Neonatal Convulsions Research Articles

معدل انتشار تشنجات حديثي الولادة في الأطفال اليمنيين - دراسة معتمدة على المستشفى.

الخلفية: التشنج هو مشكلة عصبية مشتركة في الأطفال الصغار، ينظر أساسا في فترة حديثي الولادة. وكانت تشنجات حديثي الولادة دائما موضوع اهتمام بسبب حدوثها العالمي. ويساهم بشكل كبير في اعتلال المواليد والوفيات وخاصة في البلدان النامية بما في ذلك اليمن. وهناك عدد متنوع من الظروف تكون قادرة على التسبب في النوبات في فترة الوليد. الأهداف : دراسة لتحديد نمط، حدوث ونتائج التشنجات لحديثي الولادة. التصميم : دراسة وصفية مستقبلية. الإعداد : وحدة طب الأطفال، مستشفى السلام، صعدة، اليمن. إطار الحالة: جميع الأطفال حديثي الولادة الملاحظ عليهم التشنجات أثناء رقودهم في المستشفى بين يوليو 2013 - أغسطس 2015 . الطريقة: أجريت دراسة مراقبة مستقبلية مستندة إلى المستشفى في وحدة طب الأطفال مستشفى السلام على مدى عامين (يوليو 2013 - أغسطس 2015)، تم قبول جميع الولدان أقل من 28 يوماً من العمر مع مراقبة الحركات الغير طبيعية (التشنجات) في هذه الوحدة. تم أخذ تاريخ مفصل لفترة ما قبل الولادة والولادة وبعد الولادة وفحص الطفل. ثم أجريت تحقيقات ذات صلة بما في ذلك الفحوصات الكيميائية الحيوية. تم تحليل البيانات باستخدام جهاز نظام الإحصاء لنظام التشغيل ويندوز الإصدار10 . النتائج: بينت النتائج أن من بين 1732 من الأطفال المرقدين حديثي الولادة، كان 62.6 في المائة من الذكور و 37.4 في المائة من الإناث. وكانت نسبة معدل حدوث نوبات التشنج للولدان في هذه الوحدة 68 لكل 1000حالة رقود ومن أصل 1732 رقود لحديثي الولادة، 118 (6.8٪) كانت لديهم تشنجات. ومن بين هؤلاء 86 (72.9٪) قد ولدوا خارج المستشفى .كان معدل إصابة الأطفال حديثي الولادة في وحدة طب الأطفال بمستشفى السلام بالتشنجات كان لديهم وزن أعلى مقارنه بالمواليد من غير تشنجات ، ومن أصل 118 مولود مع تشنجات كانت 74 (62.7٪) اعتبر لديهم الاختناق الوليدي، 14 (11.9٪) التهاب السحايا، 12 (10.2٪) نقص السكر في الدم، 4 (3.4٪) نقص عنصر الكالسيوم في الدم و 14 (11.9٪) أسباب غير مشخصة. وكان من بين 118 مولود 84 (71.2٪) لديهم تشنجات دقيقة وعامة. وقد توفي 54 مولود مع تشنجات (45.8٪) مقارنة مع 262 من 1614 طفل دون تشنجات (16.2٪). وكان المواليد مع التشنجات والاختناق الوليدي أو من المواليد خارج المستشفى كانت لديهم مخاطر الموت أعلى (59.5٪ و 48.8٪) على التوالي. الاستنتاج: اختناق الولادة كان السبب الرئيسي للأطفال الذين يعانون من التشنجات. وجميع التشنجات في ال 24 ساعة الأولى من الحياة كانت مصاحبة للاختناق الوليدي. وكانت التشنجات المتبوعة للعدوى تميل إلى أن تحدث في أي عمر بعد 24 ساعة من الحياة. وبالعرض الرئيسي للأطفال مع التشنجات كانت تلك التشنجات دقيقة وعامة. وكانت نسبة ارتفاع معدل الوفيات بين الأطفال المواليد خارج المستشفى أعلى من المواليد بداخل المستشفى.

Peripartum events associated with severe neurologic morbidity and mortality among acidemic neonates.

