Pathogenesis of Chronic Subdural Hematoma

Trotter,¹in 1914, first emphasized the traumatic etiology of Virchow's pachymeningitis hemorrhagica interna.²Following Putnam and Cushing's study³in 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,⁴in 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 Gross⁵modified 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