“…Anakinra, an IL-1 receptor blocker, had also shown mild short-term improvements in a subset of patients in the first series [ 27 ] and in a later study of 15 patients [ 28 ]. Because of the common presence of a cricopharyngeal bar, invasive procedures including balloon dilatation and myotomy can lead to improvement of symptoms in patients with serious dysphagia and weight loss prior to PEG insertion [ 20 , 29 – 33 ], although this effect was not long lasting after 5 years [ 17 ]. In our experience, Botox injections have not been helpful.…”
Section: Autoimmune Neurological Disorders With Dysphagiamentioning
Autoimmune neurogenic dysphagia refers to manifestation of dysphagia due to autoimmune diseases affecting muscle, neuromuscular junction, nerves, roots, brainstem, or cortex. Dysphagia is either part of the evolving clinical symptomatology of an underlying neurological autoimmunity or occurs as a sole manifestation, acutely or insidiously. This opinion article reviews the autoimmune neurological causes of dysphagia, highlights clinical clues and laboratory testing that facilitate early diagnosis, especially when dysphagia is the presenting symptom, and outlines the most effective immunotherapeutic approaches. Dysphagia is common in inflammatory myopathies, most prominently in inclusion body myositis, and is frequent in myasthenia gravis, occurring early in bulbar-onset disease or during the course of progressive, generalized disease. Acute-onset dysphagia is often seen in Guillain–Barre syndrome variants and slowly progressive dysphagia in paraneoplastic neuropathies highlighted by the presence of specific autoantibodies. The most common causes of CNS autoimmune dysphagia are demyelinating and inflammatory lesions in the brainstem, occurring in patients with multiple sclerosis and neuromyelitis optica spectrum disorders. Less common, but often overlooked, is dysphagia in stiff-person syndrome especially in conjunction with cerebellar ataxia and high anti-GAD autoantibodies, and in gastrointestinal dysmotility syndromes associated with autoantibodies against the ganglionic acetyl-choline receptor. In the setting of many neurological autoimmunities, acute-onset or progressive dysphagia is a potentially treatable condition, requiring increased awareness for prompt diagnosis and early immunotherapy initiation.
“…Anakinra, an IL-1 receptor blocker, had also shown mild short-term improvements in a subset of patients in the first series [ 27 ] and in a later study of 15 patients [ 28 ]. Because of the common presence of a cricopharyngeal bar, invasive procedures including balloon dilatation and myotomy can lead to improvement of symptoms in patients with serious dysphagia and weight loss prior to PEG insertion [ 20 , 29 – 33 ], although this effect was not long lasting after 5 years [ 17 ]. In our experience, Botox injections have not been helpful.…”
Section: Autoimmune Neurological Disorders With Dysphagiamentioning
Autoimmune neurogenic dysphagia refers to manifestation of dysphagia due to autoimmune diseases affecting muscle, neuromuscular junction, nerves, roots, brainstem, or cortex. Dysphagia is either part of the evolving clinical symptomatology of an underlying neurological autoimmunity or occurs as a sole manifestation, acutely or insidiously. This opinion article reviews the autoimmune neurological causes of dysphagia, highlights clinical clues and laboratory testing that facilitate early diagnosis, especially when dysphagia is the presenting symptom, and outlines the most effective immunotherapeutic approaches. Dysphagia is common in inflammatory myopathies, most prominently in inclusion body myositis, and is frequent in myasthenia gravis, occurring early in bulbar-onset disease or during the course of progressive, generalized disease. Acute-onset dysphagia is often seen in Guillain–Barre syndrome variants and slowly progressive dysphagia in paraneoplastic neuropathies highlighted by the presence of specific autoantibodies. The most common causes of CNS autoimmune dysphagia are demyelinating and inflammatory lesions in the brainstem, occurring in patients with multiple sclerosis and neuromyelitis optica spectrum disorders. Less common, but often overlooked, is dysphagia in stiff-person syndrome especially in conjunction with cerebellar ataxia and high anti-GAD autoantibodies, and in gastrointestinal dysmotility syndromes associated with autoantibodies against the ganglionic acetyl-choline receptor. In the setting of many neurological autoimmunities, acute-onset or progressive dysphagia is a potentially treatable condition, requiring increased awareness for prompt diagnosis and early immunotherapy initiation.
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