ORCID Profile
0000-0002-2714-5387
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: SAGE Publications
Date: 07-02-2017
Abstract: The R3 component of the electrically evoked blink reflex may form part of a startle reaction. Acoustic startle responses are augmented by yohimbine, an α 2 -adrenoceptor antagonist that blocks α 2 -autoreceptors, and are potentiated by opioid receptor blockade. To investigate these influences on electrically evoked startle responses, 16 mg yohimbine, with (16 participants) or without 50 mg naltrexone (23 participants), was administered in separate double-blind placebo-controlled cross-over experiments. In each experiment, R3 (a probable component of the startle response) was examined before and after high-frequency electrical stimulation of the forearm, a procedure that initiates inhibitory pain controls. Anxiety and somatic symptoms were greater after yohimbine than placebo, and were potentiated by naltrexone. Pain ratings for the electrically evoked startle stimuli decreased after high-frequency electrical stimulation in the placebo session but remained stable after drug administration. Yohimbine with naltrexone, but not yohimbine alone, also blocked an inhibitory effect of high-frequency electrical stimulation on electrically evoked sharp sensations and R3. Together, the findings suggest that adding naltrexone to yohimbine potentiated anxiety and blocked inhibitory influences of high-frequency electrical stimulation on electrically evoked sensations and startle responses. Thus, opioid peptides could reduce activity in nociceptive and startle-reflex pathways, or inhibit crosstalk between these pathways. Failure of this inhibitory opioid influence might be important in chronically painful conditions that are aggravated by startle stimuli.
Publisher: Wiley
Date: 14-08-2012
DOI: 10.1002/J.1532-2149.2012.00208.X
Abstract: In healthy humans, analgesia to blunt pressure develops in the ipsilateral forehead during various forms of limb pain. The aim of the current study was to determine whether this analgesic response is induced by ultraviolet B radiation (UVB), which evokes signs of peripheral sensitization, or by high-frequency electrical stimulation (HFS), which triggers signs of central sensitization. Before and after HFS and UVB conditioning, sensitivity to heat and to blunt and sharp stimuli was assessed at and adjacent to the treated site in the forearm. In addition, sensitivity to blunt pressure was measured bilaterally in the forehead. The effect of ipsilateral versus contralateral temple cooling on electrically evoked pain in the forearm was then examined, to determine whether HFS or UVB conditioning altered inhibitory pain modulation. UVB conditioning triggered signs of peripheral sensitization, whereas HFS conditioning triggered signs of central sensitization. Importantly, ipsilateral forehead analgesia developed after HFS but not UVB conditioning. In addition, decreases in electrically evoked pain at the HFS-treated site were greater during ipsilateral than contralateral temple cooling, whereas decreases at the UVB-treated site were similar during both procedures. HFS conditioning induced signs of central sensitization in the forearm and analgesia both in the ipsilateral forehead and the HFS-treated site. This ipsilateral analgesia was not due to peripheral sensitization or other non-specific effects, as it failed to develop after UVB conditioning. Thus, the supra-spinal mechanisms that evoke central sensitization might also trigger a hemilateral inhibitory pain modulation process. This inhibitory process could sharpen the boundaries of central sensitization or limit its spread.
Publisher: Springer Science and Business Media LLC
Date: 26-11-2013
DOI: 10.1007/S00221-013-3776-X
Abstract: In healthy participants, high-frequency electrical stimulation of the forearm not only evokes local hyperalgesia but also inhibits sensitivity to pressure-pain in the ipsilateral forehead, possibly due to activation of ipsilateral inhibitory pain modulation processes. The aim of this study was to compare the effects of high- and low-frequency electrical stimulation of the forearm on sensitivity to pressure-pain in the ipsilateral forehead, as inhibitory pain modulation may be stronger after low- than high-frequency electrical stimulation. Before and after high- and low-frequency electrical stimulation, sensitivity to heat and to blunt and sharp stimuli was assessed at and adjacent to the electrically conditioned site in the forearm. In addition, sensitivity to blunt pressure was measured bilaterally in the forehead. Pain was more intense after high- than low-frequency electrical stimulation and was followed by primary and secondary hyperalgesia to mechanical stimulation after high- but not low-frequency electrical stimulation. Nevertheless, sensitivity to pressure-pain decreased to the same extent in the ipsilateral forehead after both forms of electrical stimulation. This decrease was associated with heightened sensitivity to pressure-pain at the electrically conditioned forearm site and with diminished sensitivity to heat around this site. These findings suggest that sensitisation of pressure-sensitive nociceptive afferents at the site of electrical stimulation is associated with generation of an ipsilateral pain-inhibitory process. This ipsilateral pain-inhibitory process may decrease sensitivity to pressure-pain in the ipsilateral forehead and suppress secondary hyperalgesia to heat.
