✓ Intrinsic insular tumors are frequently excluded from surgical treatment. The authors propose a more extensive approach to these lesions based on the results of this prospective series. From September 1993 to January 1995, 30 patients (18 males and 12 females; mean age 42 years) harboring benign (15 patients) or malignant (15 patients) tumors involving the insula underwent surgical treatment. The dominant and nondominant hemispheres were both affected in 15 cases. Two groups were defined on the basis of preoperative magnetic resonance (MR) imaging: 14 lesions were restricted to the insula and the corresponding opercula; the other 16 lesions also involved other mesocortical and/or allocortical areas. Most patients displayed only mild preoperative symptoms. The median score according to the Karnofsky performance scale was 90. Microsurgical removal was achieved via a transsylvian approach in nine cases and via a frontal and/or temporal approach in 21 cases. According to early postoperative MR imaging, complete tumor removal (100%) was seen in five patients, nearly complete (> 80%) in 21, and incomplete resection (50%–80%) in four patients. There was no operative mortality; 19 patients (63%) experienced immediate postoperative morbidity, including reduced performance. After a mean follow-up review of 8.5 months two of 21 patients suffered permanent deficits, accounting for an overall operative morbidity of 10%. At the mean time of review, three patients with Grade IV tumors had died of tumor recurrence. The authors conclude that low-grade intrinsic insular tumors, as well as Grade III tumors, can be removed with favorable results in the majority of patients. Surgery to excise glioblastomas should only be considered for patients with good preoperative performance and young age.
Josef Zentner, Bernhard Meyer, Armin Stangl and Johannes Schramm
Bernhard Meyer, Armin P. Stangl and Johannes Schramm
✓ In this article the authors report the case of a mixed cerebrovascular malformation in which a true arteriovenous malformation (AVM), harboring a nidus, is associated with a venous malformation that serves as the draining vein for the nidus. Despite the authors' preoperative rationale for exclusive extirpation of the AVM, an inadvertent injury and the obliteration of the venous malformation generated delayed postoperative neurological deterioration, which could clearly be attributed to venous hemorrhagic infarction. Because this is only the second instance of this type of mixed vascular malformation of the brain reported, which also underscores the concept of nonsurgical treatment of venous malformations, the authors discuss the diverse literature regarding mixed vascular malformations and the treatment of venous malformations.
Armin P. Stangl, Ruth Wellenreuther, Doris Lenartz, Jürgen A. Kraus, Anil G. Menon, Johannes Schramm, Otmar D. Wiestler and Andreas von Deimling
✓ A significant number of patients with meningiomas develop multiple tumors without anatomical bridges. To understand the mechanism by which multiple meningiomas arise, the authors analyzed DNA from 39 multiple meningiomas in 12 patients to locate alterations in the neurofibromatosis type 2 (NF2) gene. This gene has been shown to be inactivated in meningiomas. No patient in our series had a family history of meningiomas or NF2. All tumors were investigated by single-strand conformation polymorphism analysis of the entire coding region of the NF2 gene and by direct DNA sequencing of altered fragments. The DNA from meningiomas in 10 patients carried NF2 gene mutations. In six of the 10 patients with NF2 mutations, all tumors in the respective individual exhibited the identical DNA alteration in the NF2 gene, thus indicating clonal origin. All four patients with more than two lesions had clonal meningiomas and four patients with two meningiomas each carried different mutations in their tumors. Analysis of constitutional DNA revealed a wild-type NF2 sequence in all 12 patients, thus excluding a forme fruste of NF2 in these cases. Our data demonstrate that the majority of multiple meningiomas with NF2 gene mutations are of somatic and clonal origin. Spread of tumor cells via the cerebrospinal fluid is the most likely mechanism to account for the development of these multiple meningiomas.