Surgical Management of Parasagittal and Convexity Meningiomas

Sporadic

The etiology of sporadic meningiomas is not yet known. Although head injury, viral infection, and cell phone use have been implicated in the development of intracranial meningiomas, ^, the data are inconclusive and conflicting for each of these potential etiologies. The strongest support for an etiologic role in the development and progression of sporadic meningiomas is hormonal. Specifically, studies have shown a potential progesterone influence in the development of meningiomas based on the propensity of these tumors to occur in females and the presence of progesterone receptors in the majority of meningiomas. Although few definitive etiologic correlations have been made for meningiomas, several iatrogenic, environmental, and genetic causes have been linked to their development. These tumorigenic etiologies have significant implications for the management of a meningioma patient who presents for treatment.

Radiation-Induced Meningioma

Ionizing radiation is the most robustly associated risk factor for acquired meningioma. ^, This association was established by two large cohorts of individuals exposed to radiation who subsequently developed tumors, including meningiomas. Studies published on a group of almost 11,000 Israeli children treated with low-dose (approximately 1.5 Gy) radiation for tinea capitis revealed a 9.5 times greater risk for the development of meningioma compared with matched controls and untreated siblings. ^, Similarly, the incidence of meningioma formation among 68 survivors of the Hiroshima atomic bomb blast within a 2-km radius of the hypocenter identified a 2.9 times greater risk for the development of meningioma, with a higher risk for patients within a 1-km radius (6.7 times greater risk). Other iatrogenic forms of exposure to ionizing radiation have also been linked to the subsequent development of intracranial meningiomas, including higher-dose, full-mouth dental radiographs and radiotherapy provided for treatment of other cancers. Radiation-induced meningiomas generally have a dose-dependent latency to development of 10 to over 30 years, with significant morbidity and mortality, and have a higher propensity than other meningiomas to recur after resection.

Radiation-induced meningiomas tend to be of a higher pathologic grade as compared with their sporadic counterparts, but even World Health Organization (WHO) grade I radiation-induced meningiomas exhibit more aggressive clinical behavior and have an increased proclivity to recur is compared with their sporadic counterparts. ^{, ,} Patients with radiation-induced meningiomas also have an increased incidence of multiple tumors, which must be considered in planning placement of the surgical incision. ^{, ,} Further, atrophic changes in the scalp that commonly accompany cranial irradiation can require modification of standard multilayer scalp closure. Because radiation exposure can result in other delayed side effects, patients with radiation-induced meningiomas require close medical follow-up for other sequelae, including pituitary dysfunction, visual disturbances (optic atrophy), radiation necrosis, and the development of other neoplasms (sarcoma, glioma).

Neurofibromatosis Type 2

Neurofibromatosis type 2 (NF2) is an autosomal dominant heritable tumor predisposition syndrome that leads to the development of central and peripheral nervous system tumors (meningiomas, schwannomas, ependymomas), ophthalmologic findings (cataracts, epiretinal membranes, retinal hamartomas), and cutaneous findings (skin plaques, subcutaneous tumors). Intracranial meningiomas are identified in approximately half of NF2 patients and are a significant source of morbidity and mortality. NF2-associated intracranial meningiomas are frequently multiple and develop at a younger age as compared with sporadic cases of meningiomas. Up to 20% of children presenting with a meningioma will have NF2, necessitating full clinical screening and longitudinal follow-up. ^, The presence of intracranial meningiomas is associated with a 2.5-fold rise in relative risk of mortality in patients with NF2. Meningiomas associated with NF2 frequently have increased proliferative activity and a greater rate of atypical and anaplastic grades than do sporadic meningiomas. ^, Because of the frequent multiplicity of lesions, we perform a resection of tumors based on the development of symptoms rather than radiographic tumor growth.

Multiple Meningiomas

Examination of a large series reporting on the presence of multiple meningiomas found that 1% to 10.5% of patients may present with multiple tumors. ^, Identification of patients with multiple meningiomas has increased significantly with the advent of improved imaging techniques. Both sporadic and familial forms of multiple meningiomas independent of NF2 or history of radiation exposure have been described in the literature. Familial forms of the disease follow an autosomal dominant inheritance pattern and are caused by a mutation independent of the NF2 gene. ^, Tumors in patients with multiple sporadic meningiomas appear to originate from a single clone (suggesting metastatic spread), whereas others may develop these tumors independently based on cytogenetic differences between tumors. Patients with sporadic or familial forms of multiple meningiomas present dilemmas in management similar to patients with NF2; resection is often reserved until the development of symptoms rather on the basis of radiographic tumor growth.

Convexity Meningiomas

Convexity meningiomas are tumors of the supratentorial space that have their sole attachment to the dura covering the convexity of the cerebral hemispheres. The original classification of convexity meningiomas by Cushing included temporal, frontal, paracentral, parietal, and occipital locations. Several studies examining the distribution of convexity tumors reveal that the frontal region is the most common site of origin (over 50%), with the posterior locations least frequent (7% to 11%) and the remainder equally distributed between the temporal and paracentral locations. ^, Because of improvements in the ability to localize tumors and their relationship to functional cortices based on anatomic and functional imaging studies, it is possible to classify convexity tumors preoperatively as well as to anticipate clinical symptoms and the specific risks associated with their management.

Parasagittal Meningiomas

Parasagittal meningiomas have an attachment to the dura, which forms the outer layer of the superior sagittal sinus (SSS) ( Fig. 23.1 ). Olivecrona classified parasagittal meningiomas based on their anatomic location (anterior, middle, posterior) along the SSS due to the consequences of sinus occlusion during complete removal of meningiomas in each location. The most common site in which parasagittal meningiomas arise is the middle third of the SSS (from coronal suture to bregma; 37% to 70% of parasagittal meningiomas). Fifteen to 42% of parasagittal meningiomas are located along the anterior third of the SSS (from the glabella to the coronal suture) and 9% to 16% are located along the posterior third of the SSS (between the bregma and the torcula). ^,

For preoperative evaluation and surgical planning, it is critical to differentiate parasagittal meningiomas from convexity and falcine meningiomas. Convexity meningiomas are distinguished from parasagittal tumors by the presence of brain tissue at the parasagittal angle and lack of attachment to the dura of the SSS. Falcine meningiomas are delineated from parasagittal tumors by their sole dural attachment to the falx cerebri. Parasagittal meningiomas can vary in the amount of attachment to convexity dura and the falx cerebri, but all have an attachment to the SSS dura (see Fig. 23.1 ).

Convexity Meningiomas

Similar to other mass-occupying lesions in the central nervous system, convexity meningiomas can present with a variety of signs and symptoms based on their anatomic location. Symptomatic convexity meningiomas are most commonly associated with headache (39% to 48%), seizures (20% to 34%), and/or hemiparesis (10% to 21%). ^{, ,} Other specific symptomatology—such as dysphasia, sensory changes, and visual disturbances—occur less frequently but develop when tumors are located specifically over the respective eloquent cortices.