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Sensory hypoaesthesia is a feature of chronic whiplash but not chronic idiopathic neck pain
Manual Therapy 15 (2010) 48–53
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Original Article
Sensory hypoaesthesia is a feature of chronic whiplash but not chronic idiopathic neck pain Andy Chien a, b, Michele Sterling a, c, * a
Division of Physiotherapy and National Health and Medical Research Council Centre for Clinical Research Excellence in Spinal Pain, Injury and Health (CCRE Spine), School of Health and Rehabilitation Sciences, The University of Queensland, Australia b School of Physiotherapy, The University of Melbourne, Parkville, Victoria 3010 Australia c CONROD, Mayne Medical School, The University of Queensland, Herston Road, Herston, Brisbane QLD 4006, Australia
a r t i c l e i n f o
a b s t r a c t
Article history: Received 29 December 2008 Received in revised form 15 May 2009 Accepted 26 May 2009
Both sensory hypersensitivity and hypoaesthesia are features of chronic whiplash associated disorders (WAD). Sensory hypersensitivity is not a consistent feature of chronic idiopathic (non-traumatic) neck pain but the presence of hypoaesthesia has not been investigated. This study compared the somatosensory phenotype of whiplash and idiopathic neck pain. Comprehensive Quantitative Sensory Testing (QST) including both detection and pain thresholds as well as psychological distress were measured in 50 participants with chronic WAD, 28 participants with chronic idiopathic neck pain and 31 healthy controls. The whiplash group demonstrated lowered pressure pain thresholds (PPTs) at all sites compared to the controls (p < 0.01) but there was no difference between the two neck pain groups (p > 0.05) except at the tibialis anterior site (p ¼ 0.02). The whiplash group demonstrated lowered cold pain thresholds compared to idiopathic and control groups (p < 0.03). For detection thresholds, the whiplash group showed elevated vibration (p < 0.04), heat (p < 0.02) and electrical (p < 0.04) thresholds at all upper limb sites compared to the idiopathic neck pain group and the controls (p < 0.04). Sensory hypoesthesia whilst present in chronic whiplash is not a feature of chronic idiopathic neck pain. These findings indicate that different pain processing mechanisms underlie these two neck pain conditions and may have implications for their management. Crown Copyright Ó 2009 Published by Elsevier Ltd. All rights reserved.
Keywords: Whiplash Neck pain Quantitative Sensory Testing
1. Introduction Whiplash associated disorders (WAD) are heterogeneous with some individuals demonstrating widespread sensory hypersensitivity that is associated with both higher levels of pain and disability and poor functional recovery (Sterling et al., 2003). This phenomena is not unique to WAD and has been shown to be present in patients with cervical radiculopathy (Chien et al., 2008b) but in contrast does not appear to be a feature of chronic neck pain of a non-traumatic nature (idiopathic neck pain) (Scott et al., 2005; Elliott et al., 2008). Sensory hypersensitivity likely reflects augmented central pain processing mechanisms (Curatolo et al., 2001; Sterling et al., 2003) and its presence or not may indicate that different pain processes underlie various neck pain conditions.
* Corresponding author. CONROD, Mayne Medical School, The University of Queensland, Herston Road, Herston, Brisbane QLD 4006, Australia. Tel.: þ61 7 3365 3444; fax: þ61 7 3346 4603. E-mail address: [email protected] (M. Sterling).
We have recently demonstrated that in addition to sensory hypersensitivity, increased detection thresholds or sensory hypoaesthesia is also present in individuals with chronic whiplash (Chien et al., 2009). Similar findings have been demonstrated in other musculoskeletal conditions such as chronic diffuse upper limb pain and patellofemoral pain (Jensen et al., 2007b; Tucker et al., 2007) and may indicate the involvement of central inhibitory processes related to nociceptive input (Voerman et al., 2000; Tucker et al., 2007; Chien et al., 2008b). Apkarian et al. (1994) suggested that prolonged nociceptive input into the central nervous system (CNS) may cause an inhibitory effect which in turn ‘‘dampens’’ the CNS’s ability to perceive and interpret afferent sensory input. If central inhibitory mechanisms are involved in the somatosensory dysfunction seen in neck pain subsequent to whiplash injury, it could be expected that patients with chronic idiopathic neck pain would also demonstrate similar sensory changes. However, previous studies have examined only sensory hypersensitivity (decreased pain thresholds) and not hypoaethesia (increased detection thresholds) in chronic idiopathic neck pain. The aim of the current study was to compare the somatosensory phenotype of non-traumatic (idiopathic neck pain) to that of
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A. Chien, M. Sterling / Manual Therapy 15 (2010) 48–53
patients with chronic whiplash as well as healthy asymptomatic controls, particularly with respect to detection thresholds to various sensory stimuli. This may provide further insight into the underlying mechanisms of the two neck pain conditions.
2. Materials and methods 2.1. Participants A cross sectional study design was used to allow comparison between the two neck pain groups (chronic whiplash and chronic idiopathic neck pain) and a control group. The whiplash group comprised 50 participants (39 females; mean age 37.2 10.4 years) with persistent neck pain as a result of a motor vehicle crash (MVC) (>3 months but less than 2 years). All of the participants with whiplash injury fulfilled the criteria of WAD II (without clinical neurological signs) as defined by the Quebec Task Force (Spitzer et al., 1995). Participants were excluded if they experienced concussion, loss of consciousness or head injury as a result of the MVC and if they had been diagnosed with a psychiatric disorder. The participants with whiplash were recruited via primary care practises and through print media advertisement. The idiopathic neck pain group comprised of 28 participants (20 females; mean age 32.3 8.7 years) reporting ongoing, insidiousonset (non-traumatic) neck pain for more than 3 months and less than 3 years in duration. Participants were excluded if the onset of their neck pain was related to a MVC or other forms of trauma or if they had been diagnosed with any neurological or musculoskeletal disorders and/or a diagnosed psychiatric disorder that may influence Quantitative Sensory Testing (QST) results. The participants were recruited via local medial advertisement. Thirty-one healthy volunteers (25 females) were also recruited from the general community provided they had no complaints of spinal, upper or lower limb pain and had never experienced trauma or injuries to the cervical spine, head, and upper quadrant or knee regions requiring medical treatment. The mean age of the control group was 31.4 8.9 years. The study was approved by the institutional medical research ethics committee. All the participants were unpaid volunteers and all gave written informed consent before inclusion.
2.2. QST measures The QST measures utilised in the current study are sub-divided into 2 types: pain threshold measures and detection threshold measures. We have used these measures in previous studies of whiplash and neck pain and their validity and reliability is established (Chien et al., 2008a, b, Chien et al., 2009).
2.3. Pain threshold measures 2.3.1. PPTs PPT’s were determined using a pressure algometer with a probe size of 1 cm2 and application rate of 40 kPa/s (Somedic AB, Farsta, Sweden). Bilateral test sites included the articular pillars of C5/6, nerve trunk of the median nerve near the elbow and at the muscle belly of tibialis anterior (Sterling et al., 2003). The participants were asked to press a button when the sensation under the probe changed from being pressure alone to pressure and pain. The procedure was repeated 3 times at each site with the mean score used for analysis.
