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Luxury perfusion, also sometimes referred to as post-ischemic hypoperfusion, is a neuroradiological term used to describe regional cerebral blood flow in excess of local metabolic requirements. It is most commonly seen in the setting of reperfused cerebral infarction. Although luxury perfusion per se is not harmful, as it occurs in areas of more severe damage it implies a poorer prognosis for the affected brain 9. It is also associated with increased swelling and rate of hemorrhagic transformation 11.
The term luxury perfusion is sometimes also used to denote cerebral hyperperfusion syndrome encountered following treatment of long-standing severe carotid stenosis by carotid endarterectomy or carotid artery stenting. Although there are some similarities (namely a failure of normal microvascular autoregulation resulting in blood flow in excess of metabolic requirements) the time course and prognostic implications are entirely different. As such reserving the term luxury perfusion for cases of cerebral ischemia avoids confusion.
Additionally, post-ischemic hyperperfusion has been divided into early and late forms which overlap substantially with other imaging findings. The early form, seen immediately following reperfusion is closely related, if not identical, to the angiographic blush seen during thrombolysis or endovascular clot retrieval and contrast staining seen post-procedure whereas the late form is seen hours and days later on perfusion studies 9-11.
For this article, we are restricting the term luxury perfusion to denote perfusion findings obtained following reperfused cerebral infarcts.
Luxury perfusion is represents a mismatch between cerebral blood flow and local metabolic requirement that are usually tightly coupled 7. As neuronal and glial cells succumb to ischemia, their metabolic requirements also reduce. This should result in a reduction in cerebral blood flow, instead, in luxury perfusion, this is not the case, presumably due to a failure of autoregulation 1-4. Instead, there is an overabundance of blood supplied to infarcted tissue. This, in turn, results in a decrease in the regional oxygen extraction fraction 7.
CT and MR perfusion
CT perfusion usually will demonstrate elevated cerebral blood flow (CBF) and cerebral blood volume (CBV) in the affected region. Mean transit time (MTT) and time to peak (TTP) are variable but are often shortened due to arteriovenous shunting 1,6.
The corresponding non-contrast CT or MRI typically shows changes of an evolving established stroke 1.
Treatment and prognosis
The primary importance of luxury perfusion is recognizing that it implies a poor outcome for the affected brain, despite reperfusion. These regions will typically go on to infarct. Furthermore because of the abundant perfusion and disrupted blood-brain barrier, cerebral swelling and likelihood of hemorrhagic transformation are increased 11.
History and etymology
The term "luxury perfusion" was coined by N Larsen in 1966 who demonstrated a regional mismatch between local oxygen uptake and cerebral blood flow as measured by xenon-133 injection, and confirmed the previous observation of "bright-red cerebral venous blood" in cases of infarction 8.
cerebral hyperperfusion syndrome
patients presenting with stroke-like symptoms post-seizure (e.g. Todd paresis) can have a similar pattern of hyperperfusion with increased CBV and CBF and shortened MTT 3,5
it should be noted that this is generally seen in status epilepticus or when scanned during seizures; in the post-ictal phase, CBV and CBF are decreased and MTT somewhat prolonged 5