Book Review

VERHANDLUNGEN DER DEUTSCHEN GESELLSCHAFT FUR KREISLAUFFORSCHUNG, 19. TAGUNC. HAUPTTHEMA: KREISLAUF AND GEHIRN. Dr. Rudolf Thauer, Editor. 324 pages, Darm- stadt, 19.53, Dr. Dietrich Steinkopff.

The book is a collection of 34 papers with discussions, presented at the 19th meeting (April 9-12, 1953) of the Deutsche Gesellschaft fiir Kreislaufforschung, with cerebral circulation as the main topic.

Kety and Schmidt’s method seems to have been generally accepted for measurement of the cerebral circulation and oxygen uptake. Bodechtel (pages 109-131) reports in his review on the clinical picture of disturbances of cerebral circulation, an impressive material of 800 pat,ients in whom this method was used. The cerebral blood flow is severely reduced in the Adams-Stokes syndrome, during cardiac decompensation (11 cases), and cerebra1 arteriosclerosis (26 cases). Impairment of cerebral circulation is more common in right than in left ventricular insufficiency. On the other hand, it is significantly increased in car pulmonale due to the increased arterial CO:, content, producing increase of intracranial pressure with the concomitant syndrome. However, as soon as cardiac decompensation develops, the cerebral blood flow drops below normal.

The decreased cerebra1 blood flow is the basis of acute (convulsions, loss of consciousness) or more chronic disturbances of the central nervous system. Forty per cent of cyanotic patients with congenital heart disease, in a material of 650 cases of the University Hospital in Boon (Grosse- Brockhoff) had neurologic symptoms. The drop of blood pressure in myocardial infarct may pro- duce the dominating syndrome of a cerebral accident, and only the routinely taken electrocardio- gram (ECG) may reveal a myocardial infarct as the underlying cause.

Schneider (pages l-25) review’s the experimental basis of brain circulation and oxygenation in its application to clinical problems. Extensive animal work in Germany on the effect of CO, and 02 tension, blood pressure, and other fundamental variables on cerebral circulation has paralleled similar investigations in the United States. Section of the neck sympathetic fibers, block of the ganglion stellatum, and sympathicolytic drugs increase the normal cerebral circulation only slightly, if at all, but may increase a previously decreased cerebral circulation very sub- stantially.

A minimum level of cerebral oxygen uptake necessary for maintenance of function is differ- entiated from the minimum level necessary for maintenance of the structure. The latter is very much lower and approximately 10 per cent of the normal metabolic rate of the brain. Such low level is accompanied with deep coma, but sufficient to keep the structure intact so that the recover? is complete. If the oxygen supply falls below that critical level, irreparable damage occurs de- pending on the time and degree of ischemia. The critical time for complete arrest of circulation is about 3 to 4 minutes, but a trickle of blood flow has a tremendous effect on the survival time. In one typical experiment with the isolated head of a cat, increase of the cerebral blood flow from 3.3 to 3.8 C.C. per minute shortened the time from the release of ischemia to the appearance 01

electroencephalographic (EEG) action potentials from 20 to 4.5 seconds. It is concluded that in the reports of revival after cardiac standstill up to 10 minutes, the arrest of cerebra1 circulation was not quite complete.

There is a remarkable adaptation of the central nervous system to chronic hypoxia; ambul- atory patients with pernicious anemia may have values of cerebral 02 uptake which would pro- duce deep coma in an acute condition.

Of great interest is the finding of an optimum brain temperature between 28 and 32” C. for recovery from ischemia. The recovery time was increased at higher or lower temperatures and was equally long at 38” and 22”. It seems that nothing is gained by cooling the brain below 32”.

Opitz (pages 26-44) discusses the effect of cerebral ischemia on the metabolic changes in the brain. Frequently, the abolishment of reflexes in cerebral ischemia occurs in two phases, separated by an interval of about 20 seconds. The first phase is due to the exhaustion of aerobic and the second one is due to the exhaustion of anerobic energy (glycolysis). The energetic efficiency of glycolysis, however, is very poor. The extreme vulnerability of the brain to oxygen deprivation, as compared to other organs, is due to the very low level of aerobic as well as anaerobic reserves,

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in view of its high metabolic rate. It is of interest that, in contrast to the heart or skeletal muscle, the glycogen in the brain is not utilized in the condition of acute ischemia. The cumulative effect of hypoglycemia and impairment of cerebral circulation is discussed more specifically by Hiipker (pages 241-246).

