Browsing by Author "Jovic, Nebojsa (56367047200)"

Purpose: To get more insight into molecular mechanisms underlying oxidative stress and its role in different types of seizure, in this study, oxidative byproducts of proteins, lipids and DNA, as well as, antioxidant enzyme activities were studied in adult patients with epilepsy. Methods: Study was performed in 60 patients with epilepsy and in 25 healthy controls. Plasma protein reactive carbonyl derivatives (RCD) and protein thiol groups (P-SH), byproducts of oxidative protein damage, as well as antioxidant enzyme activities, superoxide dismutase (SOD) and glutathione peroxidase (GPX) were studied spectrophotometrically. Urinary 8-epi-prostaglandin F2α (8-epi-PGF2α) and 8-hydroxy-2′-deoxyguanosine (8-OHdG), representative byproducts of lipid and DNA oxidative damage, respectively, were determined by enzyme immunoassay. Results: RCD levels were significantly increased (p = 0.001), while P-SH content was decreased in patients with first seizure (p = 0.052) compared to controls, independently of the seizure type. Urinary 8-epi-PGF2α and 8-OHdG were significantly increased in patients with epilepsy (p = 0.001 and p = 0.001). Rise in 8-epi-PGF2α was more pronounced in patients with generalized tonic-clonic seizure (GTCS) compared to those with partial seizure (PS). Both SOD and GPX activity were significantly increased in epileptic patients compared to controls (p = 0.001 and p = 0.001), but only SOD activity was significantly higher in patients with GTCS than in those with PS. Conclusions: Data on enhanced protein, lipid and DNA oxidation, together with upregulated antioxidant enzyme activities, confirm the existence of systemic oxidative stress in patients with epilepsy. It might be speculated that post-translational modification to existing functional proteins, particularly alterations to ion channels, might be at least partially responsible for acute early changes in neuronal networks. © 2010 British Epilepsy Association.

Purpose: To get more insight into molecular mechanisms underlying oxidative stress and its role in different types of seizure, in this study, oxidative byproducts of proteins, lipids and DNA, as well as, antioxidant enzyme activities were studied in adult patients with epilepsy. Methods: Study was performed in 60 patients with epilepsy and in 25 healthy controls. Plasma protein reactive carbonyl derivatives (RCD) and protein thiol groups (P-SH), byproducts of oxidative protein damage, as well as antioxidant enzyme activities, superoxide dismutase (SOD) and glutathione peroxidase (GPX) were studied spectrophotometrically. Urinary 8-epi-prostaglandin F2α (8-epi-PGF2α) and 8-hydroxy-2′-deoxyguanosine (8-OHdG), representative byproducts of lipid and DNA oxidative damage, respectively, were determined by enzyme immunoassay. Results: RCD levels were significantly increased (p = 0.001), while P-SH content was decreased in patients with first seizure (p = 0.052) compared to controls, independently of the seizure type. Urinary 8-epi-PGF2α and 8-OHdG were significantly increased in patients with epilepsy (p = 0.001 and p = 0.001). Rise in 8-epi-PGF2α was more pronounced in patients with generalized tonic-clonic seizure (GTCS) compared to those with partial seizure (PS). Both SOD and GPX activity were significantly increased in epileptic patients compared to controls (p = 0.001 and p = 0.001), but only SOD activity was significantly higher in patients with GTCS than in those with PS. Conclusions: Data on enhanced protein, lipid and DNA oxidation, together with upregulated antioxidant enzyme activities, confirm the existence of systemic oxidative stress in patients with epilepsy. It might be speculated that post-translational modification to existing functional proteins, particularly alterations to ion channels, might be at least partially responsible for acute early changes in neuronal networks. © 2010 British Epilepsy Association.

