Clinical and radiological features of MS, NMOSD, and MOGAD, and evolution of the diagnostic processes in Thailand

Abstract

Thailand and other Asian countries have experienced an increase in the prevalence of multiple sclerosis (MS), neuromyelitis optica spectrum disorder (NMOSD), and myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD). 1 This is probably due to both the increasing disease awareness and accessibility to diagnostic serological testing and magnetic resonance imaging (MRI). Although MS, NMOSD, and MOGAD have distinct mechanisms, prognoses, and treatments, they share common clinical features or even mimic other conditions. It is not uncommon for the diagnostician to be unconfident to make a definite diagnosis at the first presentation, especially with the lack of the typical presentations, MRI findings, and positive serological markers. Moreover, other mimic diseases in Asia, which are somewhat different from Western countries, also need excluding. Herein, we summarize the typical presentations of MS, NMOSD, and MOGAD along with the evolution and obstacles in diagnosing these diseases in Thailand. We also highlight the essential practical points to discriminate between them. | UTILIZING THE D IAG NOS TI C CRITERIA OF MS , NMOS D, AND MOG ADThe diagnostic criteria for both MS and NMOSD have been revised many times as our understanding of the diseases has improved.Revised criteria have enabled earlier diagnosis, provided prompt treatment, and potentially prevented future disability. However, MS and NMOSD are only diagnosed if the current criteria are met, and alternative diagnoses are excluded. A significant milestone in improving diagnosis was the 2001McDonald criteria incorporating MRI findings to serve as surrogates

MOG‐antibody‐associated disorder with hypothalamic lesions associated with hypersomnia and decrease of orexin in CSF: A case report

“…7,[16][17][18][19][20] Lesions surrounding the third ventricles and cerebral aqueduct including the thalamus and hypothalamus have been reported in NMOSD patients and similar lesions have been reported in a small number of patients with MOGAD. [3][4][5] There has been no report of symptomatic hypersomnia caused by MOGAD. This report describes an important case in which hypersomnia caused by hypothalamic lesions with MOGAD were confirmed with the reduction of the orexin level in CSF.…”

“…In addition, several neurological diseases with hypothalamic lesions, central demyelinating diseases, encephalitis, and brain tumors were reported to cause symptomatic narcolepsy 7,16–20 . Lesions surrounding the third ventricles and cerebral aqueduct including the thalamus and hypothalamus have been reported in NMOSD patients and similar lesions have been reported in a small number of patients with MOGAD 3–5 . There has been no report of symptomatic hypersomnia caused by MOGAD.…”

“…MOG‐antibody can sometimes produce radiological findings similar to those of MS and neuromyelitis optica spectrum disorder (NMOSD) 4,5 . MOGAD shares similar characteristics and MRI features with NMOSD; however, sleep arousal disorder has not been reported in MOGAD.…”

Clinical and neuroimaging phenotypes of autoimmune glial fibrillary acidic protein astrocytopathy: A systematic review and meta‐analysis

“…Clinically, GFAP-A shows a resemblance with MOG antibodyassociated disease (MOGAD) and acute disseminated encephalomyelitis (ADEM), with its prodromal state and psychiatric symptoms in conjunction with altered consciousness. Although GFAP-A causes longitudinally extensive myelitis, permanent paraor tetraplegia was seldom reported in GFAP-A, as opposed to AQP4-positive neuromyelitis optica spectrum disorder (NMOSD) [49,50]. Similarly, visual involvement in GFAP-A is typically painless and of a mild character compared to AQP4-positive NMOSD, with only rare cases of long-term visual impairment or blindness [8,33,36].…”