Isolated dysphagia due to aquaporin-4 autoimmunity

Türkoğlu, Recai; Kıyat-Atamer, Aslı; Tüzün, Erdem; Akman‐Demir, Gülşen

doi:10.4318/tjg.2012.0437

Cited by 4 publications

(2 citation statements)

References 5 publications

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“…The dysphagia was thought due to the involvement of the nucleus ambiguous, which is more ventrally located than the area postrema. This case highlights that the spectrum of NMO brainstem symptoms are not necessarily confined to the dorsal medulla, but may extend ventrally (104). …”

Section: Anatomical Distribution Of Nmo Lesions In the Cnsmentioning

confidence: 91%

The Pathology of an Autoimmune Astrocytopathy: Lessons Learned from Neuromyelitis Optica

et al. 2013

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Neuromyelitis optica (NMO) is a disabling autoimmune astrocytopathy characterized by typically severe and recurrent attacks of optic neuritis and longitudinally-extensive myelitis. Until recently, NMO was considered an acute aggressive variant of multiple sclerosis (MS), despite the fact that early studies postulated that NMO and MS may be two distinct diseases with a common clinical picture. With the discovery of a highly specific serum autoantibody (NMO-IgG), Lennon and colleagues provided the first unequivocal evidence distinguishing NMO from MS and other CNS inflammatory demyelinating disorders. The target antigen of NMO-IgG was confirmed to be aquaporin-4 (AQP4), the most abundant water channel protein in the central nervous system (CNS), mainly expressed on astrocytic foot processes at the blood brain barrier, subpial and subependymal regions. Pathological studies demonstrated that astrocytes were selectively targeted in NMO as evidenced by the extensive loss of immunoreactivities for the astrocytic proteins, AQP4 and glial fibrillary acidic protein (GFAP), as well as perivascular deposition of immunoglobulins and activation of complement even within lesions with a relative preservation of myelin. In support of these pathological findings, GFAP levels in the cerebrospinal fluid (CSF) during acute NMO exacerbations were found to be remarkably elevated in contrast to MS where CSF-GFAP levels did not substantially differ from controls. Additionally, recent experimental studies showed that AQP4 antibody is pathogenic, resulting in selective astrocyte destruction and dysfunction in vitro, ex vivo, and in vivo. These findings strongly suggest that NMO is an autoimmune astrocytopathy where damage to astrocytes exceeds both myelin and neuronal damage. This chapter will review recent neuropathological studies that have provided novel insights into the pathogenic mechanisms, cellular targets, as well as the spectrum of tissue damage in NMO.

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Section: Anatomical Distribution Of Nmo Lesions In the Cnsmentioning

confidence: 91%

The Pathology of an Autoimmune Astrocytopathy: Lessons Learned from Neuromyelitis Optica

et al. 2013

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“…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.…”

Section: Neuromyelitis Optica Spectrum Disorder (Nmosd)mentioning

confidence: 98%

Dysphagia in Neuroinflammatory Diseases of the Central Nervous System

Ghadiri¹,

Moghadasi²

2022

Dysphagia - New Advances

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Neuroinflammatory disorders of the central nervous system (CNS) consist of a relatively heterogeneous group of diseases that share the autoimmune activity against different parts of the system. Swallowing problems could happen in many of these cases. Its effect on the patients’ quality of life is undeniable. It could be an important cause of morbidity and mortality. Detailed medical history and physical exam are important. Several questionnaires could help monitor dysphagia. Radiographic and endoscopic evaluations may be necessary to detect overlooked swallowing problems. The main treatment appears to be treating the underlying disease, besides general supplementary options like rehabilitation and speech therapy.

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Comparative clinical characteristics of neuromyelitis optica spectrum disorders with and without medulla oblongata lesions

Wang

Zhang

et al. 2014

J Neurol

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Brainstem involvement, especially the medulla oblongata (MO), has been reported in neuromyelitis optica spectrum disorders (NMOSDs). The purpose of this study was to investigate retrospectively and compare clinical, laboratory, and imaging features of NMOSDs with and without MO lesions. A total of 170 patients with NMOSDs were enrolled, including 44 patients with MO lesions and 126 patients without MO lesions. Clinical features, laboratory tests, and magnetic resonance imaging findings among these patients were assessed. MO lesions were found in 25.9 % of the NMOSDs patients. The mean duration was 13 months. Patients with MO lesions had a higher Annualized relapse rate and Expanded Disability Status Score Scale. Headache, dizziness, nystagmus, dysarthria, intractable hiccup and nausea, choking cough or dysphagia, movement disorders, and neuropathic pain were more common in MO lesion patients. Patients with MO lesions were more frequently complicated with thyroid diseases. Multiple brain involvement, More importantly, Longitudinally extensive transverse myelitis were more frequently found in patients with MO lesions. MO lesions might be a symbol of more severe neurologic deficits and worse prognosis of NMOSDs.

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Isolated dysphagia due to aquaporin-4 autoimmunity

Cited by 4 publications

References 5 publications

The Pathology of an Autoimmune Astrocytopathy: Lessons Learned from Neuromyelitis Optica

The Pathology of an Autoimmune Astrocytopathy: Lessons Learned from Neuromyelitis Optica

Dysphagia in Neuroinflammatory Diseases of the Central Nervous System

Comparative clinical characteristics of neuromyelitis optica spectrum disorders with and without medulla oblongata lesions

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