AANEM Connect

Hi all,
I wanted to ask for community/expert input on how you approach interpretation of distal latency with regards to demyelination, in the setting of severe axonal loss and muscle atrophy?
 
I believe it’s generally accepted that distal latency can be prolonged up to about ~130% of the upper limit of normal in the setting of axonal loss (without implying superimposed demyelination)-- largely due to loss of the fastest fibers.  For more proximal conduction velocities, ~75% of the lower limit of normal is used, which seems roughly commensurate.
 
However, when amplitudes are extremely low (e.g., 0.1 mV for a motor NCS), it seems plausible that other factors (beyond loss of fastest fibers) could cause further latency prolongation (without implying demyelination). Some of these include:
(a) distal collateral sprouting: increased NMJ transmission time
(b) distal collateral sprouting: more slowly conducting immature myelin (and decreased spacing of nodes of Ranvier)
(c) increased electrical transmission time through muscle due to atrophy
(d) inability to accurately measure motor onset latency (only seeing "tip of the iceberg" of the motor response
 
Importantly, it seems to me that all of these factors would affect the terminal portion of the study (distal latency) disproportionately (relative to the more proximal conduction velocity measurements)-- without implying demyelination-- and that these mechanisms bring us beyond what's expected for loss of the fastest fibers. In this context, 130% of the upper-limit-of-normal as a threshold seems too low/lax (might overcall demyelinating disease in the setting of end-stage axonal loss?).  I don't know if this has systematically been explored: the range of latency prolongations expected in extreme axonal loss.  
 
In this context, do you have a threshold for assessing distal latencies potentially concerning for focal demyelination in the setting of extreme axonal loss?  (A relevant clinical application would be looking for evidence of superimposed ulnar neuropathy at the wrist in a patient with established ulnar neuropathy at the elbow with severe and chronic end-stage axonal loss).   
Sandra