Pain medicine : the official journal of the American Academy of Pain Medicine
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Complex regional pain syndrome I (CRPS I) is defined by the International Association for the Study of Pain (IASP) criteria to include pain that is disproportionate to the inciting event, sensory disturbances such as allodynia/ hyperalgesia, autonomic dysfunction, and motor dysfunction that usually occurs after trauma that is frequently trivial and generally expressed in an extremity. These symptoms are well described in the adult population, but there are relatively few data or reports of its prevalence in the pediatric population. Recent studies have demonstrated that unlike the adult population, about 90% of the cases reported are females in a range of 8 to 16 years, the youngest being 3 years old. ⋯ Behavioral management is a mandatory accompaniment of any program of exercise therapy and the sometimes extreme sensory disturbances and parental enmeshment do distinguish the clinical presentation from that in the adult. Interventional procedures may be required in the face of extreme allodynia preventing exercise therapy, and in occasional cases interruption of the sympathetic nerves may reverse this symptom in a few children. Occasionally, continuous analgesia techniques such as that which can be delivered by tunneled epidural catheter or an externalized neurostimulator (spinal cord stimulation) for short periods of time are effective.
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Complex regional pain syndrome (CRPS) patients exhibit multiorgan pathology and inflammatory changes after limb trauma. The objective of this study was to identify how neuro-cutaneous signaling is facilitated after fracture and examine how this altered signaling contributes to the development of CRPS-like changes in the injured limb. ⋯ Collectively, these data suggest that neuro-cutaneous signaling is up-regulated and can mediate inflammatory changes observed in the hindpaw skin of the fracture rat model and in human CRPS skin. Future translational and clinical studies mapping these inflammatory changes may identify novel therapeutic targets for preventing post-traumatic pain from transitioning into chronic CRPS.
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The primary aim of this pilot study was to identify structural and functional brain differences in older adults with self-reported disabling chronic low back pain (CLBP) compared with those who reported nondisabling CLBP. ⋯ Brain structure and function is different in older adults with disabling CLBP compared with those with nondisabling CLBP. Deficits in brain morphology combining groups are associated with pain duration and poor physical function. Our findings suggest brain structure and function may play a key role in chronic pain related disability and may be important treatment targets.
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Case Reports
Painful medial branch neuroma treated with minimally invasive medial branch neurectomy.
Case report. ⋯ Deafferentation injury is a rare but recognized complication of chemical, surgical, and thermal neuroablation. This case report presents a rare instance of presumed neuroma formation following multiple radiofrequency ablations for the treatment of facet-generated mechanical back pain. Open and minimally invasive medial branch neurectomy resulted in complete resolution of pain and return to baseline function.
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Complex regional pain syndrome-type I (CRPS-I; reflex sympathetic dystrophy) is a chronic pain condition that usually follows a deep-tissue injury such as fracture or sprain. The cause of the pain is unknown. We have developed an animal model (chronic post-ischemia pain) that creates CRPS-I-like symptomatology. ⋯ These data, and a large body of clinical evidence, suggest that in at least a subset of CRPS-I patients, the fundamental cause of the abnormal pain sensations is ischemia and inflammation due to microvascular pathology in deep tissues, leading to a combination of inflammatory and neuropathic pain processes. Moreover, we suggest a unifying idea that relates the pathogenesis of CRPS-I to that of CRPS-II. Lastly, our hypothesis suggests that the role of the sympathetic nervous system in CRPS-I is a factor that is not fundamentally causative, but may have an important contributory role in early-stage disease.