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The effect of cerebral anoxia on leucine incorporation into proteins of various subcellular fractions from rabbit brain was studied by using a previously reported in vitro model. Although the decrease in leucine incorporation was observed earlier in nuclei and microsomes, other fractions also demonstrated a rapid decrease. These results were quite different from the pattern of leucine incorporation observed in a type of reversible suppression produced with diphenylhydantoin.

Until a few years ago, it was generally thought that irreversible brain damage would result from any condition that produced a profound cerebral anoxia of greater than eight to ten minutes' duration. This conclusion was based on observations made by physicians during clinical emergencies and by investigators using experimental models in which the onset, degree, and duration of anoxia could be controlled. 1-6 Most techniques for producing anoxia in the intact animal also produce ischemia and there is some evidence to suggest that cerebral anoxia is exacerbated by ischemia. 7 However, the results of recent studies with totally ischemic brain tissue suggest that many of the variables measured approach normal after reoxygenation. This has led some workers to question whether cerebral anoxia actually causes irreversible brain damage within so short a period as ten minutes. 8-11 If proper protocols are to be established for the treatment of cardiac arrests and

Es wird die schwereanoxisch-vasale Hirnschadigung eines 8 Monate alten Kindes beschrieben, bei dem gut uber 1 Monat hindurch Bewustlosigkeit bestand und bei einer Muskelstarre (Decortikation bzw. Decerebration) sich zeitweilig Zuckungen und eine extrapyramidale Hyperkinese zeigten. Schon fruhzeitig entsprach das Elektrencephalogramm der schweren Bewustlosigkeit, wahrend Krampfpotentiale fehlten.

Varying degrees of heart block may occur in the presence of congenital heart disease, and cause mild Stokes-Adams attacks which conceivably could be more severe, with convulsions. The symptoms then are not due to the congenital heart disease but to the cerebral anoxia that follows the ventricular standstill. This condition may occur in congenital heart disease where no evidence of an interventricular septal defect is apparent. A case is presented with definite evidence of a patent ductus arteriosus, and no evidence of a patent interventricular septum, in which mild Stokes-Adams attacks occurred associated with the sudden onset of heart block, which varied in degree, was transient and followed by normal rhythm. This occurred following exertion, and was not of nervous origin. This is the first case to be reported of congenital heart disease with Stokes-Adams attacks in which an electrocardiogram taken during the attack is presented.

The convulsant threshold of 24 corpus-callotomized Sprague–Dawley rats exposed to Indoklon vapor once a week was found to be significantly lower than that of 24 sham-operated controls in the second, third, and fourth exposures; the sensitivity of both groups of animals increased progressively and levelled out at the fifth exposure. Repetition of the experiment after 3 weeks of rest, with exposures spaced at 48-hour intervals, further lowered the convulsant threshold of the animals, both groups exhibiting a similar, and possibly maximal, sensitivity to Indoklon at the second exposure. When in another series, 60 corpus-callotomized rats and 60 sham-operated controls were injected intraperitoneally with CD10 of Indoklon at weekly intervals, the susceptibility of both groups to convulsions again increased rapidly during the first four injections; at the second injection, the corpus-callotomized rats were significantly more sensitive to Indoklon than the controls. During the fifth to eighth injection, the convulsibility of the animals reached a plateau, 62.2% to 78.5% of the rats convulsing; the difference between the two groups at this stage became less marked, though the convulsions in corpus-callotomized animals continued to be of longer duration than in the controls. Repetition of the injections, spaced at 48-hour intervals, after 3 months of rest, demonstrated a continuing high and equal sensitivity of the two groups of rats to Indoklon with some depression setting in during the second half of a series of 12 injections.

Fifteen episodes of acute postoperative psychoses were observed in eleven elderly patients. All cases were classified as acute brain syndrome or acute delirium. The psychosis occurs in predisposed persons in the presence of various toxic factors which cause cerebral anoxia. The treatment consists of elimination of toxic factors, correction of anemia or fluid-electrolyte imbalance, accident prevention and securing the uninterrupted administration of the postoperative care. The prognosis is good. In the presence of persistent provoking agents, irreversible mental changes may develop.

1. An Meerschweinchen (und Mausen) wird das Verhalten der Schnappatmung bei perakuter, totaler Hirnischaemie untersucht und deren Beeinflussung durch Narkose sowie Unterkuhlung.

