Amplitude-dependent slowing of conduction in amyotrophic lateral sclerosis and polyneuropathy

✍ Scribed by Daniel M. Feinberg; David C. Preston; Jeremy M. Shefner; Eric L. Logigian

• Publisher: John Wiley and Sons
• Year: 1999
• Tongue: English
• Weight: 97 KB
• Volume: 22
• Category: Article
• ISSN: 0148-639X
• DOI: 10.1002/(sici)1097-4598(199907)22:7<937::aid-mus19>3.0.co;2-6

✦ Synopsis

The mechanism of motor nerve conduction slowing in amyotrophic lateral sclerosis (ALS) is thought primarily to be loss of large, fastconducting motor fibers; this is less certain in axonal polyneuropathy. We compared motor conduction studies in 64 patients with axonal polyneuropathy with 72 patients with ALS. Compound motor action potential amplitude, distal motor latency, and conduction velocity were converted to a percentage of the upper or lower limit of normal and then represented as a square root (SQRT) transformation, plotted with SQRT amplitude as the independent variable and SQRT latency or SQRT conduction velocity as the dependent variables. Regression analysis of the lower extremity nerve data showed that prolongation of latency and slowing of velocity were amplitudedependent and were virtually identical in ALS and polyneuropathy. In the upper extremity, amplitude-dependent prolongation of latency was similar in both groups, but amplitude-dependent slowing of velocity was seen in ALS and not in axonal polyneuropathy. Our data support the hypothesis that the major mechanism of slowing is similar in both polyneuropathy and ALS and is the loss of large, fast-conducting fibers. However, the presence of distal but not proximal slowing in the upper extremity of axonal polyneuropathy suggests that additional mechanisms may be contributory.