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Igor Papalia, Aurelio Cardaci, Francesco Stagno d'Alcontres, Jennifer M. Lee, Pierluigi Tos and Stefano Geuna


The authors of other studies have reported that the selection of an agonistic donor nerve is required for recovering voluntary motor control after end-to-side nerve repair. In this experimental investigation, the authors' goal was to verify this assumption by performing end-to-side neurorrhaphy of the rat median nerve on its antagonistic radial nerve.


The left median nerve in 10 adult female rats was repaired by end-to-side neurorrhaphy after epineuriotomy on the radial nerve at the middle of the brachium. The time course of median nerve functional recovery was then assessed using the grasping test until postoperative Week 30. Before removing the nerve, the surgical site was carefully explored to exclude contamination by the proximal nerve stump, and the functional anatomy of median and radial nerves was assessed by electrical stimulation. Repaired nerves were then processed for resin embedding, and semithin sections were obtained for nerve fiber histomorphometry by using the dissector method.


Repaired median nerves were repopulated by nerve fibers regenerating from the radial donor nerve as previously shown. Moreover, voluntary motor control of the flexor muscles innervated by the median nerve was progressively recovered beginning in postoperative Week 10 and reaching 42% of normal by Week 30.


Contrary to previously reported data, recovery of voluntary motor function after end-to-side nerve repair can also be expected when an antagonistic nerve is used as a donor nerve.

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Luca Basaldella, Enrico Orvieto, Angelo Paolo Dei Tos, Mila Della Barbera, Marialuisa Valente and Pierluigi Longatti

✓Arachnoid cysts are frequent incidental findings on neuroimaging studies and in clinical practice. Theories of their origin, still matter for debate, compose four categories: 1) a ball-valve mechanism; 2) an osmotic gradient between the intra- and extracystic medium; 3) primary malformation of the arachnoid membrane or cerebral lobe agenesis; and 4) fluid hypersecretion by the lining cells of the cyst wall. The cause of cyst enlargement is also debatable, although there is strong controversial evidence supporting the last two theories rather than the former. Brain water homeostasis and its regulatory pathways are weakly understood at the molecular level. In this brief report the authors attempt to add new insights into the pathogenesis of arachnoid cysts by considering aquaporin expression in the cyst wall and discuss possible future research directions and molecular targets.

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Giulia Ronchi, Michele Cillino, Giovanna Gambarotta, Benedetta Elena Fornasari, Stefania Raimondo, Pierfrancesco Pugliese, Pierluigi Tos, Adriana Cordova, Francesco Moschella and Stefano Geuna


Multiple factors may affect functional recovery after peripheral nerve injury, among them the lesion site and the interval between the injury and the surgical repair. When the nerve segment distal to the lesion site undergoes chronic degeneration, the ensuing regeneration (when allowed) is often poor. The aims of the current study were as follows: 1) to examine the expression changes of the neuregulin 1/ErbB system during long-term nerve degeneration; and 2) to investigate whether a chronically denervated distal nerve stump can sustain nerve regeneration of freshly axotomized axons.


This study used a rat surgical model of delayed nerve repair consisting of a cross suture between the chronically degenerated median nerve distal stump and the freshly axotomized ulnar proximal stump. Before the suture, a segment of long-term degenerated median nerve stump was harvested for analysis. Functional, morphological, morphometric, and biomolecular analyses were performed.


The results showed that neuregulin 1 is highly downregulated after chronic degeneration, as well as some Schwann cell markers, demonstrating that these cells undergo atrophy, which was also confirmed by ultrastructural analysis. After delayed nerve repair, it was observed that chronic degeneration of the distal nerve stump compromises nerve regeneration in terms of functional recovery, as well as the number and size of regenerated myelinated fibers. Moreover, neuregulin 1 is still downregulated after delayed regeneration.


The poor outcome after delayed nerve regeneration might be explained by Schwann cell impairment and the consequent ineffective support for nerve regeneration. Understanding the molecular and biological changes occurring both in the chronically degenerating nerve and in the delayed nerve repair may be useful to the development of new strategies to promote nerve regeneration. The results suggest that neuregulin 1 has an important role in Schwann cell activity after denervation, indicating that its manipulation might be a good strategy for improving outcome after delayed nerve repair.