Elsevier

Brain and Development

Volume 34, Issue 2, February 2012, Pages 124-127
Brain and Development

Oxidative stress in patients with clinically mild encephalitis/encephalopathy with a reversible splenial lesion (MERS)

https://doi.org/10.1016/j.braindev.2011.04.004Get rights and content

Abstract

We examined oxidative stress markers, tau protein and cytokines in the cerebrospinal fluid (CSF) in six patients with clinically mild encephalitis/encephalopathy with a reversible splenial lesion (MERS). In the CSF, 8-hydroxy-2′-deoxyguanosine (8-OHdG) and hexanoyl-lysine adduct levels increased over the cutoff index in four and one out of six MERS patients, respectively. The CSF IL-6 and IL-10 levels were increased in three out of six patients, two of which had extended lesion of the cerebral white matter. The CSF value of tau protein, marker of the axonal damage, was not increased, and neuron specific enolase (NSE) in the CSF was not increased. The increased 8-OHdG levels in the CSF, DNA oxidative stress marker, in four MERS patients, suggesting involvement of oxidative stress in MERS. MERS is occasionally accompanied with hyponatremia, although our patients lacked hyponatremia. It is possible that the disequilibrium of systemic metabolism including electrolytes may lead to facilitation of oxidative stress and reversible white matter lesion in MERS. The increase of cytokine production seems to be involved in the distribution of lesions in MERS.

Introduction

The patients with clinically mild encephalitis/encephalopathy with a reversible splenial lesion (MERS) showed the magnetic resonance imaging (MRI) findings of a reversible lesion in the central portion of the splenium of corpus callosum (SCC) with transient reduced diffusion, and had mild clinical courses and recovered completely without sequelae [1], [2]. Intramyelinic edema, hyponatremia and axonal damage have been hypothesized for pathogenesis in MERS [2], [3], [4]. However, the detailed reasons for the transiently reduced diffusion are unknown. Levels of oxidative stress markers [5] and tau protein [6], a marker of axonal injuries, have been examined in the cerebral spinal fluids (CSF) in the patients with developmental brain disorders. We reported the involvement of oxidative stress in a patient with limbic encephalopathy [7]. Here we examined the oxidative stress markers, tau proteins and neuron specific enolase (NSE) in CSF in six MERS patients to clarify the pathogenesis.

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Materials and methods

Six patients (four female and two male, age 1–13 years) diagnosed as MERS with clinical course and MRI findings were included (Table 1). Six controls aged from 11 months to 8 years, in which the CSF was tested for the examination of fever, and no neurological symptoms such as convulsions were observed. Parent consent was obtained in all subjects in accordance with the Helsinki Declaration and all protocols were approved by the institutional ethics committee of the Tokyo Metropolitan Institute of

Results

There were no abnormalities in serum levels of sodium (136–141 mmol/l) and other electrolytes. Patient 5 showed delirium, whereas other five patients did not. Five patients except patient 6 had generalized tonic seizures, and anticonvulsants were given temporally. Patient 1 subsequently developed cluster of the similar convulsion, and continuous intravenous infusion of midazolam. Patients 2 and 4 were given antibiotics for a few days. Hyponatremia or hypoglycemia was not seen in patients.

Discussion

The causes of transient and reduced diffusion in the SCC are unknown in MERS patients [2]. The SCC consists of commissural fibers from the occipital, temporal and parietal lobes, the changes in which tend to affect the SCC more frequently than the genu or body of corpus callosum. The difference in arterial vascularization and/or water content in the corpus callosum may lead to the frequent occurrence of SCC lesion [8], [9]. Reversible diffusion changes in the SCC are also observed in patients

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