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AIM: To study clinical and neuroimaging signs of cardioembolic stroke (CES) in children. MATERIAL AND METHODS: Ten children (mean age 3.5±3.5 years) were examined. Eight children met the diagnostic criteria of CES CASCADE, two children were diagnosed with CES based on the complex of symptoms. A comparison group consisted of 90 children with other subtypes of ischemic stroke (IS). The diagnosis was confirmed by MRI and magnetic-resonance angiography; symptom severity was assessed with PedNIHSS and PSOM. RESULTS AND CONCLUSION: The PedNIHSS score in the acute stage of CES was higher (18.4±9.34) compared to patients with other subtypes of IS (12.6±6.2; p=0.0065). Six patients had large cerebral infarctions with the involvement of basal ganglia, internal capsule, white matter and cerebral cortex. In two patients, the infarction affected the cerebral cortex and underlying white matter, in one patient it affected the cortex from one side and the basal ganglia from the other. A damage of the cortex was noted in one patient. The frequency of recurrent CES was 30%, of fatal cases 20%. Recurrent IS and severe residual neurological deficit were more frequent in CES. CONCLUSION: Early disease onset, acute development and progression of neurological deficit up to the maximal level in the first 5 min, marked severity of the acute stage (PedNIHSS score >15), early onset of neurological function recovery, marked residual neurological deficit (PSOM score >2) are the additional signs of CES.

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AIM: To study clinical and neuroimaging signs of cardioembolic stroke (CES) in children. MATERIAL AND METHODS: A group of 100 patients with arterial ischemic stroke (AIS), aged from 1 month to 15 years, was stratified into the main group (10 patients with CES) and the comparison group (90 patients with other subtypes of AIS). CT and MRI, MR-angiography, ultrasound study as well as assessment of clinical symptoms on PedNIHSS were performed. The duration of follow-up was from 2 month to 14 years. The follow-up allowed the assessment of occurrence of secondary strokes, severity of residual neurological symptoms on the PSOM and fatal outcomes. Special attention was drawn to the use of CASSADE criteria for CES. RESULTS AND CONCLUSION: Clinical features that help to diagnose CES, even in the absence of adequate neuroimaging, in patients with heart disease, which is a potential high risk factor for cardioembolia, were established. These factors include early disease onset, acute development and progression of neurological deficit to the maximal level in the first 5 min., marked severity of the acute period (PedNIHSS > 15), early recovery of neurological functions, significant residual neurological symptoms (PSOM > 2). These symptoms should be used in addition to the CASCADE criteria in the diagnosis of CES of AIS type in children.

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A total of 60 patients aged 6-16 years with tics and Tourette's syndrome were studied. Antibodies to caudate nucleus proteins were assayed by western blot hybridization. Ten patients with Tourette's syndrome were found to have antibodies to caudate nucleus protein. Seven patients with neuroleptic-resistant types of Tourette's syndrome received single transfusions of immunoglobulin preparations, which produced regression of vocal and motor hyperkinesias and improvement in behavior (remission for more than six months). The observation of antibodies to caudate nucleus proteins and the positive effects seen on administration of immunoglobulins to patients with Tourette's syndrome support previous data on the possibility of using immunoglobulin therapy in the treatment of tic-type hyperkinesias and provide evidence of the involvement of autoimmune mechanisms inducing damage to the dopaminergic system of the striatum.

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Sixty children, aged from 6 to 16 years, with tics and Tourette syndrome have been studied. Western immunoblotting techniques has been used to evaluate the serum antibodies against the caudate nucleus. These antibodies have been detected in 10 cases. Seven patients with Tourette syndrome who were treated with neuroleptics for a long time without any therapeutical effect received the immunomodulatory therapy with intravenous immunoglobulin. The regression of motor and vocal tics as well as improvement of behavioral symptoms were observed (duration of remission was more than 6 months). These findings and successful immunomodulatory therapy of patients with Tourette syndrome confirm previous reports in the literature and support the idea of immunologically triggered disturbance of the striatal dopaminergic system.

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In experiments on dogs, application of the cross-over circulation method revealed that mildronate increased coronary blood flow due to active coronary dilation. In experiments on cats, a cardioprotective effect of mildronate was found, which prevented the development of acute ischemic heart failure by stabilizing the major hemodynamic parameters. Clinical studies of patients with Functional Classes I-III angina provided evidence for positive effects of mildronate on coronary blood flow.

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Acute dog experiments involving the perfusion of donor coronary arteries demonstrated that alpha-adrenoreceptor stimulation in the presence of a beta-adrenergic block resulted in a 30% drop of coronary flow. This response is maintained at low perfusion coronary blood pressure values (up to 25 +/- 13 mmHg, p less than 0.02), whereas coronary dilatation reserve is already fully depleted at 60 +/- 8 mmHg, suggesting that the degree of coronary arterial stenosis associated with coronary insufficiency may be a decisive factor shaping coronary response to alpha-adrenoreceptor stimulation.

