Cerebral Cortical Encephalitis and Other Meningocortical Manifestations of Myelin Oligodendrocyte Glycoprotein Antibody-Associated Disease in Children: Case Series and Review of the Literature.

Myelin oligodendrocyte glycoprotein (MOG) antibody-associated disease is a neuroinflammatory disorder (MOGAD) with heterogeneous phenotype including paroxysms of optic neuritis, transverse myelitis, acute disseminated encephalomyelitis, brainstem demyelination, and encephalitis. Fluid-attenuated inversion recovery hyperintense cortical lesions in MOG-associated encephalitis with seizures, or FLAMES, is a manifestation of cerebral cortical encephalitis seen less frequently than other typical MOG antibody-associated disease presentations. Cases of FLAMES are rarer in children, and frequently initially misdiagnosed with infectious meningoencephalitis.

NMOSD and MOGAD: an evolving disease spectrum.

Neuromyelitis optica (NMO) spectrum disorder (NMOSD) is a relapsing inflammatory disease of the CNS, characterized by the presence of serum aquaporin 4 (AQP4) autoantibodies (AQP4-IgGs) and core clinical manifestations such as optic neuritis, myelitis, and brain or brainstem syndromes. Some people exhibit clinical characteristics of NMOSD but test negative for AQP4-IgG, and a subset of these individuals are now recognized to have serum autoantibodies against myelin oligodendrocyte glycoprotein (MOG) - a condition termed MOG antibody-associated disease (MOGAD). Therefore, the concept of NMOSD is changing, with a disease spectrum emerging that includes AQP4-IgG-seropositive NMOSD, MOGAD and double-seronegative NMOSD.

Thunderclap headache as a first manifestation of acute disseminated encephalomyelitis: case report and literature review.

Background: Acute Disseminated Encephalomyelitis (ADEM) is an acute demyelinating disorder of the central nervous system, characterize by multiple white matter hyperintensities on T2 MRI. Patients usually present with subacute progressive encephalopathy and polyfocal neurological deficits. Possible treatments are corticosteroids, immunoglobulins and plasma exchange.

[Modern pathogenetic treatment of rare demyelinating diseases].

Rare demyelinating diseases are a group of diseases whose pathogenesis is based on the process of demyelination. This group of diseases includes acute multiple encephalomyelitis (ADEM), opticoneuromyelitis spectrum diseases (NMOSD) and anti-myelin-oligodendrocyte glycoprotein-associated diseases (MOG-antibodies-associated diseases - MOGAD). Recently, new biological drugs for pathogenetic therapy have been developed, which have shown their effectiveness and good tolerability in comparison with therapy with first- and second-line drugs.

Bilateral Cerebellar Hemorrhages: An Atypical Presentation of Acute Hemorrhagic Encephalomyelitis.

Hurst disease, or Weston-Hurst syndrome, or acute hemorrhagic encephalomyelitis (AHEM), is an infrequent condition that usually gets provoked after a viral infection (respiratory tract infection) or, as reported in many case reports, post-vaccination. Hurst disease is a difficult-to-diagnose condition because it mimics common presentations such as stroke, decreased or loss of consciousness, brain abscess, and seizures, making clinical diagnosis challenging. Radiological imaging, such as magnetic resonance imaging (MRI) of the brain with diffusion-weighted imaging, now serves as the primary modality to identify such conditions, despite its lack of specificity.

Evaluating Therapeutic Plasma Exchange in Pediatric Acute Disseminated Encephalomyelitis: A Comprehensive Review.

Acute disseminated encephalomyelitis (ADEM) is a rare autoimmune disorder characterized by brain and spinal cord inflammation. In pediatric patients, ADEM presents unique challenges due to its potential for rapid progression and long-term neurological sequelae. Therapeutic plasma exchange (TPE) has emerged as a potential treatment option by targeting the underlying autoimmune process and modulating the inflammatory response.