Pain
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Using latent class analysis (LCA), a previous study on patients attending primary care identified four courses of low back pain (LBP) over the subsequent 6 months. To date, no studies have used longitudinal pain recordings to examine the "natural" course of recurrent and chronic LBP in a population-based sample of individuals. This study examines the course of LBP in the general population and elaborates on the stability and criterion-related validity of the clusters derived. ⋯ Three of the four clusters describing the typical course of pain matched the clusters described previously for patients in primary care. Due to the population-based design, this study achieves, for the first time, a close insight into the "natural" course of chronic and recurrent low back pain, including individuals that did not necessarily visit the general practitioner. The findings will help to understand better the nature of this pain in the general population.
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We aimed to study the quality of communication between health care providers and patients with low back pain with emphasis on information giving in a back pain clinic, including if characteristics of patients could be associated with communication quality. We videotaped 79 encounters in which 21 providers informed patients about the results of magnetic resonance imaging of the back. Background information about the patients was collected by questionnaires and interview after the encounter. ⋯ The results were significant for all professional subgroups (doctors, physiotherapists, chiropractors). Communication quality in encounters with back pain patients is worse, the longer the patient has suffered pain. Poor communication quality also seems to be associated with patients being older.
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In patients with distal symmetric polyneuropathy we assessed non-nociceptive Abeta- and nociceptive Adelta-afferents to investigate their role in the development of neuropathic pain. We screened 2240 consecutive patients with sensory disturbances and collected 150 patients with distal symmetric polyneuropathy (68 with pain and 82 without). All patients underwent the Neuropathic Pain Symptom Inventory to rate ongoing, paroxysmal and provoked pains, a standard nerve conduction study (NCS) to assess Abeta-fibre function, and laser-evoked potentials (LEPs) to assess Adelta-fibre function. ⋯ In patients with ongoing pain the severe LEP suppression and the correlation between pain intensity and LEP attenuation may indicate that this type of pain reflects damage to nociceptive axons. The partially preserved LEPs in patients with provoked pain suggest that this type of pain is related to the abnormal activity arising from partially spared and sensitised nociceptive terminals. Because clinical and neurophysiological abnormalities followed similar patterns regardless of aetiology, pain should be classified and treated on mechanism-based grounds.
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The aim of mindfulness meditation is to develop present-focused, non-judgmental, attention. Therefore, experience in meditation should be associated with less anticipation and negative appraisal of pain. In this study we compared a group of individuals with meditation experience to a control group to test whether any differences in the affective appraisal of pain could be explained by lower anticipatory neural processing. ⋯ Meditation was also associated with lower activity in S2 and insula during the pain-evoked response, although the experiment could not disambiguate this activity from the preceding anticipation response. Our data is consistent with the hypothesis that meditation reduces the anticipation and negative appraisal of pain, but effects on pain-evoked activity are less clear and may originate from preceding anticipatory activity. Further work is required to directly test the causal relationship between meditation, pain anticipation, and pain experience.
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The enzyme 3alpha-hydroxysteroid oxido-reductase (3alpha-HSOR) catalyzes the synthesis and bioavailability of 3alpha,5alpha-neurosteroids as allopregnanolone (3alpha,5alpha-THP) which activates GABA(A) receptors and blocks T-type calcium channels involved in pain mechanisms. Here, we used a multidisciplinary approach to demonstrate that 3alpha-HSOR is a cellular target the modulation of which in dorsal root ganglia (DRG) may contribute to suppress pain resulting from peripheral nerve injury. Immunohistochemistry and confocal microscope analyses showed 3alpha-HSOR-immunostaining in naive rat DRG sensory neurons and glial cells. ⋯ Most importantly, in vivo knockdown of 3alpha-HSOR expression in healthy rat DRG using 6-carboxyfluorescein-3alpha-HSOR-siRNA exacerbated thermal and mechanical pain perceptions. This paper is the first to show that siRNA-induced knockdown of a key neurosteroid-synthesizing enzyme directly affects an important function as nociception. Hopefully, these results may be useful for the development of novel analgesics.