Between January 1975 and April 2001, 8,225 patients with ovarian cancer were seen at The University of Texas M.D. Anderson Cancer Center. Brain metastases developed in 72 of these patients (0.9%). The medical records of these patients were reviewed to assess the incidence of these metastases and their correlates of survival, as well as to describe the various treatment modalities used against them and their respective outcomes. The mean age of patients at the time of brain metastasis diagnosis was 53.7 years. The median interval between the diagnosis of the primary cancer and brain metastasis was 1.84 years. Neurological deficit, headache, and seizure were the most common symptoms. The brain was the only site of metastasis in 43% of patients. Multiple metastases were seen in 65% of them, although this may be a slight underestimate, as brain metastases in 17% of patients were evaluated prior to the magnetic resonance imaging era. The median survival time after the diagnosis of brain metastases was 6.27 months (95% CI, 4.48-8.06 months). The combination of surgical resection and whole-brain radiation therapy (WBRT) resulted in a longer survival time (median, 23.07 months) than did WBRT alone (median, 5.33 months) or surgery alone (median, 6.90 months) (p < 0.01 in both instances, multivariate Cox proportional hazards model analysis). The prognosis for patients with brain metastases from ovarian cancer appears to be poor. The existence of systemic dissemination at the time of brain metastasis was associated with a worse survival trend. The only significant predictor of survival in our series was the treatment modality. In particular, the resection of brain metastasis from ovarian cancer followed by WBRT appeared to be superior to resection alone or WBRT alone.
We conclude that radical surgical resection of spinal cord ependymomas can be safely achieved in the majority of patients. A trend toward neurological improvement from a postoperative deficit can be expected between 1 and 3 months after surgery and continues up to 1 year. Postoperative dysesthesias begin to improve within 1 month of surgery and are significantly better by 1 year after surgery. The best predictor of outcome is the preoperative neurological status.
c c n s . o r gCysts of the ligamentum flavum are unusual causes of spinal compression. Their etiology and histopathologic classification have yet to be fully elucidated. We report our experience of four cases of ligamentum flavum cysts occurring in the lumbar spine and discuss some of the etiologies and possible pathophysiologic mechanisms for their development. CASE REPORTSAn outline of the cases is contained in the Table, and imaging examples are shown in Figure 1. Case 1The patient was an 82-year-old woman referred for recent onset of right-sided sciatica involving mostly the S1 distribution and causing major incapacitation because of severe pain. There was no pain on coughing; however, she had increased urinary frequency at night. On examination, motor function was normal and there was no sensory disturbance on examination of the legs. Reflexes were hypoactive in the right leg with plantar reflexes downgoing.Computerized tomography (CT) imaging of the lumbo-sacral spine showed significant degenerative disease in the lumbar spine, as well as an epidural mass occupying the L5-S1 region, with a small posterocentral subligamentous hernia, possibly representing a synovial or arachnoid cyst but also compatible with a benign cystic tumour such as a schwannoma. Subsequent magnetic resonance imaging (MRI) demonstrated a voluminous epidural cystic lesion compressing the cauda equina to the right of the sac at L5-S1, compatible with a synovial cyst of the ligamentum flavum. In light of the acuity and degree of incapacitation of the disease, the patient was hospitalized for urgent laminectomy with microsurgical removal of the cyst.ABSTRACT: Background: Cysts of the ligamentum flavum are rare and unusual causes of spinal compression. Methods: We report our experience of four cases of ligamentum flavum cysts occurring in the lumbar spine and discuss some of the possible etiologies and pathophysiologic mechanisms according to the available literature. Conclusion: This entity is clearly different from the synovial facetjoints or ganglion cysts.RÉSUMÉ: Sténose spinale lombaire incapacitante causée par un kyste du ligament jaune. Introduction: Les kystes du ligament jaune sont rares et causent très rarement une compression spinale. Méthodes: Nous rapportons notre expérience au sujet de quatre cas de kystes du ligament jaune au niveau lombaire et nous discutons de l'étiologie et de la physiopathologie de cette entité à la lumière de la littérature actuelle. Conclusion: Cette pathologie est nettement différente des kystes synoviaux des articulations facettaires ou des kystes ganglionnaires.
Ganglioneuromas are benign slow-growing masses that can be treated with complete surgical extirpation without any adjuvant therapy. Such lesions involving the sacrococcygeal region are exceedingly rare. The authors present the case of a 70-year-old woman with a sacrococcygeal ganglioneuroma treated by total en bloc resection. This patient also had a previous coccygeal fracture. To the authors' knowledge, there are no other reports of ganglioneuroma in association with a history of trauma.
A 29-year-old woman was found lying unconscious in the shower. There was a two-day history of headache and dizziness. In the emergency room, she was initially stuporous (Glasgow Coma Scale 10/15), afebrile, bradycardic and hypertensive. She exhibited roving, conjugate eye movements, left facial paresis (including frontalis), left ptosis, diffuse hypotonia, extensor plantar responses bilaterally and a 1.5 cm warm, fluctuant mass with surrounding erythema behind the left ear (Figure 1). Otoscopy revealed a bulge in the posterior wall of the left external auditory canal.A CT scan without contrast revealed an oval lesion with a hypodense centre and surrounding edema in the left cerebellar hemisphere, non-communicating hydrocephalus with compression of the fourth ventricle, a right midline shift, and effacement of cisterns (Figure 2). There was a 1.5 cm area of complete erosion on the posterior aspect of the left temporal bone and rupture of the anterior wall of the petrous bone in the left middle fossa (Figure 3). Infused CT showed ring enhancement of the cerebellar lesion. The petrous bone appeared THE CANADIAN JOURNAL OF NEUROLOGICAL SCIENCES 317
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