[We have read several publications of great authority on the neurological profession in the last two years in which were expressed assessments of the current situation combined with opinions about neurology and the necessity to reorganize neurological patient care. These articles took up the question of neurorehabilitation too. The authors, who on a daily basis, deal with the rehabilitation of people with disabilities as a consequence of neurological conditions, summarize some important definitions of rehabilitation medicine and the present system of neurological rehabilitation, as it is defined by the rehabilitation profession.]

[Non-valvular AF is the most common cardiac arrhytmia. Its incidence increases with age. AF is an independent risk factor for ischaemic stroke, representing a five times higher risk for it, associated with a high mortality rate. Beside AF, there are several other risk factors which influence the risk of stroke. Stroke risk calculator can be used to assess the risk of patient having a stroke. The most endangered group of patients with AF are those who have already suffered from cerebrovascular event. The only effective medication for prevention of stroke due to AF had been the application of vitamin K antagonists (VKA) which considerably decrease the rate of ischaemic event in a patient with AF providing that the INR is in the therapeutic range. VKA have several limitations of use in clinical practice and the fear of bleeding complications results an underusing of these drugs. Only 50% of all patients treated with VKA reaches the therapeutic range of INR. The breakthrough of prevention of stroke in recent years is undisputedly the coming out of novel oral anticoagulants (NOACs, thrombin and Xa-factor inhibitors). Recent studies suggest that these novel drugs prove the same efficacy as VKA drugs, furthermore dabigatran in a dose of 2×150 mg or apixaban in 2×5mg was statistically superior to warfarin in the prevention of stroke. NOACs have shown a large reduction in intracranial hemorrhage compared with warfarin. They are given as a fixed dose and do not require persistent monitoring making them much more convenient. NOACs at guidelines of European Society of Cardiology act as a preferable drugs in case of ischaemic stroke with AF. Probably the extended use of NOACs in clinical practice will be the mainstream of stroke prevention in the future.]

[Background and purpose - Neurodegenerative diseases eg. ischemic stroke causes lifelong disabilities in cognitive functions and movement, furthermore high frequency of death. Antiapoptotic, or growth factor gene targeting to cortical structures could be a useful tool for neuroprotection in ischemic brain diseases. In present study we examined the feasibility of the gene therapy of the cortex and hippocampus via transfecting brain with recombinant adenovirus containing LacZ reporter gene in normal and postischemic condition. Since translation of proteins can be inhibited following ischemia by the phosphorylation of ribosomal subunit eIF2α, phosphor-eIF2α immunohystochemistry were performed. Methods - Our adenovirus vector was introduced via the cisterna magna into control and postischemic gerbil brain. After 48 hours of transfection the brains were examined for X-gal staining. LacZ expressing cells showed blue colour. Five min. transient global ischemia was induced by clipping the vertebral and carotid arteries of gerbil. Phosphor-eIF2α immunohystochemistry were performed following 48 hours of ischemia. Results - Administration of adenoviral vector resulted in transfection of hippocampal CA1, CA2, CA3 cell layers while gyrus dentatus remained untransfected. Cortical pyramidal cell layers were also transfected. In postischemic brain the lack of LacZ gene expression were detected in the CA1 and CA2 layer of hippocampus. Ischemia caused eIF2α phosphorylation in hippocampal CA1, CA2, CA3 and most neuronal layers in the cortex. Conclusion - Introducing adenovirus vector via the cisterna magna may results in effective gene therapy of cortex and hippocampus. To develop effective gene therapy in postischemic hippocampal CA1 and CA2 cell layers needs further investigation. eIF2α phosphorylation probably doesn’t interfere with transgene expression.]