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childhood stroke, participated in the study. Population-based control-group for perinatal stroke consisted of 150 and for childhood stroke of 84 healthy individuals. DNA testing for MTHFR C677T and A1298C mutations was performed, genotypes were determined by PCR using specific primers. Association analysis (p-values with Fisher exact test, odds ratios with 95% confidence intervals) was performed using Terminal software. Results: The 677T allele carrier status (p=0.9, OR=1.0) did not show relevance as a genetic risk factor for perinatal stroke. An interesting observation was the fact that minor allele frequency of A1298C was higher in healthy controls than in patients with either perinatal (p=0.08, OR=0.63) or childhood (p=0.14, OR=0.6) AIS. On the other hand, minor allele frequency of C677T demonstrated a weak association with childhood AIS (p=0.09, OR=1.7, 95% CI: 0.9– 3.2). Conclusion: Our data support the hypothesis that functional MTHFR polymorphism C677T may represent a genetic risk factor for childhood AIS, representing 1.7-times higher risk. The A1298C polymorphism was not found as genetic risk factor for perinatal nor for childhood stroke.
P203 - 2949 Seizures persistence’s prognosis in children with arterial ischemic stroke L. Shalkevich, O. Lvova, M. Lukashchuk, A. Dolmatova, A. Kudlatch. Department of Pediatric Neurology, Belarusian Medical Academy of Post-Graduate Education, Minsk, Belarus Objective: To investigate clinical and electroencephalographic features of seizures during acute and recovery periods of arterial ischemic stroke (AIS) in children. Methods: Type of study: case series. Inclusion criteria: Children 0–15 y.o. with seizures during AIS’s debut. We identified the type of episodes and EEG features in acute and recovery periods after one year. Results: 152 children with AIS were examined. Seizures occurred during the acute period of stroke in 39 (25.7%) cases and antiepileptic therapy was prescribed for all of them. Generalized seizures type was registered in 56.4% (n=22), focal type in 23% (n=9), focal type with secondary generalization – in 20.6% (n=8) children. Epileptiform activity was registered in 31% (n=9) patients. Disorganized changes on background EEG without signs of paroxysmal activity were predominant in most children – 75.9% (n=22) as well as background activity was normal only in 13.8% (n=4) of them. In the recovery period seizures persisted in 10.5% (n=16). Generalized seizures of acute period pass to recovery period in 27.2% (n=6, RR=0.56 95%CI 0.3–1.0), and focal seizures with secondary generalization – in 75% (n=6, RR=2.75 95%CI 1.2–6.0). Seizures accompanied by epileptiform activity on EEG during acute period persisted in the recovery period in 55.6% (n=5, RR=2.7 95%CI 1.1– 6.1), without activity – in 30% (n=9, RR=0.5 95%CI 0.2–1.1). At the same time generalized seizures of acute period combined with epileptiform activity on EEG persist in recovery period in 50% (n=2, RR=2.2 95%CI 0.6–8.3), without it – in 22.2% (n=4, RR=0.6 95%CI 0.2–1.7). Conclusion: The presence of epileptiform activity on EEG and the development of focal with secondary generalization seizures type in children with AIS and seizures in the acute period increase the risk of seizure persistence in the recovery period in spite of antiepileptic therapy have been prescribed.
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31 had hemorrhagic stroke). The patients were between infants to 14 years old. We were observation all patients along year. 5 children (6.41%) were died: 2 children after IS, 3 – after HS. Since one year 21 patients (28.77%) were healthy and 52 (71.23%) had outcomes symptoms (motor abnormalities, epilepsy, mental retardation (include speech and cognitive problems)). 44 children (60.27%) had problems with motor function, 27 (36.99%) – seizures, 34 (46.57%) – mental retardation. 18 patients (24.66%) had one outcome symptom, 15 children (20.55%) – had two symptoms, 19 patients (26.02%) – had three symptoms together. Results: Children with motor abnormalities since one year in the acute period had hemoglobin 104.70±2.66 g/l, the average level of hemoglobin in group without motor problems in future was 114.60±4.11 g/l (p<0.05). In the group of children who had seizers since one year level of hemoglobin in acute period was 101.52±3.5 g/l to compared with group of children without seizers – 112.83±2.95 g/l (p<0.05). Patients who had mental retardation since one year in the acute period of stroke had hemoglobin 96.71±2.59 g/l and children without mental problem in future had 119.05±2.87 g/l in the acute period (p<0.05). Conclusion: Children who had outcome symptoms since one year after stroke had a lower hemoglobin level in the acute period than children without neurological problems in future.
