Cerebral vasomotor paralysis produced by intracranial hypertension.

TLDR: The first purpose of the present experiments was to determine the sequence of events which ultimately lead to neurological deterioration and death during gradual expansion of an intracranial mass lesion.

Abstract: THE SIGNS and symptoms of increased intracranial pressure and cerebral compression have occupied the interest of numerous investigators since earliest times. Although changes in vital signs in response to alterations in intracranial dynamics have long been recognized, the importance of these changes in the diagnosis and management of patients with expanding intracranial lesions has been questioned. In particular, the arterial hypertension which is readily produced experimentally by increased intracranial pressure has been considered to be of limited clinical significance because it has been assumed that blood pressure does not increase until the intracranial pressure approaches the diastolic pressure and that this rarely occurs. This conclusion was based primarily on periodic recording of the lumbar subarachnoid pressnre and thus requires the additional assumption that the spinal fluid pressure at all times approximates the intracranial pressure. In a previous report we presented experimental evidence that obstruction at the tentorial incisura during expansion of a supratentorial mass prevents communication of pressure to the posterior fossa and spinal cana1.l Also, as the pressure gradient across the incisura increases, the vasopressor threshold decreases, and arterial hypertension may then occur, with absolute intracranial pressures far below the diastolic pressure.? The first purpose of the present experiments was to extend these observations in an attempt to determine the sequence of events which ultimately lead to neurological deterioration and death during gradual expansion of an intracranial mass lesion. The history of the investigation of cerebral compression before 1900 was reviewed by