To identify peripartum events that may predict the development of short-term neurologic morbidity and mortality among acidemic neonates. Retrospective case-control study conducted at a single-teaching hospital on data from January 2010 to December 2015. The study cohort group included all acidemic neonates (cord artery pH≤7.1) born at≥34weeks. Primary outcome was a composite including any of the following: neonatal encephalopathy, convulsions, intra-ventricular hemorrhage, or neonatal death. The study cohort was divided to the cases group, i.e., acidemic neonates who had any component of the primary outcome, and a control group, i.e., acidemic neonates who did not experience any component of the primary outcome. Of all 24,311 neonates born≥34weeks during the study period, 568 (2.3%) had a cord artery pH≤7.1 and composed the cohort study group. Twenty-one (3.7%) neonates composed the cases group. Multivariate logistic regression analysis revealed that cases were significantly more likely to have experienced placental abruption (OR 18.78; 95% CI 5.57-63.26), born≤2500g (OR 13.58; 95% CI 3.70-49.90), have meconium (OR 3.80; 95% CI 1.20-11.98) and cord entanglement (OR 5.99; 95% CI 1.79-20.06). The probability for developing the composite outcome rose from 3.7% with isolated acidemia to 97% among neonates who had all these peripartum events combined with intrapartum fetal heart rate tracing category 2 or 3. Neonatal acidemia carries a favorable outcome in the vast majority of cases. In association with particular antenatal and intrapartum events, the short-term outcome may be unfavorable.

Current Overview of Neonatal Convulsions.

Neonatal convulsions are one of the most common emergency neurological events in the early period after birth. The frequency has been reported to be 1.5 to 3 in 1000 live births. It has been established that the convulsion threshold is lower in infants due to immature neonatal neurons and differences in neurotransmitters. Hypoxic ischemic encephalopathy is the most common etiology in neonatal convulsions. Other causes vary, and may be related to the level of development of the country. Convulsions are classified into 4 different types according to the clinical findings. The most common is the subtle (undefined) type of seizure; the other types are defined as clonic, tonic, and myoclonic seizures. Non-epileptic paroxysmal movements frequently seen in the neonatal period, should not be confused with seizures. The most common non-epileptic paroxysmal movements are jitteriness, benign neonatal sleep myoclonus, and hyperekplexia. A newborn that experiences convulsions should be hospitalized and monitored with continuous video electroencephalogram, if possible. If an initial rapid evaluation detects an acute metabolic disorder, treatment is provided, and, if warranted, it will be followed by a plan for further treatment with anticonvulsant drugs. Phenobarbital is still currently recommended as first-line therapy, though there are studies of other anticonvulsant drugs. Levetiracetam and phenytoin are commonly used as second-step anticonvulsant drugs. The aim of treatment should be not only to stop acute symptomatic seizures, but also to reduce the risk of brain damage and to minimize the possible negative effects of epilepsy and neurological deficits.

A Study of Magnesium Levels in Neonatal Convulsions

A Study of Magnesium Levels in Neonatal Convulsions

A Review on Pharmacokinetics of Levetiracetam in Neonates.

Neonatal seizures are the most common clinical manifestation of Central Nervous System (CNS) dysfunction and are associated with various neurological sequelae. There are currently no evidence-based guidelines for the management of neonatal seizures and currently used drugs such as phenobarbital, and phenytoin have limited efficacy and potential toxicities. Newer second line anticonvulsant, levetiracetam, has been used in refractory neonatal seizures despite limited data and off-label use. In this review, we will discuss various pharmacological properties of levetiracetam when used in neonatal population. A PubMed search for MEDLINE was undertaken to look for studies using the terms "Levetiracetam", AND "Neonates" as key words from year 1995 to January 2017. Relevant articles were selected and information was extracted about pharmacokinetics, pharmacodynamics and clinical uses of levetiracetam in neonates. Levetiracetam is an active, water-soluble S-enantiomer of racemic pyrrolidine acetamide which exerts its antiepileptic action by binding to the synaptic vesicle protein within the brain. Metabolism of levetiracetam does not include the CYP P450 system and it is mainly eliminated through kidneys after rapid absorption. Also, no significant interactions with other drugs have been identified. Unlike other commonly used antiepileptic drugs, levetiracetam is not bound to plasma proteins, thereby, reducing the chances of toxicity and severe, life threatening side effects have not been reported. In fact, it has been shown to prevent neuro-degeneration after hypoxia/ischemia in rodent models of epilepsy. Levetiracetam has been emerging as a potential therapeutic option for refractory neonatal convulsions owing to its non-hepatic elimination, linear pharmacokinetics, low protein binding and better safety profile.

