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Journal Article

Citation

Chien A, Eliav E, Sterling M. Clin. J. Pain 2010; 26(8): 722-728.

Affiliation

*Division of Physiotherapy, CCRE: Spinal Injury, Pain and Health, The University of Queensland, St Lucia §Centre of National Research on Disability and Rehabilitation Medicine (CONROD), Herston, Queensland †Department of Physiotherapy, The University of Melbourne, Parkville, Victoria, Australia ‡Department of Diagnostic Sciences, Division of Orofacial Pain, University of Medicine and Dentistry New Jersey, Newark, NJ.

Copyright

(Copyright © 2010, Lippincott Williams and Wilkins)

DOI

10.1097/AJP.0b013e3181f096ac

PMID

20842004

Abstract

OBJECTIVES: (1) To investigate the development of hypoesthesia from soon after the whiplash injury to 6 months postinjury and (2) to determine differences in detection thresholds between those with initial features of poor recovery and those without these signs. METHODS: Fifty-two participants with acute whiplash-associated disorders (WAD) (<1 mo) were classified as either "high-risk" (n=17; Neck Disability Index >30; sensory hypersensitivity) or "low risk" (n=35; without these signs). Detection thresholds to electrical, thermal, and vibration stimuli and psychological distress were prospectively measured within 1 month of injury and then 3 and 6 months postinjury. Detection thresholds were also measured in the 38 controls. RESULTS: Both WAD groups showed hypoesthesia (vibration, electrical, and cold) at 1 month postinjury. Vibration and electrocutaneous hypoesthesia persisted to 3 and 6 months only in the high-risk WAD group. Heat detection thresholds were not different between the groups at 1 month postinjury but were elevated in the high-risk group at 3 and 6 months. Both WAD groups were distressed at 1 month but this decreased by 3 months in the low-risk group. The differences in the Impact of Event Scale did not impact on any of the sensory measures. DISCUSSION: Sensory hypoesthesia is a feature of acute WAD but persists only in those at higher risk of poor recovery. These findings suggest the involvement of the central inhibitory mechanisms that may be sustained by ongoing nociception.


Language: en

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