Pain
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For years, physical deconditioning has been thought to be both a cause and a result of back pain. As a consequence physical reconditioning has been proposed as treatment-goal in patients with chronic low back pain (LBP). However, it is still unclear whether a patient's physical fitness level really decreases after pain-onset. ⋯ Results showed that only in a subgroup of patients a PAL-decrease had occurred after the onset of pain, whereas no signs of physical deconditioning were found. Negative affect and the patients' perceived physical activity decline in the subacute phase predicted a decreased level of PAL over one year. Based on these results, we conclude that as to the assumption that patients with CLBP suffer from disuse and physical deconditioning empirical evidence is still lacking.
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Complex regional pain syndrome (CRPS) may lead to movement disorders (MDs) in some patients. Reliable information on the nature, chronology and clinical determinants of MDs in CRPS patients is lacking but could provide better insight in to the underlying pathophysiological mechanism. We retrospectively evaluated the clinical and temporal characteristics of MDs in patients with CRPS. ⋯ The hazard of developing dystonia in subsequent extremities increased with the number of extremities affected by dystonia. We conclude that dystonia in CRPS shows highly variable onset latency and is associated with younger age at onset and increased risk of developing dystonia in other extremities. The delayed onset and progression of dystonia in CRPS may indicate the involvement of a different underlying mechanism, possibly associated with maladaptive neuroplasticity.
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Neuropathic pain after spinal cord injury is not well understood and is difficult to treat. One possible cause is mismatch between motor commands and sensory feedback. This two-part study in five paraplegic patients investigated whether a visual illusion aimed to correct this mismatch reduces pain. ⋯ Mean (95% CI) decrease in pain was 53 mm (45-61 mm) at post training and 43 mm (27-58 mm) at 3-month follow-up. Virtual walking may be a viable treatment for pain after spinal cord injury. A clinical trial seems warranted.
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Using a gene expression analysis approach we found that the mRNA encoding the lysosomal cysteine protease cathepsin S (CatS) was up-regulated in rat dorsal root ganglia (DRG) following peripheral nerve injury. CatS protein was expressed in infiltrating macrophages in DRG and near the site of injury. At both sites CatS expression progressively increased from day 3 to day 14 after injury. ⋯ In nerve-injured rats, mechanical hyperalgesia, but not allodynia, was significantly reversed for up to 3h by systemic administration of a non-brain penetrant, irreversible CatS inhibitor (LHVS, 3-30 mg/kg s.c.). Depletion of peripheral macrophages by intravenous injection of liposome encapsulate clodronate (1ml, 5 mg/ml) partially reduced established mechanical hyperalgesia but not allodynia, and abolished the anti-hyperalgesic effect of LHVS. Our results demonstrate a pro-nociceptive effect of CatS and indicate that endogenous CatS released by peripheral macrophages contributes to the maintenance of neuropathic hyperalgesia following nerve injury.