Various inflammatory diseases of central nervous system, including subacute sclerosing panencephalitis, could cause epilepsia partialis continua. Two boys with epilepsia partialis continua with onset in terminal phase of atypical subacute sclerosing panencephalitis have been reported. Children were not vaccinated against measles, and the second case had history of measles at an early age. In both cases, the onset of subacute sclerosing panencephalitis was characterized by altered behavior and cognitive decline with very fast mental and neurological deterioration. One boy was suffering from complex partial seizures and myoclonic jerks synchronous with periodic electroencephalographic pattern. Diagnosis was proved by increased titers of antimeasles antibodies in both serum and cerebrospinal fluid. In terminal phase of the disease, epilepsia partialis continua of localized group of the muscles was diagnosed, with good response to intravenous infusion of midazolam. Surface electroencephalographic recordings during epilepsia partialis continua did not show the epileptic discharges. During the terminal phase of the disease, no other type of seizures and movement disorders were recognized, except epilepsia partialis continua. In spite of the treatment, period from the onset of disease to death lasted less than 3 months, suggesting very fulminant course of subacute sclerosing panencephalitis. © Springer-Verlag 2011.

The objective of the study was to evaluate etiology, clinical characteristics and outcome in children with epilepsia partialis continua (EPC).The investigation included 51 children with EPC aged 0.2-18 years treated in the period 1993-2009. The median period from the onset of underlying disorder to EPC was 6 months (0-72 months). EPC was caused by different pathologies: inflammatory and immune-mediated (52%), metabolic (13.7%), structural brain abnormalities (11.8%), cryptogenic (7.8%), vascular (5.9%), dual (5.9%), postoperative (2%). Median duration of EPC was 15 days (1-200 days). EPC involved more frequently the right side of the body comparing to the left one. The outcome was assessed at the end of the follow up period (mean 6.5 years, ranged 0.2-16 years). Unchanged neurological status was observed in 10 (19.6%) children, neurological consequences in 33 (64.7%) children and lethal outcome in 8 (15.7%) children.The most frequent etiology in our cohort was inflammatory and immune-mediated disease of central nerve system including Rasmussen's encephalitis. The duration of EPC was prolonged, most frequently involving the right upper limb. The outcome of EPC in children was unfavorable. © 2012 Elsevier B.V.

The objective of the study was to evaluate etiology, clinical characteristics and outcome in children with epilepsia partialis continua (EPC).The investigation included 51 children with EPC aged 0.2-18 years treated in the period 1993-2009. The median period from the onset of underlying disorder to EPC was 6 months (0-72 months). EPC was caused by different pathologies: inflammatory and immune-mediated (52%), metabolic (13.7%), structural brain abnormalities (11.8%), cryptogenic (7.8%), vascular (5.9%), dual (5.9%), postoperative (2%). Median duration of EPC was 15 days (1-200 days). EPC involved more frequently the right side of the body comparing to the left one. The outcome was assessed at the end of the follow up period (mean 6.5 years, ranged 0.2-16 years). Unchanged neurological status was observed in 10 (19.6%) children, neurological consequences in 33 (64.7%) children and lethal outcome in 8 (15.7%) children.The most frequent etiology in our cohort was inflammatory and immune-mediated disease of central nerve system including Rasmussen's encephalitis. The duration of EPC was prolonged, most frequently involving the right upper limb. The outcome of EPC in children was unfavorable. © 2012 Elsevier B.V.

