The incidence of intracranial meningioma in Manitoba, Canada, was reviewed from 1980 through 1987. During that time, 193 tumors were diagnosed, with a male:female ratio of 1:2. This occurrence corresponded to crude incidence rates of 2.3/100,000 for all meningiomas and 0.17/100,000 for malignant meningiomas. Among malignant meningiomas, the male:female ratio was 1:1. The age-specific annual incidence rate increased with age up to the eighth decade where it peaked at 8.4/100,000. The distribution of histopathological subtypes was: 74 meningotheliomatous (38%), 64 transitional (33%), 14 malignant (7%), 14 fibroblastic (7%), seven psammomatous (4%), four angioblastic (2%), and 16 unknown (8%). The diagnosis of malignant meningioma was based on the World Health Organization criteria, with only Grade III and IV tumors included in this subtype. Clinical features did not allow for differentiation of benign from malignant neoplasms. Individuals with malignant tumors were, however, more likely to suffer paresis (50%) and less likely to be without deficit (14%) than their benign counterparts. The radiographic appearance of "mushrooming" was observed only in patients with malignant meningioma. All malignant tumors showed evidence of peritumoral edema; however, none exhibited calcification. During the 8-year study interval, the tumor recurred in 10 (71%) of the 14 patients with malignant meningioma. Tumor recurrence was accompanied by dedifferentiation from a more benign histology in four patients (2% of the total material).

The authors have demonstrated that high-quality MR images can be obtained in the operating room within reasonable time constraints. Procedures can be conducted without compromising or altering traditional neurosurgical, nursing, or anesthetic techniques. It is feasible that within the next decade intraoperative MR imaging may become the standard of care in neurosurgery.

In humans, three isoforms of the T-type (Ca(v)3.1) calcium-channel alpha(1) subunit have been reported as a result of alternate splicing of exons 25 and 26 in the III-IV linker region (Ca(v)3.1a, Ca(v)3.1b or Ca(v)3.1bc). In the present study, we report that human glioma express Ca(v)3.1 channels in situ, that splicing of these exons is uniquely regulated and that there is expression of a glioma-specific novel T-type variant (Ca(v)3.1ac). Seven human glioma samples were collected at surgery, RNA was extracted, and cDNA was produced for RT-PCR analysis. In addition, three glioma cell lines (U87, U563, and U251N), primary cultures of human fetal astrocytes, as well as adult and fetal human brain cDNA were used. Previously described Ca(v)3.1 splice variants were present in glioma samples, cultured cells and whole brain. Consistent with the literature, our results reveal that in the normal adult brain, Ca(v)3.1a transcripts predominate, while Ca(v)3.1b is mostly fetal-specific. RT-PCR results on glioma and glioma cell lines showed that Ca(v)3.1 expression in tumor cells resemble fetal brain expression pattern as Ca(v)3.1bc is predominantly expressed. In addition, we identified a novel splice variant, Ca(v)3.1ac, expressed in three glioma biopsies and one glioma cell line, but not in normal brain or fetal astrocytes. Transient expression of this variant demonstrates that Ca(v)3.1ac displays similar current-voltage and steady-state inactivation properties compared with Ca(v)3.1b, but a slower recovery from inactivation. Taken together, our data suggest glioma-specific Ca(v)3.1 gene regulation, which could possibly contribute to tumor pathogenesis.

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Breadboard testing of the prototype components has shown spatial resolution of 30 microm, greatly exceeding our expectations. Neurosurgeons will not only be able to perform current procedures with a higher margin of safety but also must speculate on techniques that have hitherto not even been contemplated. This includes coupling the robot to intelligent tools that interrogate tissue before its manipulation and the potential of molecular imaging to transform neurosurgical research into surgical exploration of the cell, not the organ.

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We speculate regarding malignant transformation as a possible consequence of this decline in antioxidant capacity, as well as regarding the role of seizures and astrocytoma glutamate receptors in the initiation of free radical cascades. The therapeutic and teleological implications are considerable.