In this single-institution cohort of patients with SAH, onset seizures were an independent risk factor for late seizures and a predictor of poor outcome.

Thirteen patients with schwannomas of the jugular foramen were operated on at the Cleveland Clinic between 1974 and 1983. The authors' experience in managing these rare tumors is presented. Three major growth patterns of jugular foramen schwannoma were seen, and it is postulated that the position of the tumor depends on its point of origin from the nerves as they pass through the pars nervosa of the jugular foramen. The more distal lesions will expand inferiorly out of the base of the skull, and the more proximal lesions will enlarge into the posterior fossa. Tumors in the mid region will tend to expand primarily into bone. The schwannoma was primarily intracranial in six patients. In five patients the tumor expanded the bone at the base of the skull, with only a small intracranial component, and in two patients the tumor was primarily extracranial, with a small extension into the bone or posterior fossa. The presentation of the patients varied according to the tumor growth pattern. Deafness, vertigo, and ataxia were present in all patients with a major intracranial component, and in most of these there were only minimal deficits of the jugular foramen nerves. By contrast, lower cranial nerve involvement, including hoarseness and weakness of the trapezius and sternocleidomastoid muscles, occurred in patients in whom the tumor was primarily, within the bone or extracranial. Three of the five patients with the major component of the schwannoma within the bone also had deafness. Symptomatic history was longest in those with tumor mainly involving the bone at the base of the skull, and shortest in patients with entirely extracranial tumor. Surgical resection was accomplished with a joint neurosurgical-otological approach, usually combining a posterior fossa exploration with either a translabyrinthine transcochlear or infralabyrinthine procedure. The exact nature of the operation depended upon the presence of intracranial tumor and on the extent of bone or extracranial involvement. Total excision was performed in all cases. There was no operative mortality, and surgery resulted in loss of function of the ninth, 10th, and 11th cranial nerves in most patients. The major postoperative morbidity consisted of swallowing difficulties and sputum aspiration.

The in vitro subcellular distribution patterns of 10 porphyrins, varying in hydrophobicity and charge, were studied using confocal laser scanning microscopy on two cell lines (V79 and C6 glioma cells) for incubation times up to 24 h. All of the porphyrins were taken up rapidly by both cell lines and distinct classes of subcellular distribution patterns were observed: general cytoplasmic staining; localization in lysosomes (usually associated with general cytoplasmic staining); localization in mitochondria (and general cytoplasmic staining); localization in mitochondria with subsequent uptake into lysosomes. Structure-localization relationships which have emerged are that porphyrins with dominantly cationic side chains localize in mitochondria, whereas those with a more anionic character tend to localize in lysosomes.

The prognosis for patients with high-grade cerebral glioma is poor. Most treatment failures are due to local recurrence of tumor, indicating that a more aggressive local therapy could be beneficial. Adjuvant treatments such as porphyrin-sensitized photodynamic therapy (PDT) or boron neutron capture therapy (BNCT) have the potential to control local recurrence. The selective tumor uptake of a boronated porphyrin was studied in CBA mice bearing an implanted intracerebral glioma. Biopsy samples of tumor, normal brain, and blood were analyzed by a fluorometric assay following intraperitoneal and intravenous administration of boronated protoporphyrin (BOPP). This compound was selectively localized to tumor at ratios as high as 400:1 relative to normal brain.Confocal laser scanning microscopy of glioma cells in vitro and in vivo showed that BOPP was localized within mitochondria and excluded from the nucleus of these cells. This discrete subcellular localization was confirmed by density gradient ultracentrifugation after homogenization of mouse tumor biopsies. The selective discrete localization of these compounds within the tumor suggests that this compound may be used as a dual PDT/BNCT sensitizer.Primary cerebral tumors are responsible for -2% of all cancer deaths, with =10,000 persons dying per annum in the United States (1). The majority of these deaths are due to the high-grade gliomas-anaplastic astrocytoma and glioblastoma multiforme. At present there is no satisfactory treatment for these tumors. Surgery provides a definitive histological diagnosis and relief of symptoms of raised intracranial pressure. Radiotherapy and adjuvant chemotherapy are of limited value and most studies utilizing these treatments report median survival times of <1 year (1, 2). Most treatment failures are due to local recurrence of the tumor, suggesting that more aggressive local therapy could be beneficial. Two adjuvant therapies with the potential to control local recurrence are photodynamic therapy (PDT) and boron neutron capture therapy (BNCT).PDT relies on the selective uptake or retention of a photosensitizing chemical in the tumor relative to surrounding normal tissue, followed by treatment with light of the appropriate wavelength to activate the photosensitizer (3). The photoactivation of this sensitizer results in generation of a cytotoxic chemical species, probably singlet excited state oxygen, which leads to selective tumor necrosis (3). Photosensitizers that have been used in most clinical and experimental studies to date are hematoporphyrin derivative (HpD) and its enriched commercial preparation Photofrin II (3), both of which have been shown to selectively localize in glioblastoma multiforme (4, 5). Reports of PDT in the treatment of animal (5-7) and human (5, 7-9) gliomas have been encouraging, although the use of a more tumor-selective photosensitizer than HpD or Photofrin II would be desirable.Like PDT, BNCT is based on selective tumor localization of a sensitizing agent, a compound containing 10B atoms, fo...

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