Epidemiology of Multiple Sclerosis in Western Herzegovina and Herzegovina – Neretva Canton, Bosnia and Herzegovina

The aim of this study was to investigate the selected indicators of multiple sclerosis (MS) in Herzegovina (Western Herzegovina Canton and Herzegovina-Neretva Canton). By using all available health and medical sources in the studied area and using McDonald’s criteria, a total of 96 patients were identified in the period from 1996 to 2006. Results of the study show that the crude prevalence of MS was 30.99/100,000 (95% confidence interval [CI] 24.8–37.2), the highest one in the municipality of Posu{je (49.6/100,000) and the lowest one in the municipalities of Neum and Ravno (no recorded cases); the female/male ratio was 1.5; the mean age of the patients on the prevalence day was 41.4±10.2 years and the mean age at the disease onset was 30.7±6.4 years; the most often clinical course of the disease was relapsing-remitting (58%), secondary progressive course was present in 28% patients, primary progressive in 9% and progressive relapsing in 1% of patients; the most frequent initial signs of the disease were motor (33%) and sensory ones (24%). According to the results of the study, the south-western part of Bosnia and Herzegovina is an area on the crossing from moderate risk to high risk zone for MS. The distribution of MS is heterogeneous. MS was more prevalent in the municipalities with colder climate and more winter precipitation and it is not present in the coastal region with warmer climate and almost without winter precipitation

Trends in stroke thrombolysis rate in Bosnia and Herzegovina: a hospital-based observation study

Aim To assess trends in thrombolysis rates and door-to-needle times in University Hospital Mostar. Methods Data from the University Hospital Mostar Registry were used. Information on the number of ischaemic stroke patients, intravenous thrombolysis rates and „door-to-needle times“ (DNT) were collected between January 2013 and December 2021. Results Out of the total of 3100 ischaemic stroke patients, alteplase was given to 130 patients giving a thrombolysis rate of 4.2%. The mean hospital thrombolysis rate increased from 2.4% in 2013 to 10.6% in 2021. Conclusion Although the hospital thrombolysis rate more than quadrupled, there is still a low proportion of acute ischaemic stroke patients who received intravenous thrombolysis therapy. Education and interventions indicating the importance of recognition and treatment of acute ischemic stoke are necessary for all physicians

Neurological Complications of COVID-19

Koronavirusna bolest u 2019. godini (COVID-19) uzrokovana je novootkrivenim korona virusom tipa 2 koji uzrokuje teški akutni respiratorni sindrom (SARS-CoV-2). Virus je otkriven u prosincu 2019. godine, a od strane Svjetske zdravstvene organizacije je, zbog broja oboljelih i proširenosti širom svijeta, proglašena pandemija. Klinička prezentacija COVID-19 varira od asimptomatskog do teškog oblika i smrtnog ishoda. Iako kliničkom slikom dominiraju respiratorne smetnje, mnogobrojne studije ukazuju na pojavu akutnih i kroničnih neuroloških komplikacija u skoro trećine oboljelih. Najčešći neurološki simptomi akutne faze COVID-19 su glavobolja, gubitak njuha i okusa, poremećaji stanja svijesti, encefalopatije, encefalitisi, moždani udar, bolovi u mišićima, epileptički napadaji, poliradikulopatije (GBS) te pojačan umor i netolerancija napora, poremećaji vegetativnih funkcija, kognitivne i psihičke smetnje u postinfekcijskoj fazi oboljenja. Potencijalni patofiziološki mehanizam nastanka neuroloških poremećaja u akutnoj fazi uključuje koagulopatije s udruženim hipoksično-ishemijskim oštećenjima, poremećajem krvno-moždane barijere, endoteliopatijama i neuroinvazijom virusa, udruženom s neuro-imunim odgovorom. Cilj ovog članka je prikazati najčešće akutne i kronične neurološke poremećaje vezane uz COVID-19 kod odraslih bolesnika kao i potencijalni patofiziološki mehanizam nastanka neuroloških poremećaja, a buduće epidemiološke studije o bolesnicima s COVID-19 bi trebali utvrditi pravu incidenciju neuroloških komplikacija COVID-19, razgraničiti specifične neurološke sindrome, postaviti dijagnostičke i terapijske protokole ta razjasniti mehanizam nastanka poremećaja.Coronavirus disease in 2019 (COVID-19) is caused by the newly discovered coronavirus type 2 which causes severe acute respiratory syndrome (SARS-CoV-2). The virus was discovered in December 2019, and the World Health Organization has declared a pandemic due to the number of cases and the spread around the world. The clinical presentation of COVID-19 varies from asymptomatic to severe and lethal outcome. Although the clinical picture is dominated by respiratory disorders, numerous studies indicate the occurrence of acute and chronic neurological complications in almost a third of patients. The most common neurological symptoms of the acute phase of COVID-19 are headache, loss of smell and taste, disturbances of consciousness, encephalopathies, encephalitis, stroke, muscle pain, epileptic seizures, polyradiculopathy (GBS) and increased fatigue and intolerance to stressful and mental disorders in the postinfectious phase of the disease. Potential pathophysiological mechanisms of the development of neurological disorders in the acute phase include coagulopathies with associated hypoxic-ischemic damage, blood-brain barrier disorder, endotheliopathies and neuroinvasion of viruses with associated neuro-immune response. The objective of this paper is to present the most common acute and chronic neurological disorders related to COVID-19 in adult patients as well as the potential pathophysiological mechanism of neurological disorders, and future epidemiological studies on patients with COVID-19 should determine the true incidence of specific neurological syndromes, to establish diagnostic and therapeutic protocols and to clarify the mechanism of disorder development

The role of TPA I/D and PAI-1 4G/5G polymorphisms in multiple sclerosis.