Purpose Oxidative stress is recognized as an important factor in progressive myoclonus epilepsy (PME). Genetic polymorphism of glutathione S-transferases (GSTs), which are involved in both protection from oxidative damage and detoxification, might alter the capacity for protecting tissues from exogenous and endogenous oxidants. We aimed to assess a possible association between GST polymorphism and PME, as well as, correlation between GST genotypes and oxidative phenotype in PME patients. Methods GSTA1, GSTM1, GSTP1 and GSTT1 genotypes were determined in 26 patients with PME and 66 controls. Byproducts of protein oxidative damage (thiol groups (P-SH) and nitrotyrosine), superoxide dismutase (SOD) and glutathione peroxidase (GPX) activities were determined. Results The frequency of GSTA1, GSTM1 and GSTP1 genotypes was not significantly different between PME patients and controls, while individuals with GSTT1-null genotype were at 5.44-fold higher risk of PME than carriers of GSTT1-active genotype. Moreover, significant risk of PME was obtained in carriers of both GSTT1-null and GSTM1-null genotypes. Carriers of combined GSTA1- active and GSTT1-null genotype were at highest, 7.55-fold increased risk of PME. Byproducts of protein damage did not reach statistical significance, while SOD and GPX activities were significantly higher in PME patients then in controls. When stratified according to GST genotype, P-SH groups were significantly lower only in patients with GSTT1-null genotype in comparison to carriers of active genotype. Only SOD activity was increased in GSTT1-null when compared to corresponding active genotype. Conclusions GSTT1-null genotype might be associated with the increased risk and enhanced susceptibility to oxidative stress in PME patients. © 2015 British Epilepsy Association. Published by Elsevier Ltd. All rights reserved.

Purpose Oxidative stress is recognized as an important factor in progressive myoclonus epilepsy (PME). Genetic polymorphism of glutathione S-transferases (GSTs), which are involved in both protection from oxidative damage and detoxification, might alter the capacity for protecting tissues from exogenous and endogenous oxidants. We aimed to assess a possible association between GST polymorphism and PME, as well as, correlation between GST genotypes and oxidative phenotype in PME patients. Methods GSTA1, GSTM1, GSTP1 and GSTT1 genotypes were determined in 26 patients with PME and 66 controls. Byproducts of protein oxidative damage (thiol groups (P-SH) and nitrotyrosine), superoxide dismutase (SOD) and glutathione peroxidase (GPX) activities were determined. Results The frequency of GSTA1, GSTM1 and GSTP1 genotypes was not significantly different between PME patients and controls, while individuals with GSTT1-null genotype were at 5.44-fold higher risk of PME than carriers of GSTT1-active genotype. Moreover, significant risk of PME was obtained in carriers of both GSTT1-null and GSTM1-null genotypes. Carriers of combined GSTA1- active and GSTT1-null genotype were at highest, 7.55-fold increased risk of PME. Byproducts of protein damage did not reach statistical significance, while SOD and GPX activities were significantly higher in PME patients then in controls. When stratified according to GST genotype, P-SH groups were significantly lower only in patients with GSTT1-null genotype in comparison to carriers of active genotype. Only SOD activity was increased in GSTT1-null when compared to corresponding active genotype. Conclusions GSTT1-null genotype might be associated with the increased risk and enhanced susceptibility to oxidative stress in PME patients. © 2015 British Epilepsy Association. Published by Elsevier Ltd. All rights reserved.

During routine examination of a patient with posttraumatic stress disorder, a large cavum septi pellucidi was noted on CT scan. Cava septi pellucidi were seldom reported as a finding in posttraumatic stress disorders. In our opinion, large cava are only the marks of the brain susceptibility for various neuropsychiatric diseases and disorders. © neuroanatomy.org.

Purpose: Evaluation of the etiology, clinical characteristics and outcome of the first status epilepticus (fSE) event in children. Method: The patients with fSE hospitalized in our Institute from 1995 to 2011 were included. The etiology was characterized as either known (symptomatic) or unknown (cryptogenic). Outcome was assessed at the end of hospitalization. Logistic regression analyses were used to assess predictors of the outcome, with odds ratio adjusted by age as a measure effect. Results: The study included 236 patients with a median age of 2.0 years (IQR 4.0). Etiology was identified as secondary to: defined electroclinical syndromes 108 (45.8), acute symptomatic conditions 63 (26.7%), unknown 24 (10.1%), progressive encephalopathy 23 (9.7%), or remote symptomatic 18 (7.6%). Recurrence rate was 16.9%, neurological consequences were in 24.6% and case-fatality ratio was 4.7%. The main predictors were for: a) death – progressive encephalopathy (OR = 14.68, 95% CI 4.06–23.11. p = 0.001); b) neurological sequelae – acute symtomatic (OR 3.44, 95% CI 4.82–6.47) p = 0.001, remote symptomatic (OR = 13.84, 95% CI 4.34–44.12. p = 0.001), progressive encephalopathy (OR = 3.94, 95% CI 1.64–9.56. p = 0.002), seizure duration >60 min (OR = 0.44, 95% CI 0.24–0.81. p = 0.001); c) seziure recurrence – acute symptomatic etiology (OR = 3.59, 95% CI 41.76–7.21. p = 0.001), seizure duration >60 min (OR = 0.30, 95% CI 0.15–0.61. p = 0.001). Conclusions: In children with fSE, exploring acute disorders and immediate etiological treatment is essential. The outcome of fSE is favorable concerning the recurrence rate, while neurological sequelae are seen in one quarter of the patients. The etiology and fSE duration are the main determinants of outcome. © 2018 British Epilepsy Association

