ORCID Profile
0000-0002-3711-8737
Current Organisation
Murdoch University
Does something not look right? The information on this page has been harvested from data sources that may not be up to date. We continue to work with information providers to improve coverage and quality. To report an issue, use the Feedback Form.
Publisher: Ovid Technologies (Wolters Kluwer Health)
Date: 19-08-2022
DOI: 10.1097/J.PAIN.0000000000002764
Abstract: Alpha-1 adrenoceptors are overexpressed in the epidermis of a subgroup of patients with complex regional pain syndrome (CRPS). Activating α 1 -adrenoceptors in epidermal cells increases production of the proinflammatory cytokine interleukin-6 (IL-6), a mediator of inflammation. To investigate whether this might exacerbate inflammation in CRPS, primary keratinocytes or dermal fibroblasts were cultured from skin biopsies obtained from the affected limb of 25 patients and a similar site in 28 controls. The fundamental proinflammatory cytokine, tumor necrosis factor alpha, was administered for 24 hours to initiate inflammation. After this, cells were incubated for 6 hours with the α 1 -adrenoceptor agonist phenylephrine. Exposure to tumor necrosis factor alpha induced proinflammatory cytokine mRNA production and protein secretion in keratinocytes and fibroblasts and enhanced α 1B -adrenoceptor mRNA expression in keratinocytes. Additional stimulation of α 1 adrenoceptors with phenylephrine increased the production of IL-6 mRNA and protein secretion in both cell types. Under all conditions, gene and protein α 1 -adrenoceptor levels and cytokine gene expression and protein secretion were similar, overall, in patients and controls, except for abnormally high α 1 -adrenoceptor protein levels in the keratinocytes of 3 of 17 patients. These findings suggest that persistent inflammation in CRPS is not due to dysfunction of skin cells but is a normal response to extrinsic signals. After α 1 -adrenoceptor stimulation of keratinocytes, increases in IL-6 mRNA but not protein were proportional to basal α 1 -adrenoceptor protein levels. Skin cells play an important role in persistent inflammation in CRPS. Potentially, a positive feedback loop between α 1 -adrenoceptors and IL-6 production in skin cells contributes to this inflammatory state.
Publisher: Oxford University Press (OUP)
Date: 21-11-2022
DOI: 10.1093/PM/PNAC180
Abstract: Complex regional pain syndrome (CRPS) is associated with a range of sensory disturbances on the symptomatic side of the body but whether this includes olfaction is uncertain. To clarify this, the aims of this study were to compare ratings of intensity and hedonic appeal of household odorants in CRPS patients and controls, and to determine whether ratings differed between the symptomatic and contralateral sides within the s le of patients. Six odorants (vanilla, fish sauce, vinegar, eucalyptus, almond essence and acetone) were presented sequentially in random order on cottonwool buds held in the midline approximately 1 cm from both nostrils in 37 CRPS patients and 21 pain-free controls. Each odor was rated for intensity and hedonic appeal, and participants reported whether the odor was stronger and/or smelt different on one side than the other. The odorants smelt worse for patients than controls (P & .05 for the symptomatic and contralateral sides) but neither the intensity nor the unpleasantness of the odorants was greater on the symptomatic than contralateral side in the group as-a-whole. These findings suggest that the trigeminal component of olfaction interacts bilaterally with pain-sensitized circuits in the thalamus or higher cortical centers to distort odor perception in patients with CRPS. This aberrant process appears to differ from the mechanism that underlies hemilateral hyperalgesia in other sensory modalities.