Previous studies have shown impaired fibrinolysis in multiple sclerosis (MS) and implicated extracellular proteolytic enzymes as important factors in demyelinating neuroinflammatory disorders. Tissue-type plasminogen activator (t-PA) and its inhibitor (PAI-1) are key molecules in both fibrinolysis and extracellular proteolysis. In the present study, an association of the TPA Alu I/D and PAI-1 4G/5G polymorphisms with MS was analyzed within the Genomic Network for Multiple Sclerosis (GENoMS). METHODS: The GENoMS includes four populations (Croatian, Slovenian, Serbian, and Bosnian and Herzegovinian) sharing the same geographic location and a similar ethnic background. A total of 885 patients and 656 ethnically matched healthy blood donors with no history of MS in their families were genotyped using PCR-RFLP. RESULTS: TPA DD homozygosity was protective (OR = 0.79, 95% CI 0.63-0.99, P = 0.037) and PAI 5G5G was a risk factor for MS (OR = 1.30, 95% CI 1.01-1.66, P = 0.038). A significant effect of the genotype/carrier combination was detected in 5G5G/I carriers (OR = 1.39 95% CI 1.06-1.82, P = 0.017). CONCLUSIONS: We found a significantly harmful effect of the combination of the PAI-1 5G/5G genotype and TPA I allele on MS susceptibility, which indicates the importance of gene-gene interactions in complex diseases such as MS

The Role of TPA I/D and PAI-1 4G/5G Polymorphisms in Multiple Sclerosis

Background. Previous studies have shown impaired fibrinolysis in multiple sclerosis (MS) and implicated extracellular proteolytic enzymes as important factors in demyelinating neuroinflammatory disorders. Tissue-type plasminogen activator (t-PA) and its inhibitor (PAI-1) are key molecules in both fibrinolysis and extracellular proteolysis. In the present study, an association of the TPA Alu I/D and PAI-1 4G/5G polymorphisms with MS was analyzed within the Genomic Network for Multiple Sclerosis (GENoMS). Methods. The GENoMS includes four populations (Croatian, Slovenian, Serbian, and Bosnian and Herzegovinian) sharing the same geographic location and a similar ethnic background. A total of 885 patients and 656 ethnically matched healthy blood donors with no history of MS in their families were genotyped using PCR-RFLP. Results. TPA DD homozygosity was protective (OR = 0.79, 95% CI 0.63–0.99, P=0.037) and PAI 5G5G was a risk factor for MS (OR = 1.30, 95% CI 1.01–1.66, P=0.038). A significant effect of the genotype/carrier combination was detected in 5G5G/I carriers (OR = 1.39 95% CI 1.06–1.82, P=0.017). Conclusions. We found a significantly harmful effect of the combination of the PAI-1 5G/5G genotype and TPA I allele on MS susceptibility, which indicates the importance of gene-gene interactions in complex diseases such as MS

The lack of association between angiotensin-converting enzyme gene insertion/deletion polymorphism and nicotine dependence in multiple sclerosis

Blood-borne angiotensin II is generated from angiotensinogen via cleavage by renin and angiotensin-converting enzyme (ACE), an enzymatic cascade known as the renin–angiotensin system (RAS). Several lines of evidence indicate that ACE, beyond its classical role of mediating blood pressure regulation, might contribute to the etiology of substance addictions by influencing dopaminergic signaling. A functional insertion/deletion (I/D) polymorphism of the ACE gene was associated with risk for being a smoker among individuals with depression and with smoking severity in studies comprising patients with depression and healthy controls. Several reports have described significantly increased ACE activity in cerebrospinal fluid and serum among MS patients. Furthermore, in our previous work with MS patients from Croatian and Slovenian populations, we demonstrated that the ACE-I/D polymorphism contributes to an elevated MS risk among male patients. Here we investigated whether the ACE-I/D polymorphism might influence smoking behavior among patients with MS. Patients and Methods Genotyping was performed in 521 patients (males/females: 139/382) using polymerase chain reaction. Results We revealed no significant differences in ACE genotype and allele frequencies between smokers and nonsmokers and no significant association between the ACE-I/D polymorphism and either pack-year smoking history or number of cigarettes smoked daily (p > .05, respectively). Conclusion The ACE-I/D polymorphism does not contribute either to risk for nicotine dependence or to smoking severity among MS patients. In the context of reports on the ACE-I/D polymorphism and nicotine dependence among healthy controls and patients with depression, we may speculate that the mechanism by which this polymorphism influences nicotine dependence risk differs in MS compared to depression, although not compared to a healthy population. In addition to angiotensin II, other potential ACE substrates, such as substance P and neurotensin, which also influence dopaminergic neurotransmission (and are proposed to be associated with MS), may deserve study in future