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2.3.2. Cold pain thresholds Thermotest (Somedic AB, Farsta, Sweden) was used to determine cold pain thresholds. The thermode was applied directly over the skin of mid-cervical region as well as the dorsal aspect of the hand bilaterally. The temperature was preset to decrease at a rate of 1 C/s from a baseline of 30 C. The participant was given a switch to identify when the cold sensation first became painful (Sterling et al., 2003). The Thermotest had a cut-out temperature of 5 C. If the cold pain threshold was not reached before the minimum cutout temperature, the minimum cut-out temperature was recorded for that trial. The mean of three trials at each site was calculated for analysis. 2.4. Detection threshold measures 2.4.1. Vibration thresholds (VTs) A vibrometre (Somedic AB, Stockholm, Sweden) with a tissue displacement range of 0.1 400 was used to supply vibration stimulation to the hand. In order to familiarise the participants with the vibration stimulus, 3 trials of the test stimuli, or until the participant was able to consistently indicate the onset of the stimulus, were applied over the muscle belly of brachioradialis. Readings were then taken over areas of the hand innervated by distal aspect of the C6 (palmar aspect of the 1st metacarpal), C7 (palmar aspect of 2nd metacarpal) and C8 dermatomes (dorsum of the 5th metacarpal) (Chien et al., 2008b). These tests were done bilaterally for all groups. Participants indicated when the vibration first appeared (the perception threshold (VPT)) and when it disappeared (the disappearance threshold (VDT)). The VT was then noted as the average of VPT and VDT. 2.4.2. Thermal (hot, cold) detection thresholds (TDTs) Utilising the method of limits, the Thermotest (Somedic AB, Farsta, Sweden) with a 25 50 thermode was used. Detection thresholds were measured over areas of the hand innervated by the C6 and 7 (dorsum over the 1st and 2nd metacarpal) and C8 (dorsum of the 5th metacarpal) dermatomes (Chien et al., 2008b). The temperature was preset to either increase or decrease at a rate of 1 C/s from a baseline of 30 C. The participant was asked to press a button as soon as they first detected the sensation of warmth or cold. 2.4.3. Current perception thresholds (CPTs) A non-noxious method of electrocutaneous stimulation was used in a method of limits procedure to allow determinations of CPT. The Neurometer CPT/C device (Neurotron., Baltimore, USA) delivers continuous trains of constant current electrical stimuli to the skin through a pair of 1 cm diameter gold electrodes coated with a thin layer of conductive gel and taped to the test site. Sites tested were those innervated by C5/6 (lateral elbow, inferior to elbow joint line), C7 (distal phalanx of index finger); C8 (distal phalanx of 5th digit) and tibialis anterior as a remote site (Chien et al., 2008b). The method of limits at a frequency of 250 Hz was utilised where the participants were asked to report when they first perceive the sensation (perception threshold). The intensity was then decreased until participants identified the threshold at which they can no detect the sensation (VDT). The detection threshold was calculated as the mean of the perception and VDT. The procedure was repeated three times and recorded for analysis. 2.5. Questionnaires All participants with neck pain completed the Neck Disability Index (NDI) (Vernon and Mior, 1991) as a measure of self-reported pain and functional disability. In order to account for the potential
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A. Chien, M. Sterling / Manual Therapy 15 (2010) 48–53
Table 1 Mean, SD and the p-values for pain threshold measures. QST parameter
Site
PPT (kPa)
Cx Med Tibant
Cold pain ( C)
Cx Hand
Control
Control vs idiopathic
Control vs whiplash
Idiopathic vs whiplash
Mean
SD
Mean
SD
Mean
SD
p-Value
p-Value
p-Value
313.9 301.0 592.0
46.2 45.0 125.3
215.0 222.1 471.8
78.6 61.7 164.5
178.6 187.9 425.9
74.8 87.9 168.2
0.01* 0.02* 0.31
<0.00* <0.00* <0.00*
0.17 0.46 0.02*
0.2 0.6
<0.00* <0.00*
0.03* 0.02*
8.03 9.00
Idiopathic
2.36 2.12
12.18 11.96
Whiplash
4.64 5.27
15.25 17.11
6.99 7.30
PPT ¼ Pressure pain threshold, Cx ¼ Cervical spine, Med ¼ Median nerve trunk, Tibant ¼ Tibialis anterior. *p < 0.05 on post hoc tests of group difference.
influence of psychological distress on pain responses (Rhudy and Meagher, 2000), all participants completed The Symptom Check List 90-Revised (SCL-90-R).
the tibialis anterior site compared to the idiopathic group (p ¼ 0.02) and controls (p < 0.01) with no difference between the latter two groups (p ¼ 0.31) (Table 1).
2.6. Statistical analysis
3.3.2. Cold pain thresholds MANCOVA revealed significant differences between the three groups (p < 0.01) at both the cervical and hand sites. Post hoc tests showed that the whiplash group demonstrated significantly decreased cold pain thresholds when compared to both the idiopathic neck pain and control groups at these sites (p < 0.03). There was no significant difference between the idiopathic neck pain group and the controls at any sites (p > 0.05) (Table 1).
The SPSS 16.00 statistical package for Macintosh was used for analyses. The Mann-Whitney test was firstly used to determine within participant side to side differences and followed by the exploratory analysis for all the measures and in all groups. Multivariate analysis of covariance (MANCOVA) was then performed as a global test for group comparison. Age, gender and the global severity index (GSI) from the SCL-90-R were entered as covariates. For the variables that demonstrated significant difference on MANCOVA, a LSD (least significant difference) post hoc test was used to identify specific group differences. The Mann-Whitney test was also used to compare between the two neck pain groups on SCL-90 subscale scores. For all analyses a p-value of <0.05 was considered significant. 3. Results 3.1. Participants For the whiplash group, the mean time post injury was 15 11 months. The mean NDI score of the whiplash group was 47.4 (out of 100) 16.4, which is rated as a moderate level of disability (Vernon and Mior, 1991). Forty-five percent of whiplash participants reported varying degrees of arm pain radiating past the shoulder and 66% experienced headache. The idiopathic neck pain group presented with a mean NDI score of 27.3 11.9 and the mean symptom duration was 28.3 11.2 months.
3.4. Detection threshold measures 3.4.1. VTs MANCOVA revealed significant group differences at all test sites (p < 0.05). Post hoc tests revealed that the whiplash group had elevated vibration detection thresholds at all test sites compared to both the idiopathic neck pain group and controls (p < 0.04). The idiopathic neck pain group was not significantly different to controls at any site (p > 0.12) (Fig. 1). 3.4.2. TDTs MANCOVA revealed significant group differences for heat detection thresholds at both sites (p < 0.01). Heat detection thresholds were significantly higher in the whiplash group when compared to other groups (p < 0.02). No significant difference was found between the idiopathic neck pain group and the controls for both test sites (p > 0.12). There was no main effect for group for cold detection thresholds (p > 0.1) (Fig. 2).
