Such a dissociation of CBF and metabolism was postulated by Lassen,34 who described a “luxury perfusion syndrome” in patients with acute brain disorders. This syndrome is characterized by cerebral hyperemia, defined as excessive blood flow relative to the brain's metabolic requirements. Lassen argued that the hyperemia was due to impaired CBF autoregulation secondary to ischemia or hypoxia, and speculated that it could lead to disruption of the blood-brain barrier and edema formation. Since then, hyperemia has been observed in a number of acute clinical conditions, including ischemic stroke35,51 and head injury.7,11,13,53
Of particular relevance to head injury is the related concept of “vasomotor paralysis” introduced by Langfitt and coworkers31–33 to explain brain swelling and intracranial hypertension in experimental studies of cerebral compression and trauma. They postulated an acute reduction in vasomotor tone that resulted in cerebral vasodilatation, increased blood volume, and elevated intracranial pressure (ICP). When arterial hypertension followed trauma, massive brain swelling occurred that was associated with both hyperemia and edema.38,64 These findings suggested that brain trauma impairs CBF autoregulation, which was subsequently confirmed.36,42,62
It is apparent that the concepts of luxury perfusion and vasomotor paralysis refer to different aspects of the same phenomenon; namely, an acute derangement of the cerebral circulation manifested by hyperemia and a potential for brain swelling. Although repeatedly observed in human and animal studies, the pathophysiological significance of this syndrome remains obscure, including its relevance to the management of clinical head injury. Thus, the incidence and time course of hyperemia following head injury is not fully known, nor is its relationship to intracranial hypertension. Furthermore, it is not clear whether therapy should be aimed at reducing the hyperemia. Although hyperventilation therapy has been widely used to control ICP, its effect on acute hyperemia has not been systematically evaluated.
The present study was undertaken to elucidate the role of acute CBF alterations in the pathophysiology of clinical head injury. Special emphasis was placed on the occurrence of hyperemia, its time course and relationship to ICP, and its response to hyperventilation. Serial observations were made in 75 comatose patients studied as soon as possible after trauma. Advantage was taken of the noninvasive intravenous xenon-133 (Xe133) technique, which allowed repeated bilateral determinations of CBF in the intensive care unit. This was supplemented by measurements of arteriojugular venous oxygen difference (AVDO2), from which global estimates of CMRO2 were derived. Because AVDO2 represents the ratio of metabolism to blood flow, it also provided independent confirmation of cerebral ischemia and hyperemia.
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Dastur DKLane MHHansen DBet al: Effects of aging on cerebral circulation and metabolism in manBirren JEButler RNGreenhouse SWet al (eds): Human Aging. A Biological and Behavioral Study. Washington, DC: U.S. Government Printing Office196359–76Human Aging. A Biological and Behavioral Study.
Hjelm MOvergaard JLassen NAet al: Brain tissue lactacidosis of hyperemic regions around brain tumorsHarper MJennett BMiller Det al (eds): Blood Flow and Metabolism in the Brain. Edinburgh: Churchill Livingstone197513.41–13.42Blood Flow and Metabolism in the Brain.
Lassen NA: The luxury-perfusion syndrome and its possible relation to acute metabolic acidosis localised within the brain. Lancet 2:1113–11151966Lassen NA: The luxury-perfusion syndrome and its possible relation to acute metabolic acidosis localised within the brain. Lancet 2:
Obrist WDDolinskas CAJaggi JLet al: Serial cerebral blood flow studies in acute head injury: application of the intravenous 133Xe methodMagistretti PL (ed): Functional Radionuclide Imaging of the Brain. New York: Raven Press1983145–150133Functional Radionuclide Imaging of the Brain.
Co-oximeter manufactured by Instrumentation Laboratory, Inc., 113 Hartwell Avenue, Lexington, Massachusetts.
This research was supported by Grant NS 08803 from the National Institute of Neurological and Communicative Disorders and Stroke.