P205 - 2992 Dyslipidemia as the possible risk factor for arterial ischemic stroke in children O. Lvova, I. Gavrilov, I. Astryuhina, E. Orlova, O. Kenzina, Y. Kuznetsov. Child Neurology Unit, Clinic Paediatric City Hospital 9, Departament of Clinical Psychology and Psychophysiology, Ural Federal University, Yekaterinburg, Russia Background: Arterial Ischemic Stroke (AIS) in children is very rare and can be caused by huge number of diseases. Dyslipidemia seems to be the risk factors of AIS in children. But interaction between dyslipidemia and pediatric AIS is not investigated thoroughly. Objective: To investigate the incidence and the possible variants of dyslipidemias in children with Arterial Ischemic Stroke (AIS). Methods: Type of study: case series. Inclusion criteria: 76 boys or girls under the age of 15 y.o. with AIS’s debut and confirmed by brain CT (MRI) scan; slavic origin; informed consent form. We identified cholesterol level in 76; HDL, Triglycerides in 37; LDL, VLDL in 32 children (mmol/l was the unit for all data) and KA in AIS acute period (during first 3 days). Results: We found dyslipidemias in more than quarter cases. The average level for exceeding indicators were: triglycerides 2.5±0.21 (n=10), cholesterol 5.62±0.11 (n=20), LDL 3.55±0.2 (n=6), VLDL 1.29±0.12 (n=6), KA 3.9±0.2 (n=19). The low level of HDL was in 15 cases (0.75±0.05). In 24 cases we identified isolated hypo-α-cholesterolemia, in 18 – IIa Fredrickson phenotype, in 6 – IV and in 2 patients IIb Fredrickson phenotype. Conclusion: We assume dyslipidemias to have the diagnostic value in early life stroke’s debut. The maximum possible set of lipid and lipoproteins must be assigned and the reason of dyslipidemias has to be investigated. Detection of dyslipidemia may become a starting point for therapy and secondary prevention in those patients.
P206 - 2993 P204 - 2990 Correlations between hemoglobin level in the debut of pediatric stroke and outcome since one year N. Smulska. Neurology Department, Pediatric Hospital 1, Kiev, Ukraine Objective: We were analyses associated with level of hemoglobin in the debut of pediatric stroke and presence outcome symptoms since one year after acute stroke. Methods: The main group include 78 children with stroke (47 children had ischemic stroke,
Outcome after pediatric stroke: Investigation genes polymorphism N. Smulska. Neurology Department, Pediatric Hospital 1, Kiev, Ukraine Objective: We were analyses associated with genes polymorphism and presence outcome symptoms since one year after acute stroke. Methods: 78 children with stroke (47 children had ischemic stroke, 31 had hemorrhagic stroke) had genetic investigation (we were tasting polymorphism of six genes: MTHFR
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C677T, MTHFR A1298C, MTRR, FV, FII, ACE I/D). The patients were between infants to 14 years old. We were observation all patients along year. 5 children (6.41%) were died. Since one year 21 patients (28.77%) were healthy and 52 (71.23%) had outcome symptoms (motor abnormalities, epilepsy, mental retardation (include speech and cognitive problems)). 44 children (60.27%) had problems with motor function, 27 (36.99%) – seizures, 34 (46.57%) – mental retardation. Results of investigation were expressed as pooled odds ratios (OD) and χ2 in children with or without outcome since one year after stroke. Statically was the results p<0.05. Results: In group of children with motor abnormalities since one year we had more frequently mutation 1298AC of MTHFR gene – 54.55%, without motor problems this mutation was in 31.03% cases (χ2 =3.90, p=0.048, OR=2.67, 95% CI: 1.00– 7.14). 1298AA polymorphism of MTHFR gene had a protective effect about motor dysfunctions (χ2 =4.21, p=0.040, OR=0.36, 95% CI: 0.13–0.97). Presence 1298AA polymorphism of MTHFR gene in group of seizers outcome had also protective effect – 18.52% children with seizers since one year had 1298AA polymorphism and in 43.48% cases without seizers had the same genotype (χ2 =4.71, p=0.03, OR=0.30 95% CI: 0.10–0.92). In group of mental retardation we had frequently mutation 1298AC of MTHFR gene – 52, 94%, but we had not statistically difference compare of group without mental retardation (38.46%). We had not statistically difference among other genes. Conclusion: Children with or without outcome symptoms since one year after stroke could have different genotypes.
19s (2015) S1 – S152
P207 - 3052 Brain T2-weighted signal intensity ratio in children with sickle cell disease with and without stroke J. McSwiggan, J. Collinson, R. Bhadresha, C. Nielsen, A. Darekar, F. Kirkham. UCL Institute of Child Health Objective: Iron is paramagnetic, accumulates with age, is higher in the deep gray matter in neurodegeneration and if increased in tissues, shortens MRI T1 and T2. There are few data in children with sickle cell disease (SCD). Our aims were to measure T2-weighted signal intensity ratio (T2SIR), a ratio comparing regional T2 with CSF T2, as a proxy for brain iron status in children with SCD and controls and to compare T2SIR with serum Ferritin. Methods: Using ImageJ, 2 masked observers (coefficient variation <5%) measured T2 in regions of interest from archived 1.5T MRI data (Siemens Vision; TR=3.458 ms, TE=96 ms) in controls and children with haemoglobin (Hb) SS and SC and generated T2SIR and Pearson correlations with serum ferritin. Controls (n=23) and children with HbSC (HbSC) or HbSS with no (HbSS-NL), covert (HbSS-CL, n=17) or overt (HbSS-OL; n=5) lesions were compared (one way analysis of variance; post hoc Dunnett’s test). Results: Serum ferritin significantly correlated (p<0.05) with T2SIR in right (R) and left (L) caudate and putamen. Compared with controls, T2SIR for R/L caudate, R putamen, R/L globus pallidus, and R/L red nucleus was lower in HbSS-OL (p<0.01) and in R/L globus pallidus and R/L red nucleus in HbSS-CL (p<0.05) Discussion: The significant correlations with serum Ferritin suggest that T2SIR is a proxy measure of brain iron. Reasons for brain iron accumulation in SCD include regular blood transfusions and neurodegeneration, perhaps related to hypoxic exposure. Studies quantitating and comparing brain and liver iron measurements are warranted.