Vol 1, No 3 (2007)

Original articles

Metabolic syndrome and ischemic stroke

Tanashyan M.M., Orlov S.V., Domashenko M.A., Ionova V.G.

Abstract

Metabolic syndrome is multifactorial (hyperinsulinaemia, arterial hypertension, dyslipidaemia, obesity) condition with the increased risk of cerebrovascular diseases. In the majority of cases it is associated with its influence on the system оf haemorrheology and haemostasis. In our study we investigated two groups of patients with ischemic stroke: 20 with and 20 without metabolic syndrome. Patients with metabolic syndrome had slower recovery and worse outcome after stroke compared to patients without metabolic syndrome. It was showed that metabolic syndrome makes worse common macro and microrheological blood parameters: increases thrombocyte and erythrocyte aggregation, decreases erythrocyte deformability. The exhaustion of all components of atherombogenic (antiaggregation, anticoagulation and fibrinolytic) potential of the vessels’ wall was also demonstrated. All revealed changes stimulate forming of thrombi and make worse microcirculation in patients with metabolic syndrome. The monitoring of haemorrheological and haemostatic parameters is essential for improving of the treatment of patients with ischemic stroke, especially patients with metabolic syndrome background.
Annals of Clinical and Experimental Neurology. 2007;1(3):
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Psychiatric disorders in epilepsy. Communication II

Karlov v.a.

Abstract

Аnalysis of various chronic psychiatric disturbances in epilepsy – characteristic personality changes, aggressiveness and cognitive abnormalities – is presented. Relevant risk factors and mechanisms of chronic psychiatric disorders in different clinical variants of epilepsy are assessed. An extensive personal experience of the author and literature data are summarized concerning urgent therapy of acute psychotic manifestations and severe depressive disorders in patients with epilepsy. Psychiatric syndromes that are in cause and effect relation with current medication of epilepsy and with prescription of particular antiepileptic drugs are discussed in detail.
Annals of Clinical and Experimental Neurology. 2007;1(3):
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Partial thrombosis of carotid arteries in acute ischemic stroke

Chechetkin A.O., Lagoda O.V.

Abstract

We have conducted the analysis of 6 patients (5 males/1 female) with acute ischemic stroke due to partial thrombosis of the carotid arteries (CA). Duplex scanning showed that in 4 cases thrombus was located in carotid bifurcation and internal carotid artery, in 2 cases thrombi were found only in internal carotid artery. In 3 cases thrombus was immobile (one of them had small floating fragments on the thrombus’ surface) and in 3 cases was mobile (floating). In 3 cases thrombi were located on the small atherosclerotic plaques. In all patients the haemorrheological and haemostatic changes typical for hypercoagulation state were revealed. Hyperhomocy steinemia could be probably the cause of thrombi formation in 2 cases. In 2 cases thrombectomy was performed. Re-thrombosis occurred in 1 case and was explained by the absence of definite diagnosis. Once the diagnosis of hyperhomocysteinemia was set and the proper treatment was administrated the recurrent thrombus was completely exposed to lysis. In 1 patient thrombi formed both in CA and profound veins of the leg that caused lethal pulmonary thromboembolism. 3 patients demonstrated the effectiveness of conservative treatment which led to complete lysis of thrombi in 2 patients and the partial lysis of the thrombus in 1 patient.
Annals of Clinical and Experimental Neurology. 2007;1(3):
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Histochemical changes of NADPH-diaphorase in Guillain–Barre syndrome

Sakharova A.V., Lozhnikova S.M., Piradov M.A., Pirogov V.N.

Abstract

The distribution of NADPH-diaphorase activity in peripheral nerve biopsy was studied to evaluate the role of nitric oxide in demyelination. NO is an important inflammatory mediator which appears to exert significant effects in number of demyelinating diseases, and sometimes is established a direct causal link between NO and demyelination. Till now there wasn’t any description for the involvement of nitric oxide in GBS cellular immune reactions. We have studied cellular and subcellular histochemistry of NADPHdiaphorase in GBS. Peripheral nerve biopsy tissues were examined with regard to disease duration, from 6 patients who were 11 to 52 days after onset of symptoms. Tetrazolium method in our modification was used to visualize NADPHdiaphorase reaction in the successive tissue sections on the cellular and ultrastructural levels. We have shown that specific pattern of histochemical reaction was characteristic for each distinct time point of disease duration. Up and downregulation mode of histochemical reaction was different for Schwann cells (SC) and mononuclear inflammatory cells. During demyelination reduced NADPH-diaphorase activity was found in SCs associated with degrading myeline sheath. During remyelination that characterized by proliferation of SCs and enlarge of its cell volume we observed an increase in NADPH-diaphorase reaction that indicated on the rise of the NO production in it. In that activated SCs the intracellular distribution of NADPH-diaphorase is changed. Maximum of reaction intensity was shifted in nucleus. It suggests the appearance of the expressional regulation in SCs, which characteristic for the highoutput iNOS, and directed to increase of NO production The levels of NADPH-diaphorase activity varied in large extend in different recruited macrophages in the same tissue sample. It reflects the cyclic character proper to macrophagal iNOS. Intensive reaction was found in cytoplasm and nuclear envelop of the mononuclear cells, that migrate throw the blood vessel walls where NO may enhancing local nerve blood flow and serve simultaneously as important effector in the clearance of the myelin/axonal debris. High intensive NADPH-diaphorase activity was detected in distinct cytoplasm regions of the macrophage on the territory of the injured myelin sheath. Hyperproduction of nitric oxide and cytotoxic effect may take place in such districts. All this findings suggest that endogenous nitric oxide is involved in pathogenesis of GBS.
Annals of Clinical and Experimental Neurology. 2007;1(3):
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Endovascular interventions of stenosing brachiocephal arteries

Protsky S.V., Dobzhansky N.V.

Abstract

This article is devoted of surgical endovascular reconstraction of brachiocephal arteries as one of methods of cerebral ischemia prevention. Description of world experience of endovascular interventions is described. High efficacy of stenting discovers a huge perspectives in future.
Annals of Clinical and Experimental Neurology. 2007;1(3):
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Hypertension disturbances of cerebral blood circulation

Kistenev B.A., Maksimova M.Y., Bryukhov V.V.

Abstract

Hypertension is the main cause and the most important risk factor of various forms of temporary as well constant acute disturbances of cerebral blood circulation. Patients with more than 25 years hypertension and frequent increases of blood pressure have damages of brain vessels with plasmorrhage and fibrinoid necrosis
of capillaries walls. This damage in their turn being “hypertonic stenosis or occlusion” of brain vessels can lead to a disturbance of blood flow in the supplied regions and result in forming small lacunar brain infarctions, the most typical for arterial hypertension. From the other hand, necrosis of media vessels myocytes can lead to their sharp thinning, forming microaneurysm, that breaks and causes intracerebral hemorrhage. The presented clinical observation states different types of hypertension angiopathy in one patient and as a result different types of disturbances of cerebral blood circulation: cerebral hypertension stroke, repeated intracerebral hemorrhage and small lacunar brain infarctions.
Annals of Clinical and Experimental Neurology. 2007;1(3):
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