3.2. Within participants side to side differences There were no significant side to side differences for any measures (both pain threshold and detection thresholds) for all of the groups (all p > 0.05). As a result, the mean of left and right sides were calculated and used for further analysis for all the groups. 3.3. Pain threshold measures 3.3.1. PPTs MANCOVA revealed a significant difference between the three groups for all test sites (p < 0.05). Post hoc tests showed that the whiplash and idiopathic neck pain groups demonstrated lower PPTs at both the cervical and median nerve site when compared to controls (p < 0.05) and there was no difference between the two neck pain groups at these sites (p > 0.05). The whiplash group also demonstrated significantly lowered pain thresholds at
Fig. 1. Mean (SE) VTs of the control, idiopathic and whiplash groups. The stimulus was applied over areas of the hand innervated by C6 (Palm 1st), C7 (Palm 2nd) and C8 dermatomes (Dor 5th). *p < 0.05.
A. Chien, M. Sterling / Manual Therapy 15 (2010) 48–53
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Fig. 3. Electrocutaneous detection thresholds at a frequency of 250 Hz (means SE) of the control, idiopathic and whiplash groups. Sites tested were those innervated by C6 (lateral elbow, Elb), C7 (distal phalanx of index finger, Ind); C8 (distal phalanx of 5th digit, Lit) with Tibialis anterior (TibAnt) as a remote site. *p < 0.05.
Fig. 2. TDTs (means SE) of the control, idiopathic and whiplash groups. The stimulus was applied over the dorsum aspect of the hand corresponding to the C6 and 7 (Ind: dorsum over the 2nd metacarpal) and C8 (Lit: dorsum of the 5th metacarpal) dermatomes. *p < 0.05.
3.4.3. CPTs MANCOVA revealed significant group differences at all test sites (p < 0.01) except at the tibialis anterior site (p > 0.4). Posts hoc tests revealed that the whiplash group showed significantly higher detection thresholds at all the upper limb sites compared to the idiopathic neck pain group and the controls (p < 0.04). No significant difference was found between the idiopathic neck pain group and controls (p > 0.19) with the exception of the elbow site which was increased compared to controls (p ¼ 0.03) (Fig. 3). 3.5. Psychological distress (SCL-90-R) The mean raw scores and standard deviation for each of the SCL90-R subscales are presented in Table 2. The whiplash and idiopathic neck pain groups demonstrated significantly higher scores for the subscales of somatization and Generalized Severity Index GSI compared to controls (p < 0.03) with no difference between the two neck pain groups (p > 0.05). The whiplash group also demonstrated elevated scores for the subscale of depression when compared to the other two groups (p ¼ 0.02). When GSI, age and gender were entered as covariates in MANOVA, group differences for all variables remained unchanged. 4. Discussion The results of the current study demonstrate that the sensory presentation of chronic WAD is distinctly different to that of idiopathic neck pain. Participants with chronic idiopathic neck pain showed mechanical (pressure) hyperalgesia over the cervical and median nerve sites that were comparable to the chronic WAD group. However, mechanical hyperalgesia at the remote site
(tibialis anterior) and cold hyperalgesia over the cervical spine were unique to participants with chronic whiplash. These findings are consistent with those previously reported by Scott et al. (2005) and Elliott et al. (2008). Not all studies have demonstrated a lack of widespread sensory hypersensitivity and cold hyperalgesia in individuals with chronic idiopathic neck pain. Johnston et al. (2008) reported increased sensitivity to pressure pain at the tibialis anterior site together with cold hyperalgesia over the cervical spine in office workers with mild to moderate/severe neck pain (non-traumatic). However, on closer inspection of Johnston et al.’s data, the actual threshold values reported for their neck pain group were, although statistically significant, very close to control values. The pain thresholds were certainly much higher than those of our whiplash sample as well as previous whiplash data (Scott et al., 2005; Elliott et al., 2008) and thus may not represent actual hyperalgesia. Additionally, values for cold pain threshold were lower than 15 C (Johnston et al., 2008), a value proposed by Bennett (2006) to be considered abnormal. It is of interest to note that patients with tennis elbow also demonstrate cold and PPTs that are different from asymptomatic controls (Fernandez-Carnero et al., in press) but are not so affected as those seen in whiplash. Similarly, our idiopathic neck pain group showed lower PPTs at the median nerve site of the upper limb compared to previous data (Scott et al., 2005; Elliott et al., 2008) but whilst these thresholds were lower than controls, they were also not as hyperalgesic as those of the whiplash group. Thus it appears that sensory hypersensitivity is not an ‘all or nothing’ phenomena but rather may represent a continuum of Table 2 SCL-90-R psychological subscales (mean SD) for the whiplash, idiopathic neck pain and control groups. SCL-90-R subscale
Whiplash
Idiopathic
Control
Somatizationa Obsessive compulsive Interpersonal sensitivity Depressionb Anxiety Hostility Phobic anxiety Paranoid ideation Psychoticism General severity indexa
72 57 51 73 54 51 50 48 52 66
61 44 45 52 39 46 48 48 51 54
41 42 42 43 41 41 45 42 42 46
(8) (8) (6) (12) (8) (6) (10) (4) (10) (10)
(7) (6) (6) (9) (10) (5) (6) (6) (10) (9)
(10) (8) (8) (8) (10) (14) (12) (8) (8) (10)
a The whiplash and idiopathic neck pain groups demonstrated significantly higher scores compared to controls. b The whiplash group demonstrated significantly higher scores compared to the idiopathic and control groups.
