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It consists of pain perception of a previously amputated limb. The exact pain mechanism is disputed and includes mechanisms involving cerebral, peripheral, and spinal origins. Such controversy limits researchers' and clinicians' ability to develop consistent therapeutics or management. Neuroimaging is an essential tool that can address this problem. This review explores diffusion tensor imaging, functional magnetic resonance imaging, electroencephalography, and magnetoencephalography in the context of PLP. These imaging modalities have distinct mechanisms, implications, applications, and limitations. Diffusion tensor imaging can outline structural changes and has surgical applications. Functional magnetic resonance imaging captures functional changes with spatial resolution and has therapeutic applications. Electroencephalography and magnetoencephalography can identify functional changes with a strong temporal resolution. Each imaging technique provides a unique perspective and they can be used in concert to reveal the true nature of PLP. Furthermore, researchers can utilize the respective strengths of each neuroimaging technique to support the development of innovative therapies. PLP exemplifies how neuroimaging and clinical management are intricately connected. This review can assist clinicians and researchers seeking a foundation for applications and understanding the limitations of neuroimaging techniques in the context of PLP.

C39X and C44X channel proteins are trafficking defective. We show that C39X and C44X channels undergo translation reinitiation at M60 which deletes the hERG N-terminus including the first 34 residues of the Per, Arnt, and Sim (PAS) domain. In contrast to the reinitiation of Q81X channels at M124, in which the PAS domain is nearly completely deleted, reinitiation at M60 disrupts the folding of this highly structured domain, precluding the efficient folding and trafficking of the mutant channels. The RNase protection assay, western blot analysis and electrophysiology were used to characterize the LQT2 mutants at the RNA, protein, and functional level. Our findings indicate that translation reinitiation may give rise to trafficking as well as functional defects of mutant hERG channels associated with LQT2 nonsense mutations.

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