Fluid-Attenuated Inversion Recovery Vascular Hyperintensities: An Important Imaging Marker for Cerebrovascular Disease

Identification of FVH

The key to identification of FVH is to be aware of its appearance and of the clinical conditions in which it appears with greater frequency. Although the most frequent location is within the Sylvian fissure, FVH has been noted within distal branches of the anterior, middle, and posterior cerebral arteries, as well as more proximally within the intracranial carotid artery and the proximal MCA (Fig 1). When present, the intravascular hyperintensity can be subtle. It is unclear whether FVH is seen in the posterior fossa, though cerebellar collateral circulation has been described. In most cases, FVH is unilateral, and in bilateral arterial disease, it is often asymmetric. This comparison of one half with the other can aid in identification of hyperintense vessels. Unfortunately the presence of FVH can be missed when images are degraded by motion.

There are conditions that should warrant the clinician's particular attention to the presence of FVH, including acute ischemic stroke and intracranial steno-occlusive disease. There will be cases in which the findings of FVH will be unexpected, such as in a reported case in the setting of trauma.¹¹ In this case, the presence of FVH was not noted, and the patient later had a stroke in the same vascular territory. In the authors' experience, FVHs can sometimes be seen in individuals undergoing MR imaging sequences for vague neurologic symptoms and are often not described. Further imaging with MRA may reveal underlying cerebrovascular disease, or the patient may present with a neurologic event (Fig 2).

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Fig 2.

FVH is often transient and is a marker of collateral flow. A, In case 1 (top row), preangiogram FLAIR image demonstrates FVH in the left temporal lobe. B, The angiogram obtained soon after demonstrates MCA occlusion and very good leptomeningeal collateral flow. The MR image obtained at 24 hours after presentation (C) demonstrates absence of FVH, the presence of T2 signal-intensity abnormality in the basal ganglia and subcortical white matter consistent with acute infarction, and a normal flow-related enhancement in the left MCA on a concurrent MR angiogram (D). The absence of FVH on follow-up imaging is consistent with restoration of normal flow. In case 2 (bottom row), preangiogram FLAIR image (E) demonstrates FVH in the left temporal lobe, and an angiogram (F) obtained soon after shows MCA occlusion and very good collateral flow. G, MR image obtained the day after demonstrates continued presence of FVH and T2 signal-intensity abnormality in the basal ganglia, consistent with acute infarction. There is reduced flow-related enhancement in the left MCA territory on a concurrent MR angiogram (D), indicating continued abnormal arterial flow.

Pathophysiology Resulting in FVH

The typical FLAIR sequence used in MR imaging of the brain is a heavily T2-weighed pulse sequence with a long TE spin-echo acquisition with reduction or elimination of the very high signals from CSF. Blood vessels on FLAIR sequences are normally dark due to a loss of signal intensity from blood protons moving out of the imaging section before the section-selective 180° pulse is applied, so that a spin-echo is not formed.⁹ This is also referred to as the “flow void” phenomenon. FVH represents the relative absence of this flow void.

Initially, there were postulations that FVH represented clot¹² or hemodynamic stress^4,13 within intracerebral arteries. Others have related the phenomenon to alterations in blood flow.^4,7,9 When FLAIR images were compared with catheter angiograms obtained in <6 hours of the MR imaging acquisition, FVHs were noted in areas of retrograde leptomeningeal collateral flow and just proximal to large-vessel occlusion.⁹ Further evidence for FVH representing impaired hemodynamics and retrograde collateral blood flow includes its presence in acute stroke, due to large-vessel stenosis⁸ or occlusion,¹² its transient nature,^9,12 and the fact that it was not seen in the hemisphere contralateral to cerebral ischemia.⁹

Retrograde leptomeningeal collateral flow is a predictor of clinical outcome in the setting of acute stroke,¹⁴ and when well-developed, it can sustain ischemic regions where the primary source of arterial inflow is blocked.¹⁵ The extent and variability of collaterals among patients presenting with acute stroke should be better characterized.¹⁶ In conditions in which arterial blockage occurs gradually, such as atherosclerosis, there is the opportunity to gradually develop more extensive collaterals, which prove beneficial during acute cerebral ischemia. There are likely to be a host of yet unidentified factors, which promote collateral formation and further account for collateral variability.¹⁷ FVHs are seen in some but not all cases of collateral flow, but it is not clear which additional factors are associated with their presence and extent.

