressive enlargement of the hematoma. Gardner,⁴ in 1932, proposed that expansion of an original subdural clot occurred through osmotic attraction of cerebrospinal fluid by blood within the semipermeable hematoma neomembranes. Zollinger and Gross⁵ modified this theory by postulating that the osmotic pressure in the subdural hematoma was maintained by gradual disintegration of erythrocytes into oncotically active substances. Eventually, after a "latent interval," enough fluid would be absorbed from the plasma to compress the cerebral hemisphere and cause symptoms. Other theories have since been published, but through . . . [Full Text PDF of this Article]

Author Affiliations
INDIANAPOLIS

From the Surgical Experimental Laboratories and the Section of Neurological Surgery, Department of Surgery, Indiana University Medical Center.

Footnotes
Received for publication Dec. 6, 1962.

Supported by a grant from the John A. Hartford Foundation, Inc., to L. W. Freeman, M.D.

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