BACKGROUND AND PURPOSE: The selectins play a role in the initiation of endothelium-leukocyte interaction; endothelial expression of E-selectin is induced by ischemia-reperfusion-like conditions in vitro. Neutrophils accumulate in post-hypoxic-ischemic neonatal rat brain prior to the evolution of necrosis and neutrophil depletion attenuates hypoxic-ischemic brain injury; the mechanisms leading to post-hypoxic-ischemic neutrophil accumulation are unknown. We hypothesized that E-selectin might mediate post-hypoxic-ischemic injury in the immature brain, thus, we evaluated E- selectin gene expression by RT-PCR and protein accumulation by immunocytochemistry in post-hypoxic-ischemic neonatal (postnatal day 7) rat brain. METHODS: Neonatal rats (n=48) underwent right carotid ligation followed by 2h in 8% O2; this procedure typically produces ipsilateral striatal, hippocampal and cortical infarction. Controls included carotid ligation alone, hypoxia alone, and neither hypoxia nor ligation. For RNA extraction, rats were killed 0, 1, 2, 4, 8, 12, 24 and 48 h post-hypoxia-ischemia. For immunocytochemistry, rats were killed at 4 and 8 h. RESULTS: Ipsilateral(right-sided) E-selectin mRNA was markedly elevated in cortex, striatum and hippocampus at 4 and 8 h post-hypoxia-ischemia; expression decreased at 12 and 24 h and was no longer detectable at 48 h. E-selectin protein was detected predominantly in right striatum 8 h post-hypoxia-ischemia, in a pattern consistent with a vascular distribution. E-selectin mRNA was barely detectable in any controls. CONCLUSION: The temporal and spatial profiles of post-hypoxic-ischemic E-selectin mRNA and protein expression are consistent with a role in post-hypoxic-ischemic neutrophil recruitment and in the evolution of subsequent brain injury.
Animals ; Anoxia ; Brain ; Brain Injuries ; E-Selectin* ; Gene Expression ; Hippocampus ; Hypoxia-Ischemia, Brain* ; Immunohistochemistry ; Infarction ; Ligation ; Necrosis ; Neutrophil Infiltration ; Neutrophils ; Rats* ; RNA ; RNA, Messenger* ; Selectins

PURPOSE: Platelet-activating factor (PAF) is overproduced in ischemic brain. Although post-ischemic PAF antagonist administration protects the mature brain in some models, little is known about the effects of PAF antagonists in the immature brain. We hypothesized that the PAF antagonist BN 52021 would attenuate perinatal cerebral hypoxic-ischemic injury. METHODES: To elicit focal hypoxic-ischemic brain injury, seven day old (P7) rats(n=111) underwent right carotid ligation, followed by 2.5-3.25 h hypoxia (FiO2=0.08). BN 52021 neuroprotection was evaluated in 3 groups of experiments: (1) 25mg/kg/dose, 0 and 2 h post-hypoxia, (2) 25mg/kg/dose immediately before and 1 h after hypoxia, (3) post-hypoxia-ischemia treatment with BN 52021 12.5, 25 or 50mg/kg/dose in 2 doses 0 and 2 h after hypoxia. All experiments included concurrent vehicle-injected controls. To quantitate severity of injury, bilateral regional cross-sectional areas (groups 1 and 2) or hemisphere weights (group 3) were evaluated on Pl2. RESULTS: Both pre- and post-hypoxic treatment with BN 52021 (25mg/kg/dose, 2 serial doses) decreased the incidence of cerebral infarction from 90% to about 30%(p<0.02, Fisher's exact test). Measurement of cross-sectional areas confirmed neuroprotection and indicated some benefit of pre- over post-hypoxic-ischemic treatment in hippocampus and cortex. Over the dose range tested, the neuroprotective effect of BN 52021 administration was not dose-dependent. In contrast, BN52021 did not attenuate NMDA-induced hippocampal excitotoxic injury in P7 rats. CONCLUSIONS: Either prophylactic or "rescue" administration of PAF antagonists decreases the incidence and severity of brain injury associated with an episode of perinatal cerebral hypoxia-ischemia.
Animals ; Anoxia ; Brain Injuries* ; Brain* ; Cerebral Infarction ; Hippocampus ; Hypoxia-Ischemia, Brain ; Incidence ; Ligation ; Neuroprotective Agents* ; Rats* ; Weights and Measures