Purpose: Evaluation of the etiology, clinical characteristics and outcome of the first status epilepticus (fSE) event in children. Method: The patients with fSE hospitalized in our Institute from 1995 to 2011 were included. The etiology was characterized as either known (symptomatic) or unknown (cryptogenic). Outcome was assessed at the end of hospitalization. Logistic regression analyses were used to assess predictors of the outcome, with odds ratio adjusted by age as a measure effect. Results: The study included 236 patients with a median age of 2.0 years (IQR 4.0). Etiology was identified as secondary to: defined electroclinical syndromes 108 (45.8), acute symptomatic conditions 63 (26.7%), unknown 24 (10.1%), progressive encephalopathy 23 (9.7%), or remote symptomatic 18 (7.6%). Recurrence rate was 16.9%, neurological consequences were in 24.6% and case-fatality ratio was 4.7%. The main predictors were for: a) death – progressive encephalopathy (OR = 14.68, 95% CI 4.06–23.11. p = 0.001); b) neurological sequelae – acute symtomatic (OR 3.44, 95% CI 4.82–6.47) p = 0.001, remote symptomatic (OR = 13.84, 95% CI 4.34–44.12. p = 0.001), progressive encephalopathy (OR = 3.94, 95% CI 1.64–9.56. p = 0.002), seizure duration >60 min (OR = 0.44, 95% CI 0.24–0.81. p = 0.001); c) seziure recurrence – acute symptomatic etiology (OR = 3.59, 95% CI 41.76–7.21. p = 0.001), seizure duration >60 min (OR = 0.30, 95% CI 0.15–0.61. p = 0.001). Conclusions: In children with fSE, exploring acute disorders and immediate etiological treatment is essential. The outcome of fSE is favorable concerning the recurrence rate, while neurological sequelae are seen in one quarter of the patients. The etiology and fSE duration are the main determinants of outcome. © 2018 British Epilepsy Association

Purpose: The aim of the study was to evaluate the outcome of status epilepticus (SE) in children and to define predictors for morbidity, mortality, and SE recurrence. Methods: The study included 302 children (age 2 months to less than 18 years; mean age ± SD 4.7 ± 4.2 years) with 489 episodes of SE. Etiology, treatment, and clinical and electroencephalography (EEG) features of SE and their impact on the outcome were analyzed. The outcome was classified into three categories: unchanged neurologic status, neurologic consequences, and lethal outcome. Univariate and multivariate Cox hazard regression analyses were used to define predictors of mortality, morbidity, and SE recurrence. Key Findings: Neurologic status was unchanged in 235 children (77.8%) and neurologic consequences occurred in 39 patients (12.9%); case-fatality ratio was 9.3% and recurrence rate was 21%. Mortality was related to progressive encephalopathy, preexisting neurologic abnormalities, specific EEG findings, and generalized convulsive type of SE. Neurologic consequences were associated with younger age, progressive encephalopathy, duration of SE >24 h, prior epilepsy, and specific EEG findings. Multivariate analyses showed that etiology of SE and prior neurologic abnormalities were independent predictors of mortality, whereas younger age, etiology, and very long duration of SE were predictors of morbidity. Significance: Outcome of SE in children is favorable in most of the cases, but mortality and morbidity rates are still high. Etiology and prior neurologic abnormalities were the main predictors of mortality, whereas the main predictor of morbidity was underlying etiology. © 2011 International League Against Epilepsy.