Publisher: Springer Science and Business Media LLC
Date: 12-05-2018
DOI: 10.1007/S00221-018-5255-X
Abstract: Exposure to moderate levels of ultraviolet B radiation (UVB) is painless but nevertheless induces an inflammatory response that sensitizes primary afferent nociceptors. Subsequently, heating the UVB-treated site can sensitize spinal nociceptors. We used a repeated-measures design to determine whether heating the UVB-treated site also triggers ipsilateral inhibitory controls. Specifically, a 2-cm diameter site on the forearm of 20 participants was exposed to UVB at twice the minimum erythema dose. 48 h later mechanical and thermal sensitivity had increased at the UVB-treated site, indicating primary hyperalgesia. In addition, sensitivity to blunt pressure had increased in the ipsilateral forehead, implying activation of an ipsilateral supra-spinal pro-nociceptive mechanism. Despite this, the area under the curve of the ipsilateral nociceptive blink reflex decreased when the UVB-treated site was heated to induce moderate pain. Together, these findings suggest that the UVB treatment sensitized primary nociceptive afferents and generated an ipsilateral supra-spinal pro-nociceptive mechanism. In addition, sensitization to heat induced by the UVB treatment strengthened an ipsilateral anti-nociceptive process elicited by heat-pain. Infrequent but enduring discharge of sensitized primary nociceptive afferents, driven by inflammation after UVB exposure, might initiate a lateralized supra-spinal pro-nociceptive influence that heightens awareness of impending harm on the sensitized side of the body. In addition, a lateralized anti-nociceptive response triggered by an intense barrage of nociceptive signals may help to differentiate stronger from weaker sources of pain.
Publisher: Wiley
Date: 29-05-2015
DOI: 10.1002/EJP.736
Abstract: In healthy humans, high-frequency electrical stimulation (HFS) of the forearm not only produces hyperalgesia at the site of stimulation but also reduces sensitivity to pressure-pain on the ipsilateral side of the forehead. In addition, HFS augments the ipsilateral trigeminal nociceptive blink reflex and intensifies the ipsilateral component of conditioned pain modulation. The aim of this study was to determine whether α2-adrenoceptors mediate these ipsilateral nociceptive influences. The α2-adrenoceptor antagonist yohimbine was administered to 22 participants in a double-blind, placebo-controlled crossover study. In each session, thermal and mechanical sensitivity in the forearms and forehead was assessed before and after HFS. In addition, the combined effect of HFS and yohimbine on the nociceptive blink reflex and on conditioned pain modulation was explored. In this paradigm, the conditioning stimulus was cold pain in the ipsilateral or contralateral temple, and the test stimulus was electrically evoked pain in the forearm. Blood pressure and electrodermal activity increased for several hours after yohimbine administration, consistent with blockade of central α2-adrenoceptors. Yohimbine not only augmented the nociceptive blink reflex ipsilateral to HFS but also intensified the inhibitory influence of ipsilateral temple cooling on electrically evoked pain at the HFS-treated site in the forearm. Yohimbine had no consistent effect on primary or secondary hyperalgesia in the forearm or on pressure-pain in the ipsilateral forehead. These findings imply involvement of α2-adrenoceptors both in ipsilateral antinociceptive and pronociceptive pain modulation processes. However, a mechanism not involving α2-adrenoceptors appears to mediate analgesia in the ipsilateral forehead after HFS.
Publisher: Elsevier BV
Date: 11-2016
DOI: 10.1016/J.JPAIN.2016.07.004
Abstract: In healthy humans, high-frequency electrical stimulation (HFS) of the forearm not only evokes local signs of central sensitization but also triggers broader ipsilateral inhibitory influences on pain akin to a lateralized form of conditioned pain modulation. Paradoxically, some of these inhibitory influences are augmented by α HFS not only evokes local signs of central sensitization but also triggers a broader ipsilateral antinociceptive mechanism mediated by opioid receptors. Dysfunction of this lateralized pain modulation process might contribute to painful unilateral disorders such as migraine or complex regional pain syndrome.
