Axon injury in the peripheral nervous system (PNS) induces a regeneration-associated gene (RAG) response. Atf3 (activating transcription factor 3) is such a RAG and ATF3's transcriptional activity might induce ‘effector’ RAGs (e.g. small proline rich protein 1a (Sprr1a), Galanin (Gal), growth-associated protein 43 (Gap43)) facilitating peripheral axon regeneration. We provide a first analysis of Atf3 mouse mutants in peripheral nerve regeneration. In Atf3 mutant mice, facial nerve regeneration and neurite outgrowth of adult ATF3-deficient primary dorsal root ganglia neurons was decreased. Using genome-wide transcriptomics, we identified a neuropeptide-encoding RAG cluster (vasoactive intestinal peptide (Vip), Ngf, Grp, Gal, Pacap) regulated by ATF3. Exogenous administration of neuropeptides enhanced neurite growth of Atf3 mutant mice suggesting that these molecules might be effector RAGs of ATF3's pro-regenerative function. In addition to the induction of growth-promoting molecules, we present data that ATF3 suppresses growth-inhibiting molecules such as chemokine (C-C motif) ligand 2. In summary, we show a pro-regenerative ATF3 function during PNS nerve regeneration involving transcriptional activation of a neuropeptide-encoding RAG cluster. ATF3 is a general injury-inducible factor, therefore ATF3-mediated mechanisms identified herein might apply to other cell and injury types.

A thorough knowledge of the anatomy of the vulnerable nerves and of variants in their course can lessen the risk of iatrogenic nerve injury. When such injuries arise, early diagnosis and planning of further management are the main determinants of outcome. If adequate nerve regeneration does not occur, surgical revision should optimally be performed 3 to 4 months after the injury, and 6 months afterward at the latest. On the other hand, if postoperative high resolution ultrasound reveals either complete transection of the nerve or a neuroma in continuity, surgery should be performed without any further delay. If the surgeon becomes aware of a nerve transection during the initial procedure, then either immediate end-to-end suturing or early secondary management after three weeks is indicated.

High-resolution ultrasonography is a noninvasive, readily applicable imaging modality, capable of depicting real-time static and dynamic morphological information concerning the peripheral nerves and their surrounding tissues. Continuous progress in ultrasonographic technology results in highly improved spatial and contrast resolution. Therefore, nerve imaging is possible to a fascicular level, and most peripheral nerves can now be depicted along their entire anatomical course. An increasing number of publications have evaluated the role of high-resolution ultrasonography in peripheral nerve diseases, especially in peripheral nerve entrapment. Ultrasonography has been shown to be a precious complementary tool for assessing peripheral nerve lesions with respect to their exact location, course, continuity, and extent in traumatic nerve lesions, and for assessing nerve entrapment and tumors. In this article, the authors discuss the basic technical considerations for using ultrasoniography in peripheral nerve assessment, and some of the clinical applications are illustrated.

• MR neurography (MRN) can aid the diagnosis of thoracic outlet syndrome (TOS). • Identifiable causes of TOS in MRN include fibrous bands and bony anomalies. • Increased T2W signal within brachial plexus elements indicate relevant nerve compression. • High positive predictive value allows confident and targeted indication for surgery.

Glucose deprivation strongly affected NP cell metabolism. The effects of an altered glucose supply on gene expression were more pronounced than the mechanically induced effects. Data in this study demonstrate that the glucose environment is more critical for disc cell metabolism than mechanical loads. In individual human donors, however, adequate mechanical stimuli might have a beneficial effect on matrix turnover during IVD degeneration.