4.6 Article

HARM revisited: Etiology of subarachnoid hyperintensities in brain FLAIR MRI

Journal

INTERNATIONAL JOURNAL OF STROKE
Volume 17, Issue 10, Pages 1121-1128

Publisher

SAGE PUBLICATIONS LTD
DOI: 10.1177/17474930211064754

Keywords

Magnetic resonance imaging; MRI; FLAIR; subarachnoid hyperintensities; stroke; gadolinium

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This study retrospectively analyzed 23,948 cerebral MRIs and found that 84 images from 61 patients showed HARM-positive results. HARM was observed not only in stroke patients, but also in other neurological conditions, and it was not dependent on therapy.
Background: The hyperintense acute reperfusion marker (HARM) describes a phenomenon with a hyperintense signal in the subarachnoid space in Fluid-Attenuated Inversion Recovery (FLAIR) magnetic resonance imaging (MRI) sequences, presumably based on blood-brain barrier breakdown in acute stroke with reperfusion. However, this imaging phenomenon was described in other medical conditions. Aim: Determination of the prevalence and associated clinical findings of this phenomenon in a large sample of patients with different neurological conditions. Methods: This is retrospective, single-center, observational study of 23,948 cerebral MRIs acquired in a Neurological University Clinic over 5 years. The prevalence of HARM, the underlying diagnosis, and damage pattern were examined by chart analysis; MRI was analyzed regarding the type of acute lesions, extent of microangiopathic lesions, and whether gadolinium-based contrast agent (GBCA) was given. Results: Among the MRI data, 84 images (0.35%) from 61 patients were HARM-positive without a subarachnoid signal abnormality in any other sequence. Etiologies were heterogeneous; 35 patients had a cerebrovascular disease (CVD; 19 patients received recanalization therapy), 12 patients had an inflammatory central nervous system (CNS) disease and 14 patients had epilepsy. GBCA was applied to 64% of the patients. Conclusion: HARM was a rare radiological finding in a range of different neurological pathologies, not limited to stroke, or to previous reperfusion therapy and was not dependent on previous GBCA administration. Our data suggest that the term is too narrow in terms of the concepts of the underlying pathology. We propose to use the term FLAIR Subarachnoid Hyperintensity (FLASH) phenomenon which might better reflect the observation that the radiological sign can be associated with a variety of central neurological conditions without a straightforward association with therapy.

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