This definition appears very rarely
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Our patient presented with the syndrome of chronic ataxic neuropathy with ophthalmoplegia IgM paraprotein, cold agglutinins and anti‐GD1b disialosyl antibodies (CANOMAD). His disturbance of eye movements comprised A pattern exotropia and convergence movements with upward saccades, including convergence nystagmus. Thus the clinical presentation (see video clip; the video clip can be viewed on the J Neurol Neurosurg Psychiatry website at http://www.
Fisher syndrome and ataxic GBS are more strongly associated with IgG anti-GQ1b and anti-GT1a than with anti-GD1b antibodies, whereas the association is reversed in the case of acute sensory ataxic neuropathy. Chronic ataxic neuropathy with disialosyl antibodies is associated with IgM paraprotein to GD1b and GQ1b, which occasionally reacts with GT1a. The clinical, electrophysiological, and pathological features, along with experimental findings, suggest that acute and chronic ataxic neuropathies with disialosyl antibodies form a continuous clinical and pathophysiological spectrum characterized by a complement-mediated disruption at the nodal region and are better classified in the new category of nodo-paranodopathies.
CANOMAD stands for Chronic Ataxic Neuropathy Ophtalmoplegia IgM paraprotein Cold Agglutinins Disialosyl antibodies. Signs and symptoms of CANOMAD may include loss of muscle, tendon, and joint sensation, abnormal gait (walk), ataxia, tingling sensation on the skin around the mouth or extremities, paralysis of eye muscles, difficulty swallowing and speaking, and rarely respiratory muscle weakness. This condition is caused by the presence of anti-diasialosyl antibodies in the body.
Chronic sensory ataxic neuropathy with anti-dyalosyl IgM antibodies symptoms, causes, diagnosis, and treatment information for Chronic sensory ataxic neuropathy with anti-dyalosyl IgM antibodies (CANOMAD syndrome) with alternative diagnoses, full-text book chapters, misdiagnosis, research treatments, prevention, and prognosis.
In 17 out of 18 cases, the serum contained benign IgM paraproteins, and in four of these cases at least two IgM paraproteins were present. The IgM antibodies were also cold agglutinins in 50% of cases. The clinical picture comprised a chronic neuropathy with marked sensory ataxia and areflexia, and with relatively preserved motor function in the limbs. In addition, 16 out of 18 cases had motor weakness affecting oculomotor and bulbar muscles as fixed or as relapsing-remitting features. When present in their entirety, these clinical features have been described previously under the acronym CANOMAD: chronic ataxic neuropathy.