The incidence and risk factors of epilepsy in children born preterm: A nationwide register study

ObjectivesThe aim was to compare the incidence of epilepsy between very preterm (VP) (<32+0 weeks), moderately preterm (MP) (32+0–33+6 weeks), late preterm (LP) (34+0–36+6 weeks) and term infants (≥37 weeks) and to establish and compare risk factors of epilepsy in these groups. MethodsThe national register study included all live born infants in Finland in 1991–2008. Excluding infants with missing gestational age, a total of 1,033,349 infants were included in the analysis and they were analyzed in four subgroups (VP, MP, LP and term) and three time periods (1991–1995, 1996–2001 and 2002–2008). Results5611 (0.54%) children with epilepsy were diagnosed. The incidence of epilepsy was 2.53% in the VP, 1.08% in the MP, 0.75% in the LP and 0.51% in the term group. Intracranial hemorrhage (OR 3.48; 95% CI 2.47–4.89) and convulsions in the neonatal period (OR 13.4; 95% CI 10.2–17.6) were associated with an increased risk of epilepsy. Compared to the term group, preterm birth (VP OR 4.59; 95% CI 3.79–5.57, MP 1.97; 1.48–2.63, LP 1.44; 1.25–1.68) was associated with an increased risk of epilepsy after adjusting for maternal, pregnancy, delivery and sex variables. ConclusionsThe incidence of epilepsy decreased by advancing gestational age at birth and preterm birth predicted an increased risk of epilepsy in childhood. Intracranial hemorrhage and neonatal convulsions were strongly associated with an increased risk of epilepsy.

P 85 KCNQ-2 missense mutations and phosphatidylinositol 4,5-bisphosphate in familial epilepsy

The KCNQ2/3 channel is a slowly activating, non-inactivating voltage-gated potassium channel. It causes the M-current and sustains the resting membrane potential. Therefore, it is crucial for the regulation of neuronal plasticity. If a neuron does not reach the resting-potential after activation, excitation may spread throughout the neuronal network and a seizure may follow. In this work we study the influence of the intracellular second messenger phosphatidylinositol 4,5-bisphosphate (PIP2) on channels containing mutant KCNQ2 subunits associated with Benign Familial Neonatal Convulsions (BFNC). We hypothesize that mutations in the KCNQ2 C-terminus are characterized not only by constitutive changes, but also by changes in their modulation by second messengers. We examined the following missense-mutations: R333G, L339R, R353G, R553Q, K554N and L637Q, all located in the C-terminus of KCNQ2. Measurements were performed in whole-cell gigaseal voltage-clamp technique in HEK293t cells transfected with wildtype (WT) or mutant KCNQ2 and WT KCNQ3. We first characterized channel activation in IV curves. To examine the modulation of channels by PIP2, we perfused cells intracellularly with Neomycin by adding it to the patch pipette; the aminoglycoside-antibiotic agent acts as a PIP2 sponge and reduces PIP2 binding to KCNQ2. In addition, we activated muscarinic M1 receptors using oxotremorine, leading to PIP2 depletion through activation of phospholipase C (PLC). Our work showed. • Voltage dependence of channel activation was similar as WT for all mutants. • Two of the examined mutants have smaller currents (L339R, L637Q), four have similar currents (R333G, R553Q, K554N), and one has higher currents(R353G) as compared to the wildtype channel. • The evaluated mutants did not have a higher sensitivity to Neomycin. • Unexpectedly, activation of M1 receptors by very low agonist concentrations led to an initial, short-lasting increase in currents followed by the known decrease in current at higher concentrations. This phenomenon was observed in the wildtype and in mutants. Previous research by others described an impaired binding between Calmoduline and KCNQ2 R353G being associated with a smaller number of channels reaching the cellular membrane (Richards et al., 2004). Conversely, our results showed increased whole-cell currents with the R353G mutant. Yet we were able to confirm a hypersensibility of R353G to Oxotremorine recently described by others (Kosenko et al., 2012). These findings support the hypothesis that C-terminal missense mutations can influence channel regulation by second messengers in the absence of constitutive changes in the channel activity itself. Conceivably, the development of epileptogenic activity may even in sporadic forms of epilepsy be caused not only by structural changes, but also by alterations in intracellular second messenger pathways affecting ion channel regulation.

