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Matthew J. McGirt, Alan T. Villavicencio, Ketan R. Bulsara, Henry S. Friedman, and Allan H. Friedman

✓ Adjuvant use of 1,3-bis(2-chloroethyl)-1-nitrosourea (BCNU) wafers with surgical resection is becoming common for the treatment of malignant gliomas. Cyst formation in the tumor resection cavity is a recently described complication associated with the use of BCNU wafers. There is currently no report in which successful management of this complication without additional surgical intervention is described.

The authors describe four patients in whom postoperative cysts developed in the tumor resection cavity after placement of BCNU wafers. These include a 38-year-old man with a left frontoparietal tumor, a 48-year-old man with a right frontal lobe tumor, a 78-year-old man with a left parietooccipital tumor, and a 61-year-old woman with a left frontotemporal tumor. Histopathological studies of biopsy samples revealed malignant glioma in each patient. All four patients had unremarkable perioperative courses, were discharged within 3 to 8 days of surgery, and subsequently returned with acute neurological deterioration. Follow-up magnetic resonance (MR) imaging demonstrated cyst formation with significant mass effect at the previous resection site. Three patients were treated with high-dose dexamethasone and returned to their neurological baseline over an 8-day period. The fourth patient improved after surgical drainage and biopsy sampling of the cyst, which revealed no evidence of infection or recurrent tumor, but again sought medical care 2 weeks later with cyst recurrence necessitating high-dose steroid therapy. On MR images at least a 30% reduction in cyst size was demonstrated in all four patients, each of whom remained clinically stable at 2, 6, 6, and 4 months of follow-up review.

Neurosurgeons should be aware of the potential for postoperative cyst formation accompanied by clinically significant mass effect after BCNU wafer implantation, as well as the potential for successful nonsurgical management leading to clinical and radiological improvement.

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Matthew J. McGirt, Ketan R. Bulsara, Thomas J. Cummings, Kent C. New, Kenneth M. Little, Henry S. Friedman, and Allan H. Friedman

Object. The prognostic value of differentiating between recurrent malignant glioma and a lesion due to radiation effect by performing stereotactic biopsy has not been assessed. Thus, this study was undertaken to determine such value.

Methods. Between 1995 and 2001, 114 patients underwent magnetic resonance (MR) imaging—guided stereotactic biopsy to differentiate lesions caused by a recurrence of malignant astrocytoma and by radiation effect. All patients had previously undergone tumor resection (World Health Organization Grade III or IV) followed by radiotherapy. Disease diagnosis based on biopsy and patient characteristics were assessed as predictors of survival according to results of a multivariate Cox regression analysis. The diagnosis determined with the aid of biopsy was compared with that established during a subsequent resection in 26 patients.

Survival following stereotactic biopsy was markedly increased in patients suffering from radiation effect compared with those harboring recurrent malignant glioma (p < 0.0001). In patients with radiation effect on biopsy, an increasing patient age (p < 0.05), having had two compared with one prior resection (p < 0.05), and a decreasing time from radiotherapy to biopsy (p < 0.001) were factors associated with decreased survival. Nevertheless, in patients with biopsy-defined radiation effect at second progression or with an age younger than 50 years the survival rate remained higher than that in patients with recurrent tumor on biopsy (p < 0.01). A biopsy-based diagnosis of radiation effect obtained less than 5 months after radiotherapy was not associated with an increased rate of patient survival compared with a diagnosis of recurrent malignant glioma on biopsy (p = 0.286). Eighty-six percent of lesions initially determined to be due to radiation effect on biopsy fewer than 5 months after radiotherapy were characterized as recurrent glioma by a mean of 11 months later. In contrast, only 25% of lesions initially diagnosed as attributable to radiation effect on biopsy more than 5 months after radiotherapy were classified as recurrent glioma a mean of 12 months later (p < 0.05).

Conclusions. With the aid of stereotactic biopsy the authors demonstrated prognostic significance in differentiating recurrent malignant astrocytoma from a lesion due to radiation effect in patients presenting more than 5 months after having undergone radiotherapy. In patients who presented earlier than 5 months after radiotherapy, radiation effect on biopsy was not associated with an improved rate of survival compared with that in patients harboring recurrent malignant astrocytoma.

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Ketan R. Bulsara, Matthew J. McGirt, Lawrence Liao, Alan T. Villavicencio, Cecil Borel, Michael J. Alexander, and Allan H. Friedman

Object. Differentiating myocardial infarction (MI) from reversible neurogenic left ventricular dysfunction (stunned myocardium [SM]) associated with aneurysmal subarachnoid hemorrhage (SAH) is critical for early surgical intervention. The authors hypothesized that the cardiac troponin (cTn) trend and/or echocardiogram could be used to differentiate between the two entities.

Methods. A retrospective study was conducted for the period between 1995 and 2000. All patients included in the study met the following criteria: 1) no history of cardiac problems; 2) new onset of abnormal cardiac function (ejection fraction [EF] < 40% on echocardiograms); 3) serial cardiac markers (cTn and creatine kinase MB isoform [CK-MB]); 4) surgical intervention for their aneurysm; and 5) cardiac output monitoring either by repeated echocardiograms or invasive hemodynamic monitoring during the first 4 days post-SAH when the patients were euvolemic.

