Acute spinal epidural abscess is a disease unfamiliar to most physicians. It is rarely diagnosed before the onset of irreparable damage to the spinal cord, and the true nature of the process is often discovered only at postmortem examination. We are reporting the following case to illustrate a sequence of symptoms and signs important in arriving at an early diagnosis. Prompt treatment will save the patient from lifelong disability or death. REPORT OF CASE I. P., a white girl aged 18, was admitted to the Montefiore Hospital July 7, 1937. The history was significant in that the patient had been operated on for acute and recurrent osteomyelitis eight times between February 1930 and December 1936. The right scapula, a rib, the left femur and the right femur had been involved. The patient was first seen on July 4, when she complained of severe pain in both loins and in the

ArticleFURTHER OBSERVATIONS ON FLEXOR RIGIDITY IN THE HINDLEGS OF THE SPINAL CATJ. G. Dusser De Barenne, and Y. D. KoskoffJ. G. Dusser De BarenneFrom the Laboratory of Neurophysiology, Yale University, New Haven, Conn., and Y. D. KoskoffFrom the Laboratory of Neurophysiology, Yale University, New Haven, Conn.Published Online:31 Jan 1934https://doi.org/10.1152/ajplegacy.1934.107.2.441MoreSectionsPDF (793 KB)Download PDF ToolsExport citationAdd to favoritesGet permissionsTrack citations ShareShare onFacebookTwitterLinkedInWeChat Previous Back to Top Next Download PDF FiguresReferencesRelatedInformation More from this issue > Volume 107Issue 2January 1934Pages 441-446 Copyright & PermissionsCopyright © 1934 by American Physiological Societyhttps://doi.org/10.1152/ajplegacy.1934.107.2.441History Received 5 October 1933 Published online 31 January 1934 Published in print 31 January 1934 Metrics

ArticleFLEXOR RIGIDITY OF THE HIND LEGS AND PRIAPISM IN THE "SECONDARY" SPINAL PREPARATION OF THE MALE CATJ. G. Dusser de Barenne, and Y. D. KoskoffJ. G. Dusser de BarenneFrom the Laboratory of Neurophysiology of Yale University, New Haven, Conn., and Y. D. KoskoffFrom the Laboratory of Neurophysiology of Yale University, New Haven, Conn.Published Online:30 Sep 1932https://doi.org/10.1152/ajplegacy.1932.102.1.75MoreSectionsPDF (2 MB)Download PDF ToolsExport citationAdd to favoritesGet permissionsTrack citations ShareShare onFacebookTwitterLinkedInWeChat Previous Back to Top Next Download PDF FiguresReferencesRelatedInformation More from this issue > Volume 102Issue 1September 1932Pages 75-86 Copyright & PermissionsCopyright © 1932 by American Physiological Societyhttps://doi.org/10.1152/ajplegacy.1932.102.1.75History Received 19 May 1932 Published online 30 September 1932 Published in print 30 September 1932 Metrics

In a previous report it was shown that resting muscle of normal dogs may liberate lactic acid into the blood stream. The lactic acid may thus reach the liver where it is removed and converted to carbohydrate. It may be retained in the liver as glycogen or leave the liver, appearing in the blood as glucose. In the present study on diabetic dogs it was found that this lactic acid-glucose cycle involving muscle and liver was one of the mechanisms for maintaining hyperglycemia after the glycogen stores of the liver were reduced by fasting. Fourteen large female dogs were fasted for 3 days or more and were then depancreatized under aseptic precautions. When the respiratory quotient and the D/N ratio indicated that the dogs had become completely diabetic, they were put under amytal anesthesia, the femoral vessels were exposed and the abdomen was opened by a longitudinal incision. Samples of blood were drawn practically simultaneously from the femoral artery, femoral vein, portal vein and hepatic vein. These blood samples were analyzed for glucose and lactic acid. The results may be presented as 3 links in a chain of evidence: First as seen in Table I, both during rest and exercise there is greater concentration of lactic acid in the blood of the femoral vein than in that of the femoral artery. Taking differences of 5 mg. % or more as significant, this occurred in 13 of 25 observations. Only once did the muscles take out lactic acid from the blood.

The following research was undertaken to determine the factors regulating the concentration of lactic acid in the blood of mammals. Observations were made on 32 dogs most of which were decerebrate. The amount of lactic acid in the arterial blood was compared with that of the blood draining the liver, spleen, portal system, kidney, testicle, lower extremities, brain, thyroid, lungs and heart. Lactic acid was estimated by the method of Shaffer, Cotonio and Friedemann. Sugar was determined by the Shaffer-Hartmann method. A difference of 5 mg. % or more between the lactic acid content in the arterial and venous samples was considered significant. Typical results are found in Table I, where the muscle poured lactic acid in the blood stream and the liver removed it. Thus, in 27 of 51 observations the muscles added to the lactic acid content of the blood passing through them. In 19 cases the difference between arterial and venous blood was not considered significant, and in 5 instances only did the muscles remove lactic acid. On the other hand, in 21 of 34 observations the liver removed lactic acid. However, in 6 instances the liver was adding lactic acid to the blood and therefore could not explain the lower arterial level. It is clear that some organ other than the liver was removing lactic acid. Results from many of the organs were not constant. Sometimes they would remove lactic acid from the blood though in decerebrate animals they usually added lactic acid. We next studied the heart. As seen in Table I1 the heart, in 6 observations, was removing lactic acid from the blood passing through it. Even small differences are significant in the heart because of its relatively large vascular supply.