Terminal latency index in neuropathy with antibodies against myelin-associated glycoproteins
Autor: | Jim Dambrosia, Vitalie D. Lupu, Marinos C. Dalakas, Jacob Meer, Mary Kay Floeter, Carlos A. Mora |
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Rok vydání: | 2006 |
Předmět: |
Adult
Male medicine.medical_specialty Pathology Physiology Neural Conduction Action Potentials Electromyography Antibodies Central nervous system disease Cellular and Molecular Neuroscience Myelin Degenerative disease Charcot-Marie-Tooth Disease Physiology (medical) Immunopathology medicine Reaction Time Humans Latency (engineering) Ulnar Nerve Aged Myelin-associated glycoprotein medicine.diagnostic_test business.industry Peripheral Nervous System Diseases Middle Aged medicine.disease Surgery Median Nerve Myelin-Associated Glycoprotein medicine.anatomical_structure nervous system Female Neurology (clinical) business Polyneuropathy |
Zdroj: | Musclenerve. 35(2) |
ISSN: | 0148-639X |
Popis: | Neuropathy with antibodies against myelin-associated glycoproteins (MAG/SGPG-N) and hereditary sensorimotor neuropathy type 1 (HMSN1) are characterized by chronic demyelination with little conduction block. Electrodiagnostic studies suggest that in HMSN1 conduction slowing occurs uniformly along the nerve, whereas in MAG/SGPG-N it is predominantly distal. Some but not all previous reports have shown that the terminal latency index (TLI) was useful to distinguish MAG/SGPG-N from chronic idiopathic demyelinating polyneuropathy. We compared median TLI from 21 patients with MAG/SGPG-N with those obtained from 26 patients with HMSN1, 20 with HMSN2, and 12 healthy volunteers. All patients with TLI0.26 had MAG/SGPG-N, and all patients with TLIor =0.32 had HMSN1. In the remaining patients with intermediate TLI values, ulnar distal motor latency (DML) aided in differentiation between MAG/SGPG-N and HMSN1 with an overall sensitivity of 100% and specificity of 98%. In conclusion, median TLI in combination with ulnar DML can further guide the demyelinating neuropathy evaluation toward hereditary or autoimmune causes. |
Databáze: | OpenAIRE |
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