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The effects of ongoing nociceptor discharge on sensory and autonomic activity and the relationship between psychophysiological factors and the subjective experience of pain in reflex sympathetic dystrophy

Blockey, Paul (1996) The effects of ongoing nociceptor discharge on sensory and autonomic activity and the relationship between psychophysiological factors and the subjective experience of pain in reflex sympathetic dystrophy. Professional Doctorate thesis, Murdoch University.

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Abstract

Complex neural mechanisms are thought to underlie the development of reflex sympathetic dystrophy. Evidence in the literature to date suggests the involvement of interactive changes at the level of both the peripheral and central nervous systems. Exactly how these changes account for the various autonomic and sensory disturbances accompanying reflex sympathetic dystrophy, or how psychological factors impinge on these pathophysiological mechanisms, is still not fully understood. To investigate these issues, four studies were carried out; the first three on healthy subjects and the last on patients who met the diagnostic criteria for reflex sympathetic dystrophy.

In Study 1, the reliability of autonomic responses over time in the presence of capsaicin-induced C-nociceptor activity, and the symmetry of autonomic responses to stimulation were examined. The capsaicin was topically applied to the forearm in some subjects and to the dorsal surface of the hand in others. The autonomic stimuli comprised of a deep breath and presentation of a loud tone though earphones (also used in subsequent studies). In Study 1, as in each of the studies, vascular responses and sweat gland activity in the fingers were assessed using photoplethysmography and skin conductance recordings respectively. A high degree of symmetry in vasoconstriction and skin conductance responses was found between the limbs of healthy subjects in the presence of acute chemogenic pain in one limb.

Study 2 was carried out to assess whether autonomic responses within the ulnar nerve distribution on the capsaicin-inflamed hand would differ from those observed within the same nerve distribution on the contralateral limb. Pulse transducers were attached to the palmar side of the fifth finger and skin conductance electrodes were placed on the palmar surface of each hand (all within the ulnar nerve distribution). The capsaicin was applied to the dorsal surface of the right hand, within the ulnar nerve distribution. Study 2 also set out to determine the symmetry of sensory responses in each of the nerve distributions of both hands and to assess the reliability of touch thresholds over time, in the presence of capsaicin-induced C­nociceptor activity. A thermocouple-controlled Peltier device was used to present the heat stimulus during the collection of warmth and heat-pain thresholds. Two­point discrimination thresholds were assessed by dragging two metal points across the skin. Touch thresholds were assessed using six graded Von Frey filaments. In addition, the Peltier device was used to heat the capsaicin-inflamed cutaneous region. This was done to determine the symmetry of vascular and sweating responses during thermal hyperalgesia. There were three separate heating conditions: two experimental conditions during which either the tone or breath stimulus was presented, and a control condition. Subjective pain ratings were obtained throughout each of the conditions using a ten-point verbal analogue scale. Pain ratings were obtained to determine whether an increase in sympathetic activity following the presentation of the autonomic stimuli was associated with any change in the level of pain experienced. Study 2 found that chemogenic pain in the hand had no effect on pulse amplitude and skin conductance responses to the autonomic stimuli. However, the investigation of sensory responses identified asymmetries between the limbs, typically corresponding to greater sensitivity on the left side in right-handed subjects. The presence of capsaicin-induced C-nociceptor activity within the ulnar nerve distribution one hand was associated with higher touch thresholds within that nerve distribution, but touch thresholds in the median and radial nerve distributions did not change after the application of capsaicin. Heating the capsaicin-inflamed skin resulted in a bilateral vasoconstrictor response, but was not associated with any increase in sweat gland activity. Subjective pain ratings were not found to differ across the heating conditions, suggesting that increases in autonomic activity did not increase C-nociceptor activity.

In Study 3, a range of sensory thresholds (warmth, heat-pain, touch, pressure­pain, two-point discrimination) were measured before and after topical application of capsaicin. In addition, the symmetry of vascular and sweating responses were assessed during a stepped increase in the heat applied to the capsaicin-inflamed skin. Two heating conditions were employed: a control condition and one in which the tone was presented. Subjective pain ratings were collected every five seconds. The presence of capsaicin-induced C-nociceptor activity was associated with higher touch thresholds and lower pressure-pain thresholds within the cutaneous nerve distribution to which the caspaicin was applied. No changes were observed in other sensory modalities. Vasoconstrictor responses increased in a stepwise fashion with corresponding increases in the heat stimulus intensity, while there was no fluctuation in skin conductance responses. The absence of sweat gland activity suggests that decreases in pulse amplitude did not reflect a nonspecific stress response. The findings supported the hypothesis that ongoing C-nociceptor stimulation induces a bilateral vasoconstrictor reflex at the spinal level. A decrease in subjective pain ratings following the presentation of a startling stimulus (tone) was observed in healthy subjects with acute chemogenic pain. It was hypothesised that this decrease in subjective pain ratings may have been due to mechanisms of pain inhibition that may involve the central or peripheral modulation of nociceptive transmission.

In Study 4, the symmetry between autonomic responses (this time including a cold stimulus: a bronze bar refrigerated to 5 degrees Celsius) in the affected and unaffected limbs of a sample of reflex sympathetic dystrophy sufferers was assessed. In subjects with pain in an upper limb, pulse tranducers and electrodes were placed on the palmar side of the fingers. In those with pain in a lower limb, recordings were taken from the ventral side of the toes. Vasoconstrictor responses to the breath and tone stimuli were significantly greater in the affected limb in comparison to the contralateral unaffected limb. Vasoconstrictor responses to the autonomic stimuli were independent of skin conductance fluctuations, suggesting that reflex sympathetic dystrophy is associated with aberrations of specific autonomic mechanisms. The results supported the hypothesis that reflex sympathetic dystrophy is not associated with a general increase in sympathetic outflow to the affected extremity. The observed asymmetry between the affected and unaffected limb in subjects with reflex sympathetic dystrophy may be due to peripheral structures developing a hypersensitivity to circulating or neurally-released vasoconstrictive agents. Study 4 also examined whether autonomic activity induced through presentation of the breath, tone and cold stimuli impacted on the subjective experience of pain in subjects with reflex sympathetic dystrophy. The presentation of these stimuli was accompanied by increases in subjective pain ratings in some, but not all subjects with reflex sympathetic dystrophy. The findings support the notion that multiple mechanisms involving both nociceptive and non-nociceptive afferents may underlie continuous pain in reflex sympathetic dystrophy. The lack of any decrease in subjective pain ratings following autonomic arousal suggests that reflex sympathetic dystrophy may also involve a failure in the modulation of pain. These results support the notion that emotional states such as anxiety may lead to an increase in the pain experienced by individuals with reflex sympathetic dystrophy.

Taken together, the results of the four studies indicate that the sensory and autonomic abnormalities of reflex sympathetic dystrophy do not seem to be a product of ongoing peripheral nociceptor input alone. Nevertheless, capsaicin appears useful for investigating the acute effects of nociception on sensory and autonomic activity.

Item Type: Thesis (Professional Doctorate)
Murdoch Affiliation: School of Social Sciences
Notes: Note to the author: If you would like to make your thesis openly available on Murdoch University Library's Research Repository, please contact: repository@murdoch.edu.au. Thank you.
Supervisor(s): Drummond, Peter
URI: http://researchrepository.murdoch.edu.au/id/eprint/52213
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