No abstract available.
Child* ; Humans ; Mycoplasma pneumoniae* ; Mycoplasma* ; Pneumonia* ; Pneumonia, Mycoplasma*

Headaches are common in children and become more common and increase in frequency during adolescence. There are various causes of headaches. The majority of cases are considered as primary and include migraine and tension headaches. The rational evaluation of headache begins with careful history. Migraine is genetically determined recurrent pain syndrome accompanied by neurological and gastrointestinal features, involving interaction of external triggers and internal pathophysiology and the causes of considerable disability to suffers. Establishing the correct diagnosis is essential for successful treatment. Treatment of pediatric migraine includes an individually tailored regimen of both nonpharmacologic and pharmacologic measures.
Adolescent ; Child* ; Diagnosis ; Headache* ; Humans ; Migraine Disorders ; Tension-Type Headache

Attention deficit hyperactivity disorder (ADHD) is a neurobehavioral developmental disorder characterized by a persistent pattern of inattention and/or hyperactivity, as well as forgetfulness, poor impulse control or impulsivity, and distractibility. The recommended evaluation includes documenting the type and severity of ADHD symptoms, verifying the presence of normal vision and hearing, screening for comorbid psychological conditions, reviewing the child's developmental history and school performance, and applying objective measures of cognitive function. Prevailing opinion characterizes ADHD as a disorder of executive function attributable to abnormal dopamine transmission in the frontal lobes and frontostriatal circuitry. A clearly defined etiology remains unknown, but studies suggest a strong genetic link. The aim of treatment is to decrease symptoms, enhance functionality, and improve well-being for the child and his or her close contacts. Stimulants remain the pharmacological agents of first choice for the management of ADHD, and psychosocial, behavioral and educational strategies that enhance specific behaviors may improve educational and social functioning in children with ADHD.
Aluminum Hydroxide ; Attention Deficit Disorder with Hyperactivity ; Carbonates ; Child ; Dopamine ; Executive Function ; Frontal Lobe ; Hearing ; Humans ; Mass Screening ; Vision, Ocular

Attention deficit hyperactivity disorder (ADHD) is a neurobehavioral developmental disorder characterized by a persistent pattern of inattention and/or hyperactivity, as well as forgetfulness, poor impulse control or impulsivity, and distractibility. The recommended evaluation includes documenting the type and severity of ADHD symptoms, verifying the presence of normal vision and hearing, screening for comorbid psychological conditions, reviewing the child's developmental history and school performance, and applying objective measures of cognitive function. Prevailing opinion characterizes ADHD as a disorder of executive function attributable to abnormal dopamine transmission in the frontal lobes and frontostriatal circuitry. A clearly defined etiology remains unknown, but studies suggest a strong genetic link. The aim of treatment is to decrease symptoms, enhance functionality, and improve well-being for the child and his or her close contacts. Stimulants remain the pharmacological agents of first choice for the management of ADHD, and psychosocial, behavioral and educational strategies that enhance specific behaviors may improve educational and social functioning in children with ADHD.
Aluminum Hydroxide ; Attention Deficit Disorder with Hyperactivity ; Carbonates ; Child ; Dopamine ; Executive Function ; Frontal Lobe ; Hearing ; Humans ; Mass Screening ; Vision, Ocular

