Editor’s Update and Selected Articles From JNS

By John D. England, MD

John D. England, MD

Readers of the Journal of the Neurological Sciences will soon notice a few changes between the covers. The Editorial Board and I are gradually changing the way in which case reports are handled and published. JNS continues to receive a large number of manuscripts submitted from around the world.

Because of publication limitations, we can accept only a minority of these manuscripts for publication. Although case reports are usually considered reports of “anecdotal” observations, most clinical neurologists find them educational and interesting. Rather than reject all of these case reports, we have decided to publish many of them as “Letters to the Editor.” In this way, we can accommodate them within JNS.

The journal also will be featuring more “editorials” to highlight and enhance important original articles, which will be published simultaneously. These will usually be solicited by invitation from one of the associate editors or me. However, if you are asked to review a manuscript for JNS and believe that an accompanying editorial would be useful, please provide this as a recommendation in your review.

In our ongoing attempt to enhance accessibility of JNS articles to members of the World Federation of Neurology (WFN), we have selected two “free–access” articles, which are profiled in this issue of World Neurology.

In this issue, we feature two paired articles:

1) In the first article, Dennis Paul and colleagues provide new observations about the ubiquitous and important Na⁺-K⁺ ATPase pump. This research team previously documented that inflammation results in an up-regulation of sodium channels (especially Nav1.7) in dorsal root ganglia (DRG). Using the same experimental paradigm, they have now demonstrated that there is a simultaneous up-regulation of the Na⁺-K⁺ ATPase pump. The researchers had hypothesized that this would occur since without an up-regulation of the Na⁺-K⁺ ATPase to pump Na⁺ out of the cells, an increase in Na⁺ influx would lead to an osmotic influx of water. Consequently, the DRG cells would swell and burst. As proof of the protective mechanism provided by an increase in the Na⁺-K⁺ ATPase pump, the authors blocked the activity of the pump with ouabain. This pharmacologic blockade resulted in the swelling and death of the DRG cells which had an inflammation-induced increase in Na⁺ channels. These observations have important implications for the pathophysiology of inflammatory conditions and concomitant neuropathic pain. They may have broader importance for the pathophysiology of other diseases such as diabetes mellitus, which is known to interfere with Na⁺-K⁺ ATPase pump expression and function. Specifically, interference with the function or blockade of the Na⁺-K⁺ ATPase pump might cause premature cell death in susceptible cells. Paul D, Soignier RD, Minor L, Tau H, Singu-Mize E, Gould HJ. Regulation and pharmacological blockade of sodium-potassium ATPase: A novel pathway to neuropathy. J Neurol Sci 2014;340:139-143.

2) In the second article, Craig Stevens provides a thoughtful and comprehensive editorial about the biological importance of the Na⁺-K⁺ ATPase pump. This paper serves as a brief primer on the importance of the Na⁺-K⁺ ATPase pump for maintaining the resting membrane potential and volume in all cells. He also highlights the growing evidence that Na⁺-K⁺ ATPase dysfunction may be involved in several neurological diseases in addition to peripheral neuropathy. Stevens CW. New pathways for an old molecule: The role of the Na+-K+ ATPase pump in peripheral neuropathy. J Neurol Sci 2014;340:3-4.