Pain
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Anatomical and physiological studies in animals, as well as functional imaging studies in humans have shown that multiple cortical areas are activated by painful stimuli. The view that pain is perceived only as a result of thalamic processing has, therefore, been abandoned, and has been replaced by the question of what functions can be assigned to individual cortical areas. The following cortical areas have been shown to be involved in the processing of painful stimuli: primary somatosensory cortex, secondary somatosensory cortex and its vicinity in the parietal operculum, insula, anterior cingulate cortex and prefrontal cortex. ⋯ The affective-motivational component is close to what may be considered 'suffering from pain'; it is clearly related to aspects of emotion, arousal and the programming of behaviour. This dichotomy, however, has turned out to be too simple to explain the functional significance of nociceptive cortical networks. Recent progress in imaging technology has, therefore, provided a new impetus to study the multiple dimensions of pain.
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Randomized Controlled Trial Clinical Trial
The effects of disclosure on pain during dental hygiene treatment: the moderating role of catastrophizing.
Catastrophizers and non-catastrophizers were asked to disclose about their dental worries prior to undergoing dental hygiene treatment. It was hypothesized that the effects of emotional disclosure would vary as a function of the level of catastrophizing; where catastrophizers would be more likely than non-catastrophizers to show reductions in pain and emotional distress. The study also examined whether emotional disclosure influenced subsequent levels of catastrophizing and dental anxiety. ⋯ The interaction between condition and level of catastrophizing remained significant even when controlling for emotional distress and the emotional content of the thought records. While catastrophizers benefited from disclosure in regard to their immediate physical and emotional experience, their levels of catastrophizing and dental anxiety remained essentially unchanged. Theoretical and clinical implications of the findings are discussed.
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Recently, Cervero and Laird (NeuroReport, 7 (1996) 526-528; Pain, 68 (1996) 13-23) proposed a new pathophysiological mechanism of dynamic mechanical allodynia in skin. Using the capsaicin pain model in humans, they showed that light mechanical stimulation within an area of secondary mechanical allodynia induces vasodilatation measured by laser-Doppler flowmetry. They suggested that the low-threshold A beta-mechanoreceptive fibres depolarize the central terminals of nociceptive primary afferent neurons via interneurons. ⋯ In conclusion, electrical stimulation of A beta-fibres in allodynic skin does not induce antidromic vasodilatation. Consequently, interaction of A beta-mechanoreceptive fibres and nociceptive C-fibres at a presynaptic level is unlikely to produce antidromically conducted impulses and therefore cannot explain the pathophysiology of mechanical allodynia. Alternatively, it is much more likely that under pathophysiological conditions, activity in A beta-fibres may activate nociceptive second-order neurons, i.e. in the spinal cord.
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Recent animal models of experimental nerve injury have proven useful in evaluating potential sympathetic involvement in neuropathic pain syndromes. We have employed a widely adopted unilateral L5/L6 spinal nerve ligation model to compare the development of mechanical allodynia with neurochemical changes both at the site of peripheral nerve injury and in the dorsal root ganglia (DRG). We have focused on the expression of neuropeptide Y (NPY), a well-studied regulatory peptide and phenotypic marker of sympathetic neurons, and functionally related Y-receptor binding sites following nerve injury. ⋯ Newly established functional interactions of spatially segregated sensory- and sympathetically-derived end bulbs in developing neuromas may enhance neuronal hyperexcitability engendered by aberrant electrical activity at the site of injury. Injury-related alterations in the regulatory activities of NPY released within the DRG at somally-distributed Y-receptors may also contribute to the development and/or persistence of symptoms characteristic of sympathetically-maintained pain. Finally, at later times NPY-mediated modulation of NE release from invading sympathetic axon terminals within the DRG may affect the extent of alpha2 rece
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Case Reports
A case of reflex sympathetic dystrophy (complex regional pain syndrome, type I) resolved by cerebral contusion.
We present a case of refractory reflex sympathetic dystrophy (RSD) (complex regional pain syndrome, type I) whose symptoms (ongoing pain, allodynia, hyperhydrosis and temperature abnormalities) were resolved after the patient suffered a traumatic cerebral contusion in the left temporal lobe, which caused no neurological deficit. This case suggests that symptoms of some RSD patients may largely sustained by a complex network involving the brain.