ABSTRACT
Purpose: To investigate multidimensional pain intensity and quality after collagenase Clostridium histolyticum (CCH) injection in patients with Dupuytren contracture using a pain visual analog scale (VAS) and the revised version of the Short-Form McGill Pain Questionnaire (SF-MPQ-2). Methods: This prospective observational study was carried out from 2015 to 2017. As a primary end point, patients completed the pain VAS (range, 0 [no pain] to 100) and SF-MPQ-2 before and after CCH injection; 3, 9, and 24 hours after CCH injection; after the extension procedure; and 3 and 7 days after CCH injection. In addition, they reported the dose and duration of supplementary analgesic use during this period. Results: A total of 41 patients were enrolled in this study (51 joints). Mean pain VAS score (mean ± SD, 34 ± 21) was maximal 9 hours after CCH injection and decreased within the following 7 days. The total score of the SF-MPQ-2 significantly increased after CCH treatment and decreased in the 7 days after the injection. Among the SF-MPQ-2 subscales, the highest and lowest scores after CCH injection were recorded for continuous pain and affected descriptors, respectively. Nonsteroidal anti-inflammatory drugs were most frequently self-administered during 7 days after the extension procedure compared with any other study period. Conclusions: The pain VAS and SF-MPQ-2 revealed acute pain after CCH injection. However, all examined pain aspects dramatically improved within 7 days after injection. Pain after CCH injection is characterized by low scores in the Affective Descriptors subscale of the SF-MPQ-2. Type of study/level of evidence: Prognostic â £.
ABSTRACT
No clinically applicable drug is currently available to enhance neurite elongation after nerve injury. To identify a clinically applicable drug, we screened pre-approved drugs for neurite elongation in the motor neuron-like NSC34 cells. We found that zonisamide, an anti-epileptic and anti-Parkinson's disease drug, promoted neurite elongation in cultured primary motor neurons and NSC34 cells in a concentration-dependent manner. The neurite-scratch assay revealed that zonisamide enhanced neurite regeneration. Zonisamide was also protective against oxidative stress-induced cell death of primary motor neurons. Zonisamide induced mRNA expression of nerve growth factors (BDNF, NGF, and neurotrophin-4/5), and their receptors (tropomyosin receptor kinase A and B). In a mouse model of sciatic nerve autograft, intragastric administration of zonisamide for 1 week increased the size of axons distal to the transected site 3.9-fold. Zonisamide also improved the sciatic function index, a marker for motor function of hindlimbs after sciatic nerve autograft, from 6 weeks after surgery. At 8 weeks after surgery, zonisamide was protective against denervation-induced muscle degeneration in tibialis anterior, and increased gene expression of Chrne, Colq, and Rapsn, which are specifically expressed at the neuromuscular junction. We propose that zonisamide is a potential therapeutic agent for peripheral nerve injuries as well as for neuropathies due to other etiologies.
