Human neuronal cells can be produced in culture and implanted stereotactically into the brains of patients with motor deficits due to stroke. Although a measurable improvement was noted in some patients and this translated into improved activities of daily living in some patients as well, this study did not find evidence of a significant benefit in motor function as determined by the primary outcome measure. This experimental trial indicates the safety and feasibility of neuron transplantation for patients with motor stroke.

Background and Purpose-Mild hypothermia is possibly the single most effective method of cerebroprotection developed to date. However, many questions regarding mild hypothermia remain to be addressed before its potential implementation in the treatment of human stroke. Here we report the results of 2 studies designed to determine the optimal depth and duration of mild hypothermia in focal stroke and its effects on infarct size, neurological outcome, programmed cell death, and inflammation. Methods-Rats underwent a 2-hour occlusion of the left middle cerebral artery. In the first study (I) animals were kept (intraischemically) at either 37°C (nϭ8), 33°C (nϭ8), or 30°C (nϭ8). Study II consisted of 4 groups: (1) controls (37°C, nϭ10), (2) 30 minutes of hypothermia started at ischemic onset (33°C, nϭ9), (3)1 hour (33°C, nϭ8), and (4) 2 hours (33°C, nϭ8). Brain temperature was measured by a thermocouple probe placed in the contralateral cortex. After suture removal, all animals were rewarmed and reperfused for 22 hours (I) or 70 hours (II). Results-Mild hypothermia to 33°C or 30°C was neuroprotective (17Ϯ7% and 27Ϯ6%, respectively) relative to controls (53Ϯ8%, PϽ0.02), but 33°C was better tolerated and recovery from anesthesia was faster. The neurological score of hypothermic animals was significantly better than that of controls (I & II) at both 24 and 72 hours postischemia except for the 30-minute group (II), which showed no improvement. In Study II, 2 hours of hypothermia reduced injury by 59%, 1 hour reduced injury by 84% whereas 30 minutes did not reduce injury. Normalized for infarct size, 2 hours of mild hypothermia decreased neutrophil accumulation by 57% whereas both 1 hour and 30 minutes had no effect. At 72 hours, 1 and 2 hours of mild hypothermia decreased transferase dUTP nick-end labeling (TUNEL) staining by 78% and 99%, respectively, and 30 minutes of hypothermia had no effect. Conclusions-Intraischemic mild hypothermia must be maintained for 1 to 2 hours to obtain optimal neuroprotection against ischemic cell death due to necrosis and apoptosis. (Stroke. 1998;29:2171-2180.)

Arteriovenous malformations of the brain are congenital vascular lesions that affect 0.01-0.50% of the population, and are generally present in patients aged 20-40 years. The usual clinical presentations are haemorrhage, seizures, progressive neurological deficit, or headache. Results of natural history studies have shown a yearly haemorrhage rate of 1-4%. Frequency of rebleeding has increased over the years, and several factors that increase risk of haemorrhage have been identified. Although substantial, the morbidity associated with haemorrhages could be less than previously thought. Over the past decade, great advances have been made in application of endovascular embolisation techniques, stereotactic radiosurgery, and microsurgery, allowing effective multidisciplinary treatment of arteriovenous malformations, including those previously deemed to be untreatable. Increasing attention has been paid to management of flow-related aneurysms associated with these malformations. Finally, many reports of recurrent arteriovenous malformations have coincided with new theories regarding the embryogenesis of these disorders and laboratory work suggesting their proliferative potential.

A small (< 1 mm in diameter) or absent ipsilateral posterior communicating artery is a risk factor for ischemic cerebral infarction in patients with internal-carotid-artery occlusion.