Publisher: Wiley
Date: 11-12-2022
DOI: 10.1002/EJP.2061
Abstract: Applying an ice cube to the temple (the conditioning stimulus) inhibits electrically evoked pain in the forearm. The present study aimed to determine whether temple cooling also inhibits pressure‐ and heat‐pain test stimuli in the upper limb and, if so, to investigate the intra‐session test–retest reliability of this response. Additional aims were to establish whether pain inhibition evoked by temple cooling was associated with parasympathetic activity and to explore sex differences in response. The s le consisted of 40 healthy adults (24 females). Heart rate was recorded continuously throughout the session. An ice cube (3 × 4 cm contact area) was applied for 1 min to the temple on the dominant side. Before and immediately afterwards, the pressure pain threshold was measured from the dorsal hand and sensitivity to heat (in idually adjusted at baseline to elicit moderate pain) was measured from the ventral forearm. The procedures were repeated 15 min later. Temple cooling inhibited pressure pain on the hand but not heat pain on the forearm. However, test–retest reliability of pressure pain inhibition was poor. Heart rate decreased during temple cooling, consistent with a “ ing” reflex. Males had stronger pressure pain inhibition, lower heart rate and higher overall autonomic activity than females. However, cardiac parasympathetic activation during temple cooling was comparable in both sexes and was unrelated to pain inhibition. These findings indicate that temple cooling evokes pain inhibition that is stronger in males than in females. Cardiac parasympathetic activity does not appear to mediate this response. The conditioning stimulus in the conditioned pain modulation paradigm is often applied to the upper or lower limbs. This may confound pain‐inhibitory effects in people with peripheral neuropathy who typically have enhanced or diminished sensation in the extremities. Applying an ice cube at the temple area induces pain‐inhibitory effects on the upper limb after the ice is removed. Future research examining pain modulation in people with peripheral neuropathy may consider adopting temple cooling as the conditioning stimulus.
Publisher: SAGE Publications
Date: 17-11-2021
DOI: 10.1177/03331024211058204
Abstract: Trigeminal autonomic cephalalgias and complex regional pain syndrome are rare conditions, and their co-occurrence has not been reported previously. Clinical findings: In two patients, ipsilateral trigeminal autonomic cephalalgias developed after the onset of upper limb complex regional pain syndrome. Hyperalgesia to thermal and mechanical stimuli extended beyond the affected limb to encompass the ipsilateral forehead, and was accompanied by ipsilateral hyperacusis and photophobia. In addition, examination of the painful limb and bright light appeared to aggravate symptoms of trigeminal autonomic cephalalgias. Detailed examination of the association between facial and upper limb pain indicated that both sources of pain cycled together. Furthermore, in one case, stellate ganglion blockade inhibited pain for an extended period not only in the affected limb but also the face. These findings suggest some overlap in the pathophysiology of complex regional pain syndrome and trigeminal autonomic cephalalgias. Specifically, central sensitization and/or disruption of inhibitory pain modulation on the affected side of the body in complex regional pain syndrome might trigger ipsilateral cranial symptoms and increase vulnerability to trigeminal autonomic cephalalgias.
Publisher: Wiley
Date: 14-01-2021
DOI: 10.1111/PSYP.13757
Abstract: Acoustic startle stimuli inhibit pain, but whether this is due to a cross-modal inhibitory process or some other mechanism is uncertain. To investigate this, electrical stimulation of the sural nerve either preceded or followed an acoustic startle stimulus (by 200 ms) or was presented alone in 30 healthy participants. Five electrical stimuli, five acoustic startle stimuli, 10 startle + electrical stimuli, and 10 electrical + startle stimuli were presented in mixed order at intervals of 30-60 s. Effects of the startle stimulus on pain ratings, pupillary dilatation and nociceptive flexion reflexes to the electric shock were assessed. The acoustic startle stimulus inhibited electrically evoked pain to the ensuing electric shock (p < .001), and the electrical stimulus inhibited the perceived loudness of a subsequent acoustic startle stimulus (p < .05). However, the startle stimulus did not affect electrically evoked pain when presented 200 ms after the electric shock, and electrically evoked pain did not influence the perceived loudness of a prior startle stimulus. Furthermore, stimulus order did not influence the pupillary responses or nociceptive flexion reflexes. These findings suggest that acoustic startle stimuli transiently inhibit nociceptive processing and, conversely, that electrical stimuli inhibit subsequent auditory processing. These inhibitory effects do not seem to involve spinal gating as nociceptive flexion reflexes to the electric shock were unaffected by stimulus order. Thus, cross-modal interactions at convergence points in the brainstem or higher centers may inhibit responses to the second stimulus in a two-stimulus train.
