Clinical Neuroscience

[Mental disorders after stroke]

VARGA Dániel

APRIL 20, 2002

Clinical Neuroscience - 2002;55(03-04)

[Stroke represents a major public health problem in Hungary, but relatively little attention is directed toward poststroke neuropsychiatric disturbances. Stroke patients frequently represent mood disturbances, cognitive decline, anxiety disorders, and sometimes serious schizophorm or paranoid states. Poststroke depression is the most common and possibly amenable form to therapeutic intervention. Depressiv symptoms have negativ effect on the rehabilitation process, quality of life and even on long-term survival. Considering drug therapy, in the past decade tricyclic drugs have been replaced by newly developed antidepressants with milder side-effects profile. Our knowledge on the relationship among vascular and other types of dementia has been extended in the recent years. This development also has some therapeutic implications. It seems likely that other psychiatric disorders, psychoses, pathological affect and personality disorders also inhibit recovery and limit long-term quality of life, but abvailable data on this topic is limited.]



Further articles in this publication

Clinical Neuroscience

[Marker molecules of endothelial cell dysfunction in acute ischemic stroke]

SZEGEDI Norbert, MAY Zsolt, ÓVÁRY Csaba, SKOPÁL Judit, NAGY Zoltán

[Introduction - In spite of all similarities, ischemic stroke cases representing 80% of the acute cerebrovascular accidents, different steps of platelet activation, coagulation and fibrinolytic cascade are involved in the patomechanism of the different stroke subtypes. The differentiation of the atherothrombotic, cardioembolic and lacunar forms of acute ischemic stroke is based on the comprehensive evaluation of clinical signs, neuroimaging technics, and diagnostic ultrasound, but also a significant effort was made to characterize the specifities of the underlying processes of the coagulation system by signal molecules, in order to clarify their possible role and to support the diagnostic and therapeutic decisions. Patients and methods - The von Willebrand factor was studied as the marker of endothelial injury in 34 acute ischemic stroke patients within 24 hours after the onset of their stroke, and repeatedly 2, 4, and 12 weeks thereafter. To determine the probable source of the von Willebrand factor, usually released not only by endothelial cells, but also by platelets, the authors simultaneously measured the levels of an additional endothelial marker, thrombomodulin, and a platelet activation marker, β-thromboglobulin. Results - The mean of von Willabrend factor levels measured in stroke patients on the first day was 123%, whereas the mean of the control group 72% (p<0.05). There was no significant difference according to stroke subtype. Von Willebrand values determined two weeks later showed a further 60% increase in stroke patients, and after a gradual fall their level remained above the concentration of the control group. The β-thromboglobulin level measured in stroke group was significantly higher, than in control individuals (171 IU/ml vs. 32 IU/ml, p<0.001). This was characteristic for atherothrombotic and cardioembolic stroke, but not for lacunar infarctions. If measured repeatedly, β-thromboglobulin levels decreased rapidly in the first two weeks, than somewhat slower. Soluble thrombomodulin was slightly elevated in stroke patients (4.24 ng/ml) compared to healthy subjects (3.81 ng/ml), without statistical significance, and without major differences between subgroups. Conclusions - While early determination of β-thromboglobulin can contribute to the differential diagnoses of the subtypes of ischemic stroke, the long-lasting elevation of von Willebrand factor may reflect endothelial dysfunction caused by several factors in the microvasculature of the penumbra.]

Clinical Neuroscience


NAGY Zoltán

Clinical Neuroscience

[MR investigations in stroke]

KENÉZ József, BARSI Péter

[In the article digital imaging methods are presented with special emphasis on the use on diagnostics of cerebral circulation studies. Recently, fundamental changes have happened in this field, concerning especially the MR investigations. These changes have influenced the therapeutic strategies of ischaemic stroke. Authors give the theoretical background on the diffusion and perfusion MR imaging, emphasising the importance of their “mismatch” and its impact in the estimation of the outcome of ischaemic events. More recently, new, controversial facts arose, regarding the reasons of the introduction of the theory of so called “negative” and “positive” mismatches. As a consequence, a level of uncertainty took place in the judgement of prognostics. The leading institutions are searching the way to solve the problem which seems to be the quantitative evaluation of the diffusion, perfusion and mismatch data. The advent of the multislice spiral CT with very fast imaging and the importance of CT investigations increased. With this new kind of equipment, even perfusion studies can be performed using iodinated contrast medium.]

Clinical Neuroscience

[Regulatory mechanisms in focal cerebral ischemia. Perspectives in neuroprotective treatment]

NAGY Zoltán, SIMON László, BORI Zoltán

[Permanent or temporary disruption of cerebral blood flow rapidly depletes brain regions of their limited energy reserves (glycogen, glucose, oxygen, ATP) leading to an energy crisis. Tissue damage occurs due to the energy crisis. The central part of the damage, the ischaemic “core” region is surrounded by zones of the shell-like penumbra. Necrotic, as well as apoptotic cell death could be identified in the penumbra. Going away from the ischaemic core different neurochemical processes are occuring by space and time.“Immediate early response” genes (c-fos, fos-B, c-Jun, krox 20, 24) are activated, heatshock proteins (hsp 70, 72, HSF, HSE, HIF), cytokines (TNF-α, IL-1β), inflammatory factors (COX), adhesion and glial factors (ICAM-1, ELAM-1, P-selectin), vasoactive factors (IL -6, -10, PAF), reactive oxigen radicals and connected factors (O2, OH, NO, NOS, SOD) are produced within minutes and hours. Cell deaths, necrosis and apoptosis due to the activation of calpains, caspases and nucleases occur in days. In parallel, growth factors and plasticity proteins (BDNF, NGF, TGF-β, VEGF, PDGF, GAP-43) are activated as a basis of functional rehabilitation.]

Clinical Neuroscience

[Genetics and hemostasis in young stroke patients]


[Background and purpose - The classical risk factors did not explain all the possible ethiology of cerebral stroke. Genetic polymorphisms responsible for thrombophilia were implicated recently as risk factors of stroke. In this geneticoepidemiological study the author’s aim was to analyse the tendency of genetic polymorphisms to cluster in a cohort of young and elderly stroke patients and in healthy subjects in Hungary. Methods - 253 patients with stroke were compared with 173 healthy blood donors on the basis of genetic polymorphisms of platelet GP IIb/IIIa receptor (33 LeuPro), prothrombin gene G20210A, Factor V Leiden mutation, ACE I/D, methylenetetrahydrofolate reductase (MTHFR) and β fibrinogen gene G455A. These data were acquired using PCR. Questionnaires were used to investigate the family history and to determine the risk factor profile. The subtypes of stroke were analysed in a stroke cohort grouped according to different polymorphisms. Results - An increased frequency of GP IIIa heterozygousity was found as compared to a West-European stroke cohort (31% versus 19%). The prothrombin gene variant (2.9% European and 4.8% in Hungary) was also found to increase in frequency. In young stroke patients (age <50) compared with control subjects the odds ratios were higher: in prothrombin gene (OR: 4.9), in Leiden mutation (OR: 1.67), in fibrinogen gene (OR: 1.64) and in MTHFR(+/+) (OR: 1.58). Clustering of two polymorphisms could only be detected in young patients. These clustering polymorphisms were GP IIb/IIIa with prothrombin G20210A variant (OR: 6.74, 95% CI 1.1-18.2) and prothrombin gene variant with MTHFR (OR: 5.3, CI95 1.2-8.3). Conclusion - Selected and clustered genetic polymorphisms of haemostatic factors could be responsible for the high stroke morbidity in Central Europe. The presence and clustering tendency of these factors have been described in young stroke victims.]

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