Steady potential gradients in experimental cerebral vascular occlusion

Abstract

Resting pia-ventricular steady potential in the cat is ordinarily surface positive by values ranging from less than one to as much as 7 mV. Occlusion of one middle cerebral artery is usually followed by a prominent sustained surface negative steady potential shift in the middle of the cortical surface area of distribution of this vessel. This change may be recorded with either pia-ventricular or cortico-cortical electrode placement but not from transcortical leads alone. It is therefore presumably developed across white matter, i.e., between injured and uninjured portions of subcortical axons. The role of the cerebral white matter in the steady potential shift of such restricted cerebral vascular occlusion is shown by the subcortex to ventricle leads. When steady potential is recorded from each of several cortical loci simultaneously it is found that the magnitude of this shift decrements toward the periphery of the ischemic region. The surface negative steady potential shift produced by such vascular occlusion attains an amplitude of 5 to 11 mV. in the center of the surface area of distribution of the middle cerebral artery. This change is qualitatively identical in the cat and monkey. With permanent occlusion of the vessel the steady potential shift may be transient, lasting only a few minutes or may continue at maximal value for as long as one hour. These findings are independent of the effects of Nembutal anesthesia. The ECG changes accompanying this steady potential shift are similar to those of sudden cerebral anoxia. A steady potential shift qualitatively indistinguishable from that of restricted vascular occlusion is produced by application of a small piece of solid carbon dioxide to the cortical surface. It is concluded that the steady potential shift of vascular occlusion is not peculiar to the latter but that it is a basic property of focal injury of the mammalian brain. The origin of steady potential gradients resulting from the focal cerebral injury is explainable in terms of the algebraically summated effects of injury of individual anatomical units. It is suggested that the term “cerebral injury potential” aptly characterizes the sustained steady potential shift of focal brain injury. When a brief steady potential shift follows occlusion of one middle cerebral artery the sequence of events at a given locus bears a striking similarity to that of a spreading depression.