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A. Chien, M. Sterling / Manual Therapy 15 (2010) 48–53
augmented pain processing mechanisms where conditions with greater symptom levels show more profound changes. A similar paradigm has been proposed for the recognition of neuropathic pain (Attal and Bouhissera, 2004). The discrepancy between the two neck pain groups to sensory stimuli also extended to the detection threshold measures. Hypoesthesia to vibration, heat and electrical stimulation was present in the whiplash group, with the idiopathic group having values no different from controls. These data are consistent with those reported by our previous studies of both acute and chronic whiplash (Chien et al., 2008a; Chien et al., 2009) and provide further evidence that processes underlying idiopathic neck pain are different from those of whiplash. We are not suggesting that hypoaesthesia is unique to WAD since similar sensory disturbances have been reported for other musculoskeletal conditions including diffuse upper limb pain, hip osteoarthritis and patellofemoral pain (Jensen et al., 2007b; Tucker et al., 2007). So it is interesting that our idiopathic neck pain group, arguably a comparable musculoskeletal pain condition did not show hypoaesthesia. Further investigation of these more subtle sensory disturbances in various musculoskeletal pain conditions is warranted. The widespread nature (bilateral and across dermatomes) of the sensory hypoaesthesia suggests the involvement of CNS processes. These may include central inhibitory processes subsequent to nociceptive input (Apkarian et al., 1994; Chien et al., 2009), central sensitisation (Voerman et al., 2000) and cortical reorganisation (Pleger et al., 2006). There are possible explanations for the discrepant findings in our idiopathic neck pain group. The magnitude of nociceptive input required to induce central processes may be important. Our idiopathic neck pain group reported lower levels of pain and disability than participants with whiplash and those reported for patients with diffuse upper limb pain and hypoaesthesia (Tucker et al., 2007). This proposal is contradicted by our previous findings in acute (<4 weeks) whiplash injury (Chien et al., 2008a) and those of Jensen et al. (2007a) in patellofemoral pain where reported pain and disability levels were comparable to our idiopathic neck pain group. Nevertheless, there is some evidence to indicate that the extent of some central processes, for example, cortical reorganisation correlate with pain levels (Pleger et al., 2006) and this may explain the lack of sensory hypoaesthesia found in the group with idiopathic neck pain. The duration of the nociceptive input is another factor thought to play an important role in maintaining CNS hyperexcitability (Rang et al., 1991; Woolf and Salter, 2000). However this factor cannot explain our findings as the idiopathic neck pain group reported a longer duration of symptoms (28.3 11.2 months) compared to the whiplash group (15 11 months). It is also recognised that neck pain is episodic in nature (Guzman et al., 2008) and at least clinically, it may be that idiopathic neck pain is more episodic than persistent whiplash pain. Such episodic pain may lead to interruptions in nociceptive input and this may prevent the development of the pathophysiological process within the CNS. Whilst the generalised nature of the sensory hypoaesthesia suggests involvement of central disturbances, it is noted that the deficits found in the whiplash group resemble other neuropathic conditions such as diabetes and toxin induced peripheral polyneuropathy (Jensen et al., 1991; Abad et al., 2002), and as such, peripheral nerve pathology remains a possible explanation and should not be completely overlooked. Indeed if the central processing mechanisms were the only factors involved, one would expect detection of all stimuli to be affected, however, cold detection thresholds were found to be normal in the current study. This may indicate that a-delta fibres (cold sensations) are less affected than a-beta and c-fibres. It is possible that the somatosensory disturbances seen in WAD include both central and peripheral mechanisms.
Certain psychological factors may be associated with the development of chronic WAD (Williamson et al., 2008) and may also influence the results of sensory tests (Rhudy and Meagher, 2000). In the present study, both neck pain groups demonstrated elevated psychological distress (SCL-90) when compared to controls and this was particularly with the case for the somatisization subscale. However, consistent with previous studies (Moog et al., 2002; Scott et al., 2005), the psychological scores were found to have little effect on group differences of sensory measures when entered as covariates in the analysis. Whilst it is acknowledged that other psychological constructs such as negative affectivity (Johnston et al., 2008) may also have an influence on QST results, the sensory disturbances identified in the current study should not be considered as being due to psychological distress alone but likely reflect plastic changes within the nervous system. In summary, the results of this study confirm previous findings that patients with idiopathic neck pain do not demonstrate widespread sensory hypersensitivity found to be a feature of whiplash injury. Similarly sensory hypoaesthesia whilst present in chronic whiplash is also not a feature of chronic idiopathic neck pain. These findings indicate different pain processing mechanisms, most likely within the CNS, underlie these two neck pain conditions and as such different approaches to management may be required. References Abad F, Diaz-Gomez N, Rodriguez I, Perez R, Delgado J. Subclinical pain and thermal sensory dysfunction in children and adolescents with type 1 diabetes. Diabet Med 2002;19:827–31. Apkarian AV, Stea RA, Bolanowski SJ. Heat-induced pain diminishes vibrotactile perception: a touch gate. Somatosens Mot Res 1994;11:259–67. Attal N, Bouhissera D. Can pain be more or less neuropathic? Pain 2004;110. Bennett GJ. Can we distinguish between inflammatory and neuropathic pain? Pain Res Manag 2006;11(Suppl. A):11A–5A. Chien A, Eliav E, Sterling M. Hypoaesthesia occurs in acute whiplash irrespective of pain and disability levels and the presence of sensory hypersensitivity. Clin J Pain 2008a;24:759–66. Chien A, Eliav E, Sterling M. Whiplash (grade II) and cervical radiculopathy share a similar sensory presentation: an investigation using quantitative sensory testing. Clin J Pain 2008b;24:595–603. Chien A, Eliav E, Sterling M. Hypoaesthesia occurs with sensory hypersensitivity in chronic whiplash – further evidence of a neuropathic condition. Man Ther 2009;14:138–46. Curatolo M, Petersen-Felix S, Arendt-Nielsen L, Giani C, Zbinden A, Radanov B. Central hypersensitivity in chronic pain after whiplash injury. Clin J Pain 2001;17:306–15. Elliott J, Sterling M, Noteboom JT, Darnell R, Galloway G, Jull G. Fatty infiltrate in the cervical extensor muscles is not a feature of chronic, insidious-onset neck pain. Clin Radiol 2008;63:681–7. Fernandez-Carnero J, Fernandez-De-Las_penas C, Sterling M, Souvlis T, ArendtNielsen L, Vicenzino B. Exploration of the extent of somato-sensory impairment in patients with unilateral epicondylalgia. J Pain, in press, doi: 10.1016/j.jpain.2009.04.015. Guzman J, Hurwitz E, Carroll L, Haldeman S, Cote P, Carragee E, et al. A new conceptual model of neck pain. Eur Spine J 2008;17:S14–23. Jensen R, Hystad T, Kvale A, Baerheim A. Quantitative sensory testing of patients with long lasting patellofemoral pain syndrome. Eur J Pain 2007a;11:665–76. Jensen R, Kvale A, Baerheim A. Is pain in patellofemoral pain syndrome neuropathic? Clin J Pain 2007b;24:384–94. Jensen T, Bach F, Kastrup J, Dejgaard A, Brennum J. Vibratory and thermal thresholds in diabetes with and without clinical neuropathy. Acta Neurol Scand 1991;84:326–33. Johnston V, Jimmieson NL, Jull G, Souvlis T. Quantitative sensory measures distinguish office workers with varying levels of neck pain and disability. Pain 2008;137:257–65. Moog M, Quintner J, Hall T, Zusman M. The late whiplash syndrome: a psychophysical study. Eur J Pain 2002;6:283–94. Pleger B, Ragert P, Schwenkreis P, Forster A-F, Wilimzig C, Dinse H, et al. Patterns of cortical reorganization parallel impaired tactile discrimination and pain intensity in complex regional pain syndrome. NeuroImage 2006;32:503–10. Rang H, Bevan S, Dray A. Chemical activation of nociceptive peripheral neurones. Br Med Bull 1991;47:534–48. Rhudy J, Meagher M. Fear and anxiety: divergent effects on human pain thresholds. Pain 2000;84:65–75. Scott D, Jull G, Sterling M. Widespread sensory hypersensitivity is a feature of chronic whiplash-associated disorder but not chronic idiopathic neck pain. Clin J Pain 2005;21:175–81.
