High signal in cerebrospinal fluid mimicking subarachnoid haemorrhage on FLAIR following acute stroke and intravenous contrast medium

Abstract

We describe five cases of high signal in the cerebrospinal fluid (CSF) on fast-FLAIR images 24-48 h after onset of stroke. All the patients had undergone perfusion-weighted MRI within 6 h of the onset of the symptoms. The CSF was far brighter than the cortical gyri. The high signal was diffusely around both cerebral hemispheres in two cases and around one hemisphere in two others; it was focal, around the acute ischaemic lesion, in one. CT was normal in all cases. The CSF high signal was transient, decreasing in extent and intensity with time and resolving completely within 3-6 days. It was not associated with worsening of the clinical state or poor outcome. Our explanation of this phenomena is hypothetical: we speculate that it could be due to disruption of the blood-brain barrier resulting in leakage of protein, gadolinium chelates, or both in to the subarachnoid space. It should not be confused with subarachnoid haemorrhage.

Increased Signal in the Subarachnoid Space on Fluid-Attenuated Inversion Recovery Imaging Associated with the Clearance Dynamics of Gadolinium Chelate: A Potential Diagnostic Pitfall

“…[1][2][3][4][5][6][7][8][9][10][11][12][13][14] This relies on the fact that FLAIR imaging is designed to null the normal CSF signal intensity, and any alteration in the CSF results in an increased signal intensity in the CSF. Postgadolinium FLAIR imaging has also shown hyperintensity in the SAS in patients with pathologies that are not specific to the SAS but rather disrupt the blood-brain barrier.…”

FLAIR with Contrast Linked to Better Correlation with Stroke Symptoms than Diffision-Weighted Imaging in a Patient: Detecting Hyperintense Acute Reperfusion Injury Marker and Cortical Enhancement

“…HARM can help in ischemic stroke prognosis since it has been observed in 73% of patients with subsequent hemorrhagic transformation versus only 25% of patients without hemorrhagic transformation [2] . HARM may be distant from the intraparenchymal lesion [3,4] and is more frequently noted after thrombolysis [6] . Theories on HARM pathophysiology focus on matrix metalloproteinase involvement in microvasculature damage, where endogenous tissue plasminogen activator release during vascular injury increases matrix metalloproteinases 2 and 9 [1,7] .…”

“…Blood-brain barrier (BBB) and blood-CSF barrier (BCSF) disruption (BBBD and BCSFD) is observed in several forms of brain injury [1] , including acute ischemic stroke [2,3] , hemorrhagic transformation [2] , intracerebral hemorrhage [4] , and carotid artery stenting [5] . This is rarely evaluated in clinical practice, while its contribution to total brain injury and its clinical significance are unclear.…”

“…Gadolinium enhancement at the BBB and BCSF border in FWC sequences of patients with vascular events has been coined 'hyperintense acute reperfusion injury marker' (HARM) [4] . HARM is usually noted over the sulcal subarachnoid space adjacent to lesioned brain parenchyma, on average 12.9 h from stroke onset, and its pathology is considered different from the leptomeningeal and parenchymal enhancement noted days to weeks after a stroke [2,3] . However, its independent contribution to symptomatic deficits is unverified.…”

3D Fluid-Attenuated Inversion Recovery Imaging: Reduced CSF Artifacts and Enhanced Sensitivity and Specificity for Subarachnoid Hemorrhage

“…Thus, we propose that additional studies should confirm our initial findings and test the potential of Cube-FLAIR for other pathologies that have high signal intensity within the CSF space. [27][28][29][30][31] Similar to authors of previous MR imaging studies on SAH, we used CT as a reference standard to determine the presence and localization of SAHs. 2,[23][24][25] To further enhance the diagnostic certainty regarding the overall presence of a SAH, we used a positive CSF result as additional inclusion criterion.…”