4.0 Article

Generalized vibratory deficits in osteoarthritis of the hip

Journal

ARTHRITIS & RHEUMATISM-ARTHRITIS CARE & RESEARCH
Volume 59, Issue 9, Pages 1237-1240

Publisher

WILEY-LISS
DOI: 10.1002/art.24004

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Funding

  1. National Institute of Arthritis and Musculoskeletal and Skin Diseases
  2. NIH [K23-A-R0-49748, P50-AR0-48941]
  3. Schweppe Foundation

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Objective. Lower extremity sensory deficits, including reduced proprioception, joint kinesthesia, and, recently, vibratory sense. have been described in subjects with osteoarthritis (OA) of the knee. However, comparable deficits in OA of the hip have not previously been evaluated. Vibratory perception threshold (VPT) is a reliable measure used to assess sensory deficits and is amenable to testing multiple body sites. This study examined VPT at the upper and lower extremities of subjects with hip OA compared with subjects without hip OA. Methods. Fourteen subjects with symptomatic and radiographic hip OA were compared with 13 age-matched controls without hip OA. VPT was assessed using a biothesiometer. Five sites in the lower extremity and 1 site in the upper extremity (radial head) were evaluated and compared between OA and control subjects. Results. VPT was significantly reduced at all 6 testing sites of the OA subjects compared with controls (P < 0.05 for all sites). VPT scores (mean +/- SEM volts) for OA subjects and controls were as follows: first metatarsophalangeal joint (13.5 +/- 1.4 versus 7.4 +/- 0.7), medial malleolus (18.1 +/- 2.6 versus 11.2 +/- 1.7), lateral malleolus (20.9 +/- 2.4 versus 10.6 +/- 1.5), medial femoral condyle (22.8 +/- 2.9 versus 12.6 +/- 1.3), lateral femoral condyle (26.7 +/- 2.6 versus 16.2 +/- 1.9), and radial head (10.2 +/- 0.8 versus 7.5 +/- 0.6). Conclusion. To our knowledge, this is the first study to evaluate sensory deficits in hip OA and to demonstrate that there is vibratory sense loss at both the upper and lower extremities in these subjects compared with controls. The noted generalized deficits may have significant implications in the neuromechanical pathophysiology of OA.

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