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Manual Therapy journal homepage: www.elsevier.com/math
Original Article
Sensory hypoaesthesia is a feature of chronic whiplash but not chronic idiopathic neck pain Andy Chien a, b, Michele Sterling a, c, * a
Division of Physiotherapy and National Health and Medical Research Council Centre for Clinical Research Excellence in Spinal Pain, Injury and Health (CCRE Spine), School of Health and Rehabilitation Sciences, The University of Queensland, Australia b School of Physiotherapy, The University of Melbourne, Parkville, Victoria 3010 Australia c CONROD, Mayne Medical School, The University of Queensland, Herston Road, Herston, Brisbane QLD 4006, Australia
a r t i c l e i n f o
a b s t r a c t
Article history: Received 29 December 2008 Received in revised form 15 May 2009 Accepted 26 May 2009
Both sensory hypersensitivity and hypoaesthesia are features of chronic whiplash associated disorders (WAD). Sensory hypersensitivity is not a consistent feature of chronic idiopathic (non-traumatic) neck pain but the presence of hypoaesthesia has not been investigated. This study compared the somatosensory phenotype of whiplash and idiopathic neck pain. Comprehensive Quantitative Sensory Testing (QST) including both detection and pain thresholds as well as psychological distress were measured in 50 participants with chronic WAD, 28 participants with chronic idiopathic neck pain and 31 healthy controls. The whiplash group demonstrated lowered pressure pain thresholds (PPTs) at all sites compared to the controls (p < 0.01) but there was no difference between the two neck pain groups (p > 0.05) except at the tibialis anterior site (p ¼ 0.02). The whiplash group demonstrated lowered cold pain thresholds compared to idiopathic and control groups (p < 0.03). For detection thresholds, the whiplash group showed elevated vibration (p < 0.04), heat (p < 0.02) and electrical (p < 0.04) thresholds at all upper limb sites compared to the idiopathic neck pain group and the controls (p < 0.04). Sensory hypoesthesia whilst present in chronic whiplash is not a feature of chronic idiopathic neck pain. These findings indicate that different pain processing mechanisms underlie these two neck pain conditions and may have implications for their management. Crown Copyright Ó 2009 Published by Elsevier Ltd. All rights reserved.
Keywords: Whiplash Neck pain Quantitative Sensory Testing
1. Introduction Whiplash associated disorders (WAD) are heterogeneous with some individuals demonstrating widespread sensory hypersensitivity that is associated with both higher levels of pain and disability and poor functional recovery (Sterling et al., 2003). This phenomena is not unique to WAD and has been shown to be present in patients with cervical radiculopathy (Chien et al., 2008b) but in contrast does not appear to be a feature of chronic neck pain of a non-traumatic nature (idiopathic neck pain) (Scott et al., 2005; Elliott et al., 2008). Sensory hypersensitivity likely reflects augmented central pain processing mechanisms (Curatolo et al., 2001; Sterling et al., 2003) and its presence or not may indicate that different pain processes underlie various neck pain conditions.
* Corresponding author. CONROD, Mayne Medical School, The University of Queensland, Herston Road, Herston, Brisbane QLD 4006, Australia. Tel.: þ61 7 3365 3444; fax: þ61 7 3346 4603. E-mail address: [email protected] (M. Sterling).
We have recently demonstrated that in addition to sensory hypersensitivity, increased detection thresholds or sensory hypoaesthesia is also present in individuals with chronic whiplash (Chien et al., 2009). Similar findings have been demonstrated in other musculoskeletal conditions such as chronic diffuse upper limb pain and patellofemoral pain (Jensen et al., 2007b; Tucker et al., 2007) and may indicate the involvement of central inhibitory processes related to nociceptive input (Voerman et al., 2000; Tucker et al., 2007; Chien et al., 2008b). Apkarian et al. (1994) suggested that prolonged nociceptive input into the central nervous system (CNS) may cause an inhibitory effect which in turn ‘‘dampens’’ the CNS’s ability to perceive and interpret afferent sensory input. If central inhibitory mechanisms are involved in the somatosensory dysfunction seen in neck pain subsequent to whiplash injury, it could be expected that patients with chronic idiopathic neck pain would also demonstrate similar sensory changes. However, previous studies have examined only sensory hypersensitivity (decreased pain thresholds) and not hypoaethesia (increased detection thresholds) in chronic idiopathic neck pain. The aim of the current study was to compare the somatosensory phenotype of non-traumatic (idiopathic neck pain) to that of
1356-689X/$ – see front matter Crown Copyright Ó 2009 Published by Elsevier Ltd. All rights reserved. doi:10.1016/j.math.2009.05.012
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patients with chronic whiplash as well as healthy asymptomatic controls, particularly with respect to detection thresholds to various sensory stimuli. This may provide further insight into the underlying mechanisms of the two neck pain conditions.
2. Materials and methods 2.1. Participants A cross sectional study design was used to allow comparison between the two neck pain groups (chronic whiplash and chronic idiopathic neck pain) and a control group. The whiplash group comprised 50 participants (39 females; mean age 37.2 10.4 years) with persistent neck pain as a result of a motor vehicle crash (MVC) (>3 months but less than 2 years). All of the participants with whiplash injury fulfilled the criteria of WAD II (without clinical neurological signs) as defined by the Quebec Task Force (Spitzer et al., 1995). Participants were excluded if they experienced concussion, loss of consciousness or head injury as a result of the MVC and if they had been diagnosed with a psychiatric disorder. The participants with whiplash were recruited via primary care practises and through print media advertisement. The idiopathic neck pain group comprised of 28 participants (20 females; mean age 32.3 8.7 years) reporting ongoing, insidiousonset (non-traumatic) neck pain for more than 3 months and less than 3 years in duration. Participants were excluded if the onset of their neck pain was related to a MVC or other forms of trauma or if they had been diagnosed with any neurological or musculoskeletal disorders and/or a diagnosed psychiatric disorder that may influence Quantitative Sensory Testing (QST) results. The participants were recruited via local medial advertisement. Thirty-one healthy volunteers (25 females) were also recruited from the general community provided they had no complaints of spinal, upper or lower limb pain and had never experienced trauma or injuries to the cervical spine, head, and upper quadrant or knee regions requiring medical treatment. The mean age of the control group was 31.4 8.9 years. The study was approved by the institutional medical research ethics committee. All the participants were unpaid volunteers and all gave written informed consent before inclusion.
2.2. QST measures The QST measures utilised in the current study are sub-divided into 2 types: pain threshold measures and detection threshold measures. We have used these measures in previous studies of whiplash and neck pain and their validity and reliability is established (Chien et al., 2008a, b, Chien et al., 2009).
