Cerebral palsy (CP) is one of the most frequent causes of motor disability in children. According to the up-to-date definition, CP is a group of permanent disorders of the development of movement and posture, causing activity limitations that are attributed to non-progressive disturbances that occurred in the developing foetal or infant brain. The CP definition has evolved over time; the problem is aetiologically and clinically very heterogeneous. According to European data, the average frequency of CP is 2.08 per 1000 live births, but in the group of children born with a body weight below 1500 g, the frequency is 70 times higher when compared with the group of children with a body weight over 2500 g at birth. The risk factors for CP can be divided into pre-conception, prenatal, perinatal and postnatal ones. CP commonly co-exists with epilepsy, in particular drug-resistant epilepsy, but also with mental retardation, visual and hearing impairment, as well as feeding and behavioral disorders. The degree of motor problem varies from mild to very severe making the child totally dependent on caregivers. Cerebral palsy is divided into forms depending on the type of motor disorders which dominate the clinical presentation; the traditional classifications by Ingram and Hagberg have now been replaced by the Surveillance of Cerebral Palsy in Europe classification which divides CP into spastic, dyskinetic and ataxic forms. Although cerebral palsy is a clinical diagnosis, modern diagnostic imaging provides information that allows the division of the results of magnetic resonance imaging in children with cerebral palsy into five groups according to the magnetic resonance imaging classification system. Just as the clinical presentation and the factors predisposing for CP are very diverse, treatment is also a very complex problem. Modern treatment of spasticity includes both botulinum toxin therapies and surgical techniques, eg, rhizotomy. The authors present current views on definitions, risk factors, diagnostics and treatment of CP as well as comorbid problems, eg, drug-resistant epilepsy.
OIon behalf of the International Pediatric Stroke Study Investigators
on behalf of the International Pediatric Stroke Study Investigators
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OBJECTIVES: Cerebrovascular disease is among the top 10 causes of death in US children, but risk factors for mortality are poorly understood. Within an international registry, we identify predictors of in-hospital mortality after pediatric arterial ischemic stroke (AIS). METHODS: Neonates (0–28 days) and children (29 days–<19 years) with AIS were enrolled from January 2003 to July 2014 in a multinational stroke registry. Death during hospitalization and cause of death were ascertained from medical records. Logistic regression was used to analyze associations between risk factors and in-hospital mortality. RESULTS: Fourteen of 915 neonates (1.5%) and 70 of 2273 children (3.1%) died during hospitalization. Of 48 cases with reported causes of death, 31 (64.6%) were stroke-related, with remaining deaths attributed to medical disease. In multivariable analysis, congenital heart disease (odds ratio [OR]: 3.88; 95% confidence interval [CI]: 1.23–12.29; P = .021), posterior plus anterior circulation stroke (OR: 5.36; 95% CI: 1.70–16.85; P = .004), and stroke presentation without seizures (OR: 3.95; 95% CI: 1.26–12.37; P = .019) were associated with in-hospital mortality for neonates. Hispanic ethnicity (OR: 3.12; 95% CI: 1.56–6.24; P = .001), congenital heart disease (OR: 3.14; 95% CI: 1.75–5.61; P < .001), and posterior plus anterior circulation stroke (OR: 2.71; 95% CI: 1.40–5.25; P = .003) were associated with in-hospital mortality for children. CONCLUSIONS: In-hospital mortality occurred in 2.6% of pediatric AIS cases. Most deaths were attributable to stroke. Risk factors for in-hospital mortality included congenital heart disease and posterior plus anterior circulation stroke. Presentation without seizures and Hispanic ethnicity were also associated with mortality for neonates and children, respectively. Awareness and study of risk factors for mortality represent opportunities to increase survival.
