Object Although there is general agreement on the methods of treatment for symptomatic supratentorial cerebral cavernous malformations (CMs) located in noneloquent areas, some controversy exists regarding the management of cerebral CMs that are asymptomatic and/or located in eloquent or deep areas. Moreover, recent advances in genetic findings could influence both standard clinical management and the follow-up strategy in affected individuals. Thus, the objective of this study was to develop, based on the authors' experience and a literature review, a management algorithm to deal with supratentorial cerebral CMs. Methods The authors retrospectively reviewed the clinical data related to 118 patients who underwent surgery for symptomatic supratentorial cerebral CMs at their institution. Twenty-eight of 118 patients harbored multiple lesions, and nine of these 28 patients had a clinically positive familial history. Genetic investigations were performed in 89 patients (75%). Conclusions Surgery for supratentorial cerebral CMs in noneloquent locations is safe and curative. In cerebral CMs located in deep and eloquent areas and with symptoms including progressive neurological deficits, evidence of hemorrhage, and uncontrolled seizures, surgical treatment according to an integrated plan based on frameless stereotactic guidance and functional magnetic resonance imaging is recommended and results in acceptably low morbidity. The data support the need for long-term imaging follow up in all patients, careful preoperative vascular studies to detect associated venous anomalies, and the importance of genetic mutational analysis. The DNA screening protocol will change the care of family members of patients with familial forms of cerebral CMs, because affected asymptomatic family members may benefit by early detection of lesions. At the same time, the exclusion of family members who are not carriers of the mutation as members of the population at risk reduces the economic and psychological burden of clinical and instrumental monitoring.

Background: Cauda equina syndromes (CESs) due to leptomeningeal metastases from primitive lung tumors are rare. Despite recent advancements in neuro-oncology and molecular biology, the prognosis for these patients remains poor. Here, we present a case in which a patient developed lumbar leptomeningeal metastases from lung carcinoma that contributed to a CES and reviewed the appropriate literature. Case Description: A 55-year-old female presented with the left lower extremity sciatica/weakness. Two years ago, a then 53-year-old female had received Gamma Knife stereotactic radiosurgery (SRS) for a cerebellopontine angle schwannoma. Recently, she underwent resection of lung carcinoma and SRS for a right hemispheric cerebellar metastasis. Now at age 55, she presented with the left lower extremity sciatica/weakness. When her new lumbar MR was interpreted as showing a L5 schwannoma, a L4-L5 laminectomy was performed at surgery, the authors encountered multifocal leptomeningeal metastases densely infiltrating the cauda equina. Although only subtotal resection/decompression of tumor was feasible, she did well for the ensuing year. The histological diagnosis confirmed the lesion to be a poorly differentiated lung adenocarcinoma. Conclusion: Patients with a history of prior metastatic lung cancer may present with spinal leptomeningeal metastases resulting in a CES.

Background: Neurofibromatosis Type 1 (NF-1) and previous irradiation are two common risk factors that can result in malignant peripheral nerve sheath tumors (MPNSTs), extremely rare soft-tissue sarcomas. Here, a 63-year-old male with NF-1 presented with diffuse spinal metastases from a subcutaneous MPNST. Case Description: A 63-year-old male with NF-1 presented acutely with paraplegia and urinary incontinence. Both CT and MR studies of the thoracic-lumbosacral spine showed multiple metastases from a subcutaneous MPNST. In addition, the patient had a T12 vertebral body pathological fracture. Conclusion: Despite its aggressive behavior, some cases of MPNST can be managed with gross total resection and adjuvant radiotherapy. In addition, in the presence of multiple metastases, chemotherapy may play an additional, although questionable role.

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