2.3. Pain threshold measures 2.3.1. PPTs PPT’s were determined using a pressure algometer with a probe size of 1 cm2 and application rate of 40 kPa/s (Somedic AB, Farsta, Sweden). Bilateral test sites included the articular pillars of C5/6, nerve trunk of the median nerve near the elbow and at the muscle belly of tibialis anterior (Sterling et al., 2003). The participants were asked to press a button when the sensation under the probe changed from being pressure alone to pressure and pain. The procedure was repeated 3 times at each site with the mean score used for analysis.
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2.3.2. Cold pain thresholds Thermotest (Somedic AB, Farsta, Sweden) was used to determine cold pain thresholds. The thermode was applied directly over the skin of mid-cervical region as well as the dorsal aspect of the hand bilaterally. The temperature was preset to decrease at a rate of 1 C/s from a baseline of 30 C. The participant was given a switch to identify when the cold sensation first became painful (Sterling et al., 2003). The Thermotest had a cut-out temperature of 5 C. If the cold pain threshold was not reached before the minimum cutout temperature, the minimum cut-out temperature was recorded for that trial. The mean of three trials at each site was calculated for analysis. 2.4. Detection threshold measures 2.4.1. Vibration thresholds (VTs) A vibrometre (Somedic AB, Stockholm, Sweden) with a tissue displacement range of 0.1 400 was used to supply vibration stimulation to the hand. In order to familiarise the participants with the vibration stimulus, 3 trials of the test stimuli, or until the participant was able to consistently indicate the onset of the stimulus, were applied over the muscle belly of brachioradialis. Readings were then taken over areas of the hand innervated by distal aspect of the C6 (palmar aspect of the 1st metacarpal), C7 (palmar aspect of 2nd metacarpal) and C8 dermatomes (dorsum of the 5th metacarpal) (Chien et al., 2008b). These tests were done bilaterally for all groups. Participants indicated when the vibration first appeared (the perception threshold (VPT)) and when it disappeared (the disappearance threshold (VDT)). The VT was then noted as the average of VPT and VDT. 2.4.2. Thermal (hot, cold) detection thresholds (TDTs) Utilising the method of limits, the Thermotest (Somedic AB, Farsta, Sweden) with a 25 50 thermode was used. Detection thresholds were measured over areas of the hand innervated by the C6 and 7 (dorsum over the 1st and 2nd metacarpal) and C8 (dorsum of the 5th metacarpal) dermatomes (Chien et al., 2008b). The temperature was preset to either increase or decrease at a rate of 1 C/s from a baseline of 30 C. The participant was asked to press a button as soon as they first detected the sensation of warmth or cold. 2.4.3. Current perception thresholds (CPTs) A non-noxious method of electrocutaneous stimulation was used in a method of limits procedure to allow determinations of CPT. The Neurometer CPT/C device (Neurotron., Baltimore, USA) delivers continuous trains of constant current electrical stimuli to the skin through a pair of 1 cm diameter gold electrodes coated with a thin layer of conductive gel and taped to the test site. Sites tested were those innervated by C5/6 (lateral elbow, inferior to elbow joint line), C7 (distal phalanx of index finger); C8 (distal phalanx of 5th digit) and tibialis anterior as a remote site (Chien et al., 2008b). The method of limits at a frequency of 250 Hz was utilised where the participants were asked to report when they first perceive the sensation (perception threshold). The intensity was then decreased until participants identified the threshold at which they can no detect the sensation (VDT). The detection threshold was calculated as the mean of the perception and VDT. The procedure was repeated three times and recorded for analysis. 2.5. Questionnaires All participants with neck pain completed the Neck Disability Index (NDI) (Vernon and Mior, 1991) as a measure of self-reported pain and functional disability. In order to account for the potential
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Table 1 Mean, SD and the p-values for pain threshold measures. QST parameter
Site
PPT (kPa)
Cx Med Tibant
Cold pain ( C)
Cx Hand
Control
Control vs idiopathic
Control vs whiplash
Idiopathic vs whiplash
Mean
SD
Mean
SD
Mean
SD
p-Value
p-Value
p-Value
313.9 301.0 592.0
46.2 45.0 125.3
215.0 222.1 471.8
78.6 61.7 164.5
178.6 187.9 425.9
74.8 87.9 168.2
0.01* 0.02* 0.31
<0.00* <0.00* <0.00*
0.17 0.46 0.02*
0.2 0.6
<0.00* <0.00*
0.03* 0.02*
8.03 9.00
Idiopathic
2.36 2.12
12.18 11.96
Whiplash
4.64 5.27
15.25 17.11
6.99 7.30
PPT ¼ Pressure pain threshold, Cx ¼ Cervical spine, Med ¼ Median nerve trunk, Tibant ¼ Tibialis anterior. *p < 0.05 on post hoc tests of group difference.
influence of psychological distress on pain responses (Rhudy and Meagher, 2000), all participants completed The Symptom Check List 90-Revised (SCL-90-R).
the tibialis anterior site compared to the idiopathic group (p ¼ 0.02) and controls (p < 0.01) with no difference between the latter two groups (p ¼ 0.31) (Table 1).
2.6. Statistical analysis
3.3.2. Cold pain thresholds MANCOVA revealed significant differences between the three groups (p < 0.01) at both the cervical and hand sites. Post hoc tests showed that the whiplash group demonstrated significantly decreased cold pain thresholds when compared to both the idiopathic neck pain and control groups at these sites (p < 0.03). There was no significant difference between the idiopathic neck pain group and the controls at any sites (p > 0.05) (Table 1).
The SPSS 16.00 statistical package for Macintosh was used for analyses. The Mann-Whitney test was firstly used to determine within participant side to side differences and followed by the exploratory analysis for all the measures and in all groups. Multivariate analysis of covariance (MANCOVA) was then performed as a global test for group comparison. Age, gender and the global severity index (GSI) from the SCL-90-R were entered as covariates. For the variables that demonstrated significant difference on MANCOVA, a LSD (least significant difference) post hoc test was used to identify specific group differences. The Mann-Whitney test was also used to compare between the two neck pain groups on SCL-90 subscale scores. For all analyses a p-value of <0.05 was considered significant. 3. Results 3.1. Participants For the whiplash group, the mean time post injury was 15 11 months. The mean NDI score of the whiplash group was 47.4 (out of 100) 16.4, which is rated as a moderate level of disability (Vernon and Mior, 1991). Forty-five percent of whiplash participants reported varying degrees of arm pain radiating past the shoulder and 66% experienced headache. The idiopathic neck pain group presented with a mean NDI score of 27.3 11.9 and the mean symptom duration was 28.3 11.2 months.
3.4. Detection threshold measures 3.4.1. VTs MANCOVA revealed significant group differences at all test sites (p < 0.05). Post hoc tests revealed that the whiplash group had elevated vibration detection thresholds at all test sites compared to both the idiopathic neck pain group and controls (p < 0.04). The idiopathic neck pain group was not significantly different to controls at any site (p > 0.12) (Fig. 1). 3.4.2. TDTs MANCOVA revealed significant group differences for heat detection thresholds at both sites (p < 0.01). Heat detection thresholds were significantly higher in the whiplash group when compared to other groups (p < 0.02). No significant difference was found between the idiopathic neck pain group and the controls for both test sites (p > 0.12). There was no main effect for group for cold detection thresholds (p > 0.1) (Fig. 2).