Purpose: The aim of the study was to evaluate the outcome of status epilepticus (SE) in children and to define predictors for morbidity, mortality, and SE recurrence. Methods: The study included 302 children (age 2 months to less than 18 years; mean age ± SD 4.7 ± 4.2 years) with 489 episodes of SE. Etiology, treatment, and clinical and electroencephalography (EEG) features of SE and their impact on the outcome were analyzed. The outcome was classified into three categories: unchanged neurologic status, neurologic consequences, and lethal outcome. Univariate and multivariate Cox hazard regression analyses were used to define predictors of mortality, morbidity, and SE recurrence. Key Findings: Neurologic status was unchanged in 235 children (77.8%) and neurologic consequences occurred in 39 patients (12.9%); case-fatality ratio was 9.3% and recurrence rate was 21%. Mortality was related to progressive encephalopathy, preexisting neurologic abnormalities, specific EEG findings, and generalized convulsive type of SE. Neurologic consequences were associated with younger age, progressive encephalopathy, duration of SE >24 h, prior epilepsy, and specific EEG findings. Multivariate analyses showed that etiology of SE and prior neurologic abnormalities were independent predictors of mortality, whereas younger age, etiology, and very long duration of SE were predictors of morbidity. Significance: Outcome of SE in children is favorable in most of the cases, but mortality and morbidity rates are still high. Etiology and prior neurologic abnormalities were the main predictors of mortality, whereas the main predictor of morbidity was underlying etiology. © 2011 International League Against Epilepsy.

AIM: Purpose of the study was to recognize specific migraine triggers in adolescents. MATERIAL AND METHODS: Study was conducted on 20,917 adolescents in Serbia. RESULTS: Lack of sleep, passive tobacco smoking, alcohol intakes, and “not eating in time” are triggers that provoke migraine in adolescents. CONCLUSION: Avoiding migraine triggers in 68% of adolescents reduced drug therapy for 75%. © 2014 Knezevic-Pogancev et al.

Objective: To determine the risk of recurrence of ischemic stroke in children and to evaluate the influence of etiological factors and underlying mechanisms on recurrence rate. Subjects and Methods: Thirty-six children (21 boys and 15 girls) with clinically and radiographically proven ischemic cerebral infarction were prospectively followed up over a period of 1-9 years (median 5 years 5 months). The median age of onset of stroke was 8.4 years (1-16 years). Patients with hemorrhagic stroke, neonatal infarction and sinovenous thrombosis were not included. The patients were analyzed according to the mechanisms and etiology of the initial and recurrent stroke event. Results: For the initial stroke, cardioembolic (33.3%) and arteriopathic processes (36.1%) were identified as the most probable mechanisms of arterial ischemic stroke. Prothrombotic abnormalities were found in 4 children (11.1%). Underlying pathology in the remaining 7 (19.4%) was not known. Recurrent ischemic infarction was diagnosed in 5 children (13.9%) within 5 days to 18 months (median 6 months) after the first stroke manifestation. In 3 of them stroke recurrence was due to cardiac or transcardiac embolism. Cardiac abnormality prior to the first stroke was detected in 1 child. Clinically silent multiple cerebral infarcts disclosed by MRI preceded the overt stroke episode in 2 patients. Conclusion: Congenital and acquired heart diseases were the most common cause of repeated stroke in our study. The risk of recurrence appeared to be fivefold higher in children with cardiac disease irrespective of the coexistence of other risk factors. The risk factors of stroke in children were multiple and overlapping. Consequently, recognition of the major one and its underlying mechanism is crucial for both effective therapeutic approach and the prevention of recurrence. Copyright © 2004 S. Karger AG, Basel.