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CEREBRAL METABOLISM AFTER PORTACAVAL SHUNT
153 shrunken liver. Light microscopy suggested the picture of fulminant atrophy. More details on the reported observations will be given elsewhere. The purpose of this letter is to draw attention to a simple technique, which has not hitherto been applied in " viral " hepatic coma, and the value of which seems comparable with that of more expensive and extensive, and not completely harmless, methods. Medical Clinic and Polyclinic and Department of Intensive Care, Academic Hospital of the State University,
Ghent, Belgium.
L. DEMEULENAERE F. BARBIER P. VERMEIRE.
CEREBRAL METABOLISM AFTER PORTACAVAL SHUNT wish to on the article by Dr. Read and comment SIR,-We his colleagues,! which underlines the frequency of neuropsychiatric abnormalities and electroencephalographic changes in patients with cirrhosis after portacaval anastomosis. Persistently high levels of ammonia in arterial blood is one of the most accepted pathogenetic factors; on this point Dr. Read and his colleagues report the value of prophylactic treatment with neomycin and a low-protein diet in preventing the development of neuropsychiatric abnormalities after portacaval anastomosis. We also support this view, and have noted the presence of cerebral metabolic disturbances early after shunt operation even in mentally alert and oriented patients. We have studied cerebral hxmodynamics and metabolism in 13 patients who had undergone portacaval anastomosis 1-10 months before. These patients at no time had signs of hepatic encephalopathy. Significantly high values of cerebral blood-flow were observed; this resultant increase in no way correlated with arterial PC02 and with hsmatocrit variations. In most cases, moreover, the cerebral metabolic rate of oxygen was slightly higher than normal, with an even greater increase in cerebral metabolic rate of glucose; as a consequence the glucose/oxygen cerebral quotient was significantly increased
(table I). Similar haemodynamic and metabolic results were found in 20 cirrhotic patients within 24 hours of the onset of hepatic coma or of an acute episode of encephalopathy. On the contrary, in patients with chronic coma or chronic encephalopathy there was a striking decrease in both cerebral blood-flow 1.
Read, A. E., McCarthy, C. F., Ajdukiewicz, Lancet, 1968, ii, 999.
A.
and cerebral metabolism (table n). It is worth while to underline the different behaviour of these indices in cirrhotic patients, mentally alert but previously submitted to portacavalshunt ; in these patients, in fact, high values of cerebral bloodflow and cerebral metabolic rate of glucose were found even 1 or 2 years after surgery. These results support the hypothesis that some modifications of brain metabolism occur within a short period after operation, and persist, even though no neuropsychiatric disturbances are clinically evident. We support the view that presumptive mechanism of this cerebral metabolic disorder is a partial glycolysis blockade by animation of oc-ketoglutarate to form glutamic acid and glutamine. In favour of this hypothesis, we have found increased cerebral metabolic uptake of ammonia in these clinical conditions in which there are often higher levels of ammonia in the arterial blood.2 Regarding the increase in cerebral blood-flow, an acceptable hypothesis is that it is the result of modified brain metabolic requirements. Cerebral blood-flow and cerebral metabolic rates of oxygen and glucose were determined by the methods of Kety and Schmidt.3 E. POLLI Istituto di Patologia, G. BIANCHI PORRO Medica e Metodologia Clinica, A. T. MAIOLO. University of Milan, Italy.
ANALYSIS OF PSYCHIATRIC DIAGNOSIS SIR,-Your leader on analysis of psychiatric diagnosis (Jan. " 4, p. 35), remarks that this present-day pastime is still somewhere in the 1760s ". If only it were: unfortunately it is too much in the 1880s. Your comparison is unfair-to the 18th century. The case-registers of this hospital-the erstwhile York Lunatic Asylum-reveal in the 1770s three groupings. These were " flighty ", " flighty and wild ", and "melancholy". Unfortunately, matters did not rest there. Encouraged by the success of this simple and easily understood classification (with no observer variation), the clinical practice of this hospital moved on to include other matters. For example, " furious "; and, as an indication of the first appearance of the problems of old age," loss of memory ". Worse was to come-as witness the arrival of the horrid and incomprehensible paraphrenias (systematica and confabulatoria, to name but a couple). 2.
B., Brown, G. J. A. 3.
Polli, E., Bianchi Porro, G., Della Porta, P., Maiolo, A. T. 68th Congress of the Society of Italian Internal Medicine (edited by L. Pozzi); p. 463. Rome, 1967. Kety, S. S., Schmidt, C. F. J. clin. Invest. 1948, 27, 476.
TABLE I-CEREBRAL HMMODYNAMICS AND METABOLISM IN 12 NORMAL SUBJECTS, 20 MENTALLY ALERT PATIENTS WITH HEPATIC values ± S.D.) CIRRHOSIS, AND 13 PATIENTS WITH HEPATIC CIRRHOSIS AFTER PORTACAVAL SHUNT
(mean
* r<0·001. t0-05>p>0-025. t0-02>p>0-01. c.s.F.=cerebral blood-flow (ml./lOO g. tissue/min.); C.v.x.=cerebral vascular resistances (mm. Hg/ml./100 of oxygen (ml./100 g./min.) ; C.M.R.G. = cerebral metabolic rate of glucose (mg.J100 g./min.) ; c.G./O Q. =cerebral
g./min.); c.m.R.0 =cerebral metabolic glucose/oxygen quotient.
