Hypothermia has been proposed as a neuroprotective strategy. However, short-term cooling after hypoxia-ischemia is effective only if started immediately during resuscitation. The aim of this study was to determine whether prolonged head cooling, delayed into the late postinsult period, improves outcome from severe ischemia. Unanesthetized near term fetal sheep were subject to 30 min of cerebral ischemia. 90 min later they were randomized to either cooling ( n ϭ 9) or sham cooling ( n ϭ 7) for 72 h. Intrauterine cooling was induced by a coil around the fetal head, leading initially to a fall in extradural temperature of 5-10 Њ C, and a fall in esophageal temperature of 1.5-3 Њ C. Cooling was associated with mild transient systemic metabolic effects, but not with hypotension or altered fetal heart rate. Cerebral cooling reduced secondary cortical cytotoxic edema ( P Ͻ 0.001).

Delayed selective head cooling begun before the onset of postischemic seizures and continued for 3 days may have potential to significantly improve the outcome of moderate to severe hypoxic-ischemic encephalopathy.

After more than 40 years of research, visual prostheses are moving from the laboratory into the clinic. These devices are designed to provide prosthetic vision to the blind by stimulating localized neural populations in one of the retinotopically organized structures of the visual pathway - typically the retina or visual cortex. The long gestation of this research reflects the many significant technical challenges encountered including surgical access, mechanical stability, hardware miniaturization, hermetic encapsulation, high-density electrode arrays, and signal processing. This review provides an introduction to the pathophysiology of blindness; an overview of existing visual prostheses, their advantages and drawbacks; the perceptual effects evoked by electrical stimulation; as well as the role played by plasticity and training in clinical outcomes.

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The role of edema in the pathogenesis of hypoxic-ischemic injury in the immature brain is controversial. We studied 15 chronically instrumented fetal sheep following transient cerebral ischemia, to estimate changes in extracellular space using an impedance technique, to quantify the electroencephalogram with real-time spectral analysis, and to assess histologic outcome 3 days after the insult These measurements were made in the parasagittal cortex. There was a rapid loss of extracellular space from 5±2 minutes after the onset of ischemia. Following 10 minutes of ischemia (n=7) the intracellular edema peaked but then quickly resolved (6±4 minutes), and mild selective ncuronal loss was seen. In contrast, the swelling was biphasic after 30-40 minutes of ischemia (n=8). The early edema resolved slowly (28±12 minutes) but incompletely, and secondary swelling began at 7±2 hours and peaked at 28±6 hours. The early swelling was the more severe. Postinsult epileptiform activity began at 8±2 hours and peaked at 10 ±3 hours; later there was laminar necrosis of the underlying cortex. The secondary decrease of extracellular space indicates that a progressive loss of membrane function started with the onset of postischemic epileptiform activity. The increased metabolic load of the epileptiform activity may have worsened this delayed deterioration. (Stroke 1991,22:516-521)