Studies Of Cerebral Metabolism Research Articles

Cerebral hemodynamic and metabolic studies in patients with congestive heart failure. I. Observations in lucid subjects.

HomeCirculationVol. 21, No. 5Cerebral Hemodynamic and Metabolic Studies in Patients with Congestive Heart Failure Free AccessResearch ArticlePDF/EPUBAboutView PDFSections ToolsAdd to favoritesDownload citationsTrack citationsPermissions ShareShare onFacebookTwitterLinked InMendeleyReddit Jump toFree AccessResearch ArticlePDF/EPUBCerebral Hemodynamic and Metabolic Studies in Patients with Congestive Heart Failure I. Observations in Lucid Subjects WILLIS SENSENBACH, LEONARD MADISON and SEYMOUR EISENBERG WILLIS SENSENBACHWILLIS SENSENBACH From the Medical Service, Veterans Administration Hospital, Dallas, Texas, and the Department of Internal Medicine, The University of Texas Southwestern Medical School, Dallas, Tex. Search for more papers by this author , LEONARD MADISONLEONARD MADISON From the Medical Service, Veterans Administration Hospital, Dallas, Texas, and the Department of Internal Medicine, The University of Texas Southwestern Medical School, Dallas, Tex. Search for more papers by this author and SEYMOUR EISENBERGSEYMOUR EISENBERG From the Medical Service, Veterans Administration Hospital, Dallas, Texas, and the Department of Internal Medicine, The University of Texas Southwestern Medical School, Dallas, Tex. Search for more papers by this author Originally published1 May 1960https://doi.org/10.1161/01.CIR.21.5.697Circulation. 1960;21:697–703 Previous Back to top Next FiguresReferencesRelatedDetailsCited ByOlver T, Klakotskaia D, Ferguson B, Hiemstra J, Schachtman T, Laughlin M and Emter C (2016) Carotid Artery Vascular Mechanics Serve as Biomarkers of Cognitive Dysfunction in Aortic‐Banded Miniature Swine That Can Be Treated With an Exercise Intervention, Journal of the American Heart Association, 5:5, Online publication date: 6-May-2016. Kojo M, Yamada K, Yamada H, Akiyoshi K, Inutsuka M, Hamada Y and Ogawa T (1999) Two-dimensional autoregressive analysis of carotid artery blood flow waveform in children with isolated atrial septal defect, Pediatrics International, 10.1046/j.1442-200x.1999.01055.x, 41:3, (292-298), Online publication date: 1-Jun-1999. Vrobel T (1995) Psychiatric Aspects of Congestive Heart Failure: Implications for Consulting Psychiatrists, The International Journal of Psychiatry in Medicine, 10.2190/TH2G-5MVU-XR69-D4B3, 19:3, (211-225), Online publication date: 1-Sep-1990. Frisbie J (1995) Behavioral Disturbance, Embolism, and Mitral Stenosis, The International Journal of Psychiatry in Medicine, 10.2190/6Q02-Y4M5-NY0M-LWYP, 16:3, (249-256), Online publication date: 1-Sep-1987. Crean P, Pratt T, Davies G, Myers M, Lavender P and Maseri A (1986) The fractional distribution of the cardiac output in man using microspheres labelled with technetium 99m, The British Journal of Radiology, 10.1259/0007-1285-59-699-209, 59:699, (209-215), Online publication date: 1-Mar-1986. Tresch D, Dabrowski R, Fioretti G, Darin J and Brooks H (1983) Out-of-hospital pulmonary edema: Diagnosis and treatment, Annals of Emergency Medicine, 10.1016/S0196-0644(83)80291-1, 12:9, (533-537), Online publication date: 1-Sep-1983. Gottstein U (1982) Treatment and pathogenesis of cerebrocircular disturbances in patients with heart disease and arrhythmia Atherosclerosis Clinical Evaluation and Therapy, 10.1007/978-94-009-7331-2_21, (177-185), . Lavy S, Stern S, Melamed E, Cooper G, Keren A and Levy P (1980) Effect of chronic atrial fibrillation on regional cerebral blood flow., Stroke, 11:1, (35-38), Online publication date: 1-Jan-1980.SHAPIRO W and CHAWLA N (1969) Observations on the Regulation of Cerebral Blood Flow in Complete Heart Block, Circulation, 40:6, (863-870), Online publication date: 1-Dec-1969. Blachly P and Kloster F (1966) Relation of cardiac output to post-cardiotomy delirium, The Journal of Thoracic and Cardiovascular Surgery, 10.1016/S0022-5223(19)43422-3, 52:3, (422-427), Online publication date: 1-Sep-1966. Messer J and Neill W (1962) The oxygen supply of the human heart∗, The American Journal of Cardiology, 10.1016/0002-9149(62)90156-X, 9:3, (384-394), Online publication date: 1-Mar-1962. Schwab M and Motel E (1962) Das S�ure-Basen-Gleichgewicht im arteriellen Blut und Liquor cerebrospinalis bei Herzinsuffizienz und Cor pulmonale und seine Beeinflussung durch Carboanhydrase-Hemmung, Klinische Wochenschrift, 10.1007/BF01484389, 40:24, (1233-1245), Online publication date: 1-Dec-1962. Gormsen J, Dyrbye M, Eiken M and Rønnov-Jessen V (2009) Acute Cerebral Infarct, Acta Medica Scandinavica, 10.1111/j.0954-6820.1961.tb07856.x, 169:4, (455-466) EISENBERG S, MADISON L and SENSENBACH W (1960) Cerebral Hemodynamic and Metabolic Studies in Patients with Congestive Heart Failure , Circulation, 21:5, (704-709), Online publication date: 1-May-1960. May 1, 1960Vol 21, Issue 5 Advertisement Article InformationMetrics © 1960 American Heart Association, Inc.https://doi.org/10.1161/01.CIR.21.5.697 Originally publishedMay 1, 1960 PDF download Advertisement

