Clinical outcomes of suprascapular nerve decompression.

BACKGROUND: While the incidence and prevalence of suprascapular neuropathy (SSN) remains largely unknown, the evaluation and treatment of SSN appears to be increasing. Despite multiple technique articles demonstrating nerve decompression, there has been no clinical evidence to support the efficacy of SSN decompression in the absence of rotator cuff disease. METHODS: Between October 2006 and February 2010, 27 patients underwent arthroscopic suprascapular nerve decompression at the suprascapular and/or spinoglenoid notch. Eighty-nine percent (24/27) of patients had preoperative positive electromyography and nerve conduction EMG/NCV studies documenting suprascapular nerve pathology. All patients had either a computed tomography (CT) arthrogram or magnetic resonance imaging (MRI) documenting rotator cuff integrity. All patients were evaluated with pre and postoperative subjective shoulder values (SSV) and American Shoulder and Elbow Society (ASES) self-assessment scores. Additionally, patients were questioned whether they would have the procedure again and approximately at what week they experienced noticeable pain relief. RESULTS: The 27 patients were followed for an average of 22.5 months (range, 3-44). Three patients were lost to follow-up. Seventy-one percent (17/24) of patients reported pain relief (VAS [Visual Analogue Scales] pain scale) that was statistically significant (P = .0001) at an average of 9.4 weeks from surgery. Seventy-five percent (18/24) and 71% (17/24) had statistically significant improvement in ASES (P = .0001) and SSV scores (P = .0014), respectively. Seventy-one percent (17/24) would have the surgery again. CONCLUSION: The present study demonstrates a large series of patients treated for SSN without rotator cuff pathology. Our results show statistically significant improvement in VAS, ASES, and SSV.

ClC-5: ontogeny of an alternative chloride channel in respiratory epithelia.

Chloride transport is critical to many functions of the lung. Molecular defects in the best-known chloride channel, cystic fibrosis transmembrane conductance regulator (CFTR), lead to impaired function of airway defensins, hydration of airway surface fluid, and mucociliary clearance leading to chronic lung disease, and premature death, but do not cause defects in lung development. We examined the expression of one member of the ClC family of volume- and voltage-regulated channels using the ribonuclease protection assay and Western blot analysis in rats. ClC-5 mRNA and protein are most strongly expressed in the fetal lung, and expression is maintained although downregulated postnatally. In addition, using immunocytochemistry, we find that ClC-5 is predominantly expressed along the luminal surface of the airway epithelium, suggesting that ClC-5 may participate in lung chloride secretion. Identifying candidate genes for critical ion transport functions is essential for understanding normal lung morphogenesis and the pathophysiology of several lung diseases. In addition, the manipulation of non-CFTR chloride channels may provide a viable approach for treating cystic fibrosis lung disease.