3.2. Within participants side to side differences There were no significant side to side differences for any measures (both pain threshold and detection thresholds) for all of the groups (all p > 0.05). As a result, the mean of left and right sides were calculated and used for further analysis for all the groups. 3.3. Pain threshold measures 3.3.1. PPTs MANCOVA revealed a significant difference between the three groups for all test sites (p < 0.05). Post hoc tests showed that the whiplash and idiopathic neck pain groups demonstrated lower PPTs at both the cervical and median nerve site when compared to controls (p < 0.05) and there was no difference between the two neck pain groups at these sites (p > 0.05). The whiplash group also demonstrated significantly lowered pain thresholds at
Fig. 1. Mean (SE) VTs of the control, idiopathic and whiplash groups. The stimulus was applied over areas of the hand innervated by C6 (Palm 1st), C7 (Palm 2nd) and C8 dermatomes (Dor 5th). *p < 0.05.
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Fig. 3. Electrocutaneous detection thresholds at a frequency of 250 Hz (means SE) of the control, idiopathic and whiplash groups. Sites tested were those innervated by C6 (lateral elbow, Elb), C7 (distal phalanx of index finger, Ind); C8 (distal phalanx of 5th digit, Lit) with Tibialis anterior (TibAnt) as a remote site. *p < 0.05.
Fig. 2. TDTs (means SE) of the control, idiopathic and whiplash groups. The stimulus was applied over the dorsum aspect of the hand corresponding to the C6 and 7 (Ind: dorsum over the 2nd metacarpal) and C8 (Lit: dorsum of the 5th metacarpal) dermatomes. *p < 0.05.
3.4.3. CPTs MANCOVA revealed significant group differences at all test sites (p < 0.01) except at the tibialis anterior site (p > 0.4). Posts hoc tests revealed that the whiplash group showed significantly higher detection thresholds at all the upper limb sites compared to the idiopathic neck pain group and the controls (p < 0.04). No significant difference was found between the idiopathic neck pain group and controls (p > 0.19) with the exception of the elbow site which was increased compared to controls (p ¼ 0.03) (Fig. 3). 3.5. Psychological distress (SCL-90-R) The mean raw scores and standard deviation for each of the SCL90-R subscales are presented in Table 2. The whiplash and idiopathic neck pain groups demonstrated significantly higher scores for the subscales of somatization and Generalized Severity Index GSI compared to controls (p < 0.03) with no difference between the two neck pain groups (p > 0.05). The whiplash group also demonstrated elevated scores for the subscale of depression when compared to the other two groups (p ¼ 0.02). When GSI, age and gender were entered as covariates in MANOVA, group differences for all variables remained unchanged. 4. Discussion The results of the current study demonstrate that the sensory presentation of chronic WAD is distinctly different to that of idiopathic neck pain. Participants with chronic idiopathic neck pain showed mechanical (pressure) hyperalgesia over the cervical and median nerve sites that were comparable to the chronic WAD group. However, mechanical hyperalgesia at the remote site
(tibialis anterior) and cold hyperalgesia over the cervical spine were unique to participants with chronic whiplash. These findings are consistent with those previously reported by Scott et al. (2005) and Elliott et al. (2008). Not all studies have demonstrated a lack of widespread sensory hypersensitivity and cold hyperalgesia in individuals with chronic idiopathic neck pain. Johnston et al. (2008) reported increased sensitivity to pressure pain at the tibialis anterior site together with cold hyperalgesia over the cervical spine in office workers with mild to moderate/severe neck pain (non-traumatic). However, on closer inspection of Johnston et al.’s data, the actual threshold values reported for their neck pain group were, although statistically significant, very close to control values. The pain thresholds were certainly much higher than those of our whiplash sample as well as previous whiplash data (Scott et al., 2005; Elliott et al., 2008) and thus may not represent actual hyperalgesia. Additionally, values for cold pain threshold were lower than 15 C (Johnston et al., 2008), a value proposed by Bennett (2006) to be considered abnormal. It is of interest to note that patients with tennis elbow also demonstrate cold and PPTs that are different from asymptomatic controls (Fernandez-Carnero et al., in press) but are not so affected as those seen in whiplash. Similarly, our idiopathic neck pain group showed lower PPTs at the median nerve site of the upper limb compared to previous data (Scott et al., 2005; Elliott et al., 2008) but whilst these thresholds were lower than controls, they were also not as hyperalgesic as those of the whiplash group. Thus it appears that sensory hypersensitivity is not an ‘all or nothing’ phenomena but rather may represent a continuum of Table 2 SCL-90-R psychological subscales (mean SD) for the whiplash, idiopathic neck pain and control groups. SCL-90-R subscale
Whiplash
Idiopathic
Control
Somatizationa Obsessive compulsive Interpersonal sensitivity Depressionb Anxiety Hostility Phobic anxiety Paranoid ideation Psychoticism General severity indexa
72 57 51 73 54 51 50 48 52 66
61 44 45 52 39 46 48 48 51 54
41 42 42 43 41 41 45 42 42 46
(8) (8) (6) (12) (8) (6) (10) (4) (10) (10)
(7) (6) (6) (9) (10) (5) (6) (6) (10) (9)
(10) (8) (8) (8) (10) (14) (12) (8) (8) (10)
a The whiplash and idiopathic neck pain groups demonstrated significantly higher scores compared to controls. b The whiplash group demonstrated significantly higher scores compared to the idiopathic and control groups.
