• Complex regional pain syndrome
• Pain drawings
• Pain sensitization
• Prospective study
• Spatial distribution of pain

• 24-012 Australian and New Zealand College of Anaesthetists

• Cytokines
• Fibromyalgia
• Lower back pain
• Osteoarthritis
• Post surgery pain
• Rheumathoid arthritis
• Temporomandibular joint disease

• Humans
• Cytokines/metabolism
• Cytokines/immunology
• Musculoskeletal Pain/metabolism
• Musculoskeletal Pain/immunology
• Musculoskeletal Pain/drug therapy
• Chronic Pain/metabolism
• Chronic Pain/immunology
• Animals
• Acute Pain/metabolism
• Acute Pain/immunology

• complex regional pain syndrome
• evidence‐based medicine
• interventional treatment
• intrathecal treatment
• intravenous treatment
• neurostimulation
• sympathetic blockade

• Humans
• Complex Regional Pain Syndromes/therapy
• Complex Regional Pain Syndromes/diagnosis
• Complex Regional Pain Syndromes/physiopathology
• Pain Management/methods

• Botulinum toxin A
• Budapest criteria
• Complex regional pain syndrome
• amputation
• antioxidants
• dorsal root ganglion stimulation
• gabapentin
• ketamine
• spinal cord stimulation
• sympathetic blocks

• Humans
• Complex Regional Pain Syndromes/diagnosis
• Complex Regional Pain Syndromes/therapy
• Complex Regional Pain Syndromes/epidemiology
• Chronic Pain/diagnosis
• Chronic Pain/therapy
• Pain Measurement/methods

• Acrocyanosis
• Chilblains / pernio
• Complex regional pain syndrome
• Erythromelalgia
• Lupus chilblains
• Paraneoplastic acral vascular syndrome
• Raynaud's disease
• Raynaud's mimickers
• Raynaud's phenomena
• Raynaud's syndrome
• Thoracic outlet syndrome
• Thromboangiitis obliterans

• Humans
• Raynaud Disease/diagnosis
• Raynaud Disease/physiopathology
• Diagnosis, Differential
• Pain/diagnosis

• complex regional pain syndrome
• corticoids
• treatment

• CRPS
• mixed pain
• neuropathic pain
• nociceptive pain
• nociplastic pain
• personalized medicine

• No funding for

• Complex regional pain syndrome
• Subgroups
• Subtypes

• boron-containing compounds
• complex regional pain syndrome
• gut–brain axis
• gut–immune system axis
• gut–musculoskeletal axis
• microbiota
• prebiotic boron

• Humans
• Boron
• Dysbiosis
• Microbiota
• Inflammation
• Neuralgia/drug therapy
• Neuralgia/etiology
• Complex Regional Pain Syndromes/drug therapy

• POCU/993/6/13/153178 European Social Fund within the Sectorial Operational Program Human Capital 2014-2020

• Acupuncture
• Case report
• Complex regional pain syndrome
• Herbal medicine
• Moxibustion
• Traditional Chinese medicine

• complex regional pain syndrome
• glial cells
• keratinocytes
• neurogenic inflammation
• neuroinflammation

• K08 CA228039 NCI NIH HHS
• the National Natural Science Foundation of China
• National Institutes of Health of USA
• VeloSano Pilot Award, Steve and Melody Golding Foundation

• CRPS
• TNF-α inhibitors
• anti-inflammatories
• complex regional pain syndrome
• inflammation
• treatment

• Humans
• Complex Regional Pain Syndromes
• Cytokines/genetics
• Cytokines/metabolism
• Inflammation/metabolism
• Interleukin-6/metabolism
• Keratinocytes/metabolism
• Keratinocytes/pathology
• Phenylephrine/pharmacology
• Receptors, Adrenergic/metabolism
• Tumor Necrosis Factor-alpha/metabolism
• Receptors, Adrenergic, alpha-1/metabolism

Algodystrophy or complex regional pain syndrome is a chronic pain condition characterized by hyperalgesia and allodynia. Patients with algodystrophy present an amplified and persistent activation of the innate immune system, with subsequent proliferation of keratinocytes and release of proinflammatory cytokines including interleukin (IL)-6, IL-1β, and tumor necrosis factor-α (TNF-α). Chronic inflammation and increased levels of cytokines are observed also in Ph-negative myeloproliferative neoplasms, including polycythemia vera, essential thrombocythemia, and primary myelofibrosis. Chronic myeloid neoplasms are characterized by overproduction of one or more mature non-lymphoid cell lineages, with erythrocytosis, thrombocytosis, and/or myeloproliferation.

