CSF enhancement on post-contrast fluid-attenuated inversion recovery images; a systematic review

Freeze, Whitney M.; Thiel, Merel M. van der; Bresser, Jeroen de; Klijn, Catharina J.M.; Etten, Ellis S. van; Jansen, Jacobus F.A.; Weerd, Louise van der; Jacobs, Heidi I.L.; Backes, Walter H.; Veluw, Susanne J. van

doi:10.1016/j.nicl.2020.102456

Cited by 16 publications

(21 citation statements)

References 67 publications

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“…83 Delayed cerebrospinal fluid enhancement on postcontrast fluid-attenuated inversion recovery images has been recognized as a marker of BBB leakage in different neurological disorders. 84 Moreover, the retention of the contrast agent in the subarachnoid space may also inform on (deficiencies in) cerebrospinal fluid dynamics and (glymphatic) clearance mechanisms, as demonstrated with MRI in rodents after intrathecal or intracisternal infusion of a gadolinium chelate. 85,86…”

Section: Imaging Markers Of Neuroinflammationmentioning

confidence: 99%

Neuroinflammation, Stroke, Blood-Brain Barrier Dysfunction, and Imaging Modalities

Candelario‐Jalil

Dijkhuizen

Magnus

2022

Stroke

268

150

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Maintaining blood-brain barrier (BBB) integrity is crucial for the homeostasis of the central nervous system. Structurally comprising the BBB, brain endothelial cells interact with pericytes, astrocytes, neurons, microglia, and perivascular macrophages in the neurovascular unit. Brain ischemia unleashes a profound neuroinflammatory response to remove the damaged tissue and prepare the brain for repair. However, the intense neuroinflammation occurring during the acute phase of stroke is associated with BBB breakdown, neuronal injury, and worse neurological outcomes. Here, we critically discuss the role of neuroinflammation in ischemic stroke pathology, focusing on the BBB and the interactions between central nervous system and peripheral immune responses. We highlight inflammation-driven injury mechanisms in stroke, including oxidative stress, increased MMP (matrix metalloproteinase) production, microglial activation, and infiltration of peripheral immune cells into the ischemic tissue. We provide an updated overview of imaging techniques for in vivo detection of BBB permeability, leukocyte infiltration, microglial activation, and upregulation of cell adhesion molecules following ischemic brain injury. We discuss the possibility of clinical implementation of imaging modalities to assess stroke-associated neuroinflammation with the potential to provide image-guided diagnosis and treatment. We summarize the results from several clinical studies evaluating the efficacy of anti-inflammatory interventions in stroke. Although convincing preclinical evidence suggests that neuroinflammation is a promising target for ischemic stroke, thus far, translating these results into the clinical setting has proved difficult. Due to the dual role of inflammation in the progression of ischemic damage, more research is needed to mechanistically understand when the neuroinflammatory response begins the transition from injury to repair. This could have important implications for ischemic stroke treatment by informing time- and context-specific therapeutic interventions.

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Section: Imaging Markers Of Neuroinflammationmentioning

confidence: 99%

Neuroinflammation, Stroke, Blood-Brain Barrier Dysfunction, and Imaging Modalities

Candelario‐Jalil

Dijkhuizen

Magnus

2022

Stroke

268

150

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“…Anti-VZV immunoglobulin G has been described as more robust than viral DNA PCR which disappears after early infection [ 2 , 6 , 8 ]. Post-gadolinium fluid-attenuated inversion recovery MRI sequences may demonstrate leptomeningeal enhancement with 80-90% sensitivity, attributed to pathogen-induced blood-brain-barrier dysfunction and leakage of blood-borne proteins into CSF [ 9 ]. Although imaging is not required to diagnose meningitis, it plays an important role in the assessment of complications including myelitis and vasculopathy.…”

Section: Discussionmentioning

confidence: 99%

Hemorrhagic Meningitis Due to Varicella-Zoster Virus: A Case Report With Clinical, Cytologic, and Radiologic Correlation