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augmented pain processing mechanisms where conditions with greater symptom levels show more profound changes. A similar paradigm has been proposed for the recognition of neuropathic pain (Attal and Bouhissera, 2004). The discrepancy between the two neck pain groups to sensory stimuli also extended to the detection threshold measures. Hypoesthesia to vibration, heat and electrical stimulation was present in the whiplash group, with the idiopathic group having values no different from controls. These data are consistent with those reported by our previous studies of both acute and chronic whiplash (Chien et al., 2008a; Chien et al., 2009) and provide further evidence that processes underlying idiopathic neck pain are different from those of whiplash. We are not suggesting that hypoaesthesia is unique to WAD since similar sensory disturbances have been reported for other musculoskeletal conditions including diffuse upper limb pain, hip osteoarthritis and patellofemoral pain (Jensen et al., 2007b; Tucker et al., 2007). So it is interesting that our idiopathic neck pain group, arguably a comparable musculoskeletal pain condition did not show hypoaesthesia. Further investigation of these more subtle sensory disturbances in various musculoskeletal pain conditions is warranted. The widespread nature (bilateral and across dermatomes) of the sensory hypoaesthesia suggests the involvement of CNS processes. These may include central inhibitory processes subsequent to nociceptive input (Apkarian et al., 1994; Chien et al., 2009), central sensitisation (Voerman et al., 2000) and cortical reorganisation (Pleger et al., 2006). There are possible explanations for the discrepant findings in our idiopathic neck pain group. The magnitude of nociceptive input required to induce central processes may be important. Our idiopathic neck pain group reported lower levels of pain and disability than participants with whiplash and those reported for patients with diffuse upper limb pain and hypoaesthesia (Tucker et al., 2007). This proposal is contradicted by our previous findings in acute (<4 weeks) whiplash injury (Chien et al., 2008a) and those of Jensen et al. (2007a) in patellofemoral pain where reported pain and disability levels were comparable to our idiopathic neck pain group. Nevertheless, there is some evidence to indicate that the extent of some central processes, for example, cortical reorganisation correlate with pain levels (Pleger et al., 2006) and this may explain the lack of sensory hypoaesthesia found in the group with idiopathic neck pain. The duration of the nociceptive input is another factor thought to play an important role in maintaining CNS hyperexcitability (Rang et al., 1991; Woolf and Salter, 2000). However this factor cannot explain our findings as the idiopathic neck pain group reported a longer duration of symptoms (28.3 11.2 months) compared to the whiplash group (15 11 months). It is also recognised that neck pain is episodic in nature (Guzman et al., 2008) and at least clinically, it may be that idiopathic neck pain is more episodic than persistent whiplash pain. Such episodic pain may lead to interruptions in nociceptive input and this may prevent the development of the pathophysiological process within the CNS. Whilst the generalised nature of the sensory hypoaesthesia suggests involvement of central disturbances, it is noted that the deficits found in the whiplash group resemble other neuropathic conditions such as diabetes and toxin induced peripheral polyneuropathy (Jensen et al., 1991; Abad et al., 2002), and as such, peripheral nerve pathology remains a possible explanation and should not be completely overlooked. Indeed if the central processing mechanisms were the only factors involved, one would expect detection of all stimuli to be affected, however, cold detection thresholds were found to be normal in the current study. This may indicate that a-delta fibres (cold sensations) are less affected than a-beta and c-fibres. It is possible that the somatosensory disturbances seen in WAD include both central and peripheral mechanisms.
Certain psychological factors may be associated with the development of chronic WAD (Williamson et al., 2008) and may also influence the results of sensory tests (Rhudy and Meagher, 2000). In the present study, both neck pain groups demonstrated elevated psychological distress (SCL-90) when compared to controls and this was particularly with the case for the somatisization subscale. However, consistent with previous studies (Moog et al., 2002; Scott et al., 2005), the psychological scores were found to have little effect on group differences of sensory measures when entered as covariates in the analysis. Whilst it is acknowledged that other psychological constructs such as negative affectivity (Johnston et al., 2008) may also have an influence on QST results, the sensory disturbances identified in the current study should not be considered as being due to psychological distress alone but likely reflect plastic changes within the nervous system. In summary, the results of this study confirm previous findings that patients with idiopathic neck pain do not demonstrate widespread sensory hypersensitivity found to be a feature of whiplash injury. Similarly sensory hypoaesthesia whilst present in chronic whiplash is also not a feature of chronic idiopathic neck pain. These findings indicate different pain processing mechanisms, most likely within the CNS, underlie these two neck pain conditions and as such different approaches to management may be required. References Abad F, Diaz-Gomez N, Rodriguez I, Perez R, Delgado J. Subclinical pain and thermal sensory dysfunction in children and adolescents with type 1 diabetes. Diabet Med 2002;19:827–31. Apkarian AV, Stea RA, Bolanowski SJ. Heat-induced pain diminishes vibrotactile perception: a touch gate. Somatosens Mot Res 1994;11:259–67. Attal N, Bouhissera D. Can pain be more or less neuropathic? Pain 2004;110. Bennett GJ. Can we distinguish between inflammatory and neuropathic pain? Pain Res Manag 2006;11(Suppl. A):11A–5A. Chien A, Eliav E, Sterling M. Hypoaesthesia occurs in acute whiplash irrespective of pain and disability levels and the presence of sensory hypersensitivity. Clin J Pain 2008a;24:759–66. Chien A, Eliav E, Sterling M. Whiplash (grade II) and cervical radiculopathy share a similar sensory presentation: an investigation using quantitative sensory testing. Clin J Pain 2008b;24:595–603. Chien A, Eliav E, Sterling M. Hypoaesthesia occurs with sensory hypersensitivity in chronic whiplash – further evidence of a neuropathic condition. Man Ther 2009;14:138–46. Curatolo M, Petersen-Felix S, Arendt-Nielsen L, Giani C, Zbinden A, Radanov B. Central hypersensitivity in chronic pain after whiplash injury. Clin J Pain 2001;17:306–15. Elliott J, Sterling M, Noteboom JT, Darnell R, Galloway G, Jull G. Fatty infiltrate in the cervical extensor muscles is not a feature of chronic, insidious-onset neck pain. Clin Radiol 2008;63:681–7. Fernandez-Carnero J, Fernandez-De-Las_penas C, Sterling M, Souvlis T, ArendtNielsen L, Vicenzino B. Exploration of the extent of somato-sensory impairment in patients with unilateral epicondylalgia. J Pain, in press, doi: 10.1016/j.jpain.2009.04.015. Guzman J, Hurwitz E, Carroll L, Haldeman S, Cote P, Carragee E, et al. A new conceptual model of neck pain. Eur Spine J 2008;17:S14–23. Jensen R, Hystad T, Kvale A, Baerheim A. Quantitative sensory testing of patients with long lasting patellofemoral pain syndrome. Eur J Pain 2007a;11:665–76. Jensen R, Kvale A, Baerheim A. Is pain in patellofemoral pain syndrome neuropathic? Clin J Pain 2007b;24:384–94. Jensen T, Bach F, Kastrup J, Dejgaard A, Brennum J. Vibratory and thermal thresholds in diabetes with and without clinical neuropathy. Acta Neurol Scand 1991;84:326–33. Johnston V, Jimmieson NL, Jull G, Souvlis T. Quantitative sensory measures distinguish office workers with varying levels of neck pain and disability. Pain 2008;137:257–65. Moog M, Quintner J, Hall T, Zusman M. The late whiplash syndrome: a psychophysical study. Eur J Pain 2002;6:283–94. Pleger B, Ragert P, Schwenkreis P, Forster A-F, Wilimzig C, Dinse H, et al. Patterns of cortical reorganization parallel impaired tactile discrimination and pain intensity in complex regional pain syndrome. NeuroImage 2006;32:503–10. Rang H, Bevan S, Dray A. Chemical activation of nociceptive peripheral neurones. Br Med Bull 1991;47:534–48. Rhudy J, Meagher M. Fear and anxiety: divergent effects on human pain thresholds. Pain 2000;84:65–75. Scott D, Jull G, Sterling M. Widespread sensory hypersensitivity is a feature of chronic whiplash-associated disorder but not chronic idiopathic neck pain. Clin J Pain 2005;21:175–81.
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