Publisher: Elsevier BV
Date: 2023
DOI: 10.1016/J.JPAIN.2022.09.006
Abstract: To investigate links between blood glucose, body fat mass and pain, the effects of acute hyperglycaemia on pain sensitivity and pain inhibition were examined in healthy adults with normal (n = 24) or excess body fat (n = 20) determined by dual-energy X-ray absorptiometry. Effects of hyperglycaemia on heart rate variability and reactive hyperaemia were also explored. For the overall s le, ingesting 75-g glucose enhanced pain sensitivity during 1-minute cold-water immersion of both feet (conditioning stimulus) and weakened the pain inhibitory effect of cold water on pressure pain thresholds (test stimulus). Exploratory subgroup analyses not adjusted for multiple comparisons suggested that this effect was limited to people with excess fat mass. In addition, acute hyperglycaemia suppressed resting heart rate variability only in people with excess fat mass. Furthermore, regardless of blood glucose levels, people with excess fat mass had weaker pain inhibition for pinprick after cold water and reported more pain during 5-minutes of static blood flow occlusion. Neither high blood glucose nor excess body fat affected pinprick-temporal summation of pain or reactive hyperaemia. Together, these findings suggest that hyperglycaemia and excess fat mass interfere with pain processing and autonomic function. Perspective Ingesting 75-g glucose (equivalent to approximately two standard cans of soft drink) interfered with pain-processing and autonomic function, particularly in people with excess body fat mass. As both hyperglycaemia and overweight are risk factors for diabetes, whether these are sources of pain in people with diabetes should be further explored.
Publisher: Elsevier BV
Date: 05-2018
DOI: 10.1016/J.BURNS.2017.09.010
Abstract: Stimulation of α
Publisher: Elsevier BV
Date: 10-2021
Publisher: Elsevier BV
Date: 2022
DOI: 10.1016/J.JPAIN.2021.07.003
Abstract: Converging lines of evidence suggest that autonomic and nociceptive pathways linked with the locus coeruleus are disrupted in complex regional pain syndrome (CRPS). To investigate this, pupillary dilatation to arousal stimuli (which reflects neural activity in the locus coeruleus) and pupillary reflexes to light were assessed in a cross-sectional study of 33 patients with CRPS. Moderately painful electrical shocks were delivered to the affected or contralateral limb and unilateral 110 dB SPL acoustic startle stimuli were delivered via headphones. To determine whether the acoustic startle stimuli inhibited shock-induced pain, startle stimuli were also administered bilaterally 200 ms before or after the electric shock. The pupils constricted briskly and symmetrically to bright light (500 lux) and dilated symmetrically in dim light (5 lux). However, the pupil on the CRPS-affected side was smaller than the contralateral pupil before and after the delivery of painless and painful arousal stimuli. Auditory sensitivity was greater on the affected than unaffected side but acoustic startle stimuli failed to inhibit shock-induced pain. Together, these findings suggest that neural activity in pathways linked with the locus coeruleus is compromised on the affected side in patients with CRPS. This may contribute to autonomic disturbances, auditory discomfort and pain. PERSPECTIVE: The locus coeruleus is involved not only in modulation of pain but also regulates sensory traffic more broadly. Hence, fatigue of neural activity in the ipsilateral locus coeruleus might not only exacerbate pain and hyperalgesia in CRPS but could also contribute more generally to hemilateral disturbances in sensory processing.