Clinico-etiological profile of neonatal seizures in term neonates

Background: Neonatal seizures or neonatal convulsions are epileptic fits occurring from birth to the end of the neonatal period. Neonatal seizures are a common neurological problem with a frequency of 1.5-14/1000 neonates. Neonatal seizure is common in this part of the Telangana and there was paucity of data from this area. Identification of etiology will help in management there by reducing morbidity and mortality.Methods: This prospective study was done in NICU of S.V.S. Medical College and Hospital, Mahabubnagar, from Jan 2016 to Jan 2017. Term neonates with clinically identifiable seizure were included in the present study. This study was approved by institutional ethical committee and written consent was obtained from parents of the studied neonates.Results: Of 84 studied neonates, 46 were males and 38 were females. 29 neonates had seizures within first 24 hours and 22 neonates had seizures on day 2. Perinatal asphyxia was seen in 28 neonates and septicemia was seen in 21 neonates.Conclusions: Perinatal asphyxia was the most common cause for neonatal seizures in term neonates, followed by septicaemia and metabolic disturbances.

Epilepsies associated with KCNQ2: A spectrum of disorders

Epilepsies associated with KCNQ2 are a spectrum of disorders, and KCNQ2 mutations lead to a variety of phenotypes from the severest to the mildest, from early onset epileptic encephalopathy (EOEE) to benign familial neonatal convulsion (BFNC). The type and the position of KCNQ2 mutations may be associated with phenotypes, and provide a clue for assessing prognosis. KCNQ2 mutations lead to the reduced protein expression, abnormal distribution of potassium channels or decreased currents of potassium channels. It is the potential mechanism that KCNQ2 mutations cause different phenotypes. Recent studies have also found that KCNQ2 mutations may trigger seizures by enhancing potassium channel currents; however it needs further studies to verify. Key words: KCNQ2 potassium channel; Epilepsy; Review

Clinco-Biochemical Profile Of Neonatal Seizures

Background: Neonatal seizures are the most prominent feature of neurological dysfunction during neonatal period. Neonatal seizures occur within the first 4 weeks of life in a full-term infant and up to 44 weeks from conception for premature infant. Neonatal seizures are occurring in approximately 1.8 – 3.5 / 1000 live birth.Objectives: To study clinical types, time of onset and to determine the etiology of neonatal seizures.Methods: Out of eighty eight full term and preterm neonates with seizure at neonatal care unit and general wards of Babylon Gynecology and Pediatrics teaching hospital were studied prospectively in regard to clinco-biochemical profile of neonatal seizures from period 1st of May 2009 to 1st of December 2009.Results: Eighty eight full term and preterm neonates, (95.4%) of them were term and (4.6%) were preterm. The most common cause of neonatal convulsion was metabolic disturbances collectively constitute (47.7%).The other causes were asphyxia (15.4%),meningitis (6.6%),structural abnormalities (4.4%) and unknown cause (27.2%). Tonic type occurred in (100%) of preterm patients while in term patients, (31.8℅) of them were subtle type ,followed by tonic type (24.3℅) , focal clonic (16.2℅),generalized tonic clonic (11.3℅) and multi focal clonic type(11.3℅). 80℅ of hypoglycemia occurred in male patients.Conclusions: The commonest cause of seizure was metabolic abnormalities. Subtle seizures were the commonest type of seizure observed in term babies and tonic seizures were the most commonest type in preterm babies in this studyRecommendations: Metabolic abnormalities should be excluded in every case of neonatal seizure. Improving of thelaboratory services and the availability of other investigations must be available. Proper fetal monitoring during labor is recommended to avoid birth asphyxia .

