Mild encephalopathy with a reversible splenial lesion (MERS) is a clinico-radiological syndrome characterized by a transient mild encephalopathy and MRI findings of a reversible lesion in the splenium of corpus callosum (SCC). It is classified in MERS type I and MERS type II, depending on the involvement of SCC alone or also other white matter areas. The syndrome mainly affects children and young adults; the prognosis is favorable with complete or nearly complete neurological and radiological resolution within days or weeks. The vast majority of the cases described in the literature involve Asian and Australian children. The exact pathophysiology is unknown; however, infectious-related MERS (in particular virus associated MERS) remains the most common cause of reversible splenial lesions in childhood. To the best of our knowledge, there is only one published case of MERS associated with cytomegalovirus (CMV) infection involving an Australian child. We present here the first case of a CMV-related MERS in a European Caucasian child.
Epilepsy is a frequent consequence of neonatal hypoxic–ischemic encephalopathy. It is not yet known if the introduction of therapeutic hypothermia modifies the rate and the characteristics of epilepsy. We report on 59 infants who suffered from hypoxic–ischemic encephalopathy and underwent therapeutic hypothermia. Birth, physiological and biochemical data, frequent electroencephalography (EEG) recordings or continuous EEG monitoring, and magnetic resonance imaging (MRI) were documented in the neonatal period. Prechtl's General Movements evaluation was performed and the Griffiths Scales of Mental Development were applied at 3 and 24 months of age, respectively. Children were followed up for at least 3 years (mean 5 ± 1.6 years). Six children (10%) developed epilepsy. All of them had a severe hypoxic–ischemic encephalopathy and were neurologically impaired at 2 years of age. Furthermore, all of them had a severe pattern of MRI injury and poor neonatal EEG backgrounds. Four of them suffered from neonatal status epilepticus. Four out of six showed a similar epileptic pattern: their epilepsy started early; it was drug resistant; it required an aggressive polytherapy; and it showed a spontaneous improvement after 2 years. The rate of epilepsy in our cooled infants was similar to those reported in other studies on noncooled ones. Only severe hypoxic–ischemic encephalopathy predisposed the cooled infants toward epilepsy. Neonatal status epilepticus and persisting poor EEG backgrounds were predictive of the development of epilepsy in our sample.
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