Lee R. Wolin

Evoked responses in the auditory cortex of the squirrel monkey

Abstract Using a semimacroelectrode, the contralateral and ipsilateral surface auditory cortices and insular cortices were mapped using 500 Hz 4-cycle “click” stimuli. The evoked responses were largest in amplitude and shortest in latency in the contralateral insular cortex. The crest of the contralateral superior temporal gyrus had the next highest amplitude and the next shortest latency. These two areas were considered as primary auditory input regions. The secondary areas consisted of the superior bank of the sylvian fissure lying within the precentral and postcentral gyri and the inferior temporal gyrus. The contralateral auditory surface cortex, based on the extent of evoked potentials recorded, was twice as large as the ipsilateral auditory cortex.

Electrical activity of the isolated macaque brain

Abstract The completely isolated brain (vascular as well as neurologic isolation) on donor perfusion showed excellent electrical activity of the cortex and reticular formation during all phases of its preparation including 1–4 hours of donor perfusion. As the various cranial nerves and spinal cord connections were severed from the brain stem, faster moderate voltage electrical activity appeared in cortex and reticular formation. These results were found in isolated preparations where no difficulties occurred in maintaining proper blood pressure, with minimal blood loss, and normothermic brain temperature. The neurogenically isolated brain (all cranial nerves severed) was maintained with little difficulty and appeared to show electrocortical activity similar to that in the completely isolated brain. Fast electrical activity appeared after the removal of the cranial nerves and spinal cord. Control of blood pressure, blood loss, and brain temperature was a prerequisite for optimum cortical activity. Severance of the brain stem between the mesencephalon and diencephalon (cervean isole) created first: a short period of synchronized slowing of electrical activity, followed by a longer period of extremely fast, low-voltage, desynchronized activity, then by phasic slow and fast activity. The intervals of slow activity increased in number and duration as the blood pressure became difficult to maintain, finally becoming very slow with high-voltage activity in the failing preparation. It appears that the isolated primate brain shows a range of electrophysiological activity including states characteristic of the aroused brain of an intact monkey.

Tolerance to arrest of cerebral circulation in the rhesus monkey

Abstract Twenty rhesus monkeys (Macaca mulatta) were subjected to periods of arrest of cerebral blood flow varying from 4 to 15 min. Arrest was accomplished by placing ligatures around the carotid and vertebral arteries. A drainage cannula in one carotid artery served to remove blood reaching the circle of Willis via anastomotic routes. After clamping the vessels, electrocortical activity (EEG) ceased within 25 sec. After reestablishment of blood flow to the brain, the EEG reappeared anywhere from 30 min to 5 hr depending on the duration of the arrest period. Animals subjected to periods of cerebral arrest up to 13 min showed no neurologic or behavioral deficits on the second postoperative day. The animal subjected to 14-min arrest retained motor deficits even 2 months postsurgically. Three animals subjected to 15 min of arrest failed to survive. One of these lived for 20 hr, recovering normal EEG activity and consciousness. It was able to make uncoordinated body and limb movements, but could not sit or eat. Controlled cerebral arrest up to 12 or 13 min appears to be relatively safe in the primate. Periods longer than this result in permanent neurologic deficits or death.

Behavioral effects of autocerebral perfusion, hypothermia and arrest of cerebral blood flow in the rhesus monkey

Abstract Monkeys (Macaca mulatta) were subjected to extracorporeal autocerebral perfusion. Ten animals had their brains cooled to 15 C and then maintained between 10 and 15 C for an additional 30 min by continued perfusion of cold blood. In ten animals, the brains were cooled to 15 C and cerebral blood fiow was then arrested for 30 min. Nine animals were perfused at normal temperatures for 1 hour as controls. Twenty-three of the 29 animals survived these procedures. Survivors were observed for 1 wk after surgery and revealed no obvious neurological deficits. Subsequent testing on a battery of behavioral tasks showed performance deficits suggestive of brain damage in only two animals, both from the control group. The incidence of death indicates the risk inherent in extracorporeal perfusion of the brain, but the long-term behavioral results found with the survivors demonstrates that profound hypothermia of the brain in and of itself does not have any apparently deleterious effects. Furthermore, the results with the animals subjected to arrest of cerebral blood flow under conditions of profound hypothermia demonstrate the protective effects of cooling against the damage which would otherwise result from ischemia and anoxia.

Electrophysiologic and Behavioral Responses to Ketamine Hydrochloride in the Rhesus Monkey

HE neural basis of general anesthesia is T not well understood. Descriptions of gross changes in electroencephalographic (EEG) and evoked potentials add little to this understanding.1 Longo and Silvestrini2 have shown that the anesthetic state is not necessarily related to the slowing of EEG activity, blocking of the ascending reticular activating system, or alteration of the evoked responses in the reticular formation. However, it is generally believed that general anesthet ic agents cause functional changes in some neuronal systems that impinge upon other systems, thus influencing the anesthetic state in the whole brain. Circulatory changes and depression of metabolism within neuronal systems also play an important role in the anesthetic state.3 Interaction of the above factors provides effective pain control via depression of the central nervous system (CNS) .4

Electroencephalographic characteristics of brain cooling and rewarming in monkey.