Early genetic testing for neonatal epilepsy

The incidence of seizures is greatest during the neonatal period, with an estimated rate of 2–4 per 1,000 live births. Although the majority of seizures in the newborn are due to acquired brain disorders, a substantial proportion are due to metabolic and genetic disorders causing neonatal- and infantile-onset epilepsies. For decades, genetics has played a critical role in identification and treatment of seizures in the newborn and infantile period.1,2 With newborn screening, disorders such as phenylketonuria and biotinidase deficiency can be identified before patients develop seizures. Early identification and treatment prevents the development of often severe epilepsy syndromes and associated comorbidities. Detection and early treatment will continue to improve as newborn screening methods advance, whether based in genetics or clinical observation: the first channelopathy that causes epilepsy was identified in families with benign familial neonatal convulsions in the 1990s, before completion of the human genome project and modern genomics.3

Neonatal complications among 596 infants delivered by vacuum extraction (in relation to characteristics of the extraction)

Objective: To investigate the association between complicated vacuum extraction (VE) deliveries and neonatal complications.Methods: Observational study including data on the management of 596 consecutive VE-deliveries at 6 different birth clinics in Sweden in 2013. We used logistic regression to examine the association between a complicated VE and: extracranial bleeding, severe neonatal complication (intracranial hemorrhage and/or asphyxia/low Apgar score and/or convulsions, and/or encephalopathy), and brachial plexus injury. VE was considered complicated if duration exceeded 15 min, and/or more than six pulls were used, and/or more than one cup detachment occurred. Uncomplicated VE served as the reference group.Results: Ten percent of the infants were diagnosed with at least one of the investigated complications. Cephalohematoma occurred in 5.2% of the infants and 1.5% had a subgaleal hematoma. Altogether 24 (4.0%) infants were diagnosed with a severe complication; low Apgar score, neonatal convulsions, encephalopathy or intracranial hemorrhages. Brachial plexus injury occurred in eight (1.3%) infants. The crude odds ratio for extracranial hemorrhages was 2.6 (95% CI 1.17–5.77), 4.07 (1.67–9.92) for severe neonatal complications, and 4.63 (1.08–19.76) for brachial plexus injury.Conclusions: Extraction time >15 min, >6 pulls and >1 cup detachment is associated with increased risk of neonatal complications. These results support compliance with guidelines and recommendations for VE deliveries.

Foley catheterisation versus oral misoprostol for induction of labour in hypertensive women in India (INFORM): a multicentre, open-label, randomised controlled trial

Between 62 000 and 77 000 women die annually from pre-eclampsia and eclampsia. Prompt delivery, preferably by the vaginal route, is vital for good maternal and neonatal outcomes. Two low-cost interventions-low-dose oral misoprostol tablets and transcervical Foley catheterisation-are already used in low-resource settings. We aimed to compare the relative risks and benefits of these interventions. We undertook this multicentre, open-label, randomised controlled trial in two public hospitals in Nagpur, India. Women (aged ≥18 years) who were at 20 weeks' gestation or later with a live fetus and required delivery as a result of pre-eclampsia or hypertension were randomly assigned (1:1), via computer-generated block randomisation (block sizes of four, six, and eight) with concealment by use of opaque, sequentially numbered, sealed envelopes, to receive labour induction with either oral misoprostol 25 μg every 2 h (maximum of 12 doses) or a transcervical Foley catheter (silicone, size 18 F with 30 mL balloon). Randomisation was stratified by study centre. The catheter remained in place until active labour started, the catheter fell out, or 12 h had elapsed. If the catheter did not fall out within 12 h, induction continued with artificial membrane rupture and oxytocin, administered through a micro-drip gravity infusion set. Fetal monitoring was by intermittent auscultation. The primary outcome was vaginal birth within 24 h. Due to the nature of the interventions, masking of participants, study investigators, and care providers to group allocation was not possible. We analysed by intention to treat. This trial is registered with ClinicalTrials.gov, number NCT01801410. Between Dec 20, 2013, and June 29, 2015, we randomly assigned 602 women to induction with misoprostol (n=302) or the Foley catheter (n=300; intention-to-treat population). Vaginal birth within 24 h was more common in women in the misoprostol group than in the Foley catheter group (172 [57·0%] vs 141 [47·0%] women; absolute risk difference 10·0%, 95% CI 2·0-17·9; p=0·0136). Rates of uterine hyperstimulation were low in both the misoprostol and Foley catheter groups (two [0·7%] vs one [0·3%] cases; absolute risk difference 0·3%, 95% CI -0·8 to 1·5; p=0·566) and neonatal deaths did not differ significantly between groups (six [2·0%] vs three [1·0%] neonatal deaths; 1·0, -1·04 to 2·97; p=0·322). 17 serious adverse events (3%) were reported during the study: one case of intrapartum convulsion and one case of disseminated intravascular coagulation (both in the Foley group); ten perinatal deaths, including two stillbirths (both in the Foley catheter group) and eight neonatal deaths (n=5 in the misoprostol group and n=3 in the Foley catheter group); and five of neonatal morbidity, comprising birth asphyxia (n=3), septicaemia (n=1), and neonatal convulsion (n=1). Oral misoprostol was more effective than transcervical Foley catheterisation for induction of labour in women with pre-eclampsia or hypertension. Future studies are required to assess whether oxytocin augmentation following misoprostol can be replaced by regular doses of oral misoprostol tablets. Medical Research Council, Department for International Development, and Wellcome Trust Joint Global Health Trials Scheme.

