STUDY DESIGN: This study measured the incidence of calcium pyrophosphate dihydrate crystal deposition in specimens of ligamenta flava in consecutive patients undergoing decompressive laminectomy between 1984 and 1991. The results were compared to determine the difference between calcium pyrophosphate dihydrate-negative patients with lumbar canal spinal stenosis. OBJECTIVES: The results were compared with cadaver specimens and literature values to determine if calcium pyrophosphate dihydrate crystal deposition disease contributes to the thickening of the ligamentum flavum and thereby contributes to spinal stenosis. SUMMARY OF BACKGROUND DATA: Calcium pyrophosphate dihydrate crystal deposition disease has been described in the axial skeleton. Hypertrophy of the ligamentum flavum has been suggested to contribute to stenosis. The association of calcium pyrophosphate dihydrate disease and hypertrophied ligamenta flava has not been fully defined nor linked to neurologic symptoms and signs. METHODS: The incidence of calcium pyrophosphate dihydrate crystal deposition in specimens of ligamenta flava obtained from four groups was measured: specimens obtained during surgery from 102 consecutive patients undergoing decompression laminectomy between 1984 and 1991, 47 additional pathologic specimens of ligamentum flavum tested between 1984 and 1991, 222 calcium pyrophosphate dihydrate-positive Pathology Department specimens collected between 1980 and 1991, and, as control specimens from 20 cadavers. The associated patient histories were reviewed for the first two groups; no histories were available for the cadaver group. RESULTS: The incidence of calcium pyrophosphate dihydrate crystal deposition was 24.5% in the ligamentum flavum among the surgical patients, 31% among the Pathology Department specimens, 33.8% among the calcium pyrophosphate dihydrate-positive Pathology Department specimens, and 5% among the cadavers. No associated medical conditions with calcium pyrophosphate dihydrate crystal deposition were found among the medical histories. Patients with the symptoms of spinal stenosis who were also calcium pyrophosphate dihydrate-negative patients with symptoms of less than 6 months' and less than 24 months' duration (P < 0.001). Except for time to presentation, calcium pyrophosphate dihydrate-negative patients had similar signs and symptoms of lumbar canal spinal stenosis. Having previous spine surgery did not produce a statistically significant risk of having calcium pyrophosphate dihydrate crystal deposition. No specific laboratory tests were found to be of predictive value. CONCLUSIONS: These findings suggest that calcium pyrophosphate dihydrate crystal deposition may indeed be associated with the thickening of the ligamentum flavum, if so, patients may benefit from medical treatment before undergoing surgical treatment of lumbar canal spinal stenosis.
STUDY DESIGN: This study measured the incidence of calcium pyrophosphate dihydrate crystal deposition in specimens of ligamenta flava in consecutive patients undergoing decompressive laminectomy between 1984 and 1991. The results were compared to determine the difference between calcium pyrophosphate dihydrate-negative patients with lumbar canal spinal stenosis. OBJECTIVES: The results were compared with cadaver specimens and literature values to determine if calcium pyrophosphate dihydratecrystal deposition disease contributes to the thickening of the ligamentum flavum and thereby contributes to spinal stenosis. SUMMARY OF BACKGROUND DATA: Calcium pyrophosphate dihydratecrystal deposition disease has been described in the axial skeleton. Hypertrophy of the ligamentum flavum has been suggested to contribute to stenosis. The association of calcium pyrophosphate dihydrate disease and hypertrophied ligamenta flava has not been fully defined nor linked to neurologic symptoms and signs. METHODS: The incidence of calcium pyrophosphate dihydrate crystal deposition in specimens of ligamenta flava obtained from four groups was measured: specimens obtained during surgery from 102 consecutive patients undergoing decompression laminectomy between 1984 and 1991, 47 additional pathologic specimens of ligamentum flavum tested between 1984 and 1991, 222 calcium pyrophosphate dihydrate-positive Pathology Department specimens collected between 1980 and 1991, and, as control specimens from 20 cadavers. The associated patient histories were reviewed for the first two groups; no histories were available for the cadaver group. RESULTS: The incidence of calcium pyrophosphate dihydrate crystal deposition was 24.5% in the ligamentum flavum among the surgical patients, 31% among the Pathology Department specimens, 33.8% among the calcium pyrophosphate dihydrate-positive Pathology Department specimens, and 5% among the cadavers. No associated medical conditions with calcium pyrophosphate dihydrate crystal deposition were found among the medical histories. Patients with the symptoms of spinal stenosis who were also calcium pyrophosphate dihydrate-negative patients with symptoms of less than 6 months' and less than 24 months' duration (P < 0.001). Except for time to presentation, calcium pyrophosphate dihydrate-negative patients had similar signs and symptoms of lumbar canal spinal stenosis. Having previous spine surgery did not produce a statistically significant risk of having calcium pyrophosphate dihydrate crystal deposition. No specific laboratory tests were found to be of predictive value. CONCLUSIONS: These findings suggest that calcium pyrophosphate dihydrate crystal deposition may indeed be associated with the thickening of the ligamentum flavum, if so, patients may benefit from medical treatment before undergoing surgical treatment of lumbar canal spinal stenosis.