Calcium pyrophosphate arthropathy of the spine: case report and review of the literature.

Calcium pyrophosphate deposition disease is a relatively uncommon arthropathy characterized by the clinical features of pseudogout, the radiographic manifestations of chondrocalcinosis, and the pathological deposition of calcium pyrophosphate crystals in both hyaline and fibrocartilage. Symptomatic involvement of the spine by calcium pyrophosphate deposition disease is rare except by nodular deposition in the ligamentum flavum and atlanto-occipital ligament. We report a 50-year-old woman who presented with an acute herniated disc syndrome secondary to an intraspinal inflammatory calcium pyrophosphate deposition disease mass at the level of the L4-L5 interspace. The magnetic resonance image and histopathological features of the case are also discussed.

Differentiation therapy is potentiated by chemotherapy and hyperthermia in human and canine brain tumor cells in vitro.

Human glioblastoma (U-87MG) and canine glioma (canine brain tumor [CBT]) cell lines were tested in vitro for their therapeutic sensitivity to sequential treatment with differentiating agents and chemotherapy or hyperthermia. Both cell lines responded to the inducer combination dibutyryl adenosine-3',5'-cyclic monophosphate/sodium butyrate by the formation of cytoplasmic processes detectable within 7 hours and attained approximately 90% morphological differentiation within 2 days of exposure. The clonogenicity of CBT and U-87MG cells gradually decreased after 1 to 7 days of exposure to the inducer combination, but this treatment alone failed to kill the cells. After the removal of the inducers, both lines dedifferentiated and the rate of clonogenesis increased. 1,3-bis-(2-Chloroethyl)-1-nitrosourea administered to CBT and U-87MG cells before or after 3 days of treatment with inducers potentiated the antiproliferative effects of the differentiating agents. Cisplatin administered to U-87MG cells enhanced the antiproliferative effect of the differentiating agents to a greater extent when added before the inducers rather than after differentiation was stimulated. The sequential treatment of CBT cells with a 44 degrees C heat pulse for 30 minutes followed by differentiating agents produced an additive potentiation of cell killing, whereas the reverse sequence did not. Hyperthermia pretreatment at 44 degrees C for 15 minutes or at 42 degrees C for 30 minutes failed to enhance the antiproliferative effects of inducing agents.(ABSTRACT TRUNCATED AT 250 WORDS)

Long-term survival in patients with malignant astrocytoma.

From 1978 to 1988, 314 patients with malignant astrocytoma were treated by our neuro-oncology team. Twenty-five patients were excluded from further analysis because of a lack of adequate follow-up, the brain-stem location of the tumor, or an age of less than 18 years. Of the 289 remaining patients in the valid study group, 213 had Grade IV tumors (73.7%) and 76 had Grade III tumors; 167 patients were male (57.8%) and 112 were female, and 89 were less than 40 years of age (30.8%). There were 58 long-term survivors (> 36 mo) in the series (20%). Long-term survivors were much more likely to be less than 40 years of age (x = 41.8; P < 0.005), to have undergone repeated surgery (x = 17.3; P < 0.005), to have received more than 60 Gy of radiation (x = 11.6; P < 0.005), to have Grade III tumors (x = 10.6; P < 0.005), and to have received nitrosoureas (x = 6.09; P < 0.02). Neither sex nor blood type were significantly associated with long-term survival. Patients undergoing repeated surgery were more likely to be less than 40 years of age (x = 5.72; P < 0.02), but neither sex nor histological findings was associated with repeated surgery. For the series as a whole, the observed 5-year survival rate was 6%. We conclude that an aggressive multidisciplinary approach can produce sizable numbers of long-term survivors in malignant astrocytoma patients with favorable prognostic factors.

Extraskeletal myxoid chondrosarcoma of the falx.

Intracranial cartilaginous tumors are unusual lesions, of which myxoid chondrosarcoma is the rarest. We describe this tumor arising from the falx in a 28-year-old woman treated at recurrence with a second operation and a radiation implant. The behavior of classic chondrosarcoma and mesenchymal chondrosarcoma is also reviewed.

Multiple intracerebral arteriovenous malformations: report of three cases and review of the literature.

Multiple intracerebral arteriovenous malformations are thought to be exceedingly rare lesions and have usually been reported as single cases. During the past 2 years, we have treated three patients with multiple cerebral arteriovenous malformations, representing 3.2% of a consecutive series of 95 arteriovenous malformation patients seen since 1976. Details on 17 other cases are available in the literature and are summarized here. The incidence of multiple arteriovenous malformations in major series ranges from 0.3% to 3.2%; the average incidence is 1.9% based on 21 cases encountered in a total population of 1102 arteriovenous malformation patients. Patients with multiple arteriovenous malformations often have other vascular anomalies of the brain or soft tissues, but the clinical mode of presentation, age, sex, and anatomical distribution of the lesions are the same as those of patients with single arteriovenous malformations. The use of four-vessel angiography in combination with magnetic resonance imaging may result in a higher detection rate for such cases.

