BACKGROUND: The objective of this study was to determine whether differentiation between demyelinating and axonal neuropathies could be enhanced by comparing conduction time changes in defined segments of the total peripheral nerve pathway. METHODS: Compound muscle action potentials (CMAPs) were elicited by cathodal stimulation of the tibial nerve at the ankle and popliteal fossa, and by paravertebral neuromagnetic stimulation at proximal and distal cauda equina while recording from muscles of the foot, shin, and thigh. Segmental conduction times were calculated in normal subjects; in patients with lumbosacral radiculopathy, distal symmetric diabetic neuropathy, amyotrophic lateral sclerosis, acute and chronic inflammatory demyelinating polyneuropathy; and in patients with anti-myelin-associated glycoprotein, myelomatous, and Charcot-Marie-Tooth type 1a polyneuropathies. RESULTS: Distal cauda equina latency and CMAP duration and segmental conduction times in upper leg and cauda equina facilitated differentiation of demyelinating from axonal neuropathies, even in the presence of a range of reduced amplitude CMAPs. CONCLUSIONS: Within the demyelinating neuropathy spectrum, it was further possible to distinguish subtypes.
BACKGROUND: The objective of this study was to determine whether differentiation between demyelinating and axonal neuropathies could be enhanced by comparing conduction time changes in defined segments of the total peripheral nerve pathway. METHODS: Compound muscle action potentials (CMAPs) were elicited by cathodal stimulation of the tibial nerve at the ankle and popliteal fossa, and by paravertebral neuromagnetic stimulation at proximal and distal cauda equina while recording from muscles of the foot, shin, and thigh. Segmental conduction times were calculated in normal subjects; in patients with lumbosacral radiculopathy, distal symmetric diabetic neuropathy, amyotrophic lateral sclerosis, acute and chronic inflammatory demyelinating polyneuropathy; and in patients with anti-myelin-associated glycoprotein, myelomatous, and Charcot-Marie-Tooth type 1a polyneuropathies. RESULTS: Distal cauda equina latency and CMAP duration and segmental conduction times in upper leg and cauda equina facilitated differentiation of demyelinating from axonal neuropathies, even in the presence of a range of reduced amplitude CMAPs. CONCLUSIONS: Within the demyelinating neuropathy spectrum, it was further possible to distinguish subtypes.
Authors: Vera Bril; Christopher M Blanchette; Joshua M Noone; M Chris Runken; Deborah Gelinas; James W Russell Journal: J Diabetes Complications Date: 2016-05-10 Impact factor: 2.852