Abstract Monkeys were subjected to extracorporeal autocerebral perfusion hypothermia. Half of the animals were containuously perfused after brain temperature reached 15 C for 30 min. The other half were subjected to circulatory arrest for 30 min after intracerebral temperatures fell to 15 C. In either case, the electroencephalogram showed a gradual decrease in the amplitude of the major frequency, followed by a loss of the major frequency, then a decrease in amplitude of the minor frequency with continuous slowing. Finally, low amplitude theta frequencies only were present; these became isoelectric at intracerebral temperatures of 22-19 C. It took about 35 min to cool the brain from 37 to 15 C. On rewarming, but before recovery of the animal, it took approximately 3 hours before the EEG activity approached prehypothermic frequencies and amplitudes with intracerebral temperatures reaching 34 C within 25 min after initiation of rewarming. Cerebral blood flow changes and changes in cellular membrane permeability probably contribute to the long latency in return of EEG activity.

Spontaneous electrical activity of the brain in hibernators and nonhibernators during hypothermia

Abstract During induced hypothermia, electrical activity recorded from the cerebral cortex of nonhibernators (cat and guinea pig) and hibernators (prairie dog and ground squirrel) gradually fell to the isoelectric point at 25C esophageal or buccal temperature in the nonhibernators and 17C in the hibernators. Electrical activity in the mesencephalic reticular formation remained at good amplitudes to about 23C esophageal and buccal temperature in the cat and guinea pig, and was still present at 16C in the prairie dog and ground squirrel. Cats and guinea pigs did not rewarm if their esophageal temperatures fell below 24C. Even at 25C it was necessary to apply resuscitation technics and direct heart warming to recover the animal. Prairie dogs and ground squirrels rewarmed, after their esophageal temperatures dropped below 16C, without resuscitation and heart warming. The sustained electrical activity observed in the anterior reticular formation of hibernators below 16C buccal temperature suggests a special mechanism for the maintenance of minimal metabolic conditions and circulatory integrity at reduced body temperature.

Striate cortex-superior colliculus projection in squirrel monkey

Abstract The corticofugal projections from the striate cortex to the superior colliculus in the squirrel monkey were electrophysiologically investigated. The cortical afferents projected to the ipsilateral superior colliculus in a point-to-point manner and were retinotopically organized. They terminated mainly in the deep layer of the stratum griseum superficiale, the stratum opticum, and the superficial layer of the stratum griseum intermediale. In these layers photic collicular units were mostly sensitive to moving objects. Convergence of afferent pathways from the retina and striate cortex on collicular neurons could not be demonstrated.

Arrest of cerebral blood flow and reperfusion of the brain in the rhesus monkey

Abstract Rhesus monkeys were subjected to cerebral ischaemia by arresting blood flow to the brain. The carotid and vertebral arteries were temporarily occluded and a cannula inserted into one common carotid artery permitted retrodrainage of blood reaching the circle of Willis via anastomotic channels. The blood from the cerebral vessels was washed out with dextran solution for photographic recording of the arrest of cerebral blood flow and subsequent reperfusion of the cerebral vasculature. Electroencephalographic, cardiovascular and respiratory functions were monitored throughout the procedure. Occlusion of the four major vessels with retrodrainage of the circle of Willis effectively stops perfusion of the brain. Occlusion of the vessels without retrodrainage permits a slow but significant flow of blood to the cerebral vessels. Rapid and effective reperfusion of the brain was noted even after repeated and lengthy periods of ischaemia. Thus a model for studying cerebral ischaemia, and reperfusion after ischaemia, without major thoracic or intracranial intervention is demonstrated. Some implications for resuscitation in cases of cerebral ischaemia are discussed.

The effect of hypoxia on electrocortical activity in the cebus monkey

Abstract Cebus monkeys were subjected to 8, 6, 4, and 2% inspired oxygen concentrations in nitrogen to create conditions of hypoxia without complete anoxia, cardiac arrest, asphyxia, or vascular occlusion of blood supply to the brain. The ECoG, EKG, and arterial blood oxygen saturations were examined before, during, and after a 30-min period of hypoxia. The ECoG changes in the 8% hypoxic group followed the course of events described below and were reversible: (a) The prehypoxic ECoG, recorded from the precentral and post-central gyri, consisted of high amplitude 5–7 Hz activity with 15–20 Hz activity superimposed and interposed; (b) loss of the 15–20 Hz activity; (c) reduction in amplitude of 5–7 Hz activity; (d) appearance of short isoelectric periods; (e) appearance of spindle-burst activity; (f) lengthening of isoelectric periods and disappearance of spindle bursts; and (g) complete loss of activity (isoelectric). The 4 and 6% hypoxic groups followed the same course of events described above except that the loss of 15–20 Hz occurred much more rapidly, the appearance of spindle-burst activity was extremely transient, and the isoelectric periods lengthened rapidly. In the 2% hypoxic group all ECoG events occurred precipitously, reaching the isoelectric phase within 7 min. Since these animals suffered cardiac arrest, only 9 min of hypoxia was possible before the recovery phase was instituted. The cardiac picture (EKG) during the hypoxic interval showed evidence of right and left bundle branch block and arrhythmia. In some animals of the 4 and 2% hypoxic groups evidence of cardiac ischemia and arrest was noted. The percentage of oxygen saturation of blood in the 8% hypoxic group dropped to and leveled off at an average of approximately 48% in 3 min, approximately 36 and 18% in 1 min for the 6 and 4% hypoxic groups, respectively, and “off-scale” on the oximeters in 10–15 sec in the 2% hypoxic group.