Simultaneous Bilateral Versus Staged Bilateral Carpal Tunnel Release: A Cost-effectiveness Analysis.

The purpose of this study was to determine if simultaneous bilateral carpal tunnel release (CTR) is a cost-effective strategy compared with bilateral staged CTR for the treatment of bilateral carpal tunnel syndrome. METHODS: A decision analytic model was created to compare the cost effectiveness of three strategies (ie, bilateral simultaneous CTR, bilateral staged CTR, and no treatment). Direct medical costs were estimated from 2013 Medicare reimbursement rates and wholesale drug costs in US dollars. Indirect costs were derived from consecutive patients undergoing unilateral or simultaneous bilateral CTR at our institution and from national average wages for 2013. Health state utility values were derived from a general population of volunteers using the Short Form-6 dimensions (SF-6D) health questionnaire. RESULTS: Both surgical strategies were cost effective compared with the no-treatment strategy. Bilateral simultaneous CTR had lower total costs and higher total effectiveness than bilateral staged CTR, and had an incremental cost-effectiveness ratio of $921 per quality-adjusted life year compared with the no-treatment strategy. The conclusions of the analysis remained unchanged though all sensitivity analyses, displaying robustness against parameter uncertainty. CONCLUSIONS: Surgical management is cost effective for the treatment of bilateral carpal tunnel syndrome. Bilateral simultaneous CTR, however, has lower total costs and higher total effectiveness compared with bilateral staged CTR. LEVEL OF EVIDENCE: Economic and Decision Analysis I.

Factors associated with failure of nonoperative treatment in lateral epicondylitis.

BACKGROUND: Lateral epicondylitis is a common cause of elbow pain that is treated with a variety of nonoperative measures and often improves with time. Minimal research is available on patients in whom these nonoperative treatments fail. PURPOSE: To identify baseline patient and disease factors associated with the failure of nonoperative treatment of lateral epicondylitis, defined as surgery after a period of nonoperative treatment. STUDY DESIGN: Case control study; Level of evidence, 3. METHODS: A total of 580 patients treated for lateral epicondylitis at a tertiary center between 2007 and 2012 were analyzed. Disease-specific and patient demographic characteristics were compared between patient groups (nonoperative vs surgical treatment). A multivariable logistic regression model was created based on preliminary univariate testing to determine which characteristics were associated with failure of nonoperative treatment. RESULTS: Of the 580 patients, 92 (16%) underwent surgical treatment at a mean of 6 months (range, 0-31 months) from their initial visit. Univariate analysis demonstrated a potential association (P < .10) between operative management and the following factors at initial diagnosis: increased age, body mass index, duration of symptoms, presence of radial tunnel syndrome, prior injection, physical therapy, splinting, smoking, workers' compensation, a labor occupation, use of narcotics, use of antidepressant medications, and previous orthopaedic surgery. In the final multivariable model, a workers' compensation claim (odds ratio [OR], 8.1), prior injection (OR, 5.6), the presence of radial tunnel syndrome (OR, 3.1), previous orthopaedic surgery (OR, 3.2), and duration of symptoms >12 months (OR, 2.5) remained significant independent predictors of surgical treatment. CONCLUSION: This study identifies risk factors for surgical treatment for lateral epicondylitis. While these findings do not provide information regarding causal factors associated with surgery, these patient and disease-specific considerations may be helpful when counseling patients regarding treatment options and the likelihood of the success of continued nonoperative treatment.

The efficacy of 95-Hz topical vibration in pain reduction for trigger finger injection: a placebo-controlled, prospective, randomized trial.

PURPOSE: To determine whether vibratory stimulation would decrease pain experienced by patients during corticosteroid injection for trigger finger. METHODS: A total of 90 trigger finger injections were randomized to 1 of 3 cohorts. With the injection, patients received no vibration (control group), ultrasound vibration (sham control group), or vibration (experimental group). We used a commercial handheld massaging device to provide a vibratory stimulus for the experimental group. We obtained visual analog scale (VAS) pain scores before and after injection to assess anticipated pain and actual pain experienced. RESULTS: Anticipated pain and actual pain did not differ significantly among groups. Anticipated VAS pain scores were 45, 48, and 50 and actual VAS pain scores were 56, 56, and 63 for the vibration, control, and sham control groups, respectively. When normalized using anchoring VAS pain scores for "stubbing a toe" or "paper cut," no between-group differences remained in injection pain scores. CONCLUSIONS: Concomitant vibratory stimulation does not reduce pain experienced during corticosteroid injections for trigger finger. TYPE OF STUDY/LEVEL OF EVIDENCE: Therapeutic I.

Identification of plasticity-associated genes regulated by Pavlovian fear conditioning in the lateral amygdala.

Most recent studies aimed at defining the cellular and molecular mechanisms of Pavlovian fear conditioning have focused on protein kinase signaling pathways and the transcription factor cAMP-response element binding protein (CREB) that promote fear memory consolidation in the lateral nucleus of the amygdala (LA). Despite this progress, there still remains a paucity of information regarding the genes downstream of CREB that are required for long-term fear memory formation in the LA. We have adopted a strategy of using microarray technology to initially identify genes induced within the dentate gyrus following in vivo long-term potentiation (LTP) followed by analysis of whether these same genes are also regulated by fear conditioning within the LA. In the present study, we first identified 34 plasticity-associated genes that are induced within 30 min following LTP induction utilizing a combination of DNA microarray, qRT-PCR, and in situ hybridization. To determine whether these genes are also induced in the LA following Pavlovian fear conditioning, we next exposed rats to an auditory fear conditioning protocol or to control conditions that do not support fear learning followed by qRT-PCR on mRNA from microdissected LA samples. Finally, we asked whether identified genes induced by fear learning in the LA are downstream of the extracellular-regulated kinase/mitogen-activated protein kinase signaling cascade. Collectively, our findings reveal a comprehensive list of genes that represent the first wave of transcription following both LTP induction and fear conditioning that largely belong to a class of genes referred to as 'neuronal activity dependent genes' that are likely calcium, extracellular-regulated kinase/mitogen-activated protein kinase, and CREB-dependent.

A mechanism of nucleocytoplasmic trafficking for the homeodomain protein PRH.

Proline-rich homeodomain (PRH)/hematopoietically expressed homeodomain (Hex) is a homeodomain protein that plays an important role in early embryonic patterning and hematopoiesis. PRH can act as either a tumor suppressor or an oncogene and its expression is dysregulated in certain types of lymphoid and myeloid leukemias. Aberrant exclusion of PRH from the nuclei has been associated with thyroid and breast cancers and a subset of myeloid leukemias. Accordingly, nuclear localization of PRH was found to be necessary for the inhibition of eIF4E-dependent transformation. Since PRH's nuclear-cytoplasmic localization has been associated with neoplastic transformation we sought to better understand how PRH is transported to the nuclear compartment. Here, we report an essential element that controls the mechanism of PRH nucleocytoplasmic trafficking, namely that it is imported into the nuclei by Karyopherin/Importin 7. Kap7 was identified as a binding partner for PRH in a GST-pull down from a HeLa cell protein lysate, followed by mass-spectrometry. The Kap7-PRH complex is dissociated in the presence of RanGTP, as expected for a nuclear import complex. Kap7 can bind directly to PRH in a GST-pull down assay with purified proteins, as well as mediates the transport of PRH to the nuclear compartment in a digitonin permeabilized cells assay. Finally, in vivo depletion of Kap7 dramatically reduces accumulation of PRH in the nucleus. Our data open the way for investigations of the mechanism of perturbed PRH localization in tumors and possible therapeutic interventions.