Parent artery occlusion is not obsolete in giant aneurysms of the ICA. Experience with very-long-term follow-up.

INTRODUCTION: The purpose of this study was to present the long-term clinical and angiographic follow-up (FU) in 26 consecutive patients with giant/large aneurysms (G/LAs) of the internal carotid artery (ICA) treated by parent artery occlusion (PAO). METHODS: Twenty-two of 26 G/LAs of the ICA were treated by PAO when a balloon test occlusion prior to occlusion of the ICA was tolerated. Clinical and angiographic FU were available in, respectively, 20 and 18 patients with a mean delay of 6.1 years (range 1.5-11). RESULTS: At long-term FU, clinical symptoms had disappeared in 75% of the patients, partially regressed in 10%, and remained unchanged in 15% of cases. No patient presented worsening of clinical symptoms or intracranial bleeding. Fifteen patients presented a modified Rankin scale score of 0 and five patients a score of 1. On imaging FU, persistent occlusion of the PA was observed in 17/18 cases. One case of aneurysmal recanalization was observed at long-term FU. PAO was well tolerated in all patients. On angiographic FU, no new lesion was detected, except the growing of a pre-existing aneurysm located on the carotid siphon contralateral to the occluded vessel. CONCLUSION: Our study demonstrates that occlusion of the parent artery for giant/large ICA aneurysms remains a safe and effective technique with good clinical and angiographic outcome at long-term FU.

Balloon-assisted embolization of skull base meningioma with liquid embolic agent.

The authors report a novel technique of balloon-assisted embolization of a skull base meningioma supplied by a branch of the cavernous segment of the internal carotid artery using liquid embolic agent. A temporarily inflated balloon distal to the meningioma's feeding vessel may improve the access to this small branch and may reduce the chances of unintended reflux during delivery of the liquid embolic agent.

S100B as an additional prognostic marker in subarachnoid aneurysmal hemorrhage.

OBJECTIVES: Studies of new neuroprotective approaches in patients with subarachnoid aneurysmal hemorrhage and better family information would benefit from the development of laboratory markers of brain ischemia. The goal of this study was to evaluate mean 15-day S100B for predicting outcomes after subarachnoid aneurysmal hemorrhage. DESIGN: Single center prospective cohort with consecutive inclusions. SETTING: Anesthesiology and Critical Care Neurosurgical Unit of a university hospital. PATIENTS: One hundred nine patients admitted within 48 hrs after subarachnoid aneurysmal hemorrhage onset and treated by surgical clipping or coiling within 48 hrs following admission. INTERVENTIONS: We recorded initial World Federation of Neurologic Surgeons and Fisher grades; comorbidities; initial severity; aneurysm location; presence of acute hydrocephalus; presence of intraventricular hemorrhage; initial seizures and neurogenic lung edema; initial troponin values; treatment of aneurysm; and occurrence of vasospasm. MEASUREMENTS AND MAIN RESULTS: S100B was assayed daily over the first 15 days. Glasgow Outcome Scores were recorded at intensive care unit discharge and after 6 and 12 months. The main outcome criterion was the 12-month Glasgow Outcome Scale score dichotomized as poor (Glasgow Outcome Scale 1-3) or good (Glasgow Outcome Scale 4-5). Seventy percent of patients had good 12-month outcome. Poor outcome was associated with higher initial World Federation of Neurologic Surgeons and Fisher scores, neurogenic lung edema, high mean 15-day S100B but not initial, troponin initial value, intraventricular hemorrhage, angiographically documented vasospasm, all in an univariate manner. After multivariate analysis, only mean 15-day S100B value significantly predicted outcome (p < 0.0005). The best cutoff for the mean 15-day S100B value was 0.23 microg/L (specificity 0.90, 95% confidence interval [CI] 0.81-0.95; sensitivity 0.91, 95% CI 0.75-0.98; area under the curve 0.98, 95% CI 0.87-0.99). CONCLUSION: S100B elevation over the first 15 days after subarachnoid aneurysmal hemorrhage is associated with poor outcome after subarachnoid aneurysmal hemorrhage. This result supports the use of S100B as a surrogate marker for brain ischemia in patients with subarachnoid aneurysmal hemorrhage.

Predictors of 1-year outcome after coiling for poor-grade subarachnoid aneurysmal hemorrhage.

OBJECTIVE: To describe features in patients admitted to the intensive care unit (ICU) for poor-grade aneurysmal subarachnoid hemorrhage (SAH) and to identify predictors of 12-month outcome. METHODS: We conducted a controlled observational study of 51 consecutive patients treated with endovascular coiling within 96 h of rupture for poor-grade aneurysmal SAH (20 men and 31 women, age 54 +/- 12 years). We recorded co-morbidities; initial severity; aneurysm location; occurrence of acute hydrocephalus, initial seizures, and/or neurogenic lung edema; troponin values, Fisher grade; computed tomography (CT) findings; treatment intensity; and occurrence of vasospasm. The brain injury marker S100B was assayed daily over the first 8 days. Glasgow Outcome Scores (GOS) were recorded at ICU discharge, at 6 and 12 months. The main outcome criterion was the 1-year GOS score, which we used to classify patients as having a poor outcome (GOS 1-3) or a good outcome (GOS 4-5). RESULTS: Overall, clinical status after 1 year was very good (GOS 5) in 41% of patients and good (GOS 4) in 16%. Neither baseline characteristics nor interventions differed significantly between patients with good outcome (GOS 4-5) and those with poor outcome (GOS 1-3). Persistent intracranial pressure elevation and higher mean 8-day S100B value significantly and independently predicted the 1-year GOS outcome (P = 0.008 and P = 0.001, respectively). CONCLUSIONS: Patients in poor clinical condition after SAH have more than a 50:50 chance of a favorable outcome after 1 year. High mean 8-day S100B value and persistent intracranial hypertension predict a poor outcome (GOS 1-3) after 1 year.

Phase I study of dystrophin plasmid-based gene therapy in Duchenne/Becker muscular dystrophy.

Nine patients with Duchenne or Becker muscular dystrophy were injected via the radialis muscle with a full-length human dystrophin plasmid, either once with 200 or 600 microg of DNA or twice, 2 weeks apart, with 600 microg of DNA. In the biopsies taken 3 weeks after the initial injection, the vector was detected at the injection site in all patients. Immunohistochemistry and nested reverse transcription-polymerase chain reaction indicated dystrophin expression in six of nine patients. The level of expression was low (up to 6% weak, but complete sarcolemmal dystrophin staining, and up to 26% partial sarcolemmal labeling). No side effects were observed, nor any cellular or humoral anti-dystrophin responses. These results suggest that exogenous dystrophin expression can be obtained in Duchenne/Becker patients after intramuscular transfer of plasmid, without adverse effects, hence paving the way for future developments in gene therapy of hereditary muscular diseases.