Pain
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This study continued the validation of a Whiplash Specific Disability Questionnaire (WDQ) that was developed from the Neck Disability Index (NDI) using self-reported disabilities in a group of participants experiencing whiplash-associated disorders [J Manipulative Physiol Ther 14 (1991) 409]. Previous research has established the content, construct and face validity and internal consistency of the WDQ. The aim of this study was to establish the short-term and medium-term test-retest reliability and responsiveness of the WDQ. ⋯ Correlation between change in WDQ score over 1 month and participant perceived change was r(s) = 0.64, the effect size was 0.03, the SRM was 0.08 and the responsiveness statistics were 0.90 (participants who improved) and -1.60 (participants who deteriorated). The minimal detectable change of the WDQ was established at 15 points. These results demonstrate that the WDQ has excellent short- and medium-term reproducibility and responsiveness in a population seeking treatment for WAD.
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Comparative Study
Somatostatin modulates the transient receptor potential vanilloid 1 (TRPV1) ion channel.
Activation of peripheral somatostatin receptors (SSTRs) inhibits sensitization of nociceptors, thus having a short term or phasic effect [Pain 90 (2001) 233] as well as maintaining a tonic inhibitory control over nociceptors [J Neurosci 21 (2001) 4042]. The present study provides several lines of evidence that an important mechanism underlying SSTR modulation of nociceptors is regulation of the transient receptor potential vanilloid 1 ion channel (TRPV1, formerly the VR1 receptor). Double labeling of L5 dorsal root ganglion cells demonstrates that approximately 60% of SSTR2a-labeled cells are positive for TRPV1. ⋯ Furthermore, blockade of peripheral SSTRs with c-SOM dramatically enhances CAP-induced behaviors and nociceptor activity, demonstrating SSTR-induced tonic inhibitory modulation of TRPV1. Finally, TRPV1 does not appear to be under tonic opioid receptor control since the opioid antagonist naloxone does not change CAP-induced excitation and does not effect OCT-induced inhibition of CAP responses. These data strongly suggest that SSTRs modulate nociceptors through phasic and tonic regulation of peripheral TRPV1 receptors.