Three case reports described our experience in the treatment of algodystrophy and rheumatic conditions in patients with myelofibrosis; a literature search was also performed.

The first patient was a 58-year-old woman who suffered from chronic myeloproliferative neoplasm in myelofibrotic evolution, under treatment with ruxolitinib and pre-treated with hydroxyurea; she reported inflammatory pain, and swelling of the tibiotarsal joints bilaterally. She was treated with neridronate 2 mg/kg for four days and methotrexate 15 mg per os per week, achieving a clinical benefit. The second patient was a 63-year-old woman diagnosed with polycythemia vera evolving to myelofibrosis. She experienced pain and swelling of the left tibiotarsal joint and difficulty walking. A therapy with low-dose steroid per os and intramuscular clodronate was administered for four months, followed by methotrexate at 15 mg per week. After two months, tenosynovitis significantly improved, as supported by the evidence of improved bone edema of the left tibiotarsal joint revealed in the magnetic resonance imaging, and pain symptoms were clinically ameliorated. The third patient was a 70-year-old male patient affected by essential thrombocythemia with myelofibrotic evolution and a paraneoplastic polymyalgia rheumatica treated with steroids and currently in remission. The patient received ruxolitinib for about two years; after the first year of treatment, he experienced pain and swelling of the right tibiotarsal joint with difficulty in walking, with a consequent diagnosis of edema and tenosynovitis, as per algodystrophy. After consulting a rheumatologist, the patient received therapy with neridronate intramuscularly with clinical benefit.

As overlapping interactions and clinical manifestations between hematologic neoplasms and rheumatologic diseases exist, new clinical manifestations, such as algodystrophy, may emerge during myelofibrosis and need to be monitored in the long term by a multidisciplinary team.

Neuropathic pain is the most common clinical sign of complex regional pain syndrome (CRPS). Currently, lumbar sympathetic block (LSB) is commonly utilized in lower extremity CRPS that has failed to respond to medication therapy and physical therapy, but its effectiveness is unknown. The tourniquet ischemia test (IT) can distinguish between two types of CRPS: IT-positive CRPS and IT-negative CRPS.

The aim of the study was to investigate whether LSB improves pain scores in patients with lower extremity CRPS-1 and to screen factors to predict its efficacy.

Prospective clinical observational study.

Pain management center.

Forty-three patients diagnosed with lower extremity CRPS-1 using the Budapest criteria were included as participants.

Forty-three CRPS-1 patients were treated with LSB therapy, and all of them underwent a tourniquet ischemia test (IT) before undergoing LSB therapy. LSB therapy was performed using a combination of ultrasonography and fluoroscopy. Then, numeric rating scale (NRS) scores and the symptom relief rates of patients were evaluated at 1, 4, and 12 weeks. Finally, peripheral blood inflammatory cytokine samples were collected before and after the LSB treatment.

At 4 weeks after the treatment, the total effective symptom relief rate of LSB on CRPS-1 was 25.6% (11/43), with 52.6% (10/19) of IT(+) patients and 4.2% (1/24) of IT(-) patients. There was a significant difference between the IT(-) and IT(+) groups (P = 0.001). The multivariate binary logistic regression analysis revealed that the response to the tourniquet IT was the only significant independent predictor of sympathetic block success (p = 0.007).

Tourniquet IT is a simple, safe and effective test to distinguish patients with lower extremity CRPS-1. The response to the tourniquet IT is a reliable predictor of LSB effectiveness in lower extremity CRPS-1 patients.

• the Shanghai Municipal Health Commission

• Algoneurodystrophy
• Causalgia
• Complex regional pain syndrome (CRPS)
• Post-traumatic stress disorder (PTSD)
• Reflex sympathetic dystrophy (RSD)
• Sudeck atrophy

Poor sleep quality and pain were common and had been proved as an important influenced factor of quality of life for patients with COPD. The association of sleep quality with pain has been observed in other population but remains unclear in mild patients with COPD from a community setting.

