Remote cerebral hemisphere symptoms from surgically treated patients with posterior fossa brain tumors; vascular factors: a basis for a theory concerning space sickness.

Three case histories of patients with large tumors in the posterior fossa who were operated on in a sitting position subsequently developed 1 or more symptoms referable to the temporoparietooccipital regions of the brain 24 to 48 hours postoperatively. Initially, it was believed that such symptoms were due to a stimulation of the association pathways causing firing of remote association areas (See Ch. 4). Subsequent studies of the rotation of blood vessels of the brain in the developing embryo and a review of the anatomical location of the arteries supplying the temporoparietooccipital region led to the conclusion that some compromise of the posterior cerebral artery was responsible for the symptoms. The symptomatology in these brain tumor patients was not unlike that seen in the cosmonauts and astronauts in space flight, designated as "motion sickness" in the space literature. A suggestion was made as to clarification of the definitions. This author advocated that the term "motion sickness" be confined to those symptoms of dizziness, nausea, and vomiting, due to involvement of the peripheral end organ, the inner ear. "Space sickness" might include these symptoms but also might have the addition of disorientation or the inversion of image in space and formed or unformed hallucinations. These relate to the temporoparietooccipital area, the midtemporal, and the occipital regions. In such instances, there must be central involvement or a stimulation of this interpretive cortex of the brain. The remote symptoms from the supratentorial cotex were believed to be due to hypoxia related to the posterior cerebral artery compromise, resulting in delayed "luxury perfusion" and the development of local lactic acidosis. Transaxial transmission of force with an uncal tentorial herniation causing compression of the posterior cerebral artery was suggested as a mechanism responsible for the vascular compression.