HARM revisited: Etiology of subarachnoid hyperintensities in brain FLAIR MRI

 

So you documented a problem, WHAT THE FUCK IS THE SOLUTION TO PREVENT IT? My directors would never let me get away with describing a problem without having a possible solution in hand. I'd be fired in no time.

HARM revisited: Etiology of subarachnoid hyperintensities in brain FLAIR MRI

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Katharina Althaus, Martin Kasel, Albert C Ludolph, ...

First Published January 5, 2022 Research Article 

https://doi.org/10.1177/17474930211064754

Article information

Abstract

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.

Keywords

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

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Hyperintense acute reperfusion marker associated with hemorrhagic transformation in the WAKE-UP trial

 

So you documented a problem, WHAT THE FUCK IS THE SOLUTION TO PREVENT IT? My directors would never let me get away with describing a problem without having a possible solution in hand. I'd be fired in no time.

Hyperintense acute reperfusion marker associated with hemorrhagic transformation in the WAKE-UP trial

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Anke Wouters*, Lauranne Scheldeman*, Patrick Dupont, ...

First Published June 12, 2021 Research Article 

https://doi.org/10.1177/23969873211007686

Article information

Abstract

Introduction

Hyperintense acute reperfusion marker (HARM) is an indicator of early disruption of the blood-brain-barrier. Our aim was to investigate the incidence of HARM in patients with a diffusion weighted imaging (DWI) - fluid attenuated inversion recovery (FLAIR) mismatch and determine the association between this marker and hemorrhagic complications as well as clinical outcome.

Patients and Methods

We included patients from the Efficacy and Safety of MRI-Based Thrombolysis in Wake-Up Stroke (WAKE-UP) trial who underwent baseline perfusion weighted imaging (PWI). HARM was defined as a hyperintense signal in the cerebrospinal fluid space on FLAIR imaging at 24 h after baseline imaging. We compared baseline characteristics in patients with and without HARM and investigated the association between HARM and any hemorrhagic transformation (HT) and parenchymal hematoma (PH) in a multivariate logistic regression. We also explored HARM as an independent predictor of poor outcome, defined as a modified Rankin Scale of 3–6 at 90 days.

Results

HARM was present in 14 of 223 (6%) patients with a DWI-FLAIR mismatch and baseline characteristics were similar in patients with vs without HARM. HARM showed an independent relationship with any HT (OR 6.67; 95%CI 1.72–26.58) and any PH (OR 6.92; 95%CI 1.34–29.49). The rate of HARM was similar in patients with good and poor outcome (5%, p = 0.90).

Conclusion

In the WAKE-UP trial, the incidence of HARM was only 6% at 24 h. An association was present between HARM and hemorrhagic complications, but no relationship with functional outcome was observed.

Keywords Ischemic stroke, DWI-FLAIR mismatch, HARM, hemorrhage, magnetic resonance imaging

Introduction

A paradigm shift towards tissue-based treatment strategies instead of relying on rigid time-windows has reshaped the current landscape of acute stroke care. The interest in imaging markers to guide treatment decisions and to predict tissue fate is increasing. Magnetic resonance imaging (MRI) can visualize both parenchymal and hemodynamic changes in ischemic brain tissue. Evaluating a mismatch between the DWI lesion vs the penumbral tissue, as visualized by perfusion weighted imaging (PWI-DWI mismatch),^1–3 or in relation to the presence of vasogenic edema on FLAIR (the DWI-FLAIR mismatch)⁴ are selection strategies to increase the amount of acutely treated stroke patients.

