No abnormality was found on MRA, while sulcal hyperintensity in the right frontoparietal lobes was revealed on MRI ( Fig. Brain MRI and magnetic resonance angiography (MRA) were performed after admission. No focal neurological deficits were noted. This moderate to severe headache lasted all day, accompanied by vomiting, but improved after sleeping. Three days prior to the onset of seizures, she had visited the outpatient clinic due to a headache that lasted 2 weeks. Irritability, aggressive behavior, and severe headaches on the right side of the head were noted. Ipsilateral weakness and paresthesia persisted for several hours following the seizures. Focal seizures arising from the left side evolved into bilateral tonic-clonic seizures. The patient was first admitted at the age of 9 years with headache and repeated seizures. She had two discrete encephalitic episodes 1.5 years apart: the first episode was initially diagnosed as Epstein-Barr virus (EBV) encephalitis and the second was presumed to be a hemiplegic migraine. Here, we report the diagnostic journey of a girl who was ultimately diagnosed with anti-MOG-associated-CCE. ![]() Thus, clinicians need to maintain a high index of suspicion for anti-MOG-associated disease when faced with an unusual presentation of encephalitic pathologies, such as unilateral headache with or without transient hemiparesis. Furthermore, numerous magnetic resonance imaging (MRI) findings, apart from isolated cortical hyperintensities, have also been reported in anti-MOG-associated encephalitis. Viral encephalitis, small-vessel vasculitis, and hemiplegic migraine should be ruled out, but doing so poses challenges. ![]() Unilateral cortical hyperintensities on T2-weighted fluid-attenuated inversion recovery (T2-FLAIR) sequences are a characteristic finding of this phenotype. Common symptoms of anti-MOG-associated CCE include seizures, headache, encephalitic features, and cortical symptoms, such as paresis. in 2017, is a newly identified phenotype of MOG antibody-associated disease. Cerebral cortical encephalitis (CCE), first described by Ogawa et al. However, MOG antibody-associated diseases are not limited to demyelinating syndromes. Numerous studies have implicated MOG in immune-mediated demyelinating diseases, including acute disseminated encephalomyelitis, optic neuritis, and transverse myelitis. Myelin oligodendrocyte glycoprotein (MOG) is an essential component of oligodendrocyte surface membranes.
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