Low mechano-afferent fibers reduce thermal pain but not pain intensity in CRPS.

BACKGROUND: Human hairy (not glabrous skin) is equipped with a subgroup of C-fibers, the C-tactile (CT) fibers. Those do not mediate pain but affective aspects of touch. CT-fiber-activation reduces experimental pain if they are intact. In this pilot study we investigated pain modulating capacities of CT-afferents in CRPS. METHODS: 10 CRPS-patients (mean age 33 years, SEM 3.3) and 11 healthy controls (mean age 43.2 years, SEM 3.9) participated. CT-targeted-touch (brush stroking, velocity: 3 cm/s) was applied on hairy and glabrous skin on the affected and contralateral limb. Patients rated pleasantness of CT-targeted-touch (anchors: 1 "not pleasant"-4 "very pleasant") twice daily on 10 days. Pain intensity (NRS: 0 "no pain" - 10 "worst pain imaginable") was assessed before, 0, 30, 60 and 120 min after each CT-stimulation. To assess sensory changes, quantitative-sensory-testing was performed at the beginning and the end of the trial period. RESULTS: CT-targeted-touch was felt more pleasant on the healthy compared to the affected limb on hairy (p < 0.001) and glabrous skin (p 0.002), independent of allodynia. In contrast to healthy controls patients felt no difference between stimulating glabrous and hairy skin on the affected limb. Thermal pain thresholds increased after CT-stimulation on the affected limb (cold-pain-threshold: p 0.016; heat-pain-threshold: p 0.033). CONCLUSIONS: CT-stimulation normalizes thermal pain thresholds but has no effect on the overall pain in CRPS. Therefore, pain modulating properties of CT-fibers might be too weak to alter chronic pain in CRPS. Moreover, CT-fibers appear to lose their ability to mediate pleasant aspects of touch in CRPS.

Acute Lumbar Back Pain.

BACKGROUND: Back pain has many causes. In Germany, about 70% of adults have at least one episode of back pain per year. METHODS: This review is based on a selective literature search and on the German National Disease Management Guideline for Low Back Pain. RESULTS: The physician taking the history from a patient with back pain should ask about the nature, onset, course, localization, and radiation of the pain and its dependence on physical activity and/or emotional stress. In the differential diagnosis, neurologic deficits and any "red flags" suggesting dangerous conditions such as spinal fracture, bacterial infection, and tumors must be ruled out. If no specific cause of the pain can be identified, no imaging studies are indicated on initial presentation. The treatment of acute, nonspecific low back pain focuses on pain relief and functional improvement. Adequate patient education and counseling are essential. Exercise therapy is no more effective than the continuation of normal daily activities. Restriction of activity, including bed rest, is of no benefit and merely prolongs recovery and the resumption of normal activity. Further diagnostic testing is indicated if there is any suspicion of a fracture, infection, or tumor. CONCLUSION: After dangerous conditions have been ruled out, low back pain can be pragmatically classified as either nonspecific or specific. More research is needed so that the diagnostic assessment and individualized treatment of acute lower back pain can be further refined.

Illusion of pain: pre-existing knowledge determines brain activation of 'imagined allodynia'.

UNLABELLED: Allodynia means that innocuous tactile stimulation is felt as pain. Accordingly, cerebral activations during allodynia or touch should markedly differ. The aim of this study was to investigate whether the imagination of allodynia affects brain processing of touch in healthy subjects. Seventeen healthy subjects divided into 2 subgroups were investigated: The first group (n = 7) was familiar with allodynia, based on previous pain studies, whereas the second group (n = 10) had never knowingly experienced allodynia. Using functional magnetic resonance imaging, 2 experimental conditions were investigated. In one condition the subjects were simply touched at their left hand, whereas during the other condition they were asked to imagine pain (allodynia) during tactile stimulation of the right hand and to estimate the imagined pain on a numeric rating scale. Data processing and analysis were performed with the use of SPM5. The group analysis of all subjects revealed that tactile stimulation activated contralateral somatosensory cortices (S1 [primary] and S2 [secondary]), but the imagination of allodynia led to an additional activation of anterior cingulate cortex and bilateral activation of S2, insular cortex, and prefrontal cortices. Subgroup analysis using rating-weighted predictors revealed activation of the contralateral thalamus, anterior cingulate cortex, and amygdala and a bilateral activation of S1, S2, and insular cortex and prefrontal cortices in allodynia-experienced subjects. In contrast, allodynia-inexperienced subjects only activated contralateral S1 and bilateral S2. Just the imagination that touch is painful is able to partly activate the central pain system, but only when the subject has previous experience of this. According to our results, the medial pain system is involved in the encoding of imagined allodynia. PERSPECTIVE: This article reports that pain experience is able to alter central processing of sensory stimuli. Pain knowledge appears to be able to shift "normal" tactile processing to a different quality, resulting in modified brain activity. Therefore, our study may contribute to the current understanding of human pain and will promote future research on this field.

Dysynchiria is not a common feature of neuropathic pain.

Patients with chronic neuropathic pain (non-CRPS) and brush-evoked allodynia watched a reflected image of their corresponding but opposite skin region being brushed in a mirror. Unlike complex regional pain syndrome Type 1, this process did not evoke any sensation at the affected area ('dysynchiria'). We conclude that central nociceptive sensitisation alone is not sufficient to cause dysynchiria in neuropathic pain. The results imply a difference in cortical pain processing between complex regional pain syndrome and other chronic neuropathic pain.