Terminal latency index in neuropathy with antibodies against myelin‐associated glycoproteins
Abstract 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...
| Published in: | Muscle & Nerve |
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| Main Authors: | , , , , , |
| Format: | Article in Journal/Newspaper |
| Language: | English |
| Published: |
Wiley
2007
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| Subjects: | |
| Online Access: | http://dx.doi.org/10.1002/mus.20678 https://api.wiley.com/onlinelibrary/tdm/v1/articles/10.1002%2Fmus.20678 https://onlinelibrary.wiley.com/doi/pdf/10.1002/mus.20678 |
| Summary: | Abstract 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 TLI <0.26 had MAG/SGPG‐N, and all patients with TLI ≥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. Muscle Nerve, 2006 |
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