Gorolay¹,

Martens²,

Satgunaseelan³

et al. 2022

Cureus

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Although varicella-zoster virus (VZV) is known to affect the central nervous system in a protean manner, hemorrhagic VZV meningitis has not been well documented in the literature. Here, we correlate the clinical, cytologic, and radiologic findings in an immunocompromised patient presenting with subarachnoid hemorrhage associated with VZV meningitis. Clinical findings included multidermatomal zoster, myelitis, and neurapraxia. Magnetic resonance imaging findings included superficial siderosis and diffused linear and nodular leptomeningeal enhancement. Cerebrospinal fluid cytology revealed hemorrhage and lymphocytic pleocytosis. This case report adds hemorrhagic meningitis to the spectrum of complications associated with disseminated VZV infection.

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“…The hyperintense acute reperfusion marker (HARM) is characterized as the delayed contrast enhancement of the subarachnoid or subpial space on postcontrast FLAIR images in various intracranial pathologic conditions, and is believed to be associated with permeability changes in the BBB. HARM is not a specific finding for acute stroke, and has been described in other BBB-disturbing conditions, such ascarotid artery stenting, post-operative state for cardiothoracic surgery, traumatic brain injury, and seizure [9][10][11][12][13]. HARM was found in 10-40% of patients with acute stroke in the previous studies [8,14], and is considered an useful marker for BBB disruption in acute stroke [15][16][17].…”

Section: Introductionmentioning

confidence: 88%

The Clinical Significance of the Hyperintense Acute Reperfusion Marker Sign in Subacute Infarction Patients

Lee

Kim

et al. 2021

Diagnostics

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Purpose: The hyperintense acute reperfusion marker (HARM) is characterized by the delayed enhancement of the subarachnoid or subpial space observed on postcontrast fluid-attenuated inversion recovery (FLAIR) images, and is considered a cerebral reperfusion marker for various brain disorders, including infarction. In this study, we evaluated the cerebral distribution patterns of HARM for discriminating between an enhancing subacute infarction and an enhancing mass located in the cortex and subcortical white matter. Materials and methods: We analyzed consecutive patients who experienced a subacute ischemic stroke, were hospitalized, and underwent conventional brain magnetic resonance imaging including postcontrast FLAIR within 14 days from symptom onset, as well as those who had lesions corresponding to a clinical sign detected by diffusion-weighted imaging and postcontrast T1-weighted imaging between May 2019 and May 2021. A total of 199 patients were included in the study. Of them, 94 were finally included in the subacute infarction group. During the same period, 76 enhancing masses located in the cortex or subcortical white matter, which were subcategorized as metastasis, malignant glioma, and lymphoma, were analyzed. We analyzed the overall incidence of HARM in subacute ischemic stroke cases, and compared the enhancement patterns between cortical infarctions and cortical masses. Results: Among 94 patients with subacute stroke, 78 patients (83%) presented HARM, and among 76 patients with subcortical masses, 48 patients (63%) presented peripheral rim enhancement. Of 170 subcortical enhancing lesions, 88 (51.8%) showed HARM, and 78 (88.6%) were determined to be subacute infarction. Among 94 patients with subacute stroke, 48 patients (51%) had diffusion restrictions, and HARM was found in 39 patients (81.2%). Of the 46 patients (49%) without diffusion restriction, 39 patients (84.8%) showed HARM. Conclusions: The presence of HARM was significantly associated with subacute infarctions. For the masses, a peripheral rim enhancement pattern was observed around the mass rather than the cerebral sulci on postcontrast FLAIR.

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CSF enhancement on post-contrast fluid-attenuated inversion recovery images; a systematic review

Cited by 16 publications

References 67 publications

Neuroinflammation, Stroke, Blood-Brain Barrier Dysfunction, and Imaging Modalities

Neuroinflammation, Stroke, Blood-Brain Barrier Dysfunction, and Imaging Modalities

Hemorrhagic Meningitis Due to Varicella-Zoster Virus: A Case Report With Clinical, Cytologic, and Radiologic Correlation

The Clinical Significance of the Hyperintense Acute Reperfusion Marker Sign in Subacute Infarction Patients

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