Intravenous recombinant interferon beta in patients with recurrent malignant gliomas: a phase I/II study.

A multicenter phase I/II trial of a human recombinant interferon beta (Betaseron; Triton Biosciences, Alameda, CA) was conducted in patients with recurrent glioblastoma and anaplastic astrocytoma in six centers between 1986 and 1988. Betaseron was given intravenously three times per week, starting at 90 x 10(6) IU per dose and escalating by 90 x 10(6) IU every 2 weeks up to a maximum dose of 540 x 10(6) per treatment. All patients had failed prior radiotherapy, and most had failed one or more courses of chemotherapy. Of the 72 patients entered into the protocol, 65 were considered assessable. Of 65 patients, 41 had glioblastoma, and 24 had anaplastic astrocytoma. Of the 65 assessable patients, 15 (23%) had an objective response (R), and 18 (28%) had stable disease (S), with a combined R and S rate of 51%. The Kaplan-Meier median time to progression was 24 weeks for the responders, 10 weeks for the nonresponders, and 23 weeks for the whole group. These results suggest that Betaseron has definite activity in recurrent gliomas, with an R + S rate of 51%. The maximum-tolerated dose (MTD) is between 180 and 360 x 10(6) IU, with neurotoxicity being the most troublesome toxicity at higher doses. Two patients died of treatment-related complication. Since most responders showed responses at the 180 x 10(6 IU dose range, further studies using a lower dose of Betaseron aimed at decreasing toxicity and allowing chronic maintenance therapy are merited.

In vitro response of human glioblastoma and canine glioma cells to hyperthermia, radiation, and chemotherapy.

Little is known about the sensitivity of human glioblastoma cells to hyperthermia alone and in combination with other therapies. We carried out in vitro cell survival studies on the human glioblastoma cell line U-87MG and our model canine glioma canine brain tumor (CBT) cells after multimodality treatment. Ionizing radiation was administered to flasks of cells in logarithmic growth at 500 rads (5 Gy) with consecutive treatment by hyperthermia, 1,3-bis-(2-chloroethyl)-1-nitrosourea (BCNU), or cisplatin. Cells were treated with single doses of BCNU at 5 microM with sequentially added radiation or hyperthermia and at 1 to 2 micrograms/ml of cisplatin with hyperthermia. Hyperthermia was administered in a precision controlled water bath at 44 degrees C for 30 minutes in combination with chemotherapy or radiation. In general, the sensitivity of U-87MG and CBT cells was similar for all test regimens. For example, colony formation efficiency decreased by 64% in CBT cells and by 64.4% in U-87MG cells after hyperthermia alone at 44 degrees C for 60 minutes. All combinations of BCNU, hyperthermia, and radiation administered in vitro produced enhanced cell killing, but the effects of multiple modalities were generally additive in both cell lines.(ABSTRACT TRUNCATED AT 250 WORDS)

The use of anterior Caspar plate fixation in acute cervical spine injury.

Optimal management of cervical cord injury in the presence of documented instability and/or compression of neural elements remains a controversial topic. Surgery and internal stabilization of cervical spine fracture/dislocations are effective and well accepted, but controversy exists on the relative merits of the anterior versus the posterior approach as well as the optimal timing of surgical intervention. We report our experience with the Caspar technique and instrumentation for anterior stabilization in 54 patients for acute cervical spine injury. Our series consists of 38 male and 16 female patients whose ages ranged from 16 to 68 years, with a mean age of 29.2 years. Thirty-two of these patients had complete neurological sensory/motor deficits at the time of presentation, eight were neurologically intact, and 14 had preservation of some motor and sensory function. All 54 patients had radiographic evidence of posterior instability as well as anterior disruption of either a vertebral body or intervertebral disk. We found that "early" intervention (less than 24 hours after injury) was performed frequently in the neurologically compromised patients. Twelve of the 22 patients undergoing surgery less than 24 hours after admission regained significant neurological function, with 13 of 22 developing postoperative complications. In the "delayed" group (surgery more than 24 hours after injury, mean 14.3 days), 14 patients experienced postoperative complications, with 15 of 24 demonstrating neurological improvement. The eight patients who were intact did uniformly well. There was no mortality during the follow-up. All 54 patients showed a solid fusion (clinically and radiologically) within 6 months of surgery. In two cases the plates had to be removed, without risking the fusion. Our experience suggests that although anterior cervical fusion and Caspar plating remain appropriate for patients with documented anterior compromise of the canal, it should not substitute for more traditional posterior stabilization procedures. Because this route has the potential for more serious complications, it should be reserved for the cases in which anterior decompression is deemed necessary or posterior fusion was unsuccessful. With appropriate selection of patients, no adverse effect of early surgery was demonstrated. In fact, neurologically compromised patients had the benefits of increased ease of patient care and early transfer to rehabilitation.