Complex Regional Pain Syndrome-Type 1 Presenting as deQuervain’s Stenosing Tenosynovitis (original) (raw)
Related papers
Pathogenesis of tendinopathies: inflammation or degeneration?
Arthritis Research & Therapy, 2009
The intrinsic pathogenetic mechanisms of tendinopathies are largely unknown and whether inflammation or degeneration has the prominent role is still a matter of debate. Assuming that there is a continuum from physiology to pathology, overuse may be considered as the initial disease factor; in this context, microruptures of tendon fibers occur and several molecules are expressed, some of which promote the healing process, while others, including inflammatory cytokines, act as disease mediators. Neural in-growth that accompanies the neovessels explains the occurrence of pain and triggers neurogenic-mediated inflammation. It is conceivable that inflammation and degeneration are not mutually exclusive, but work together in the pathogenesis of tendinopathies.
CLINICAL MANAGEMENT : CRPS Complex regional pain syndrome F 2 : physical therapy management
2004
Part I of this article reviewed the history, etiology and underlying mechanisms of CRPS I and II. The current article reviews the available research of physical therapy treatment interventions for patients with CRPS. As outlined in Part 1 of this article, there continues to be much uncertainty about the underlying mechanisms of CRPS. It remains challenging to develop evidence-based guidelines for physical therapy or for any other discipline. There is a paucity of prospective randomized clinical trials. The majority of published reports are case reports or consensus-based. Although the article is written primarily from a physical therapy perspective, the clinical guidelines are also of interest to other health care providers. Given the complexity and scope of CRPS, an interdisciplinary management approach is recommended. & 2003 Elsevier Ltd. All rights reserved.
Complex Regional Pain Syndrome Type I: measurements and treatment
2004
Cervical and lumbar devices are comparably effective 91 Chapter 8 General discussion and conclusion Chapter 9 Summary Chapter 10 Samenvatting 121 Dankwoord Curriculum Vitae u-.v.H A : : 4 © S W ' } h* te CHAPTER 1 Intruduction in patients with CRPS I the behaviour is said to be unproportional to a known organic cause**. It is demonstrated that compared to patients with localised neuropathic pain and chronic back pain patients. CRPS I do not display an unique or unusual pattern in terms of their symptom reporting, anxiety symptoms, pain related dysfunction, illness beha\ iour. and psychological distress". However, other studies show that CRPS I patients display higher >-. •»•* emotional distress, i.e. somatisation and phobic anxiety, than non-CRPS I patients'*'"'. Although, the possibility of a psychopathological aetiology of CRPS I continues to receive support, it is still unclear whether CRPS I patients differ from non-CRPS I patients on u cognitive level. CLINICAL PRESENTATION Sensory symptoms Pain and hyperesthesia arc the predominant sensory symptoms. Hie pain is often described as aching, burning, pricking or shinning. It is localised deep in the tissue. Abnormal sensations to mechanical-and thermal stimuli or upon joint movement are frequently presented. Allodynia is often described. Sensory deficits are common in CRPS I patients'' *•• **• *'. Autonomic symptoms Autonomic signs include swelling, colour and temperature changes, and sweating abnormalities. The swelling is often aggravated by physical activities, painful stimuli, environmental and local temperature changes, and hydrostatic pressure'-2**. 41.42 Motor-and dystrophic symptoms Muscle weakness, tremor, dystonia, myoclonus and decreased range of motion often accompany CRPS I. Range of motion is decreased by joint effusion early in the disease and by contraction and fibrosis later in the disease'-^. Decreased grip strength is observed in 78% of the patients'". Tremor has been reported in 24% to 60% of the patients'*-*'•**. Change in nail and hair growth in affected extremity is frequently reported in patients suffering of CRPS I. These symptoms are often accompanies with skin changes including fibrosis, hyperkeratosis and thin glossy skin''.