Cerebral palsy (CP) is a set of etiologically diverse symptoms that change with the child’s age. It is one of the most frequent causes of motor disability in children. CP occurs at a frequency of 1.5 to 3.0 per 1000 live-born children. CP often coexists with epilepsy, which is drug-resistant in a high number of cases. The aim of the present study was to analyze the associations between preconception, prenatal, perinatal, neonatal, and infancy risk factors for epilepsy in a group of pediatric patients with CP. We retrospectively analyzed 181 children with CP (aged 4–17 years at diagnosis), hospitalized at the Department of Pediatrics and Developmental Age Neurology in Katowice in the years 2008–2016. Division into particular types of CP was based on Ingram’s classification. Data were analyzed using STATISTICA 13.0 (STATSOFT; Statistica, Tulsa, OK, USA). Epilepsy was diagnosed in 102 children (56.35%), of whom 44 (43%) had drug-resistant epilepsy; only in 15 cases (14.71%) was epilepsy susceptible to treatment. The incidence of epilepsy varied between the types of CP. It occurred significantly more often in children with tetraplegia (75%), ataxic form (83%), and mixed form (80%) in comparison to diplegia (32%) and hemiplegia (38%). Maternal hypertension was found to be a risk factor for epilepsy in CP patients (OR = 12.46, p < 0.001) as well as for drug-resistant epilepsy (the odds ratio (OR) = 9.86, p = 0.040). Delivery by cesarean section increased the risk of epilepsy in the CP patients over two-fold (OR = 2.17, p = 0.012). We observed also that neonatal convulsions significantly increased the risk for epilepsy (OR = 3.04, p = 0.011) as well as drug-resistant epilepsy (OR = 4.02, p = 0.002). In conclusion, maternal hypertension, neonatal convulsions, and delivery by cesarean section were the most important factors increasing the risk of epilepsy as well as drug-resistant epilepsy in the analyzed group of patients with CP.
Arterial ischemic stroke (AIS) experienced at a young age is undoubtedly a serious medical problem. AIS very rarely occurs at a developmental age, whereas in young adults, it occurs with a higher frequency. The etiologic mechanisms of AIS occurring in childhood and adulthood differ. However, for both age populations, neurological consequences of AIS, including post-stroke seizures, motor disability, and recurrence of the disease, are connected to many years of care, rehabilitation, and treatment. Recurrent stroke was observed to increase the risk of patients’ mortality. One of the confirmed risk factors for recurrent stroke in children is the presence of vasculopathies, especially Moyamoya disease and syndrome, and focal cerebral arteriopathy of childhood (FCA). FCA causes a 5-fold increase in the risk of recurrent stroke in comparison with idiopathic AIS. In turn, young adults with recurrent stroke were found to more often suffer from hypertension, diabetes mellitus, or peripheral artery disease than young patients with first-ever stroke. Some reports also indicate relationships between specific genetic polymorphisms and AIS recurrence in both age groups. The aim of the present literature review was to discuss available data regarding the risk factors for recurrent AIS in children and young adults.
The 677C>T polymorphism within methylenetetrahydrofolate reductase (MTHFR) gene is related to an elevated level of homocysteine. Thus it may be considered as a genetic risk factor in ischemic stroke. Apparently studies of this type of polymorphism in childhood stroke have shown conflicting results. We performed meta-analysis of all the data that are available in relation with MTHFR polymorphism and the risk of ischemic stroke in children. We searched PubMed (last search dated December 2010) using “MTHFR polymorphism”, “ischemic stroke” “child”, “children”, “pediatric stroke” as keywords and reference lists of studies and reviews on the topic. Finally, 15 case–control studies corresponded to the inclusion criteria for meta-analysis. These studies involved the total number of 822 children and adolescents after ischemic stroke and 1,552 control subjects. Fixed or random effects models were used depending on the heterogeneity between the studies. The association between ischemic stroke and 677C>T polymorphism within MTHFR gene was observed in three of the studies. The pooled analysis showed that TT genotype of MTHFR gene is more common in stroke patients than in controls (p = 0.0402, odds ratio = 1.57, 95 % confidence interval 1.02–2.41). The Egger’s test did not reveal presence of a publication bias. The results based on a sizeable group of cases and controls have proved that the 677C>T polymorphism in MTHFR gene is associated with the development of ischemic stroke in children.