Effects of Microvascular Permeability Changes on Contrast-Enhanced T1 and Pharmacokinetic MR Imagings After Ischemia

Abstract

2Contrast-enhanced T1-weighted imaging (CET1-WI) has been routinely used in cerebral stroke study. [3][4][5] The presence of parenchymal enhancement (PE) on CET1-WI is generally accepted as an indicator of contrast medium leakage across the disrupted BBB. 6 Previous studies have demonstrated an association between the risk of HT after recanalization therapy and the increased BBB permeability shown as PE on CET1-WI during the acute stage.3 However, PE in CET1-WI usually does not appear until several days after the ictus. 2 The phenomenon has been explained by BBB breakdown and luxury reperfusion at the subacute stage. 4 Because the BBB disruption is thought to be present as early as 6 hours after cerebral infarction, it is possible that PE in CET1-WI Background and Purpose-Brain enhancement on contrast-enhanced T1-weighted imaging (CET1-WI) after ischemic stroke is generally accepted as an indicator of the blood-brain barrier disruption. However, this phenomenon usually starts to become visible at the subacute phase. The purpose of this study was to evaluate the time-course profiles of K trans , cerebral blood volume (v p ), and CET1-WI with early detection of blood-brain barrier changes on K trans maps and their role for prediction of subsequent hemorrhagic transformation in acute middle cerebral arterial infarct. Methods-Twenty-six patients with acute middle cerebral arterial stroke and early spontaneous reperfusion, whose MR images were obtained at predetermined stroke stages, were included. T2*-based MR perfusion-weighted images were acquired using the first-pass pharmacokinetic model to derive K trans and v p . Parenchymal enhancement observed on maps of K trans , v p , and CET1-WI at each stage was compared. Association among these measurements and hemorrhagic transformation was analyzed. Results-Ktrans map showed significantly higher parenchymal enhancement in ischemic parenchyma as compared with that of v p map and CET1-WI at early stroke stages (P<0.05). The increased K trans at acute stage was not associated with parenchymal enhancement in CET1-WI at the same stage. Parenchymal enhancement in CET1-WI started to occur at the late subacute stage and tended to be luxury reperfusion-dependent. Patients with hemorrhagic transformation showed higher mean K trans values as compared with patients without hemorrhagic transformation (P=0.02). Conclusions-Postischemic brain enhancement on routine CET1-WI seems to be closely related to the luxury reperfusion at the late subacute stage and is not dependent on microvascular permeability changes at the acute stage. (Stroke. 2013;44:1872-1877.)

Clinical biomarkers differentiate myelitis from vascular and other causes of myelopathy

“…Any injury to the CNS has the potential to cause a secondary inflammatory response that may manifest with some degree of pleocytosis or disruption of the blood–brain barrier, causing Gd+; in addition, hemodynamic changes in the lesion such as vasodilation and “luxury perfusion” may also result in Gd+. 21 This situation is well-illustrated by Gd+ in ischemic brain strokes within 1 week of onset. 22 Thus, evidence of a Gd+ lesion on MRI or CSF pleocytosis is not definitively diagnostic of a primary inflammatory disease, and immunosuppressive therapy may not be warranted.…”

Impact of an immune modulator fingolimod on acute ischemic stroke

“…Lesion volume was manually outlined on the DWI, FLAIR, and T1 slices and then automatically calculated for each slice from the measured area and corresponding slice thickness. The degree of enhancement on CET1-WI (7 d) was expressed as rT1%, rT1% = (mean signal intensity of a region of the infarction − mean signal intensity of the contralateral homologous normal brain area)/mean signal intensity of the contra lateral homologous normal brain area (28).…”

“…4), and imply that fingolimod limited the progression of the secondary injury in acute stroke patients. Contrast-enhanced T1-weighted imaging (CET1-WI) has been used routinely in cerebral stroke studies (28). The presence of parenchymal enhancement on CET1-WI is generally accepted as an indicator of contrast medium leakage across the disrupted BBB.…”

The peripheral immune response after stroke—A double edge sword for blood‐brain barrier integrity

“…During the late phase of stroke, the BBB dysfunction becomes less severe, in which BBB restoration possibly plays an important role . Multiple processes may be involved in the restoration of BBB permeability after stroke at the late phase of stroke.…”