Pain Physician, 2016
Background: Motor impairment is an important criterion in the Clinical Diagnostic Criteria (CDC) of Complex Regional Pain Syndrome type-1 (CRPS-1) as defined by International Association for Study of Pain (IASP). Objective: To describe the changes in musculoskeletal ultrasonography (MSKUSG) in CRPS-1 before and after treatment with ultrasound-guided dry needling (USGDN) in retrospective data from 44 patients. Study Design: Patients irrespective of age, gender, or cause of CRPS were included in this retrospective data analysis; the Budapest criteria for the diagnosis of CRPS were stringently adhered to. Setting: The analysis was done at Ashirvad Institute for Pain Management and Research with the database of CRPS patients who were treated between December 2005 and December 2014. Methods: The CDC, range of motion at upper extremity joints, dynamometry, Disability of arm, shoulder and hand score (DASH) and ultrasonography were documented on days one, 15, and 45. MSKUSG demonstrated loss of myoarchitecture and reduced bulk. Results: All 44 patients received USGDN as the sole intervention with medications and physiotherapy. MSKUSG at 15 and 45 days after starting USGDN showed a return of normalcy to the myoarchitecture and muscle bulk increase that coincided with the disappearance of CDC and a progressive and predictable improvement of the DASH scores in all the 44 patients. Limitation: The analysis focuses on only 2 parameters: the musculoskeletal changes of the forearm flexors and extensors on ultrasound guidance and the efficacy of the dry needling treatment. It is not a comparative study with another accepted form of treatment or intervention. We have not looked into the age and gender predilection of the condition owing to the small sample size of the study. Analysis of long term maintenance of relief and rehabilitation of the disability were limited to one year. Conclusion: Myofascial pathology of co-contraction appears to cause CDC of CRPS and probable ischemic loss of myoarchitecture. Relief of co-contraction with USGDN allowed resolution of tenosynovitis causing the CDC and return of normal myoarchitecture.
Current opinions on tendinopathy
Journal of sports science & medicine, 2011
Tendinopathy is characterized by pain in the tendon and impaired performance sometimes associated with swelling of the tendon. Its diagnosis is usually clinical but ultrasonography and magnetic resonance imaging can refine the diagnosis. Tendinopathy is highly prevalent and is one of the most frequently self reported musculoskeletal diseases in physical workers and sports people. Nevertheless, it is very difficult to carry out general epidemiologic studies on tendinopathy because of the varying sports cultures and sports habits in different countries. The aetiology of tendinopathy seems to be multi-factorial, involving intrinsic and extrinsic factors. The role of inflammation is still debated but the absence of inflammatory cells does not mean that inflammatory mediators are not implicated. Different theories have been advanced to explain pain and chronicity mechanisms, but these mechanisms remain largely unknown. "Conventional "treatments are generally employed empiricall...
Complex regional pain syndrome-up-to-date
Complex regional pain syndrome (CRPS) was described for the first time in the 19th century by Silas Weir Mitchell. After the exclusion of other causes, CRPS is characterised by a typical clinical constellation of pain, sensory, autonomic, motor, or trophic symptoms which can no longer be explained by the initial trauma. These symptoms spread distally and are not limited to innervation territories. If CRPS is not improved in the acute phase and becomes chronic, the visible symptoms change throughout because of the changing pathophysiology; the pain, however, remains. The diagnosis is primarily clinical, although in complex cases further technical examination mainly for exclusion of alternative diagnoses is warranted. In the initial phase, the pathophysiology is dominated by a posttraumatic inflammatory reaction by the activation of the innate and adaptive immune system. In particular, without adequate treatment, central nociceptive sensitization, reorganisation, and implicit learning processes develop, whereas the inflammation moderates. The main symptoms then include movement disorders, alternating skin temperature, sensory loss, hyperalgesia, and body perception disturbances. Psychological factors such as posttraumatic stress or pain-related fear may impact the course and the treatability of CRPS. The treatment should be ideally adjusted to the pathophysiology. Pharmacological treatment maybe particularly effective in acute stages and includes steroids, bisphosphonates, and dimethylsulfoxide cream. Common anti-neuropathic pain drugs can be recommended empirically. Intravenous long-term ketamine administration has shown efficacy in randomised controlled trials, but its repeated application is demanding and has side effects. Important components of the treatment include physio-and occupational therapy including behavioural therapy (eg, graded exposure in vivo and graded motor imaging). If psychosocial comorbidities exist, patients should be appropriately treated and supported. Invasive methods should only be used in specialised centres and in carefully evaluated cases. Considering these fundamentals, CRPS often remains a chronic pain disorder but the devastating cases should become rare.
A medical mystery of complex regional pain syndrome
A B S T R A C T Complex regional pain syndrome (CRPS) is a condition of neuropathic pain, which is characterized by significant autonomic and inflammatory features. CRPS occurs in patients who have limb surgery, limb fractures, or trauma. Many patients may have pain resolve within twelve months of the inciting incident; however, a small subset progresses to the chronic form. This transitional process often happens by changing from warm CRPS with dominant inflammatory phase to cold CRPS, in which autonomic characteristics or manifestations dominate. Several peripheral and central mechanisms are involved, which might vary among individuals over a period of time. Other contributors include peripheral and central sensitization, autonomic alterations, inflammatory and immune changes, neurochemical changes, and psychological and genetic factors. Although effective management of the chronic CRPS form is often challenging, there are a few high quality randomized controlled trials that support the efficacy of the most commonly used therapeutic approaches.