Pain
-
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.
-
Widespread sensory hypersensitivity is present in acute whiplash and is associated with poor recovery. Decreased nociceptive flexion reflex (NFR) thresholds (spinal cord hyperexcitability) are a feature of chronic whiplash but have not been investigated in the acute to chronic injury stage. This study compared the temporal development of sensory hypersensitivity and NFR responses from soon after injury to either recovery or to transition to chronicity. ⋯ In contrast generalized sensory hypersensitivity (pressure and cold) was only ever present in those with persistent moderate/severe symptoms and remained unchanged throughout the study period. This suggests different mechanisms underlie sensory hypersensitivity and NFR responses. In multivariate analyses only initial NDI scores (p=0.003) were a unique predictor of persistent spinal cord hyperexcitability indicating possible ongoing peripheral nociception following whiplash injury.
-
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.
-
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.
-
Chronic pain associated with inflammation is a major clinical problem, but the underlying mechanisms are incompletely understood. Recently, we reported that GRK2(+/-) mice with a approximately 50% reduction of GRK2 develop prolonged hyperalgesia following a single intraplantar injection of the pro-inflammatory cytokine interleukin-1beta (IL-1beta). Here we show that spinal microglia/macrophage GRK2 is reduced during chronic inflammation-induced hyperalgesia. ⋯ These data establish that chronic inflammatory hyperalgesia is associated with reduced GRK2 in microglia/macrophages and that low GRK2 in these cells is sufficient to markedly prolong hyperalgesia after a single intraplantar injection of IL-1beta. Ongoing hyperalgesia is maintained by spinal microglial/macrophage activity, fractalkine signaling, p38 activation and IL-1 signaling. We propose that chronic inflammation decreases spinal microglial/macrophage GRK2, which prevents silencing of microglia/macrophage activity and thereby contributes to prolonged hyperalgesia.