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The effect of intravenous infusion of glutamic acid on cardiac contractile function during short-term ischemia and subsequent reperfusion was studied in anaesthetized dogs. Left ventricular ischemia was induced by underperfusion of the anterior descending and circumflex coronary arteries. Infusion of glutamic acid at 3 mg/kg/min resulted in less depression of cardiac function when given after a 2 min period of 60% coronary blood flow reduction: left ventricular systolic pressure decreased by 9% vs. 22%, dP/dt decreased by 16% vs. 29%, the double product (left ventricular systolic pressure by heart rate) was reduced by 16% vs. 31%. When reperfusion was carried out during glutamic acid infusion there was a significantly enhanced recovery in cardiac function. The augmentation of cardiac performance in ischemia and reperfusion caused by glutamic acid was not accompanied by changes in myocardial oxygen consumption. Glutamic acid uptake by the ischemic myocardium increased 2-fold during infusion. This led to cessation of ammonia release from the heart due to stimulation of glutamine synthesis, and an enhancement of alanine formation coupled with pyruvate uptake but it did not effect lactate production. However, glutamic acid infusion did not influence cardiac performance and metabolism under conditions of normal coronary flow. The results suggest that elevation of glutamate arterial concentration exerts a beneficial effect on ischemic heart. The mechanisms of the protective action are discussed.

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The effect of intravenous glutamic acid infusion (3 mg/kg/min) was studied during myocardial ischemia and reperfusion in anesthetized dogs. Left ventricular ischemia was induced by underperfusion of the anterior descending and circumflex coronary arteries. Glutamic acid reduced the ischemic contractile depression 2 min after a 60%-reduction of the coronary blood flow. The left ventricular systolic pressure was decreased by 9% versus 22%, dP/dt by 16% versus 29%, left ventricular systolic pressure heart rate product by 16% versus 31%. Reperfusion with glutamic acid improved the recovery of cardiac performance without any increase in myocardial oxygen consumption. Glutamic acid infusion resulted in a 2-fold augmentation of glutamate uptake by the ischemic myocardium. It led to cessation of ammonia release by the heart due to activation of glutamine synthesis, enhancement of alanine formation coupled with pyruvate utilization and did not change lactate production. The mechanisms of the protective action of glutamic acid are discussed.

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Experiments on anesthetized dogs were made to examine oxygen extraction from coronary blood during increase and decrease in cardiac rhythm frequency under varying conditions of vasomotor regulation. With an initially high tone of the coronary vessels both increase and reduction of myocardial oxygen supply occurred at the expense of vasomotor reactions. Under these conditions the coronary blood flow velocity and systolic rhythm correlated well. At the same time the oxygen level in coronary blood did not experience noticeable changes. As the initial tone of the coronary vessels dropped, vasomotor reactions were attenuated and oxygen extraction from coronary blood underwent alterations which had occurred prior to depletion of the coronary expanding reserves. The data obtained suggest that reduction of the initial tone of the coronary vessels proceeds non-uniformly, leading to a decrease in vascular sensitivity to the tissue oxygen level.

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The influence of the occlusion of one coronary artery on coronary blood flow in an intact myocardium was investigated in narcotised dogs with open chest by using the crossed circulation method. Interruption of blood inflow to one of the branches of the left coronary artery under autoperfusion of the coronary bed led to a drop in the blood flow rate in the intact branch of the same artery, which was caused by decreased perfusion pressure. Stabilization of coronary perfusion pressure made it possible to detect the dilatatory reaction of the intact coronary bed to the occlusion of one of the coronary arteries. On the basis of an analysis of the dilatatory reaction, conclusions are drawn about the reflex nature of the observed phenomenon. The results of experiments with selective pharmacological blockade of both parts of the autonomous nervous system suggest that the afferent and efferent pathways run in the sympathetic nervous system.

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Cholinergic and adrenergic components of vegetative innervation in acupuncture zones of the human skin (in acupuncture "points") were studied by the histochemical method for acetylcholine esterase and by the method of luminescent microscopy. Skin samples were obtained by means of biopsy. In 23 corporal acupuncture zones in the skin, cholinergic nerve conductors and terminals were found to be concentrated and structurally connected with multiple vessels of the skin and its derivatives: sweat glands, folliculi of the fluffy hairs and smooth muscles. In the derm, among its derivatives, numerous free varicose axons with a high positive reaction for acetylcholine esterase were found. In 7 out of 9 examined neutral areas of the human skin, a weak cholinergic innervation was revealed. In biopsies obtained from patients during operations, adrenergic nerves in acupuncture zones were found in small amount on the vessels of skin and in smooth muscles. The problem on participation of acetylcholine from the skin neural elements in the mechanism of therapeutic effect of acupuncture is discussed.

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