Publisher: Walter de Gruyter GmbH
Date: 10-02-2021
Abstract: The expression of pain in males and females involves complex socio-psychological mechanisms. Males may report lower pain to a female experimenter to appear strong, whereas females may report higher pain to a male experimenter to appear weak and to seek protection. However, evidence to support these stereotypes is inconclusive. In iduals who catastrophise about pain rate higher pain than those who do not. How pain catastrophising interacts with the effect of the experimenter’s sex on pain reports is yet to be explored. Thus, the aim of this study was to determine whether pain catastrophising moderated the effect of the experimenter’s sex on pain reports in healthy males and females. Participants (n=60, 30 males) were assigned to one of four experimental conditions: males tested by male experimenters, males tested by female experimenters, females tested by male experimenters, and females tested by female experimenters. Participants completed the Pain Catastrophising Scale, and then sensitivity to heat and to blunt (pressure-pain threshold) and sharp stimuli was assessed on both forearms, and to high frequency electrical stimulation (HFS) administered to one forearm. Females reported lower pressure-pain thresholds than males irrespective of the experimenters’ sex. Females reported lower sharpness ratings to male than female experimenters only when the test stimuli were moderately or intensely sharp. Higher pain catastrophising scores were associated with higher sharpness ratings in females but not males. Additionally, higher pain catastrophising scores were associated with greater temporal summation of pain to HFS, and with lower pressure-pain thresholds in females who were tested by male experimenters. These findings indicate that the experimenters’ sex and the participant’s pain catastrophising score influence pain reports, particularly in females. Awareness of these psychosocial factors is important in order to interpret pain responses in a meaningful way, especially when females are tested by male experimenters. A greater awareness of sex/gender role biases and their potential interaction with pain catastrophising may help researchers and clinicians to interpret pain reports in meaningful ways. In turn, this may help to improve delivery of treatments for patients with chronic pain.
Publisher: Wiley
Date: 19-07-2013
DOI: 10.1002/J.1532-2149.2013.00370.X
Abstract: High-frequency electrical stimulation (HFS) of the human forearm evokes analgesia to blunt pressure in the ipsilateral forehead, consistent with descending ipsilateral inhibitory pain modulation. The aim of the current study was to further delineate pain modulation processes evoked by HFS by examining sensory changes in the arm and forehead investigating the effects of HFS on nociceptive blink reflexes elicited by supraorbital electrical stimulation and assessing effects of counter-irritation (electrically evoked pain at the HFS-conditioned site in the forearm) on nociceptive blink reflexes before and after HFS. Before and after HFS conditioning, sensitivity to heat and to blunt and sharp stimuli was assessed at and adjacent to the conditioned site in the forearm and on each side of the forehead. Nociceptive blink reflexes were also assessed before and after HFS with and without counter-irritation of the forearm. HFS triggered secondary hyperalgesia in the forearm (a sign of central sensitization) and analgesia to blunt pressure in the ipsilateral forehead. Under most conditions, both HFS conditioning and counter-irritation of the forearm suppressed electrically evoked pain in the forehead, and the litude of the blink reflex to supraorbital stimuli decreased. Importantly, however, in the absence of forearm counter-irritation, HFS conditioning facilitated ipsilateral blink reflex litude to supraorbital stimuli delivered ipsilateral to the HFS-conditioned site. These findings suggest that HFS concurrently triggers hemilateral inhibitory and facilitatory influences on nociceptive processing over and above more general effects of counter-irritation. The inhibitory influence may help limit the spread of sensitization in central nociceptive pathways.
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: Ovid Technologies (Wolters Kluwer Health)
Date: 30-10-2020
DOI: 10.1097/AJP.0000000000000893
Abstract: In complex regional pain syndrome (CRPS), sensory deficits and/or hyperalgesia often extend beyond the affected limb to encompass other sites on the ipsilateral side of the body. The aim of this study was to determine whether hyperalgesia in the ipsilateral forehead reflects disinhibition and/or sensitization of trigeminal afferent or second-order neurons on the CRPS-affected side. To investigate this, blink reflexes to supraorbital electrical stimuli (a 2 mA triple pulse delivered using a concentric electrode) were recorded bilaterally in 30 CRPS patients and 20 controls of similar age and sex distribution. In addition, the effect of acoustic startle stimuli on pain and blink reflexes to supraorbital electrical stimuli was explored. Supraorbital electrical stimulation was more painful on the affected than unaffected side in patients ( P .05), and was more painful on both sides in patients than controls ( P .001). In addition, electrical stimulation of the ipsilateral forehead increased loudness and auditory discomfort to acoustic startle stimuli ( P .05). However, blink reflexes were similar on both sides in patients, and smaller in litude and of longer latency in patients than controls ( P .05). These findings suggest that trigeminal sensory nerve input activates sensitized and/or disinhibited nociceptive circuits in the thalamus or higher cortical centers in CRPS. This not only evokes ipsilateral supraorbital hyperalgesia but also compromises auditory perception. Hence, crosstalk between auditory and nociceptive signals at sites of convergence within the central nervous system may generate hyperacusis in CRPS.
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 Lechi Vo.