Use of antidepressant medication in pregnancy and adverse neonatal outcomes: A population-based investigation.

Untreated depression and antidepressant use during pregnancy may have negative consequences for births. There are still conflicting data on the potential harmful effects of prenatal antidepressant treatment on child health. To investigate the relationship between the use of antidepressant medication during pregnancy and selected neonatal outcomes. A population-based cohort study including 9825 deliveries exposed to an antidepressant between 9months before last menstrual date through to delivery, from January 2005 to December 2010 in the Lombardy region of Italy, was conducted. We evaluated the prevalence ratio (PR) of low Apgar score, small for gestational age, intrauterine hypoxia and birth asphyxia, neonatal convulsion, and other respiratory conditions, among infants born to mothers exposed to an antidepressant during pregnancy using log-binomial regression analysis. Fine stratification was applied to the propensity score to account for all potential confounders. Sensitivity and subgroup analyses restricted to specific types of antidepressant, time of exposure, and women with vaginal deliveries and full-term births were also performed. A total of 33.4% of women filled at least one prescription during pregnancy. Compared to infants born to mothers with exposure to antidepressants only before pregnancy, those with exposure to antidepressants during pregnancy had an increased prevalence ratio of a low Apgar score (PR, 1.63, 95% CI, 1.01-2.61), intrauterine hypoxia and birth asphyxia (aPR, 1.37, 1.08-1.73), neonatal convulsion (aPR, 2.81, 1.07-7.36), and other respiratory condition (aPR, 1.24, 1.00-1.52). Results were similar in the sensitivity and subgroup analyses. Use of antidepressants during pregnancy may have an increased risk for several neonatal outcomes.

Risk factors for epilepsy in cases with cerebral palsy: A retrospective study

Objective: Cases with cerebral palsy (CP) followed in Child Neurology Outpatient Clinic between 2008-2015 years were evaluated retrospectively. Group 1 (n:116) and Group 2(n:118) were consisted of CP cases without and with epilepsy respectively. Clinical, laboratory findings of two groups were compared to each other. Methods: Statistical analyses were performed by using SPSS programme. P value less than 0.05 was considered as statistically significant. Results: There was no significant difference between two groups in terms of gender, gestationel age, birth type, birth weight, risk factors for CP development (pre/peri/postnatal), length of NICU stay and the need for mechanical ventilation. (p>0.05). Cases were evaluated in according to SCPE definitions and subtypes in spastic group were also defined depending on Sweedish classification. These factors outlined below were found to be significant for epilepsy development in CP cases: * History of neonatal convulsion *The presence of focal clonic or generalized tonic neonatal seizures *Abnormal base rhtyhm on neonatal EEG (generalized low amplitude, amplitude asymmetry or absence of maturational properties in according to postconceptional age) *Discharge of the case from NICU with at least one antiepileptic drug * Presence of bilateral spastic (tetraplegic) CP * Abnormal paroxysmal activity on EEG obtained at the 6 months of age * Having of abnormal cranial MRI findings (cerebral atrophy, hydrocephaly, cortical dysplasia and cerebral malformations) *Having microcephaly, visual problems and mental retardation. Conclusion: CP cases having one or more these risk factors should be monitored closely in regard to epilepsy.

