2005
DOI: 10.1016/j.clinph.2005.04.003
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Pathophysiology inferred from electrodiagnostic nerve tests and classification of polyneuropathies. Suggested guidelines

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Cited by 129 publications
(104 citation statements)
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“…For this purpose, the amplitude and latency of the sensory (sural) and motor (proneal and tibial) nerves were recorded. The motor or sensory nerve conduction velocity of 39 m/s was adopted as the lower limit (cutoff value: below average = 2 standard deviation [SD] of the normal range) [16,33].…”
Section: Assessments and Measurementsmentioning
confidence: 99%
“…For this purpose, the amplitude and latency of the sensory (sural) and motor (proneal and tibial) nerves were recorded. The motor or sensory nerve conduction velocity of 39 m/s was adopted as the lower limit (cutoff value: below average = 2 standard deviation [SD] of the normal range) [16,33].…”
Section: Assessments and Measurementsmentioning
confidence: 99%
“…This reflects the challenge in distinguishing secondary axonal degeneration from segmental demyelination in patients with CIDP by measuring dCMAP amplitudes in conventional NCSs as both pathologies could result in decreased dCMAP amplitudes (Harbo et al., 2008; Kuwabara et al., 2006, 2002; Tankisi et al., 2005, 2007). Based on this perspective, MUS should be considered as a complementary tool for NCSs in patients with CIDP as it can detect axonal degeneration by assessing muscle structural changes due to denervation.…”
Section: Discussionmentioning
confidence: 99%
“…, 2008; Tankisi, Pugdahl, Johnsen, & Fuglsang‐Frederiksen, 2007 ; Tankisi et al. , 2005). In nerve conduction studies (NCSs), not only axonal degeneration but also conduction block or increased temporal dispersion due to segmental demyelination result in decreased compound muscle action potential (CMAP) amplitude (Harbo et al.…”
Section: Introductionmentioning
confidence: 99%
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“…In addition to direct, physicochemical effects, such as trapping and cross-linking of macromolecules, AGEs exert indirect, biological effects, mediated by cell surface receptors. RAGE, whose expression is positively regulated by AGEs (26), is the prototypic AGE receptor mediating AGE-induced tissue injury via induction of reactive oxygen species formation and activation of redoxsensitive signaling pathways, and CML is a major RAGE ligand (27). The finding that, despite a comparable, dramatic degree of skin denervation, patients in the KI-s groups showed a significant reduction in RAGE expression (associated with a nonsignificant decrease in CML content) in nerves and vasa nervorum compared with KD patients, supports a role for the downregulation of the AGE-RAGE pathway as a molecular mechanism underlying the improvement of neuropathy observed after successful islet transplantation.…”
Section: Limitations Of the Studymentioning
confidence: 99%