By B. Domenik. Thiel College.
J Pediatr Orthop 11: have shown that an ischemia similar to that in Legg- 419–31 Calvé-Perthes disease can be generated by increasing 85 generic 100mg viagra sublingual otc. Clin Orthop 281: 63–8 tion of transient synovitis of the hip does not appear to 86 purchase viagra sublingual 100mg line. Tucci JJ, Jay Kumar S, Guille JT, Rubbo ER (1991) Late acetabu- lar dysplasia following early successful Pavlik harness treat- be a precursor stage of Legg-Calvé-Perthes disease as ment of congenital dislocation of the hip. J Pediatr Orthop 11: the increased pressure resulting from the effusion in 502–5 transient synovitis does not lead to vessel closure. Thieme, Stuttgart Intraosseous pressure: The measurement of intraos- 88. J Bone Joint Surg Br 84: 339–43 the venous drainage in the femoral head is impaired, 89. Wagner H (1965) Korrektur der Hüftgelenkdysplasie durch die causing an increase in intraosseous pressure. Wedge JH, Munkacsi I, Loback D (1989): Anteversion of the femur and idiopathic osteoarthrosis of the hip. J Bone Joint Surg (Am) 71: Coagulation disorder: One study found a coagulation 1040–3 disorder in 75% of 44 investigated children with Legg- 91. Wilkinson A, Sherlock D, Murray G (2002) The efficacy of the Pavlik Calvé-Perthes disease. In most cases the disorder was harness, the Craig splint and the von Rosen splint in the manage- thrombophilia with an absence of factor C or S. J Bone the disorder involved elevated serum levels of lipo- Joint Surg Br 84: 716–9 92. Wingstrand H (1997) Intracapsular pressure in congenital disloca- protein, a thrombogenic substance. J Pediatr Orthop B 6: 245–7 studies have questioned the significance of clotting 93. Wong-Chung J, Ryan M, O‘Brien T (1990) Movement of the femoral factors as an etiological component [18, 22, 34].
The pathophysiology is poorly understood and treatments often are directed at managing the signs and symptoms of disease buy viagra sublingual 100mg low cost. A significant number of patients exhibit comorbid psychological dysfunction which has led some clinicians to believe incorrectly that CRPS is entirely a psychiatric disease viagra sublingual 100 mg. Animal research has improved our mechanistic understanding of neuropathic pain and this awareness may facilitate our under- standing of CRPS (particularly CRPS type II). Recent clinical investigation has resulted in an improved understanding of the biological dysfunction observed in patients with CRPS. This review will (1) summarize the historical arguments and controversy surrounding the disease, (2) describe the psychological dys- function often observed in patients with CRPS, and (3) discuss recent trends in the neurobiological understanding of CRPS. CRPS Controversy and Misunderstanding CRPS History Several authors have questioned the validity of CRPS type I as an actual organically based neurological disease and have doubted the involvement of the sympathetic nervous system in the maintenance of the pain. Many aspects of the disease, including nomenclature, etiopathogenesis, diagnosis, and treatment have generated considerable controversy. As a result, CRPS type I (RSD) has been considered by some experts an expression of somatoform disease and therefore has been designated as pseudoneuropathy of psychogenic origin. Nomenclature Causalgia was first described in 1864 as a distinct disease entity by Silas Weir Mitchell who noted extreme pain, autonomic abnormalities, trophic changes, and involuntary movements in Civil War soldiers who suffered from traumatic injury to peripheral nerves. Rene Leriche later postulated in 1916 that the sympathetic nervous system was involved in pain states involving major tissue or nerve injury. Evans to describe patients who exhibited causalgia-like symptoms but without evidence of major tissue or nerve injury. Several other terms have been used to describe this disease such as minor causalgia, algodystrophy, shoulder-hand syndrome, posttraumatic dystrophy, and Sudeck’s atrophy. In general, the disease was given different names based on the personal assump- tions, frame of reference, institutional background, or country of origin of the investigators who were describing the disease process.