g(m1)-ganglioside and Sensation-Disorders

Antiganglioside antibodies are found in various neurological disorders that constitute a continuum from peripheral neuropathy to encephalitis. However, nystagmus has rarely been described in patients with ataxia associated with antiganglioside antibodies.. From January 2008 to July 2009, we identified 3 patients with acute ataxia and nystagmus in 2 University Hospitals of Korea, who were found to have anti-GD1b, anti-GM1, or anti-GQ1b antibodies.. In addition to acute ataxia, all 3 patients showed various combinations of nystagmus, which included central positional nystagmus (n = 3), vertical nystagmus (n = 1), and periodic alternating nystagmus (n = 1). The spontaneous and positional nystagmus were mostly detectable only with the elimination of fixation and magnification of the eyes using video goggles. Two patients also exhibited gaze-evoked nystagmus that was noticeable without the aid of video goggles. Patients had serum IgG antibodies to GD1b, GM1, or GQ1b. Cerebrospinal fluid examination, nerve conduction studies, and brain MRI were normal. In all patients, the symptoms and signs resolved over 3-12 months.. Various forms of nystagmus with acute ataxia may be a sole or predominant manifestation of disorders related to antiganglioside antibodies. The nystagmus indicates a central pathology involving the cerebellum or brainstem in this antibody-associated disorder. Antiganglioside antibodies should be measured in patients with nystagmus and acute ataxia of undetermined etiology.

Topics: Acute Disease; Adolescent; Adult; Ataxia; Autoantibodies; Autoantigens; Autoimmune Diseases; Cerebrospinal Fluid; Dizziness; Enzyme-Linked Immunosorbent Assay; Female; G(M1) Ganglioside; Gangliosides; Humans; Immunoglobulin G; Male; Nystagmus, Pathologic; Postural Balance; Sensation Disorders; Vertigo

Tumor necrosis factor-alpha (TauNuFalpha) blockers are effective in the treatment of inflammatory arthritis but can induce autoimmune disorders including multiple sclerosis. Described are two patients who developed chronic inflammatory demyelinating polyneuropathy after initiation of anti-TNFalpha treatment.

Topics: Aged; Antibodies, Monoclonal; Antirheumatic Agents; Arthritis, Rheumatoid; Autoantibodies; Etanercept; Female; G(M1) Ganglioside; Humans; Immunoglobulin G; Infliximab; Male; Middle Aged; Muscle Weakness; Neural Conduction; Peripheral Nerves; Polyradiculoneuropathy, Chronic Inflammatory Demyelinating; Receptors, Tumor Necrosis Factor; Recovery of Function; Sensation Disorders; Spondylitis, Ankylosing; Tumor Necrosis Factor-alpha