The anatomic and pathologic basis for ischemic damage of the brain is reviewed by Scholz (pages 52-69) and by Meyer (pages 69-83). Of particular interest is the observation of local arterial spasms which might explain, in part, the localization of damage in general cerebral is- chemia. Other reasons for localization of damage are the different tolerance of various structural elements to hypoxia and a different distribution of the blood flow to various parts of the brain.

Bernsmeier (pages 88-93) suggests in Kety and Schmidt’s method to replace the five pairs of blood samples from an artery and the internal jugular vein by two continuous samples taken at constant speed with a motor-driven syringe over a period of ten minutes. This procedure does not only reduce the analytical work but also simplifies the calculation. The agreement of this modification with Kety and Schmidt’s original method in parallel determinations was excellent.

Polzer and Schuhfried (pages 93-96) have developed an ingenious qualitative method for measurement of cerebral circulation. A volume pulse of intracranial blood flow is recorded through resistance changes of an alternating current of 30,000 c.p.s. by means of a Wheatstone bridge. The electrodes are put on the forehead and postmastoid region. The pulse contour is similar to the photoelectric finger plethysmogram. The pulse amplitude is calibrated in units resistance. Large differences in amplitude and contour between normal individuals and patients with cerebral arteriosclerosis are demonstrated, quite similar to differences in the peripheral finger or toe volume pulse curve between normal subjects and patients with peripheral arteriosclerosis.

Electroencaphalographic (EEG) changes in experimental and pathologic hypoxia and ischemia are reviewed by Jung (pages 170-196). The EEG is indispensable for the study of functional effects of circulatory impairment, but it is, of course, a qualitative method. The results show the different tolerance of various parts of the central nervous system to oxygen deficit with the cerebral cortex and thalamus as the most vulnerable structures. It is of interest that the sensitivity to experimental hypoxia may be significantly increased in light colds or in- fections of the upper respiratory tract.

The EEG was used in a study of cerebral effects of cardiac arrest elicited by carotid pressure in patients with the carotid sinus syndrome (Franke and Hann: pages 205210). Heine (pages 196-200) reports on simultaneous determination of cerebral circulation by means of Bernsmeier’s modification of Kety and Schmidt’s method and of the EEG in 113 cardiovascular patients. In all cases with normal EEG (normal subjects or patients with decreased cerebral circulation) there was no correlation between the various items of EEG analysis and cerebral circulation. On the other hand, there was some general correlation between cerebral circulation and abnormal EEG changes, but not in all groups of patients. The correlation was best in patients with car pul- monale, and poorest in patients with cerebral arteriosclerosis. There was no correlation between blood pressure and EEG.

Krump (pages 200-205) found in 62 per cent of 140 patients with arterial hypertension ab- normal electroencephalograms, but the changes were classified in most cases as light (34 per cent) or moderate (20 per cent). However, it was definitely normal only in 18 per cent of the group.

Angiography in normal and abnormal cerebral circulation is reviewed by Riechert (pages 131-141), and Ginshirt (pages 218-224) reports on parallel determinations of cerebral circulation by means of Kety and Schmidt’s method and angiograms in thirty-three patients with various cerebral tumors.

Weigelin (pages 233-238) studied in a large material of 626 patients with arterial hypertension the correlations between arterial blood pressure, retinal arterial pressure as measured by means of a newly developed method, and changes of the retinal fundus. The correlation coefficient between the retinal and brachial arterial pressure was very high (r = 0.9). The correlation be- tween the degree of abnormal fundus changes (subdivided into four classes) and the retinal arterial pressure (r = 0.6) or the brachial arterial pressure (r = 0.53) was much lower but still statistically significant. However, advanced fundus changes were usually present when the retinal arterial pressure exceeded the level predicted from the brachial arterial pressure on the basis of the re- gression equation.

It is not possible to review all papers presented at that meeting, but this arbitrary selection is representative for the general high standard of communications and discussions. E. S.