Stimulation of the medullary reticular formation in cold-injured brain

The vasopressor response (Cushing) in patients with high intracranial pressure (ICP) has been thought to be a result of lower brainstem dysfunction. This study was carried out to study the effect of stimulation of the reticular formation of the medulla oblongata on ICP and cerebral blood volume (CBV) in injured brain with increased ICP. The CBV was measured by the photoelectric method from the uni- or bilateral parietal lobe. Seventeen hours prior to the experiments, cold-induced edema was produced to increase basal ICP. In 15 cats, electric stimulation produced temporary increases in blood pressure (BP), ICP, and CBV and progressive intracranial hypertension was never observed (group A). In 9 animals, progressive increases in CBV and ICP up to 50-100 mmHg occurred after cessation of stimulation (group B). Prestimulation ICP in group B was significantly higher than that of group A (p less than 0.01). Rapid and simultaneous increases in ICP and CBV following stimulation strongly suggested that global increments of CBV secondary to loss of cerebral vasomotor tonus were responsible for producing progressive intracranial hypertension. In group B, the stimulation electrodes were invariably located at the area of the nucleus reticularis parvocellularis and gigantocellularis. Our experimental results show that under conditions of increased ICP, a stimulated or irritable condition of the medullary reticular formation will cause temporary or progressive intracranial hypertension.