Studies evaluating FVH and concurrent perfusion MR imaging indicate an association with smaller ischemic DWI lesion volume and larger DWI-to-PWI mismatch.¹⁰ This may indicate that the collateral blood flow represented by FVH may help decrease the volume of cellular damage as indicated by the reduced size of diffusion restriction on DWI. The DWI-PWI mismatch is thought to represent ischemic penumbra or ischemia without permanent cellular damage. Thus, FVH may indicate salvageable brain parenchyma in the setting of acute stroke. This may be useful when advanced MR imaging techniques such as perfusion MR are unavailable.

Epidemiology of FVH

FVH has been observed in both large-vessel steno-occlusive disease due to atherosclerosis^4,8 and other vasculopathies such as Moyamoya disease.¹⁸ FVH is best characterized in the setting of acute ischemic stroke, and Kamran et al⁴ noted it to be present in ≤10% of MR imaging studies in this population. When the authors evaluated only the MR images obtained within 24 hours of neurologic symptom onset, FVH was noted in 45% of cases. Furthermore, in the subgroup of patients who demonstrated MCA occlusion in the first 24 hours, the incidence of FVH was >90%. Two studies looking at the presence of FVHs within the first 3 hours after symptom onset found FVHs present in 66% and 77% of patients.^10,12 Studies have found FVHs present ipsilateral and distal to an acute occlusion.⁹

FVH can also be seen the setting of chronic intracerebral arterial steno-occlusive disease. Iancu-Gontard et al⁸ compared a group of patients with known stenoses with patients with proved lack of stenoses. In the stenosis group, FVH was present on 68% of the MR imaging studies compared with only in 5% of the MR imaging studies in patients without stenosis.

FVH has been described in Moyamoya disease and is often referred to as the ivy sign. Because of the chronic progressive nature of Moyamoya disease, there is time for collateralization to form from the leptomeninges as well as from the arteries at the base of the brain. The FVH seen represents diffuse leptomeningeal collaterals, and its presence varies immensely from patient to patient and even intrahemispherically in the same patient. Particular to Moyamoya disease is the finding of Kawashima et al¹⁸ that unilateral FVH indicated decreased vascular reserve and a potentially higher risk of ischemia.

Clinical Utility

Conclusions and Future Directions

FVH is a phenomenon on MR imaging that occurs in patients with acute ischemic stroke, intracranial stenoses, Moyamoya disease, and TIA. It represents disordered blood flow from collaterals distal to arterial occlusion or stenosis. Unlike other imaging signs of vessel occlusion such as gradient-echo susceptibility or CT hyperattenuation within a vessel lumen, it indicates the status of leptomeningeal collateral perfusion to vulnerable brain tissue rather than directly visualizing thrombus. Thus, it is not an indicator of infarction but rather of tissue that is at risk for infarction. This makes it more clinically valuable than the other 2 vessel signs because it can help clinicians decide when recanalization should be attempted and whether tissue salvage can be expected. Furthermore, FVH has high specificity and sensitivity for detecting arterial occlusion and stenosis.¹² In fact, FVH is so powerful in detecting areas of collateral circulation that it can reasonably serve as a substitute for PWI sequences when these are not available or are degraded.^3,6,9,12

The prognostic value of FVH still needs to be better elucidated. The categorization of distal-versus-proximal FVH has been shown to be significant.¹⁰ Other authors have indicated that FVHs in different regions of the intracranial vasculature yield different diagnostic and prognostic values.^4,10 Thus FVH within the MCA may give the most clear and consistent prognostic information as opposed to posterior and vertebral-basilar circulation FVH. Future studies will determine in which settings the presence of FVH can be used as a valuable datum to the clinician. FVH indicates the danger of persistent vascular stenosis or occlusion, with the associated risk of future stroke and also identifies patients with favorable collateral blood flow who would benefit from aggressive revascularization therapies.