Summary 1 The effect of halothane anaesthesia on the EEG has been studied in 35 patients. 2 In contrast to earlier reports, it was found that 1 to 4% halothane in oxygen produced a widespread, relatively fast (9–14 c/sec) medium-voltage rhythm in the EEG, with a maximum in the frontal areas. The effects of pain stimuli on this rhythm are described. 3 Owing to the decreased metabolism during anaesthesia, patients are easily hyperventilated. Hyperventilation caused a decrease in the frequency of the rhythmic fast activity and the appearance of widespread, irregular slow activity within the delta and theta ranges. 4 The addition of 50–75% nitrous oxide to the halothane-oxygen mixture evoked slow activity in the EEG and substantially reduced the amount of fast activity. Failure to take into consideration the influence of nitrous oxide and unintentional hyperventilation on the EEG during halothane anaesthesia is probably the main explanation of the statement in earlier reports that halothane produces slow waves in the EEG. A brief period of induced blood-pressure fall to 40–50 mm Hg during halothane anaesthesia produced no changes in the EEG of young and middleaged healthy subjects. In one elderly patient a similar reduction in blood pressure evoked characteristic EEG changes. It is concluded that in halothane anaesthesia the EEG is of practical value as a sensitive indicator of the influence on the functional state of the brain cells of ventilation, gas mixture, depth of anaesthesia and cerebral anoxia. Zusammenfassung 1 Die Wirkungen der Halothannarkose auf das Elektroencephalogramm wurden bei 35 Patienten untersucht. 2 Im Gegensatz zu fruheren Berichten wurde dabei gefunden, dass 1 bis 4% Halothan in Sauerstoff einen weitverbreiteten, relativ schnellen (9–14 c/sec) EEG-Rhythmus von mittlerer Voltage mit einem Maximum in den Frontalbezirken erzugen. Die Wirkungen von Schmerzreizen und Anderungen des arteriellen Blutdruckes auf diesen Rhythmus werden beschrieben. 3 Auf Grand des herabgesetzten Stoffwechsels unter der Narkose werden die Patienten leicht hyperventiliert. Hyperventilation verursachte eine Fre-quenzabnehme der schnellen rhythmischen Aktivitat und Auftreten von verbreiteten irregularen langsamen Aktivitaten im Bereich der Delta-und Theta-Venen. 4 Der Zusatz von 50–75% Stickoxydul zur Halothan-Sauerstoffmischung fuhrte zu einer langsamen Aktivitat im EEG und betrachdiche Verringerung des Auftretens schneller Rhythmen. Nichtbeachtung des Einflusses von Stickoxydul und unbeabsichtigter Hyperventilation auf das EEG wahrend einer Halothannarkose ist wahrscheinlich die wesentlichste Erklarung fur die in fruheren Berichten aufgestellte Behauptung, dass Halothan im EEG langsame Wellen erzeuge. Eine kurze Periode absichtlicher Blutdrucksenkung auf 40–50 mm Hg wahrend einer Halothannarkose rief keine EEG-Veranderung bei gesunden Personen im jungen und mittleren Lebensalter hervor. Nur bei einem alteren Patienten kam es unter einer ahnlichen Blutdrucksenkung zu charakteristischen EEG-Veranderungen. Man kann den Schluss ziehen, dass das EEG wahrend der Halothannarkose von praktischer Bedeutung ist und zwar als empfindlicher Indikator fur den Einfluss von Ventilation, Gasgemisch, Narkosetiefe und cerebraler Anoxie auf den funktionellen Zustand der Gehirnzellen.

1. 1. A study of the clinical picture, the cerebral electrical activity and pO2 was carried out on rabbits with vaccinal encephalitis. 2. 2. It was found that with the development of encephalitis oxygen tension in the cerebral tissues was lowered, accompanied by diffuse reduction in the frequency of cortical and subcortical potentials. 3. 3. Disturbance of electrogenesis in rabbits with vaccinal encephalitis is explained by the development of cerebral anoxia.

Cerebral anoxia and hypoglycemia of varying severity and diverse causes commonly present neurological problems. Minor transient symptoms are readily diagnosed when they follow insulin injections or operation, but may escape recognition when due to less evident factors, such as hyperinsulinism or paroxysmal cardiac dysfunction. Severe cases with permanent cerebral damage are uncommon but are apt to occur as preventable clinical accidents. It is the purpose of this report to present some clinical and pathological data from a selected group of such severe cases. As preliminary discussion, only brief reference can be made to the vast and scattered literature. The experimental study of anoxia is as old as the subject itself and was of much interest to the philosophers and savants of the 17th and 18th centuries, but the modern era may be said to date from Astley Cooper's1effort to determine the maximum time for which the brain could