Of the 350 patients with SAH, 10 (2.9%) had severe cardiac dysfunction. Of those 10, six were women and four were men. The patients' mean age was 53.5 years (range 29–75 years) and their SAH was classified as Hunt and Hess Grade III or IV. Aneurysm distribution was as follows: basilar artery tip (four); anterior communicating artery (two); middle cerebral artery (one); posterior communicating artery (two); and posterior inferior cerebellar artery (one). The mean EF at onset was 33%. The changes on echocardiograms in these patients did not match the findings on electrocardiograms (EKGs). Within 4.5 days, dramatic improvement was seen in cardiac output (from 4.93 ± 1.16 L/minute to 7.74 ± 0.88 L/minute). Compared with historical controls in whom there were similar levels of left ventricular dysfunction after MI, there was no difference in peak CK-MB. A 10-fold difference, however, was noted in cTn values (0.22 ± 0.25 ng/ml; control 2.8 ng/ml; p < 0.001).

Conclusions. The authors determined the following: 1) that the CK-MB trend does not allow differentiation between SM and MI; 2) that echocardiograms revealing significant inconsistencies with EKGs are indicative of SM; and 3) that cTn values less than 2.8 ng/ml in patients with EFs less than 40% are consistent with SM.

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Matthew J. McGirt, John C. Mavropoulos, Laura Y. McGirt, Michael J. Alexander, Allan H. Friedman, Daniel T. Laskowitz, and John R. Lynch

Object. The identification of patients at an increased risk for cerebral vasospasm after subarachnoid hemorrhage (SAH) may allow for more aggressive treatment and improved patient outcomes. Note, however, that blood clot size on admission remains the only factor consistently demonstrated to increase the risk of cerebral vasospasm after SAH. The goal of this study was to assess whether clinical, radiographic, or serological variables could be used to identify patients at an increased risk for cerebral vasospasm.

Methods. A retrospective review was conducted in all patients with aneurysmal or spontaneous nonaneurysmal SAH who were admitted to the authors' institution between 1995 and 2001. Underlying vascular diseases (hypertension or chronic diabetes mellitus), Hunt and Hess and Fisher grades, patient age, aneurysm location, craniotomy compared with endovascular aneurysm stabilization, medications on admission, postoperative steroid agent use, and the occurrence of fever, hydrocephalus, or leukocytosis were assessed as predictors of vasospasm.

Two hundred twenty-four patients were treated for SAH during the review period. One hundred one patients (45%) developed symptomatic vasospasm. Peak vasospasm occurred 5.8 ± 3 days after SAH. There were four independent predictors of vasospasm: Fisher Grade 3 SAH (odds ratio [OR] 7.5, 95% confidence interval [CI] 3.5–15.8), peak serum leukocyte count (OR 1.09, 95% CI 1.02–1.16), rupture of a posterior cerebral artery (PCA) aneurysm (OR 0.05, 95% CI 0.01–0.41), and spontaneous nonaneurysmal SAH (OR 0.14, 95% CI 0.04–0.45). A serum leukocyte count greater than 15 × 109/L was independently associated with a 3.3-fold increase in the likelihood of developing vasospasm (OR 3.33, 95% CI 1.74–6.38).

Conclusions. During this 7-year period, spontaneous nonaneurysmal SAH and ruptured PCA aneurysms decreased the odds of developing vasospasm sevenfold and 20-fold, respectively. The presence of Fisher Grade 3 SAH on admission or a peak leukocyte count greater than 15 × 109/L increased the odds of vasospasm sevenfold and threefold, respectively. Monitoring of the serum leukocyte count may allow for early diagnosis and treatment of vasospasm.

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Matthew J. McGirt, Robert Blessing, Michael J. Alexander, Shahid M. Nimjee, Graeme F. Woodworth, Allan H. Friedman, Carmelo Graffagnino, Daniel T. Laskowitz, and John R. Lynch


Impairment of endothelial nitric oxide synthase (eNOS), endothelium-dependent relaxation, and cerebrovascular autoregulation all occur in vasospastic cerebral arteries following subarachnoid hemorrhage (SAH). The 3-hy-droxy-3-methylglutaryl coenzyme A reductase inhibitors, or statins, both improve endothelial function and increase eNOS messenger RNA, protein, and enzymatic activity threefold. Increasing experimental evidence in animal models of SAH suggests that statins may ameliorate cerebral vasospasm. The authors hypothesized that patients chronically treated with statins would have a decreased risk of symptomatic vasospasm after SAH.


The authors retrospectively reviewed the charts of 115 patients with SAH who were consecutively admitted to the Neuroscience Intensive Care Unit of Duke University between 1998 and 2001. The independent association of statin therapy to symptomatic vasospasm was assessed using multivariate logistic regression analysis. Fifteen patients (13%) admitted with SAH were receiving statin therapy for at least 1 month before admission. Forty-nine patients (43%) experienced symptomatic vasospasm a mean of 5.8 ± 3 days after onset of SAH. Current statin therapy on admission (odds ratio [OR] 0.09, 95% confidence interval [CI] 0.01–0.77) was independently associated with an 11-fold reduction in the risk of symptomatic vasospasm. Fisher Grade 3 SAH (OR 2.82, 95% CI 1.50–5.71) and rupture of anterior cerebral or internal carotid artery aneurysm (OR 3.77, 95% CI 1.29–10.91) were independently associated with an increased risk of symptomatic vasospasm.


In this retrospective case series, patients who received statin therapy for at least 1 month demonstrated an 11-fold decrease in the risk of developing symptomatic vasospasm after SAH.