title: Origin and evolution of plateau waves. Experimental observations and a theoretical model.
abstract: Laboratory observations made in cats with fluid-percussion head injuries have suggested that plateau waves or Lundberg "A-waves" are not independent of systemic circulatory events. Four distinct phases in the evolution of the plateau wave have been identified, and each related to a circulatory change in a causal manner. The first phase is the premonitory drift phase where intracranial pressure (ICP) gradually increases prior to the plateau proper. This phase is caused by a slow gradual decline in systemic arterial blood pressure (SABP) which increases ICP by autoregulatory vasodilation and reduces cerebral perfusion pressure (CPP) to a range of 70 to 80 mm Hg. The second phase is the plateau phase initiated at a CPP of about 70 to 80 mm Hg, and is characterized by a rapid increase in ICP as CPP falls further to 40 to 50 mm Hg. The plateau lasts as long as the CPP remains stable and above ischemic levels. The third phase is the ischemic response, characterized by CPP being returned toward normal by increases in SABP in response to very low CPP's. The fourth phase is the resolution, characterized by a rapid decline in the ICP to baseline levels with stabilization of the SABP and CPP, and is best explained by autoregulatory vasoconstriction. Plateau waves appear to occur as the result of intact or mostly intact autoregulation responding to changes in CPP. The series of events that follow are best explained by what is known of normal autoregulation; the various properties of plateau waves are viewed and explained as the expected and logical consequences of an unstable CPP acting upon a generally intact cerebrovascular bed in the face of elevated ICP and decreased compliance.
mesh_terms: D000818:Animals; D001794:Blood Pressure; D001930:Brain Injuries / Q000503:physiopathology*; D002415:Cats; D002536:Cerebral Arteries / Q000502:physiology; D002560:Cerebrovascular Circulation; D006706:Homeostasis; D007427:Intracranial Pressure; D008954:Models, Biological; D014661:Vasoconstriction; D014664:Vasodilation