Cerebral hemodynamic and metabolic studies in patients with congestive heart failure. II. Observations in confused subjects.

Cerebral hemodynamic and metabolic studies in patients with congestive heart failure. II. Observations in confused subjects.

Cerebral metabolism in problem drinkers under the influence of alcohol and chlorpromazine hydrochloride.

Cerebral blood flow and metabolism studies by means of the nitrous oxide method of Kety and Schmidt were made in males who had been problem drinkers for an average of 11 years. Patients having psychoses, neuropathies, hepatic insufficiency and avitaminosis were excluded prior to the first of two studies per patient. The first study was on the effect of the oral administration of 1 gm/kg of alcohol alone and the second was made after treatment with chlorpromazine for 1 week, at which time the procedure with alcohol was repeated. The chronic use of alcohol produces an alteration in the metabolism of glutamic acid in the central nervous system and in the content of glutamic and lactic acids in the arterial blood. Further, chlorpromazine administration for a week affects more cerebral and peripheral changes than have been established for a single dose before as well as after alcohol ingestion. Despite a multiplicity of effects with alcohol, including a pronounced change in behavior after chlorpromazine, the values for cerebral oxygen and glucose consumption are normal. Submitted on March 16, 1959

The cerebral physiology of controlled hypotension.

Controlled hypotension is not infrequently induced to diminish operative bleeding, and in neurosurgical procedures, for the additional purpose of decreasing brain tension. There is considerable question as to whether the advantages of the procedure may not be outweighed by the attendant hazards.* The present study of cerebral hemodynamics and metabolism during acute and relatively prolonged blood pressure reduction was undertaken in hopes that it might yield pertinent information concerning the above problem. <h3>Method</h3> The 21 subjects of the present study were hospitalized patients of various age groups, in most instances having hypertension. Scheinberg and Stead's modification³of the Kety and Schmidt procedure⁴for the determination of cerebral blood flow (CBF) was applied in this study. The gas mixtures utilized were those described by Kety.⁴Blood oxygen was determined by the manometric technique of Van Slyke and Neill.⁵Mean arterial blood pressure (MAP) was obtained directly from

