The role of neuroeffector mechanisms in cerebral hyperperfusion syndromes

Abstract

Cerebral hyperperfusion, a state in which blood flow exceeds the metabolic needs of brain, may complicate a number of neurological and neurosurgical conditions. It may account for the propensity with which hemorrhage, cerebral edema, or seizures follow embolic stroke, carotid endarterectomy, or the excision of large arteriovenous malformations, and for some of the morbidity that accompanies acute severe head injury, prolonged seizures, and acute severe hypertension. Hyperperfusion syndromes have in common acute increases in blood pressure, vasodilatation, breakdown of the blood-brain barrier, and the development of cerebral edema. These common features suggest the possibility that they share the same pathogenic mechanisms. It was believed until recently that reactive hyperemia was caused primarily by the generation of vasoactive metabolites, which induced vasodilatation through relaxation of vascular smooth muscle. However, the authors have recently established that the release of vasoactive neuropeptides from perivascular sensory nerves via axon reflex-like mechanisms has a significant bearing upon a number of hyperperfusion syndromes. In this article, the authors summarize their data and discuss possible therapeutic implications for blockade of these nerves or their constituent neuropeptides.

The Effects of Perturbed Cerebral Blood Flow and Cerebrovascular Reactivity on Structural MRI and Behavioral Readouts in Mild Traumatic Brain Injury

“…23,24 Some of these metabolites are implicated in modulating bloodbrain-barrier permeability, 25 which could potentially enhance cerebral edema. Others have suggested neurogenic vasodilation 26 and passive physiologic coupling. 27 Our findings herein suggest that hyperperfusion on day 2 coincided with the peak of T 2 hyperintensity (vasogenic edema) and was not beneficial although the tissue was able to recover substantially by day 14, in marked contrast to the outcome found in ischemic stroke.…”

Arterial spin labeling and dynamic susceptibility contrast CBF MRI in postischemic hyperperfusion, hypercapnia, and after mannitol injection

“…The mechanisms of hyperperfusion are unknown and likely multifactorial (Marchal et al, 1999). In addition to many CBF regulating factors that are released during ischemia (Macfarlane et al, 1991), ischemia also affects tissue T 1 , T 2 , delayed arterial transit time, vascular resistance, and BBB disruption (Schaller and Graf, 2004) that could affect ASL-and DSC-CBF quantification. To improve understanding of postischemic hyperperfusion, it may be helpful to accurately measure CBF and understand how various biophysical and physiological parameters affect CBF under perturbed conditions.…”

Cerebral Hyperperfusion Syndrome After Angioplasty

“…Furthermore, administering a free-radical scavenger can prevent CHS, providing additional support for this mechanism (Ogasawara et al, 2004). Finally, an axon-like trigeminovascular reflex has been implicated in the pathophysiology of CHS (Macfarlane et al, 1991). The release of vasoactive neuropeptides from perivascular sensory nerves via axon reflex-like mechanisms has a significant bearing upon a number of hyperperfusion syndromes.…”

“…We will then discuss the risk factors, diagnostic methods, and strategies for prevention and treatment. We will also discuss a 11 increased the risk of intracranial hemorrhage (ICH) Macfarlane et al, 1991;Ouriel et al, 1999;Sbarigia et al, 1993). Preoperative significant reduction in flow velocity compared with baseline values is indicative of hypoperfusion and is associated with postoperative hyperperfusion (Keunen et al, 2001).…”

“…The stimulation of these baroreceptors in the carotid bifurcation during angioplasty can cause transient bradycardia and hypotension t h a t c a n b e f o l l o w e d b y r e b o u n d hypertension. Other phenomena proposed to explain the high blood pressure include increased norepinephrine levels probably related to cerebral edema and increased intracranial pressure, the release of vasoactive neuropeptides, the use of anesthetic drugs, and perioperative stress (Bajardi et al, 1989;Benzel & Hoppens, 1991;Macfarlane et al, 1991;Towne JB & Bernhard, 1980;Skydell et al, 1987;Skudlarick & Mooring, 1982;). Another possible mediator of impaired autoregulation in CHS is nitric oxide, which causes vasodilatation and can increase the permeability of cerebral vessels.…”