The authors describe three cases of cervical radiculomyelopathy caused by calcium pyrophosphate dihydrate crystal deposition disease (CPPDcdd). Radiological investigations revealed nodular calcifications, 5 to 7 mm in diameter, in the cervical ligamentum flavum compressing the spinal cord. Light microscopic, scanning electron microscopic, and x-ray diffraction studies were performed on all three surgical specimens obtained by laminectomy. In two of the cases x-ray microanalysis and transmission electron microscope studies were also performed. This study defined the presence of two patterns of crystal deposition in the ligamentum flavum. One is a nodular deposit, in which hydroxyapatite crystals are seen in the central part of the nodules, with calcium pyrophosphate dihydrate (CPPD) being distributed thinly around them. The other pattern is a linear deposit seen in multiple ligaments and composed of pure CPPD, which causes minimal thickening of the ligaments. A transitional pattern between the two types was also observed. This study revealed details of the nodular deposition of crystals in the ligamentum flavum and demonstrates that CPPDcdd and so-called "calcification of the ligamentum flavum" are the same disease: namely, CPPDcdd. Hydroxyapatite is assumed to have been transformed from CPPD.
The aim of this study is to review the different histological and clinical characteristics of glioblastoma multiforme (GBM) with and without cysts (cystic and noncystic GBM, respectively). Thirty-seven GBM were collected; these were tumors for which more than 80% of the volume was surgically resected, including a portion of the peripheral parenchyma of the brain. Based on preoperative magnetic resonance (MR) imaging studies, tumors were tentatively classified as cystic GBM if more than 50% of their volume appeared to be liquid; otherwise, they were considered to be noncystic GBM. Tumor volumes were estimated from contrast-enhanced T1-weighted MR images. Edema was deduced from the maximum width of contrast-enhanced edges. Peritumoral pathological analysis showed distinct margins, indicating little or no infiltration of tumor cells into white matter. Five cases were classified as cystic and 32 were noncystic GBMs. There was a statistically significant difference in age (Mann-Whitney U test; P < 0.05) between the patients with cystic tumors (median, 44 years; range, 26-59 years) and those with noncystic tumors (median, 54 years; range, 26-81 years). Four of the cystic tumors and eight of the noncystic tumors were more than 5 cm in maximum diameter. Cystic GBMs had a well-defined tumor interface and less than 2-cm-thick peritumoral edema compared to the noncystic GBMs (Fisher's exact test; P < 0.05). For patients with cystic GBMs, median survival time after surgery was 19.8 months and the 2-year survival rate was 50%. Patients with noncystic GBMs had a median survival time of 12.8 months and a 2-year survival rate of only 17%. Median time to tumor recurrence was 13.3 months for patients harboring cystic GBMs and 8.5 months for those with noncystic GBMs (log-rank test; P < 0.05). Thus, the prognosis for cystic GBM was significantly better than that for noncystic GBM, possibly because cystic GBMs showed comparatively little infiltration of the peritumoral brain parenchyma.
We investigated the relationship between radiological findings and the nature of the cyst fluid and histological findings of six Rathke's cleft cysts. The results show that the majority (five of six cases) of symptomatic Rathke's cleft cysts exhibit no enlargement of the sella turcica on plain x-rays, which may be helpful in differentiating cystic pituitary adenoma in the radiological diagnostic process. Three cases with large cysts showing high-intensity T1-weighted magnetic resonance images harbored abundances of cholesterol crystal and hemosiderin pigment in the cyst walls. The high signal intensity in magnetic resonance images of Rathke's cleft cysts may be explained by hemorrhage and a deposition of cholesterol crystal and may be considered in certain cases of Rathke's cleft cyst, especially when they are large.
A case of cervical radiculomyelopathy caused by multiple calcified nodules in the ligamenta flava is presented. Roentgenological examination of the cervical spine showed radiopaque nodular lesions, 7 x 7 x 5 mm in size, located in the paramedian portion of the posterior spinal canal. The nodules were removed surgically and they were confirmed to be calcifications of ligamenta flava. Microscopic examination of the nodules with the polarized light revealed extensive deposition of crystals. By x-ray diffraction study, the crystal was determined as calcium pyrophosphate dihydrate (CPPD: Ca2P2O7 . 2H2O). Although CPPD deposition in the cartilage has been known as pseudo-gout syndrome, deposition in the ligament has been reported only in a few cases. This is the first case with radiopaque calcified nodules in the ligamenta flava causing spinal cord compression, the composition of which proved to be CPPD.
A 52-year-old male presented with calcification of the cervical ligamentum flavum manifesting as hypesthesia of the bilateral middle, ring, and little fingers and ulnar halves of both forearms, as well as motor weakness in the bilateral upper extremities and gait disturbance. Cervical x-ray tomography detected a round calcified mass on the posterior wall of the cervical canal at the C-5 level. Computed tomography showed the round, nodular calcified mass more clearly. Magnetic resonance imaging showed an epidural low intensity mass compressing and distorting the cervical cord at the C-5 level on both T1- and T2-weighted images. Administration of gadolinium-diethylenetriaminepenta-acetic acid caused marginal enhancement of the mass. The lesion was eventually removed by posterior laminectomy. The mass was composed of a very hard crystal-like calcified deposition in the ligamentum flavum. X-ray diffraction analysis of the histological specimen showed calcium pyrophosphate dihydrate (CPPD) and hydroxyapatite in the crystal-like substance, confirming that CPPD is responsible for calcification of the cervical ligamentum flavum.
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