Evaluation of current therapy in cerebral vascular disease

0 NE of the most pressing problems in medicine is the management of the increasing numbers of patients with overt manifestations of cerebral dysfunction associated with vascular disease. Numerous neurologic syndromes are the result of occlusion of diseased cerebral vessels with curtailment of blood supply below the minimum requirements of a nonsilent area of the brain.’ Not only does the central nervous system react acutely to reduction of its blood supply below critical levels, but impairment of function to a degree which might be trivial in other organs is commonly manifested in dramatic fashion in the case of the brain. It is difficult to say with certainty whether in the above instances the cerebral vessels are more severely involved by atherosclerosis than those of other organs or whether their involvement is not remarkable in degree but is simply more obvious. The precise nature of the relationship between diffuse cerebral atherosclerosis and generalized cortical dysfunction is not clear. Studies of cerebral hemodynamics and metabolism in various age groups demonstrate a progressive reduction of cerebral blood flow and oxygen consumption with advancing years, even in the absence of obvious functional impairment.2 Other data indicate that within certain limits even further acute reduction of cerebral blood flow can be induced in elderly subjects without the appearance of untoward symptoms.s The reduced cerebral blood flow of many aged individuals may therefore exist coincidentally with diminished cerebral oxygen consumption and impaired mental function due to reduced cellular activity of independent pathogenesis. At the present time there is no successful method for the prevention or reversal of cerebral atherosclerosis. The therapeutic and corrective measures employed in the management of patients with acute and chronic cerebral vascular disturbances include administration of vasodilating agents, cerebral stimulants

Cerebral oxygen uptake in chronic schizophrenic reaction.

Since Kety and associates 1 reported that the cerebral blood flow (CBF) and cerebral metabolic rate for oxygen (CMR o2 ) are in schizophrenia, patients with this disorder have commonly been used as normal for cerebral metabolic studies. In the course of such studies we have noted unusually low values for CMR o2 in approximately one-third of patients with chronic schizophrenic reactions. Using the original nitrous oxide technique of Kety and Schmidt,* we have made 29 determinations of CBF and CMR o2 upon 24 patients with chronic schizophrenic reactions of two or more years' duration and have compared these with the rates in 81 control cases. The experimental group consisted of 11 men and 13 women from 16 to 66 years of age, with an average age of 36 years. In these subjects the onset of clearly recognizable schizophrenic reactions had occurred from 2½ to 23 years prior to

The electroencephalogram in pernicious anaemia and subacute combined degeneration of the cord