A cross-sectional study was conducted to include eligible mild patients with COPD in Pudong New District of Shanghai. A structured questionnaire was used to collect general and clinical information for the patients. The Chinese version of Pittsburgh Sleep Quality Index (PSQI) and the short form of McGill Pain Questionnaire (SF-MPQ) was used to assess sleep quality and intensity of pain. Logistic regression was performed to test the association between sleeping quality and pain intensity.

Two hundred and sixty-four patients with COPD, with an average age of 64 years (SD 5.78 years), were enrolled, and of 52% were women. Seventy-one (26.9%) participants reported at least one exacerbation during the past year. About 28.2% of the patients were classified as having poor sleep quality. Sleep quality was significantly associated with PRI score (adjusted odds ratio (ORad)=2.16, 95% CI: 1.16–4.00) and PPI rank (ORad=1.90, 95% CI: 1.08–3.34). People with daytime disturbance were more likely to have pain (ORad =2.03, 95% CI: 1.18–3.50).

Poor sleep quality was common in mild patients with COPD in community and was associated with higher pain intensity. Pain may involve an impairment of sleep quality.

• Pittsburgh sleep quality index
• SF-MPQ
• chronic obstructive pulmonary disease
• pain
• sleep

• Bradykinin receptor antagonists
• Chronic pain
• Hyperalgesia
• Inflammation
• Inflammatory mediators
• Kinins

• Animals
• Bradykinin Receptor Antagonists/pharmacology
• Cholinesterase Inhibitors/pharmacology
• Chronic Pain/etiology
• Chronic Pain/genetics
• Chronic Pain/metabolism
• Disease Models, Animal
• Female
• Gene Expression Regulation/drug effects
• Gene Silencing/drug effects
• Hyperalgesia/complications
• Ischemia/complications
• Male
• Mice
• Nociception/drug effects
• Receptors, Bradykinin/genetics
• Receptors, Bradykinin/metabolism
• Spinal Cord/pathology

• Harden-Bruehl criteria
• causalgia
• complex regional pain syndrome
• confirmatory assay
• reflex sympathetic dystrophy
• relative pain reduction
• screening test
• tourniquet ischemia test

Complex regional pain syndrome (CRPS) is characterized by continuous pain that is often accompanied by sensory, motor, vasomotor, sudomotor, and trophic disturbances. If left untreated, it can have a significant impact on the quality of life of patients. The diagnosis of CRPS is currently based on a set of relatively subjective clinical criteria: the New International Association for the Study of Pain clinical diagnostic criteria for CRPS. There are still no objective laboratory tests to diagnose CRPS and there is a great need for simple, objective, and easily measurable biomarkers in the diagnosis and management of this disease. In this review, we discuss the role of inflammation in the multi-mechanism pathophysiology of CRPS and highlight the application of potential biomarkers of inflammation in the diagnosis and management of this disease.

Complex regional pain syndrome (CRPS) is a perplexing painful syndrome of the extremities usually following a harmful event. It is distinguished in two types, mainly depending on the presence of nerve injury. Although its prevalence may vary depending on social and ethnic factors, middle-aged women seem to suffer most often and the upper limb is the most commonly affected extremity. Apart from pain, which is the dominating feature, the clinical picture unfolds across several domains: sensory, motor, autonomic and trophic. This syndrome develops in two phases, the acute (warm) phase, with the classic symptoms of inflammation, and the chronic (cold) phase, often characterized by trophic changes of the soft tissues and even bones. Although the syndrome has been studied for over two decades, no imaging or laboratory test has been established for the diagnosis and recently proposed diagnostic criteria have not yet been validated and are only occasionally applied. Its pathophysiology is still quite obscure, although the most likely mechanisms involve the classic and neurogenic paths of inflammation mediated by cytokines and neuropeptides, intertwined with changes of the autonomic and central nervous system, psychological mechanisms and, perhaps, autoimmunity. Although plenty of treatment modalities have been tried, none has been proven unequivocally efficacious. Apart from information and education, which should be offered to all patients, the most effective pharmacological treatments seem to be bisphosphonates, glucocorticoids and vasoactive mediators, while physical therapy and rehabilitation therapy also make part of the treatment.

• Complex regional pain syndrome
• algoneurodystrophy
• causalgia
• neuropathic pain
• nociceptive pain
• reflex sympathetic dystrophy

• Complex regional pain syndrome
• Disability
• Pain
• Therapy