TABLE II-CEREBRAL HaeMODYNAMICS AND METABOLISM IN 13 PATIENTS ON, AND 28 PATIENTS AFTER, FIRST DAY OF HEPATIC 7 PATIENTS WITH ACUTE AND 9 WITH CHRONIC ENCEPHALOPATHY (mean values S.D.)
Abbreviations as in table *P<0.001. p
i.
rate
COMA,
Ghent, Belgium.
L. DEMEULENAERE F. BARBIER P. VERMEIRE.
CEREBRAL METABOLISM AFTER PORTACAVAL SHUNT wish to on the article by Dr. Read and comment SIR,-We his colleagues,! which underlines the frequency of neuropsychiatric abnormalities and electroencephalographic changes in patients with cirrhosis after portacaval anastomosis. Persistently high levels of ammonia in arterial blood is one of the most accepted pathogenetic factors; on this point Dr. Read and his colleagues report the value of prophylactic treatment with neomycin and a low-protein diet in preventing the development of neuropsychiatric abnormalities after portacaval anastomosis. We also support this view, and have noted the presence of cerebral metabolic disturbances early after shunt operation even in mentally alert and oriented patients. We have studied cerebral hxmodynamics and metabolism in 13 patients who had undergone portacaval anastomosis 1-10 months before. These patients at no time had signs of hepatic encephalopathy. Significantly high values of cerebral blood-flow were observed; this resultant increase in no way correlated with arterial PC02 and with hsmatocrit variations. In most cases, moreover, the cerebral metabolic rate of oxygen was slightly higher than normal, with an even greater increase in cerebral metabolic rate of glucose; as a consequence the glucose/oxygen cerebral quotient was significantly increased
(table I). Similar haemodynamic and metabolic results were found in 20 cirrhotic patients within 24 hours of the onset of hepatic coma or of an acute episode of encephalopathy. On the contrary, in patients with chronic coma or chronic encephalopathy there was a striking decrease in both cerebral blood-flow 1.
Read, A. E., McCarthy, C. F., Ajdukiewicz, Lancet, 1968, ii, 999.
A.
and cerebral metabolism (table n). It is worth while to underline the different behaviour of these indices in cirrhotic patients, mentally alert but previously submitted to portacavalshunt ; in these patients, in fact, high values of cerebral bloodflow and cerebral metabolic rate of glucose were found even 1 or 2 years after surgery. These results support the hypothesis that some modifications of brain metabolism occur within a short period after operation, and persist, even though no neuropsychiatric disturbances are clinically evident. We support the view that presumptive mechanism of this cerebral metabolic disorder is a partial glycolysis blockade by animation of oc-ketoglutarate to form glutamic acid and glutamine. In favour of this hypothesis, we have found increased cerebral metabolic uptake of ammonia in these clinical conditions in which there are often higher levels of ammonia in the arterial blood.2 Regarding the increase in cerebral blood-flow, an acceptable hypothesis is that it is the result of modified brain metabolic requirements. Cerebral blood-flow and cerebral metabolic rates of oxygen and glucose were determined by the methods of Kety and Schmidt.3 E. POLLI Istituto di Patologia, G. BIANCHI PORRO Medica e Metodologia Clinica, A. T. MAIOLO. University of Milan, Italy.
ANALYSIS OF PSYCHIATRIC DIAGNOSIS SIR,-Your leader on analysis of psychiatric diagnosis (Jan. " 4, p. 35), remarks that this present-day pastime is still somewhere in the 1760s ". If only it were: unfortunately it is too much in the 1880s. Your comparison is unfair-to the 18th century. The case-registers of this hospital-the erstwhile York Lunatic Asylum-reveal in the 1770s three groupings. These were " flighty ", " flighty and wild ", and "melancholy". Unfortunately, matters did not rest there. Encouraged by the success of this simple and easily understood classification (with no observer variation), the clinical practice of this hospital moved on to include other matters. For example, " furious "; and, as an indication of the first appearance of the problems of old age," loss of memory ". Worse was to come-as witness the arrival of the horrid and incomprehensible paraphrenias (systematica and confabulatoria, to name but a couple). 2.
B., Brown, G. J. A. 3.
Polli, E., Bianchi Porro, G., Della Porta, P., Maiolo, A. T. 68th Congress of the Society of Italian Internal Medicine (edited by L. Pozzi); p. 463. Rome, 1967. Kety, S. S., Schmidt, C. F. J. clin. Invest. 1948, 27, 476.
TABLE I-CEREBRAL HMMODYNAMICS AND METABOLISM IN 12 NORMAL SUBJECTS, 20 MENTALLY ALERT PATIENTS WITH HEPATIC values ± S.D.) CIRRHOSIS, AND 13 PATIENTS WITH HEPATIC CIRRHOSIS AFTER PORTACAVAL SHUNT
(mean
* r<0·001. t0-05>p>0-025. t0-02>p>0-01. c.s.F.=cerebral blood-flow (ml./lOO g. tissue/min.); C.v.x.=cerebral vascular resistances (mm. Hg/ml./100 of oxygen (ml./100 g./min.) ; C.M.R.G. = cerebral metabolic rate of glucose (mg.J100 g./min.) ; c.G./O Q. =cerebral
g./min.); c.m.R.0 =cerebral metabolic glucose/oxygen quotient.
TABLE II-CEREBRAL HaeMODYNAMICS AND METABOLISM IN 13 PATIENTS ON, AND 28 PATIENTS AFTER, FIRST DAY OF HEPATIC 7 PATIENTS WITH ACUTE AND 9 WITH CHRONIC ENCEPHALOPATHY (mean values S.D.)
Abbreviations as in table *P<0.001. p
i.
rate
COMA,