title: Motor conduction parameters in neuropathies associated with anti-MAG antibodies and other types of demyelinating and axonal neuropathies.
abstract: We measured residual latency (RL), motor conduction velocity (MCV), and terminal latency index (TLI) in 15 patients with neuropathy and anti-MAG or SGPG antibodies and compared these to values obtained in 103 patients with other types of polyneuropathy (PN) and to 57 normal subjects. Ten patients had anti-MAG antibody titers of 25,600 or higher, and 5 had titers between 800 and 12,600. Patients with the highest titers had longer RL, slower MCV and shorter TLI than those with lower titers, acute or chronic inflammatory demyelinating PN, hereditary neuropathy, and metabolic or axonal neuropathy. In contrast F-wave latencies did not contribute to the differentiation between the groups of demyelinating neuropathies. RL and TLI correlated best with anti-MAG antibody titers, whereas there was a poor correlation with anti-SGPG titers suggesting that MAG more than SGPG may be the antigen in PN, and that the distal nerves are affected more than their proximal segments. The RL rather than TLI turned out to be the best variable to classify the demyelinating type of anti-MAG neuropathy. Sural nerve biopsy in 5 of the patients with the highest titer of anti-MAG antibodies showed deposits of IgM and C3 on the myelin sheaths, pronounced demyelination and widening of the myelin lamellae. In 4 of the patients with lower titers demyelination was absent or less pronounced.
authors.affiliation: Department of Neurology, Columbia Presbyterian Hospital, New York, New York, USA.
authors.forename: W
authors.initials: W
authors.lastname: Trojaborg
authors.forename: A P
authors.initials: AP
authors.lastname: Hays
authors.forename: L
authors.initials: L
authors.lastname: van den Berg
authors.forename: D S
authors.initials: DS
authors.lastname: Younger
authors.forename: N
authors.initials: N
authors.lastname: Latov
mesh_terms: D000208:Acute Disease; D001323:Autoantibodies / Q000097:blood*; D001369:Axons / Q000502:physiology*; D001706:Biopsy; D002607:Charcot-Marie-Tooth Disease / Q000276:immunology / Q000473:pathology / Q000503:physiopathology*; D002908:Chronic Disease; D003711:Demyelinating Diseases / Q000276:immunology / Q000473:pathology / Q000503:physiopathology*; D003929:Diabetic Neuropathies / Q000276:immunology / Q000503:physiopathology*; D004797:Enzyme-Linked Immunosorbent Assay; D005915:Globosides / Q000276:immunology*; D006801:Humans; D007075:Immunoglobulin M / Q000097:blood; D009046:Motor Neurons / Q000502:physiology*; D009185:Myelin Proteins / Q000276:immunology*; D018992:Myelin-Associated Glycoprotein; D009431:Neural Conduction; D010525:Peripheral Nerves / Q000473:pathology / Q000503:physiopathology; D013497:Sural Nerve / Q000473:pathology / Q000503:physiopathology
chemical_list: D001323:Autoantibodies; D005915:Globosides; D007075:Immunoglobulin M; D009185:Myelin Proteins; D018992:Myelin-Associated Glycoprotein; C051917:sulfate-3-glucuronyl paragloboside