**3. Neuromyelitis optica spectrum disorder (NMOSD)**

Neuromyelitis optica spectrum disorders (NMOSD) is another member of the neuroinflammatory diseases category. Compared with MS, it is more of an antibody-based astrocytopathy. The guilt is on antiaquaporine4, an autoantibody against water channels that are mostly found in special areas of the CNS. This nonprogressive, relapsing condition could trigger necrotizing attacks on the brain, optic nerves, or spinal cord. Brainstem involvement is common. Therefore, deglutition difficulties are expected, but it seems to be rare.

Dysphagia in these patients could be the manifestation of an acute attack, and even the presenting symptom [40, 41]. It is significantly associated with lesions in the brainstem and specially medulla oblongata. In a study by Wang et al. of 170 NMOSD patients, 15 experienced dysphagia most of whom had medullary lesions. It is speculated that involvement of nucleus ambiguous, nucleus tractus solitarius, or dorsal vagus nucleus may be responsible [42]. It also can be a sign of cerebral involvement in the absence of other evidence [43, 44]. In seven NMO patients reported by Pawlitzki et al., five showed degrees of dysphagia, mostly mild to moderate. All had brainstem or high cervical lesions. Here again, FEES could be of great help in diagnosing subtle cases [43]. As in MS, NMO cases with dysphagia have problems with swallowing both solid food and liquids [6].

The fundamentals of diagnosis and treatment of dysphagia in this population are like MS. However, as the attacks are necrotizing, no time should be lost before initiating immune therapy. The only available disease-modifying treatments in NMOSD are anti CD20s (rituximab, satralizumab, eculizumab). The chosen option should be started as soon as possible after initial relapse treatment.

#### **4. Myelin oligodendrocyte glycoprotein antibody disease (MOGAD)**

Another autoimmune demyelinating disease is MOGAD. The antibody was discovered about 40 years ago [45] but its clinical relevance was found years

later [46]. There are doubts about the pathogenicity of the anti-MOG antibody but still, it is the best available biomarker of the disease to date [47]. The clinical manifestations of MOGAD overlap with NMOSD (optic neuritis, spinal lesion, brainstem involvement), although with some differences. Cortical lesions are more prevalent in MOGAD. Astrocytes are hypertrophic and reactive, not dystrophic compared with NMOSD. Besides, there is no aquaporin4 loss [47]. Acute disseminated encephalomyelitis (ADEM) like presentation is common among children with the disease [48]. It could be monophasic (70–80% in children) or relapsing. In monophasic cases, the antibody tends to become undetectable over 12 months, so follow-up is recommended [47]. The mainstay of the treatment is anti-inflammatory drugs like steroids in the acute phase and anti CD20s as maintenance treatment.

As a rare entity, there are not many reports on specific symptoms like swallowing difficulties. However, considering the CNS involvement (especially with cortical and brainstem lesions) dysphagia is expected. Of 50 patients in a European cohort of Caucasian MOGAD cases, 15 had brainstem involvement. Of these only two complained of dysphagia besides other symptoms [49]. As in NMOSD, brain involvement in MOGAD may only present with dysphagia detected by FEES [43].
