Complex regional pain syndrome (CRPS) is a chronic regional pain disorder that most frequently affects the limbs. It is characterized by hyperalgesia, allodynia, edema, motor disturbance, and vasomotor instability, and typically occurs following surgery or trauma. In type-I CRPS there is no confirmed nerve injury, while peripheral nerve injury is present in type-II CRPS. The multifactorial pathophysiological etiology of CRPS includes inflammation, autoimmune responses, abnormal cytokine production, autonomic dysfunction, altered blood flow, psychological factors, and central cortical reorganization. There are no specific laboratory diagnostic tools for CRPS, and so it is diagnosed clinically. The Budapest criteria are currently the most-accepted diagnostic criteria.

Citations

• Complex Regional Pain Syndrome: Updates and Current Evidence
  Yeng F. Her, Eva Kubrova, Marissa Dombovy-Johnson, Mariam ElSaban, Karson Mostert, Ryan S. D’Souza
  Current Physical Medicine and Rehabilitation Repor.2024; 12(1): 50.     CrossRef
• Task-based and Magnified Mirror Therapy for Unilateral Spatial Neglect among post-stroke subjects: Study protocol for a randomized controlled trial
  Kamal Narayan Arya, Shanta Pandian, Divya Pandey, G. G. Agarwal, Neera Chaudhary, Monika Halicka
  PLOS ONE.2024; 19(1): e0296276.     CrossRef
• Diagnosis and Management of Knee Arthrofibrosis and Associated Pain-Related Fear Using Multidimensional Clinical Reasoning and Exposure In Vivo Concept: A Case Report
  Mohammad Jamali, Kevin McEnroy, Logan W. Gaudette, Zafeer Baber, Ryan J. Stoddard
  JOSPT Cases.2024; 4(3): 121.     CrossRef
• Nuclear Imaging in Orthopaedic Practice
  Alvaro Ibaseta, Ahmed Emara, Ignacio Pasqualini, Benjamin Jevnikar, Ceylan Colak, Oguz Turan, Shujaa T. Khan, Matthew E. Deren, Nicolas S. Piuzzi
  JBJS Reviews.2024;[Epub]     CrossRef

A 80-year-old man was admitted due to painful paresthesia and weakness on four extremities for three months. We diagnosed chronic progressive sensorimotor polyneuropathy of unknown cause and empirically treated with oral steroid. Six-weeks later, pruritic and erythematous papules and plaques were observed on his forearms and feet, the pathologic findings by skin biopsy were compatible with Kaposi's sarcoma. We suggest that progressive sensorimotor polyneuropathy of the patient could be attributed to Kaposi's sarcoma within the context of paraneoplastic process.

Background
Recently, polyneuropathy has been been described in higher proportions for patients with Parkinson’s disease (PD) than in normal population. This finding was hypothesized to be related to the elevation of plasma homocysteine, following the management of PD with levodopa. We conducted this study to clarify the clinical value of elevated plasma homocysteine in PD patients for their relation to polyneuropathy.
Methods
A total of 37 PD patients without neuropathy (PD control) and 41 PD patients with polyneuropathy (PDP), who were recruited for this study, were compared with age and sex matched 48 healthy controls. All PD patients performed electrophysiological tests, including nerve conduction study, to diagnose polyneuropathy. Plasma homocysteine levels were measured in all subjects and compared between each groups.
Results
The homocysteine of PDP showed higher homocysteine level than those of PD control and healthy controls. However, there was no significant difference in homocysteine levels between PD control and healthy controls. In each group of PD control and PDP, there were no intercorrelations between daily levodopa dose, duration of PD symptoms and PD treatment or motor severity with homocysteine levels.
Conclusions
We could cautiously assume that plasma homocysteine level may be related with the involvement of peripheral nerve of PD patients in this study. The pathophysiologic role of homocysteine and the relationship between plasma homocysteine level and levodopa in PDP need to be confirmed.