Exceeding the Limits of the Normal Blood-Brain Barrier: Quo Vadis Gadolinium?

Levy, L. M.

doi:10.3174/ajnr.a0725

Cited by 6 publications

(6 citation statements)

References 4 publications

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“…21 Small amounts of GBCAs might be transported into the CSF via the choroid plexus because the blood-CSF barrier is leakier than the BBB. 44,45 In a recently published study in healthy rats, Jost et al 46 showed a hyperintense CSF using a sensitive FLAIR sequence and measured 4.5 hours after GBCA administration of a CSF concentration up to a maximum of 27.4 nmol Gd/mL by ICP-MS, which is equivalent to 0.006% ID/g. In humans, 500 mL of CSF is secreted at the choroid plexus each day, which is further distributed into the subarachnoid space and subsequently into the blood via bulk flow, consistent with many drug substances distributed into the CSF.…”

Section: Discussionmentioning

confidence: 99%

Histology and Gadolinium Distribution in the Rodent Brain After the Administration of Cumulative High Doses of Linear and Macrocyclic Gadolinium-Based Contrast Agents

et al. 2017

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Section: Discussionmentioning

confidence: 99%

Histology and Gadolinium Distribution in the Rodent Brain After the Administration of Cumulative High Doses of Linear and Macrocyclic Gadolinium-Based Contrast Agents

et al. 2017

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“…30 Disruption of the BBB manifests as CE on brain MRI. 31 Periependymal white matter is one of the most AQP4 rich regions of the brain and hence the high prevalence of periependymal contrast enhancement in our cohort. Furthermore, AQP4-IgG is thought to be pathogenic only when in proximity to CNS parenchyma, as evidenced by NMO-like histopathology in animal models in those that received direct administration of AQP4-IgG into the CNS.…”

Section: Discussionmentioning

confidence: 83%

Enhancing Brain Lesions during Acute Optic Neuritis and/or Longitudinally Extensive Transverse Myelitis May Portend a Higher Relapse Rate in Neuromyelitis Optica Spectrum Disorders

Orman¹,

Wang

Pekçevik³

et al. 2017

AJNR Am J Neuroradiol

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Background and purpose Neuromyelitis optica spectrum disorders (NMOSD) is an inflammatory demyelinating disorder with optic neuritis (ON) and/or longitudinally extensive transverse myelitis (LETM) episodes. We now know that NMOSD is associated with antibodies to aquaporin 4 (AQP4) which is highly concentrated on astrocytic end-feet at the blood-brain barrier. Immune-mediated disruption of blood brain barrier may manifest as contrast enhancement (CE) on brain MRI. We aim to delineate extent and frequency of CE on brain MRI within one month of ON and/or LETM attacks and to correlate CE with outcomes measures. Methods Brain MRIs of NMOSD patients were evaluated for patterns of CE (periependymal, cloud-like, leptomeningeal, etc.). Fisher’s exact test was used to evaluate differences between the proportions of CE in seropositives and seronegatives for aquaporin-4 antibodies. Mann-Whitney test was used to compare annualized relapse rate (ARR) and disease duration between patients with and without CE, and with and without seropositivity. Results Brain MRIs of 77 patients were evaluated; 59 (10 male, 49 female) were scanned within one month of ON and/or LETM attacks and were included in the analysis. Forty-eight patients were seropositive, 9 were negative and 2 were not tested. Having brain CE of any type during acute attack was significantly associated with higher ARRs (p=0.03) and marginally associated with shorter disease duration (p=0.05). Having periependymal CE was significantly associated with higher ARRs (p=0.03). Conclusion Brain MRIs of NMOSD patients with CE during an acute relapse of ON and/or LETM are associated with increased annual relapse rate.

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“…The blood-brain barrier is an anatomic and physiologic barrier separating the brain parenchyma and he intravascular space [6]. The tight junction between the epithelial cells within the brain parenchyma is relatively impermeable [11]. The impermeability can be disrupted under pathologic processes like a tumor, ischemia, an overdose of contrast material, or intra-arterial injection of contrast material [6,[10][11].…”

Section: Discussionmentioning

confidence: 99%

Subarachnoid Contrast Hyperdensity Following Pelvic Trauma Mimicking Diffuse Subarachnoid Hemorrhage

Biswas

Amin

2020

Cureus

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We present a case of a 54-year-old male who was involved in a motorcycle accident. His head computed tomography (CT) scan on arrival at our Level 1 institution was positive for hyperdensity suspicious for subarachnoid hemorrhage (SAH). Spine CT showed anterior compression fractures of T7-T9 vertebral bodies along with the presence of contrast within the subarachnoid space in the thoracic and lumbar spine, raising suspicion for a dural tear. CT of the chest, abdomen, and pelvis revealed open book pelvic fracture, left sacral ala fracture extending into the left sacroiliac joint and S1 neural foramen, coccygeal fracture, and extraperitoneal bladder rupture. This rare case report highlights the possibility of a spinal meningeal tear in severe pelvic trauma with concomitant bladder injury as a pathway of contrast entry into the normally impermeable cerebrospinal fluid (CSF) space mimicking traumatic subarachnoid hemorrhage.

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Exceeding the Limits of the Normal Blood-Brain Barrier: Quo Vadis Gadolinium?

Cited by 6 publications

References 4 publications

Histology and Gadolinium Distribution in the Rodent Brain After the Administration of Cumulative High Doses of Linear and Macrocyclic Gadolinium-Based Contrast Agents

Histology and Gadolinium Distribution in the Rodent Brain After the Administration of Cumulative High Doses of Linear and Macrocyclic Gadolinium-Based Contrast Agents

Enhancing Brain Lesions during Acute Optic Neuritis and/or Longitudinally Extensive Transverse Myelitis May Portend a Higher Relapse Rate in Neuromyelitis Optica Spectrum Disorders

Subarachnoid Contrast Hyperdensity Following Pelvic Trauma Mimicking Diffuse Subarachnoid Hemorrhage

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