In the evaluation of polyneuropathy (PNP), one of the main goals of the electrophysiological examination is to identify the primary pathophysiology as either axonal or demyelinating due to its important implications for diagnosis, treatment and prognosis. Although several electrophysiological criteria have been suggested for definition of demyelination (Buchthal and Behse 1977, Bromberg 1991, Koski et al. 2009), there is still no consensus . In earlier studies we have shown large variation in interpreting nerve conduction studies as well as classification of PNPs among European physicians (Johnsen et al. 1994, Fuglsang-Frederiksen et al. 1995, Fuglsang-Frederiksen et al. 1999, Tankisi et al. 2003).
Our department has led the development of guidelines in classification of PNPs in collaboration with neurophysiologists from six European countries (Tankisi et al. 2005). We have also shown a more uniform practice among these European neurophysiologists in the pathophysiological classification of PNPs (Pugdahl et al. 2005, Tankisi et al. 2006, Pugdahl et al. 2011).
Broadly speaking, primary demyelination is indicated by reduction in conduction velocity, while primary axonal loss is indicated by decrease in amplitude of the sensory nerve action potential (SNAP) or the compound muscle action potential (CMAP). However, when CMAP amplitudes are markedly reduced, it is often difficult to determine whether amplitude reduction is due to axonal loss or demyelination (Johnsen and Fuglsang-Frederiksen 2000, Tankisi et al. 2007, Fuglsang-Frederiksen and Pugdahl 2011). For improved understanding of the relation between electrophysiological findings and pathophysiology, other parameters such as the correlation between CMAP amplitude and CMAP duration may be of help (Tankisi et al. 2012).
Research in our department also focuses on understanding pathophysiology in especially inflammatory PNPs by use of newer electrophysiological methods such as motor unit number estimation (MUNE) and stimulus response curves.