Blood–brain barrier damage and new onset refractory status epilepticus: An exploratory study using dynamic contrast‐enhanced magnetic resonance imaging

Author:

Li Huiping1,Liu Xian2,Wang Ruihong1,Lu Aili1,Ma Zhaohui1,Wu Shibiao1,Lu Hongji1,Du Yaming1,Deng Kan3ORCID,Wang Lixin14,Yuan Fang1ORCID

Affiliation:

1. Department of Neurocritical Care Second Affiliated Hospital of Guangzhou University of Chinese Medicine Guangzhou China

2. Department of Imaging Second Affiliated Hospital of Guangzhou University of Chinese Medicine Guangzhou China

3. Philips Healthcare Guangzhou China

4. Guangdong Provincial Key Laboratory of Chinese Medicine Emergency Research Guangzhou China

Abstract

AbstractObjectiveThis study was undertaken to characterize the blood–brain barrier (BBB) dysfunction in patients with new onset refractory status epilepticus (NORSE) using dynamic contrast‐enhanced magnetic resonance imaging (DCE‐MRI).MethodsThis study included three groups of adult participants: patients with NORSE, encephalitis patients without status epilepticus (SE), and healthy subjects. These participants were retrospectively included from a prospective DCE‐MRI database of neurocritically ill patients and healthy subjects. The BBB permeability (Ktrans) in the hippocampus, basal ganglia, thalamus, claustrum, periventricular white matter, and cerebellum were measured and compared between these three groups.ResultsA total of seven patients with NORSE, 14 encephalitis patients without SE, and nine healthy subjects were included in this study. Among seven patients with NORSE, only one had a definite etiology (autoimmune encephalitis), and the rest were cryptogenic. Etiology of encephalitis patients without SE included viral (n = 2), bacterial (n = 8), tuberculous (n = 1), cryptococcal (n = 1), and cryptic (n = 2) encephalitis. Of these 14 encephalitis patients without SE, three patients had seizures. Compared to healthy controls, NORSE patients had significantly increased Ktrans values in the hippocampus (.73 vs. .02 × 10−3/min, p = .001) and basal ganglia (.61 vs. .003 × 10−3/min, p = .007) and a trend in the thalamus (.24 vs. .08 × 10−3/min, p = .017). Compared to encephalitis patients without SE, NORSE patients had significantly increased Ktrans values in the thalamus (.24 vs. .01 × 10−3/min, p = .002) and basal ganglia (.61 vs. .004 × 10−3/min, p = .013).SignificanceThis exploratory study demonstrates that BBBs of NORSE patients were impaired diffusely, and BBB dysfunction in the basal ganglia and thalamus plays an important role in the pathophysiology of NORSE.

Publisher

Wiley

Subject

Neurology (clinical),Neurology

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