Eighty cases of pernicious anaemia in relapse, of which 24 had subacute combined degeneration of the cord (one with optic atrophy), 41 mild neurological involvement and 15 none, have been studied by means of the EEG. Seven cases showed mild organic reactions and in all of these the pre-treatment record was abnormal. The pre-treatment record was also abnormal in 60 per cent of the remaining patients who showed no significant mental abnormality. In some cases abnormality was severe (delta activity, generalised, paroxysmal or focal), in some slight (slight or moderate excess of theta activity), but the degree of abnormality bore no relationship to the severity of the anaemia, the age of the patient or the degree of neurological involvement. Ten cases of anaemia of miscellaneous type were also studied before treatment; although in 3 of these the haemoglobin level was less than 40 per cent, only in one case did the EEG show a significant abnormality and this patient had severe hypertension and atherosclerosis. Seventy-six of the cases of pernicious anaemia were re-examined after treatment with vitamin B 12. In 14 of the 29 cases which gave normal records before treatment there was a significant increase in mean frequency of the alpha rhythm and diminution in overall amplitude. Forty-two of the remaining 47 cases in which the initial record was abnormal s showed a satisfactory clinical response to treatment and in 31 (74 per cent) the EEG returned to normal, so that 60 of the 76 cases (79 per cent) eventually gave normal records. Improvement in the record began as a rule 7–10 days after the beginning of treatment and was often complete within a month, although some cases showed further improvement after intervals varying from 3–16 months. In the other 11 cases (26 per cent) who responded, persisting abnormalities consisted of a slight excess of generalised theta activity, a finding which in some could possibly be accounted for by age or constitution. Another 50 cases of pernicious anaemia (including 37 with subacute combined degeneration of the cord, 8 with mild neurological involvement and one with optic atrophy) were first studied after treatment had been in progress for between 3 months and 8 years (average 18 months). Excluding 5 cases showing epileptic discharges, 38 (84 per cent) of the other 45 patients had normal records; the remaining 7 cases (16 per cent) were restudied and in all EEG showed further improvement 5 months to 3 years after the beginning of treatment. The final total of normal records was 42 (93 per cent). Eight (6 per cent) of the 130 cases of pernicious anaemia studied gave records showing epileptic discharges (usually temporal spikes or sharp waves) and of these 4 (3 per cent) gave a personal or family history of fits or faints. It is suggested that the EEG changes in pernicious anaemia are due not to the anaemia but to a specific defect in cerebral metabolism, presumably related to the deficiency state responsible for the anaemia. Though not as sensitive as studies of cerebral metabolism by the blood flow method, the EEG is a useful tool in the investigation of these cases and reveals that maximum improvement may be delayed for up to 3 years after treatment has begun. The possible relationship of the EEG changes to alterations in glucose and pyruvate metabolism is discussed.

Effects of barbiturate sedation on the brain in toxemia of pregnancy.

Recently quantitative studies of cerebral circulation and metabolism have been carried out on women with toxemia of pregnancy. 1 It was found that the cerebral blood flow was not affected by any type of toxemia. The most striking departure from normal was the presence of a greatly increased cerebrovascular resistance, thought to be due to vasospasm. In eclampsia with convulsions, there was a depression of cerebral oxygen metabolism. This knowledge has given us a new insight into the pathophysiology of the brain in toxemia of pregnancy and has opened the way to the evaluation of the effects of therapy on this organ. 2 In modern times one of the most important aspects of therapy in this disease of obscure causation has been the use of large amounts of sedatives in an attempt to prevent or allay convulsions by depressing the central nervous system. The mechanism of this cerebral depression has

Correlative observations on cerebral metabolism and cardiac output in myxedema.

Patients with myxedema present an unusual opportunity for studying the effect of lowered metabolism on organ blood flow and for observing the effect of changes in peripheral circulation on cardiac output. Studies of cerebral metabolism in myxedema are of interest to the physician because changes in cerebral metabolism may be of importance in understanding the alterations in mental status which occur with this disease (1-3). The cerebral blood flow was measured by the nitrous oxide method of Kety and Schmidt (4) in eight patients with myxedema. The cardiac output was measured by the technique of right atrial catheterization in seven other patients with myxedema.

METABOLISM OF THE BRAIN DURING INSULIN AND METRAZOL TREATMENTS OF SCHIZOPHRENIA

A previous communication 1 appearing inThe Journalwas concerned with the possible effects of insulin and metrazol in patients with schizophrenia. The conclusions were based on observations of animals, but methods were used which did not duplicate those employed in the treatment of schizophrenia. The present communication presents a brief summary of the chief results obtained in patients with schizophrenia undergoing the insulin and metrazol treatments. Sincethese treatments change cerebral function, studies of cerebral metabolism were made. The methods used for the study of the cerebral metabolism of the patients include the simultaneous collection of samples of arterial blood entering the brain and of the blood of the internal jugular vein, which represents the return flow from that organ. These samples are analyzed for oxygen and dextrose. The differences between the venous and arterial contents indicate the cerebral utilization of oxygen and dextrose. 2 Table 1 discloses the