Pellegrini–Stieda disease (PSD) is posttraumatic ossification of the proximal attachment of the medial collateral ligament of the knee, diagnosed by radiography.1 Antecedent traumas include direct and indirect injury to the medial side of the knee. Repeated microtraumas, including therapeutic manipulation of a stiff joint and postsurgical rehabilitation, have also been reported.2
Because PSD is rarely diagnosed in neurologic rehabilitation patients, only one case of spinal cord injury having this disease was reported.3 We describe a traumatic brain injury patient with clinical and radiologic findings of PSD. Our aim in this report is to show that this entity can be seen in neurological rehabilitation patients during the course of exercise treatment and must be taken into account in differential diagnosis of knee pain, swelling, and range-of-motion limitation.
A 22-yr-old man, with contusion lesions determined by cranial computerized tomography secondary to a motorcycle accident, attended our clinic for rehabilitation. The patient had a history of 3 mos of hospitalization in the intensive care unit and anesthesia clinic in another hospital for multiple traumas. The patient did not describe any known injury or trauma to the knee in the motorcycle accident.
On examination, the patient was found to have range-of-motion limitation with swelling and complaint of pain in his left knee. The patient had no history of systemic diseases such as gout, rheumatoid arthritis, systemic sclerosis, sarcoidosis, or hyperparathyroidism.
On physical examination, the left knee was limited at 60 degrees of flexion, extension was at a normal range, and the knee joint was stable. Serum calcium, phosphate, and alkaline phosphatase levels were within normal ranges. The plain radiographs demonstrated a characteristic bony formation, calcification medial to the femoral condyle (Fig. 1). Because of the characteristic radiographic findings and the clinical course, the diagnosis of PSD was considered.
PSD manifests radiographically, with ossification arising from the epicondylar portion of the medial femoral condyle.1 In the etiology of neurogenic ectopic bone formation, humoral, neural, and local factors, including tissue hypoxia, hypercalcemia, changes in sympathetic nerve activity, prolonged immobilization, and mobilization with frequent periods of exercising after prolonged immobilization, play a role. In traumatic brain injury patients, neurogenic heterotopic ossification can result in accelerated fracture healing. Reduced collagen degradation in polytraumas with traumatic brain injury causes enhanced osteogenesis.4
Radiographically, the ossification is seen as a thin crescent or curvilinear line of a few millimeters from the femoral condyle. This feature is crucial for ruling out other lesions including fracture of the femoral condyle, periostitis, and osteoma.1
In conclusion, PSD can be seen in neurologic rehabilitation patients during the course of exercise treatment, and it must be taken into account in the differential diagnosis of knee pain, swelling, and range-of-motion limitation.
1. Niitsu M, Ikeda K, Iijima T, Ochiai N, Noguchi M, Itai Y: MR imaging of Pellegrini-Stieda disease. Radiat Med
2. Wang JC, Shapiro MS: Pellegrini-Stieda syndrome. Am J Orthop
3. Altschuler EL, Bryce TN: Pellegrini-Stieda syndrome. N Engl J Med
4. Campos da Paz A, Francisco J, Carod Artal, Ricardo K, Kali l: The function of proprioceptors in bone organization: a possible explanation for neurogenic heterotopic ossification in patients with neurological damage. Med Hypotheses