Some aspects of neonatal convulsions.

The purpose of this paper is to review and evaluaute the clinical dataon incidence, sex, body-weight, morbidity and mortality and the possible etiology of convulsions occurring in the neonatal period (i.e. the first 30 days of life) and to study the outcome in follow up examination at the age of more than 6 months. The age of 6 months is taken as a limit because previous experiences and those of other authors (Billing, 1964) have shown that only after the age of 6 months neurological and mental disorders remain evident and permanent.

Intelligence, Functioning, and Related Factors in Children with Cerebral Palsy.

Cerebral palsy (CP) is the most common significant motor impairment in childhood. CP is defined as a primary disorder of posture and movement; however, intellectual impairment is prevalent in children with CP. The purpose of this study was to examine the intelligence level associated with gross motor function and hand function, type of CP, the presence of comorbid disorders such as epilepsy, and other factors. In total, 107 children with CP were included. Age, gender, prenatal/natal/postnatal risk factors, type of CP, and presence of other neurodevelopmental disorders were recorded as demographic findings. Intellectual functions of the patients were determined by clinical assessment, adaptive function of daily life, and individualized, standardized intelligence testing. The gross motor function and hand function of the patients were classified using the "Gross Motor Function Classification System" and "Bimanual Fine Motor Function" measurements, respectively. The mean age of the patients was 8.10±3.43 years (2-16 years). The study included 63 (58.9%) male patients and 44 (41.1%) female patients. During clinical typing, 80.4% of the patients were spastic, 11.2% were mixed, 4.7% were dyskinetic, and 3.7% were ataxic. Intellectual functioning tests found 26.2% of the children within the intellectual norm and that 10% of the children had a borderline intellectual disability, 16% of them had a mild intellectual disability, 17% of them had a moderate intellectual disability, and 30.8% of them had a severe intellectual disability. No significant relationship was determined between the CP type and intellectual functioning (p>0.05). Intellectual functioning was found to be significantly correlated with hand functions and motor levels (p<0.001). Factors related with intellectual functioning were neonatal convulsion, epilepsy, and speech disorders. Intelligence assessment should be an essential part of CP evaluation and research. There is not enough reliable knowledge, unanimity regarding validity data, and population-specific norms in the intelligence assessments of children with CP. Research is required to assess properly intelligence for children with CP.

