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Neuroprotective effects of nicardipine in a rat model of ischemia and reperfusion

Mamoru Kittaka, Steven L. Giannotta, Vladimir Zelman, Jorge D. Correale, Christopher M. DeGiorgio, Martin H. Weiss, and Berislav V. Zlokovic

A reversible middle cerebral artery occlusion was performed in rats to determine whether nicardipine, a dihydropyridine voltage-sensitive Ca++ channel (VSCC) antagonist, exerts neuroprotective effects when administered 10 minutes following an ischemic insult, and if it does, whether this is due to its vasodilatory action and effect on cerebral blood flow (CBF) or to direct blockade of Ca++ entry into ischemic brain cells. An increase in the intracellular calcium, [Ca++]i, plays a major role in neuronal injury during cerebral ischemia. Although a large amount of Ca++ enters neurons through the VSCC during ischemia, inconsistent neuroprotective effects have been reported with the antagonists of the VSCC. An intraperitoneal injection of nicardipine (1.2 mg/kg) was administered to rats at 10 minutes after the onset of ischemia, and 8, 16, and 24 hours after occlusion. Cortical CBF was determined by laser-Doppler flowmetry. Neurological and neuropathological examinations were performed after 72 hours. Neuron-specific enolase, a specific marker for the incidence of neuronal injury, was measured in plasma. The CBF in the ischemic core and periphery, as well as brain temperature and physiological parameters, were not affected by nicardipine during occlusion or reperfusion. However, nicardipine treatment significantly improved motor neurological outcome by 32%, and the infarction and edema volume in the pallium as well as the edema volume in the striatum were significantly reduced by 28%, 37%, and 53%, respectively. Nicardipine also significantly reduced the neuron-specific enolase plasma levels by 50%, 42%, and 59% at 24, 48, and 72 hours after the occlusion, respectively. It is concluded that nicardipine may attenuate focal ischemic brain injury by exerting direct neuroprotective and antiedematous effects that do not depend on CBF.

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Postoperative Gamma Knife surgery for benign meningiomas of the cranial base

Laurence Davidson, Dawn Fishback, Jonathan J. Russin, Martin H. Weiss, Cheng Yu, Paul G. Pagnini, Vladimir Zelman, Michael L. J. Apuzzo, and Steven L. Giannotta


The standard treatment for meningiomas is complete resection, but the proximity of skull base meningiomas to important neurovascular structures makes complete excision of the lesion difficult or impossible. The authors analyzed the mid- and long-term results obtained in patients treated with postresection Gamma Knife surgery (GKS) for residual or recurrent benign meningiomas of the cranial base.


Thirty-six patients with residual or recurrent benign meningiomas of the skull base following one or more surgical procedures underwent GKS. There were 31 women and five men, ranging in age from 22 to 73 years. The median tumor volume was 4.1 ml (range 0.8–20 ml) and the median radiation dose to the tumor margin was 16 Gy (range 15–16 Gy).


Patients were followed for a median of 81 months (range 30–141 months) after GKS. At the end of the follow-up period, overall neurological improvement was observed in 16 patients (44.4%), whereas the condition in 20 patients (55.6%) was unchanged. One patient suffered transient cerebral edema 6 months after GKS. Based on imaging documentation, a partial response was seen in five patients (13.9%), the disease remained stable in 30 patients (83.3%), and in one patient (2.8%) there was an increase in tumor size. The actuarial progression-free survival rate was 100% at 5 years and 94.7% at 10 years.


Gamma Knife surgery was shown to be an excellent adjunct to resection because of its durable rate of tumor control and low toxicity. It should be initially considered along with surgery for the treatment of complex skull base meningiomas.

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Abstracts of the 2017 AANS/CNS Joint Section on Disorders of the Spine and Peripheral Nerves Las Vegas, Nevada • March 8–11, 2017