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April 1963

Pathogenesis of Chronic Subdural HematomaExperimental Studies

Author Affiliations

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

Arch Neurol. 1963;8(4):429-437. doi:10.1001/archneur.1963.00460040099009

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

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