Another less frequently reported imaging characteristic is the hyperintense acute reperfusion marker (HARM) defined as a delayed sign of early blood-brain-barrier (BBB) disruption. Leakage of gadolinium contrast results in enhancement of the cerebrospinal fluid (CSF) compartment on postgadolinium FLAIR images; an altered function of the BBB is thought to be responsible for this phenomenon.^5–8 The reported incidence of HARM in ischemic stroke patients is highly variable and ranges from 5.5% to 40.4%.^5,6,9–12 No consensus exists on the association of HARM with hemorrhagic transformation (HT) and clinical outcome.^5,6,10,11

We investigated the presence of HARM in patients with a DWI-FLAIR mismatch from the randomized Efficacy and Safety of MRI-Based Thrombolysis in Wake-Up Stroke (WAKE-UP) trial.⁴ Furthermore, we explored the association of HARM with hemorrhagic transformation and functional outcome at 90 days.

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Frequency of Blood-Brain Barrier Disruption Post-Endovascular Therapy and Multiple Thrombectomy Passes in Acute Ischemic Stroke Patients

And why is blood brain barrier disruption being attributed to multiple passes rather than this? Inflammatory action leaking through the blood brain barrier of the neuronal cascade of death.

Multiple passes just means there is more time for that inflammatory action to occur. Bad conclusion, and the mentors and senior researchers didn't catch this and correct it? I take no prisoners in trying to get stroke to be fixed. Firings would occur under my watch. 

Oops, I'm not playing by the polite rules of Dale Carnegie,  'How to Win Friends and Influence People'. 
Politeness will never solve anything in stroke.  I call them as I see them.

 

 

Frequency of Blood-Brain Barrier Disruption Post-Endovascular Therapy and Multiple Thrombectomy Passes in Acute Ischemic Stroke Patients

Marie Luby

,

Amie W. Hsia

,

Zurab Nadareishvili

,

Kaylie Cullison

,

Noorie Pednekar

,

Malik Muhammad Adil

,

Lawrence L. Latour

Originally publishedhttps://doi.org/10.1161/STROKEAHA.119.025914Stroke. ;0

Abstract

Background and Purpose—

The high prevalence of hyperintense acute reperfusion marker (HARM) seen after endovascular therapy is suggestive of blood-brain barrier disruption and hemorrhage risk and may be attributable to multiple thrombectomy passes needed to achieve recanalization.

Methods—

Patients with acute stroke were included if they were screened from January 2015 through February 2019, received an acute ischemic stroke diagnosis involving the anterior circulation, treated with or without IV tPA (intravenous tissue-type plasminogen activator), consented to the NINDS Natural History Study, and imaged with a baseline magnetic resonance imaging before receiving endovascular therapy. Consensus image reads for HARM and hemorrhagic transformation were performed. Good clinical outcome was defined as 0–2 using the latest available modified Rankin Scale score.

Results—

Eighty patients met all study criteria and were included in the analyses. Median age was 65 years, 64% female, 51% black/African American, median admit National Institutes of Health Stroke Scale=19, 56% treated with IV tPA, and 84% achieved Thrombolysis in Cerebral Infarction score of 2b/3. Multiple-pass patients had significantly higher rates of severe HARM at 24 hours (67% versus 29%; P=0.001), any hemorrhagic transformation (60% versus 36%; P=0.04) and poor clinical outcome (67% versus 36%; P=0.008). Only age (odds ratio, 1.1; 95% CI, 1.01–1.12; P=0.022) and severe HARM at 24 hours post-endovascular therapy were significantly associated with multiple passes (odds ratio, 7.2; 95% CI, 1.93–26.92; P=0.003).

Conclusions—

In this exploratory study, multiple thrombectomy passes are independently associated with a significant increase in blood-brain barrier disruption detected at 24 hours. Patients with HARM post-endovascular therapy had a >7-fold increase in the odds of having multiple- versus single-pass thrombectomy.

Clinical Trial Registration—

URL: https://www.clinicaltrials.gov. Unique identifier: NCT00009243.

Footnotes

Presented in part at the International Stroke Conference, Honolulu, HI, February 6–8, 2019.

Correspondence to Marie Luby, PhD, Stroke Branch, National Institute of Neurological Disorders and Stroke, National Institutes of Health, 10 Center Dr, Room B1D-733, MSC 1063, Bethesda, MD 20892–1063. Email lubym@ninds.nih.gov