Publisher: Informa UK Limited
Date: 10-2021
DOI: 10.2147/JPR.S326638
Publisher: Elsevier BV
Date: 02-2022
DOI: 10.1016/J.JPAIN.2021.08.004
Abstract: The aim of the study was to determine whether transcranial direct current stimulation (tDCS) reduced pain and signs of central sensitization induced by low frequency electrical stimulation in healthy volunteers. Thirty-nine participants received tDCS stimulation under 4 different conditions: anodal tDCS of the primary motor cortex (M1), anodal tDCS of the dorsolateral prefrontal cortex (DLPFC), anodal tDCS over M1 and DLPFC concurrently, and sham tDCS. Participants were blind to the tDCS condition. The order of the conditions was randomized among participants. Pain ratings to pinpricks, the current level that evoked moderate pain, and pain induced by low frequency electrical stimulation were assessed in the forearm by an experimenter who was blind to the tDCS conditions. Anodal tDCS at M1 increased the current level that evoked moderate pain compared to sham and other conditions. Anodal tDCS of DLPFC completely abolished secondary hyperalgesia. Unexpectedly, however, concurrent anodal tDCS over M1 and DLPFC did not reduce pain or hyperalgesia more than M1 alone or DLPFC alone. Overall, these findings suggest that anodal tDCS over M1 suppresses pain, and that anodal tDCS over DLPFC modulates secondary hyperalgesia (a sign of central sensitization) in healthy participants. PERSPECTIVE: Anodal transcranial current stimulation (atDCS) at the left motor cortex and the dorsolateral prefrontal cortex increased the electrically-evoked pain threshold and reduced secondary hyperalgesia in healthy participants. Replication of this study in chronic pain populations may open more avenues for chronic pain treatment.
Publisher: Elsevier BV
Date: 11-2022
DOI: 10.1016/J.JPAIN.2022.06.008
Abstract: Increasing evidence reveals the damaging impact of having one's chronic pain symptoms invalidated through disbelief, discrediting, and critical judgement. In other instances, a caregiver's over-attentiveness to the daily tasks of in iduals with pain can be problematic, potentially undermining rehabilitation. The aim of this study was to develop an instrument to measure different aspects of invalidation perceived by people with chronic pain. Item generation was informed through literature review and a thematic analysis of narratives from 431 peer-reviewed articles. The crowdsourcing platform Prolific was used to distribute survey items to participants. In Study 1A, Principal Component Analysis was performed on data from 302 respondents, giving rise to 4 subscales, including: Invalidation by the Self, Invalidation by Immediate Others, Invalidation by Healthcare Professionals, and Invalidation by Over-attentive Others. Confirmatory Factor Analysis of data collected from another 308 in iduals in Study 1B supported the 4-factor model of the Pain-Invalidation Scale (Pain-IS) and identified a best-fit model with 24 items. The Pain-IS was further validated in another 300 in iduals in Study 2. The Pain-IS demonstrates sound psychometric properties and may serve as a valuable tool for use by clinicians in the detection of pain-invalidation issues, as a first step in patient pain management. PERSPECTIVE: Links between pain-invalidation and pain levels, as well as functional detriment, highlight the importance of having one's chronic pain experience heard, believed, and accepted. The Pain-Invalidation Scale is designed to identify domains where invalidation of the patient's pain should be addressed to promote emotional processing, treatment adherence, and improved outcomes.
Publisher: Wiley
Date: 28-10-2022
DOI: 10.1111/DME.14729
Abstract: Diabetic peripheral neuropathy (DPN) occurs in about half of people with diabetes, of whom a quarter may develop chronic pain. Pain may remain for years yet be difficult to treat because the underlying mechanisms remain unclear. There is consensus that processing excessive glucose leads to oxidative stress, interfering with normal metabolism. In this narrative review, we argue that oxidative stress may also contribute to pain. We reviewed literature in PubMed published between January 2005 and August 2021. In diabetes, hyperglycaemia and associated production of reactive species can directly increase pain signalling and activate sensory neurons or the effects can be indirect, mediated by mitochondrial damage and enhanced inflammation. Furthermore, pain processing in the central nervous system is compromised in painful DPN. This is implicated in central sensitisation and dysfunctional pain modulation. However, central pain modulatory function is understudied in diabetes. Future research is required to clarify whether central sensitisation and/or disturbances in central pain modulation contribute to painful DPN. Positive results would facilitate early detection and future treatment.
No related grants have been discovered for Peter Drummond.