Luxury perfusion

Last revised by Frank Gaillard on 03 Oct 2020

Luxury perfusion describes blood flow in excess of local metabolic requirements to regions of infarcted brain. Cerebral blood flow (CBF) typically returns to normal or elevated levels compared to normal brain. It is thought to occur secondary to blood-brain barrier permeability and dysfunctional autoregulation 1-4, and most commonly occurs in subacute strokes (>72 hours), both treated and untreated cases, but has been reported as early as within the first 24 hours 1,2,4

Although the term luxury perfusion is most commonly encountered clinically in the setting of cerebral perfusion studies (see below) that demonstrate elevated cerebral blood flow in areas of cerebral infarction, it should be noted that the hallmark of this phenomenon is not so much elevation of cerebral blood flow, but rather the 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. Usually, this should result in a reduction in cerebral blood flow. In luxury perfusion, presumably due to a failure of autoregulation, this is not the case, however, and 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 perfusion usually will demonstrate these regions to have elevated cerebral blood flow (CBF) and cerebral blood volume (CBV). Mean transit time (MTT) and time to peak (TTP) are variable but often shortened due to arteriovenous shunting 1,6.

The corresponding non-contrast CT or MRI should show changes of an established stroke 1

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

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

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