Maternal Body Mass Index in Early Pregnancy and Risk of Epilepsy in Offspring

There is growing concern about the long-term neurologic effects of prenatal exposure to maternal overweight and obesity. The causes of epilepsy are poorly understood and, in more than 60% of the patients, no definitive cause can be determined. To investigate the association between early pregnancy body mass index (BMI) and the risk of childhood epilepsy and examine associations between obesity-related pregnancy and neonatal complications and risks of childhood epilepsy. A population-based cohort study of 1 441 623 live single births at 22 or more completed gestational weeks in Sweden from January 1, 1997, to December 31, 2011, was conducted. The diagnosis of epilepsy as well as obesity-related pregnancy and neonatal complications were based on information from the Sweden Medical Birth Register and National Patient Register. Multivariate Cox proportional hazards regression models were used to estimate adjusted hazard ratios (HRs) and 95% CIs after adjusting for maternal age, country of origin, educational level, cohabitation with partner, height, smoking, maternal epilepsy, and year of delivery. Data analysis was conducted from June 1 to December 15, 2016. Risk of childhood epilepsy. Of the 1 421 551 children born between January 1, 1997, and December 31, 2011, with covariate information available, 7592 (0.5%) were diagnosed with epilepsy through December 31, 2012. Of these 3530 (46.5%) were female. The overall incidence of epilepsy in children aged 28 days to 16 years was 6.79 per 10 000 child-years. Compared with offspring of normal-weight mothers (BMI 18.5 to <25.0), adjusted HRs of epilepsy by maternal BMI categories were as follows: overweight (BMI 25.0 to <30.0), 1.11 (95% CI, 1.04-1.17); obesity grade I (BMI 30.0 to <35.0), 1.20 (95% CI, 1.10-1.31); obesity grade II (BMI 35.0 to <40.0), 1.30 (95% CI, 1.12-1.50); and obesity grade III (BMI≥40.0), 1.82 (95% CI, 1.46-2.26). The rates of epilepsy were considerably increased for children with malformations of the nervous system (adjusted HR, 46.4; 95% CI, 42.2-51.0), hypoxic ischemic encephalopathy (adjusted HR, 23.6; 95% CI, 20.6-27.1), and neonatal convulsions (adjusted HR, 33.5; 95% CI, 30.1-37.4). The rates of epilepsy were doubled among children with neonatal hypoglycemia (adjusted HR, 2.10; 95% CI, 1.90-2.33) and respiratory distress syndrome (adjusted HR, 2.43; 2.21-2.66), and neonatal jaundice was associated with more than a 50% increased risk of epilepsy (adjusted HR, 1.47; 95% CI, 1.33-1.63). The elevated risk of epilepsy in children of overweight or obese mothers was not explained by obesity-related pregnancy or neonatal complications. The rates of childhood epilepsy increased with maternal overweight or obesity in a dose-response manner. Given that overweight and obesity are modifiable, prevention of obesity may be an important public health strategy to reduce the incidence of childhood epilepsy.

Intelligence functioning and associated factors in children with cerebral palsy

ObjectivesCerebral palsy (CP) is described as a primary disorder of posture and movement; however, intellectual impairment is prevalent in children with CP.AimThe aim of the present study was to examine the association with intellectual level and gross motor function, hand function, type of CP, and the presence of co-morbid disorders in these children.MethodsA total of 107 children with CP were included in the study. Intellectual functions of the children were determined by clinical assessment, adaptive function of daily life, and individualized standardized intelligence testing. Gross motor function and hand function of the patients were classified using the gross motor function classification system and the bimanual fine motor function measurements.ResultsThe mean age of the patients were 8.10 ± 3.43 years (age: 2–16 years). During clinical typing, we observed that 80.4% of the patients were spastic, 11.2% were mixed, 4.7% were dyskinetic, and 3.7% were ataxic. No significant relationship was determined between the type of CP and intellectual functioning (P &gt; 0.05). Intellectual functioning was found to be significantly correlated negatively with both gross motor function and hand functions level (P &lt; 0.001). The factors related to intellectual functioning were neonatal convulsion (x2 = 12.97, P = 0.002), epilepsy (x2 = 29.221, P &lt; 0.001), and speech disorders (x2 = 23.29, P &lt; 0.001).ConclusionsThere is an association between intellectual functioning in children with CP and the degree of motor impairment, neonatal convulsion, epilepsy, and speech disorders. Intelligence assessment should be an essential part of CP evaluation.Disclosure of interestThe authors have not supplied their declaration of competing interest.

Unusual Presentation of Primary Hyperparathyroidism: A Rare Case Report

ABSTRACT Aim The aim of this case report is to highlight an exceptional presentation of primary hyperparathyroidism. Background Asymptomatic maternal hyperparathyroidism manifesting in the neonate as hypocalcemic convulsions is exceedingly rare. Case report: Primary hyperparathyroidism has got a varied presentations. We present a case report of neonatal hypocalcemic convulsions secondary to asymptomatic maternal hyperparathyroidism. Here, the challenge in diagnosing this condition and management will be discussed in the context of available literature. Conclusion In the event of nonfebrile seizures in the neonate due to hypocalcemia, the mother has to be evaluated for primary hyperparathyroidism. Clinical significance: Physicians’ awareness of this unique manifestation of primary hyperparathyroidism is essential for the appropriate management of both the mother and the neonate. Timely identification and treatment of this condition will prevent complications in both. How to cite this article Teja VS, Ramakrishnan R. Unusual Presentation of Primary Hyperparathyroidism: A Rare Case Report. World J Endoc Surg 2017;9(1):13-15.