Spreading Cerebral Oligemia in Classical- and Normal Cerebral Blood Flow in Common Migraine

SYNOPSIS
Regional cerebral blood flow was studied with intra-arterial ¹³³Xenon technique in 254 areas of a hemisphere during the development of classical migraine attacks in seven patients. We describe a gradual spread of reduced cerebral blood flow starting at the posterior pole of the hemisphere and advancing in a mode quite similar to the spreading depression phenomenon of Leao. In three patients the oligemia was preceeded by focal or perifocal hyperemia. Functional activation by speech etc. was usually impaired or abolished during prodromes or accompaniments. Headache was found concommitantly with cerebral blood flow reduction and cannot be caused by reactive hyperemia in these patients. Similar findings were made in two patients studied with tomographic ¹³³Xenon technique. During induced common migraine attacks repeated cerebral blood flow studies with stationary detectors (N =3) and with tomographic technique (N =4) revealed no alterations of global or cerebral blood flow. Also tomographic determination of spontaneous common migraine attacks in four patients was normal. It is concluded that the two forms of migraine are different with respect to cerebral blood flow abnormalities and that they should be studied separately in the future. Greater interest should be directed towards the phenomenon of spreading depression as a possible model of the classical migraine attack.     

Clinical trial of Nimodipine for single attacks of classic migraine

In a randomized, double-blind cross-over study, 43 patients with classic migraine received 40 mg Nimodipine and placebo as sublingual capsules. There was no significant effect on patients' preference, development of headache, need for escape medicine, duration of headache, severity of headache or headache index. Considerable methodological problems were encountered. Only 54% of the 79 patients selected for the trial could be evaluated. Suggestions for future trials are made.     

Group a streptococcal antigens cross-reactive with myocardium. Purification of heart-reactive antibody and isolation and characterization of the streptococcal antigen

Heart-reactive antibody (HRA) appears in the sera of experimental animals inoculated with group A streptococci as well as patients with acute rheumatic fever. Adsorption of either serum with group A streptococcal membranes will remove the HRA. Blocking experiments between these two types of HRAs have demonstrated that the antibodies are directed towards different antigenic determinants on either the same or different molecules. To isolate and purify the antigen from the group A streptococcus cross-reactive with sarcolemmal sheaths of cardiac myofibers, it became necessary to purify the HRA from rheumatic fever patients’ sera. Isolated gamma globulin containing all of the HRA was adsorbed onto human sarcolemmal sheaths. The specific HRA was released by using potassium iodide. Over 99 percent of the purified HRA was shown to bind the sarcolemmal sheath whereas less than 1 percent of the antibody would bind nonspecifically to other material. Preparations of group A streptococcal membrane will bind HRA purified from the sera of acute rheumatic patients at levels of 97 percent or greater. The cross-reactive antigen solubilized by nonionic detergent was purified 120-fold by column chromatography. On sodium dodecyl sulfate polyacrylamide electrophoresis, the antigen was demonstrated to be composed of four polypeptides with mol wt of 32,000, 28,000, 26,000, and 22,000 daltons, respectively. Only proteolytic enzymes could destroy the antigenic determinant whereas glycosidases and lipases had no effect. The purified antigen blocked the binding of purified HRA to normal human heart sections.     

A COMPLEX TRUE KNOT OF THE UMBILICAL CORD

SUMMARY A case of cord presentation associated with the presence of a complex true knot is described and the aetiology and risks reconsidered.     

Prevalence of cytomegalovirus antibody in hemophiliacs and homosexuals infected with human immunodeficiency virus type 1

We determined the prevalence of antibody to cytomegalovirus (CMV) in the sera of non-homosexual hemophilia patients and homosexual men infected with the human immunodeficiency virus type 1 (HIV-1). CMV antibody testing by latex agglutination revealed 33 of 58 HIV-1 infected hemophiliacs (57%) were antibody-positive compared with 54 of 54 HIV-1 infected asymptomatic non-hemophiliac homosexuals (100%) (p less than .001). Nine of 15 hemophiliacs (60%) with symptomatic HIV-1 infection were CMV antibody-positive. We also tested 22 HIV-1 antibody-negative hemophiliacs who had received non-heat treated factor concentrates. 14 of these 22 (64%) were CMV antibody-positive compared with 57% of HIV-1 antibody-positive hemophiliacs. We conclude 1) there is little correlation between transmission of HIV-1 and CMV by factor concentrates, 2) the presence of CMV antibody does not appear to be associated with clinical stage of HIV-1 infection in hemophiliacs, and 3) there may be a significant number of CMV antibody-negative hemophiliacs with HIV-1 infection at risk for primary infection and subsequent disease if CMV seronegative blood products are not provided for future transfusions.     

Redistribution of joint moments is associated with changed plantar pressure in diabetic polyneuropathy

Background  

Patients with diabetic polyneuropathy (DPN) are often confronted with ulceration of foot soles. Increased plantar pressure under the forefoot has been identified as a major risk factor for ulceration. This study sets out to test the hypothesis that changes in gait characteristics induced by DPN related muscle weakness are the origin of the elevated plantar pressures.     

The TASK background K2P channels: chemo- and nutrient sensors

Specialized chemo- and nutrient-sensing cells share a common electrophysiological mechanism by transducing low O(2), high CO(2) and low glucose stimuli into a compensatory cellular response: the closing of background K(+) channels encoded by the K(2P) subunits. Inhibition of the TASK K(2P) channels by extracellular acidosis leads to an increased excitability of brainstem respiratory neurons. Moreover, hypoxic down-modulation of TASK channels is implicated in the activation of glomus cells in the carotid body. Stimulation of both types of cell leads to an enhanced ventilation and to cardiocirculatory adjustments. Differential modulation of TASK channels by acidosis and high glucose alters excitability of the hypothalamic orexin neurons, which influence arousal, food seeking and breathing. These recent results shed light on the role of TASK channels in sensing physiological stimuli.