Ossification of the anterior longitudinal ligament and Forestier's disease: an analysis of seven cases

• Published in: Journal of neurosurgery Vol. 83; no. 1; p. 13
• Main Authors: McCafferty, R R, Harrison, M J, Tamas, L B, Larkins, M V
• Format: Journal Article
• Language: English
• Published: United States 01.07.1995
• Subjects: Aged; Aged, 80 and over; Deglutition Disorders - etiology; Follow-Up Studies; Humans; Hyperostosis, Diffuse Idiopathic Skeletal - complications; Hyperostosis, Diffuse Idiopathic Skeletal - diagnostic imaging; Hyperostosis, Diffuse Idiopathic Skeletal - surgery; Longitudinal Ligaments - diagnostic imaging; Longitudinal Ligaments - surgery; Male; Middle Aged; Radiography; Retrospective Studies
• ISSN: 0022-3085
• DOI: 10.3171/jns.1995.83.1.0013

A retrospective review was conducted on the records and radiographs of six symptomatic patients and one asymptomatic patient with Forestier's disease. No other series of patients with this disease is found in the neurosurgical literature. Forestier's disease, also known as diffuse idiopathic skeletal hyperostosis (DISH), is an idiopathic rheumatological abnormality in which exuberant ossification occurs along ligaments throughout the body, but most notably the anterior longitudinal ligament of the spine. It affects older men predominantly; all of our patients were men older than 60 years of age. The disease is usually asymptomatic; however, dyspnea, dysphagia, spinal cord compression, and peripheral nerve entrapment have all been documented in association with the disorder. Five of the six symptomatic patients presented with dysphagia due to esophageal compression by calcified anterior longitudinal ligaments, and one patient developed recurrent spinal stenosis when scar tissue from a previous decompressive laminectomy became calcified. All patients responded well to surgery. Two of the four patients who underwent removal of cervical osteophytes required several months following surgery for the dysphagia to resolve. This would support the hypothesis that not all cases of dysphagia in Forestier's disease are due to mechanical compression. Dysphagia may result from inflammatory changes that accompany fibrosis in the wall of the esophagus or from esophageal denervation. Evaluation of dysphagia even in the presence of Forestier's disease must rule out occult malignancy. The authors' experience suggests that dysphagia in the setting of Forestier's disease is an underrecognized entity amenable to surgical intervention.