SUMMARY Eighty-two infants (ages 0–3 months) were admitted because of convulsions. The etiology was infectious in 28 (intracranial 12, extracranial 16), morphological brain damage in 20 (chiefly cerebral anoxia at birth), metabolic disorder in 9 and unknown in 25 cases. Subdural effusion was present in 6 out of 11 infants with bacterial meningitis. These data stress the significance of infection as a common cause of convulsions in early infancy. Relatively short follow-up studies demonstrate a fairly high incidence of neurological and intellectual deficits as well as recurrence of seizures. Most notorious in this regard proved to be the group of “morphological brain damage.” Hence the long-term prognosis of seizures occurring in early infancy is a guarded one. RESUME Les sujets qui ont ete suzivis pendant un temps relativement bref ont montre une proportion assez elevee de troubles neurologiques et intellectuels et une tendance a la repetition des crises. Ceci etait particulierement net chez des patients presentant une lesion cerebrale. Le pronostic eloigne des crises survenant pendant les 3 premiers mois semble done devoir etre reserve. Quatre-vingt deux enfants, âges de 0 a 3 mois, ont ete admis pour des convulsions. L'etiologie etait infectieuse dans 28 cas (intra-cranienne 12 cas, extra-cranienne 16 cas), en relation avec une lesion cerebrale (principalement d'origine anoxique obstetricale) dans 20 cas, en rapport avec un desordre metabolique dans 9 cas, et inconnue dans 25 cas. Une effusion sous-durale existait chez 6 des 11 sujets qui presentaient une meningite bacterienne. Ces constatations font ressortir l'importance de Finfection dans le determinisme des convulsions de la premiere enfance.

Auf Grund der Erfahrungen mit 421 Vakuum-Extraktionen an der I. Univ.-Frauenklinik Munchen glauben wir zu der Aussage berechtigt zu sein, das es sich bei diesem Operationsverfahren im Vergleich zur Zangenextraktion um ein fur das Kind schonenderes Vorgehen mit der Moglichkeit einer masigen Ausweitung der Indikationsstellung handelt. Die Vermeidung perinataler hypoxamischer Gehirnschadigungen kann dabei im Vordergrund stehen. Einen gesonderten Indikationsbereich konnen wir der Vakuum-Extraktion nicht zuerkennen. Er ergibt sich allein aus einer richtigen Beurteilung des technisch Moglichen in Verbindung mit einem ausreichenden Verstandnis fur die einzelne geburtshilfliche Situation.

An area of cerebral cortex was asphyxiated for 30–35 min by application of a weight exerting a pressure on the tissue greater than the blood pressure. Three days later the asphyxiated region showed in most experiments a marked loss of nerve cells. The glia seemed to be better preserved. Spreading depression could not be made to pass through the area when asphyxiation had caused substantial neuronal destruction. These observations do not support a possible involvement of the glia in the propagation of spreading depression.

An attempt has been made to emphasize the importance of a neurologic complication of minor surgery. In the later decades of life the decreased adaptability and the presence of arteriosclerosis may be well tolerated until the patient is faced with the need of adjusting to a group of factors, each tending to contribute some degree of transient cerebral anoxia. The effect of these various stresses is cumulative and their sum total is capable of resulting in acute cerebral vascular insufficiency. Based on the physiologic changes involved, certain measures are suggested which would seem to lessen the risk of anoxic damage to the brain. As new drugs and technics steadily increase the human life span, physicians have a vital responsibility to try to keep the added years as free as possible of disabling neurologic symptoms. State hospitals filled with elderly patients who are psychotic due to cerebral vascular damage cannot be considered a tribute to medical progress. Until the problem of preventing the development of arteriosclerosis and hypertension is solved, no practical clinical means of postponing their effects even temporarily should be overlooked.

THE development of closed-chest cardiac resuscitation has given a second chance at life to many victims of sudden cardiac arrest in hospitals throughout the world.1 2 3 4 The extension of this second chance to cases occurring outside the hospital, however, has not followed as rapidly as some had initially anticipated.5 Although a physician occasionally witnesses an episode of cardiac arrest outside the hospital, more often he cannot reach the victim and attempt resuscitation within the time limit imposed by cerebral anoxia. Nonmedical rescue personnel are frequently available in time, but dissemination of cardiac-resuscitation technics to these groups has been impeded by the . . .

Persistent electroretinograms (ERG) in the presence of truly isoelectric EEGs were noted in five patients who had experienced cerebral anoxia which led to irreversible coma. Following termination of respiratory support of these patients, the summated ERG in response to light flashes was recorded until it was no longer present. The deterioration of the ERG followed a consistent pattern in each patient. After the initial diminution and subsequent obliteration of the b wave, a negative ERG (remnant negativity) persisted. This in turn disappeared. These events occurred over a period lasting up to 33 min. These findings demonstrate that, as in animals, the neural elements of the human retina which give rise to the ERG are less sensitive to anoxia than is the cerebral cortex.