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Background Patients with palmar midcarpal instability have symptoms of pain, combined with clinical signs of abnormal mobility on stressing the joint, an unpredictable blockade feeling, and a noticeable clunk, in the absence of an underlying trauma. No data are available on the effect of conservative treatment for these patients. Purpose The purpose of this study was to evaluate the effect and the long-term functional outcomes of a wrist exercise program in patients with palmar midcarpal instability. Patients and Methods All patients diagnosed with palmar midcarpal instability between 2005 and 2011 were included. Patients completed the Patient-Rated Wrist and Hand Evaluation (PRWHE) and the Short Form-36 health (SF-36) questionnaires, scaled their perceived pain before and after treatment, and indicated the effect of the received treatment. Results A total of 119 patients diagnosed with palmar midcarpal instability were included. The median follow-up time was 6 years (IQR 4.5-7.0). The median PRWHE score after hand therapy was 35.5 and the median mental component of the SF-36 score was 53.9 and the physical component was 45.2. The median perceived pain reduced from eight to four and the median therapeutic effect of the wrist exercise program was five. Conclusion Although palmar midcarpal instability remains to be a chronic disease, the effectiveness of our wrist exercise program is promising with acceptable long-term functional results and a good quality of life. Level of Evidence Level IV, retrospective cohort study.
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BACKGROUND: Charcot Marie Tooth type 1a (CMT1a) is a primarily demyelinating neuropathy, characterized by slowly progressive muscle weakness, atrophy, and sensory loss, and is most pronounced in both feet and hands. There is increasing evidence that muscle weakness is determined by motor axonal dysfunction. OBJECTIVE: To investigate in patients with CMT1a whether motor axon loss, as estimated with motor unit number estimation (MUNE) and compound muscle action potential (CMAP), is related to hand function and manual dexterity. METHODS: Hand function, manual dexterity, and axon loss were studied in 48 patients with proven CMT1a. Using high-density surface EMG on the thenar muscles, MUNE was determined and CMAPs were measured. RESULTS: Pinch strength, clawing of the fingers, and manual dexterity correlated significantly with MUNE and CMAP (amplitude and area), while sensory impairments did not. Grip strength correlated significantly with CMAP amplitude but did not become significant with MUNE and CMAP area. Neurophysiologic variables were particularly associated with fine motor function of the hand. CONCLUSIONS: Motor axon loss is likely to be the major cause of hand dysfunction and impaired manual dexterity in Charcot Marie Tooth type 1a (CMT1a). In a clinical setting, the evaluation of the hands of patients with CMT1a should thus be mainly directed toward the evaluation of fine motor functions.