Seizures in the neonatal period are common and frequently indicate serious underlying brain injury. Neonatal seizures continue to present a diagnostic and therapeutic challenge to pediatricians because recognition and classification of neonatal seizures remain problematic, particularly when clinicians rely only on clinical criteria. Neonatal seizures can permanently disrupt neuronal development, induce synaptic reorganization, alter plasticity, and "prime" the brain to increased damage from seizures later in life. Since neonatal seizures predict an increased risk for later epilepsy and other neurological sequelae, accurate diagnoses are needed for aggressive antiepileptic drug use. The present review summarizes the treatment and prognosis of neonatal seizures.
Brain ; Brain Injuries ; Epilepsy ; Humans ; Infant, Newborn ; Neurons ; Plastics ; Prognosis ; Seizures

Seizures in the neonatal period are common and frequently indicate serious underlying brain injury. Neonatal seizures continue to present a diagnostic and therapeutic challenge to pediatricians because recognition and classification of neonatal seizures remain problematic, particularly when clinicians rely only on clinical criteria. Neonatal seizures can permanently disrupt neuronal development, induce synaptic reorganization, alter plasticity, and "prime" the brain to increased damage from seizures later in life. Since neonatal seizures predict an increased risk for later epilepsy and other neurological sequelae, accurate diagnoses are needed for aggressive antiepileptic drug use. The present review summarizes the treatment and prognosis of neonatal seizures.
Brain ; Brain Injuries ; Epilepsy ; Humans ; Infant, Newborn ; Neurons ; Plastics ; Prognosis ; Seizures

BACKGROUND: Leukocytes, both polymorphonuclear leukocytes(PMNL) and monocytes/macrophages have been implicated in the pathogenesis of the cerebral ischemia and stroke. Neutrophils accumulate in post-hypoxic-ischemic neonatal rat brain prior to the evolution of necrosis and neutrophil depletion attenuates hypoxic-ischemic brain injury. However, the mechanisms leading to post-hypoxic-ischemic neutrophil accumulation are unknown yet. We hypothesized that Intercellular Adhesion Molecule-1 might mediate post-hypoxic-ischemic injury in the immature brain; thus, we evaluated ICAM-1 gene expression in post-hypoxic-ischemic neonatal(postnatal day 7) rat brain. METHODS: Neonatal rats(n=36) underwent right carotid ligation followed by exposure in 8% O2 for 2.5 hours; this procedure typically produces ipsilateral striatal, hippocampal and cortical infarction. Control groups are included by carotid ligation alone, hypoxia alone, and neither hypoxia nor ligation. For RNA extraction, rats were killed 0, 1, 2, 4, 8, 12, 24 and 48 h post- hypoxia-ischemia and RT-PCR was carried out. RESULTS: ICAM-1 mRNA was barely detected in the controls including normal and sham operated animals. In the cortex, striatum and hippocampus, ICAM-1 mRNA was significantly induced in the ipsilateral(right) side compared to the contralateral(left) side just after hypoxia-ischemia. The elevated ICAM-1 mRNA gradually reached a peak at 4 or 8 h and then decreased to an almost basal level by 24 to 48 h. In contrast, the less pronounced contralateral(left-sided) ICAM-1 mRNA expression appeared to peak earlier, within 2 h post-hypoxia-ischemia. CONCLUSION: The temporal profiles of post-hypoxic-ischemic ICAM-1 mRNA expression are consistent with a role in post-hypoxic-ischemic neutrophil recruitment and in the evolution of subsequent brain injury.
Animals ; Anoxia ; Brain Injuries* ; Brain Ischemia ; Brain* ; Gene Expression ; Hippocampus ; Infarction ; Intercellular Adhesion Molecule-1* ; Leukocytes ; Ligation ; Necrosis ; Neutrophil Infiltration ; Neutrophils ; Rats* ; RNA ; RNA, Messenger* ; Stroke

PURPOSE:Insulin-like growth factor-I(IGF-I) is an essential anabolic factor for postnatal rat brain development and IGF-I expression is highly abundant during the first 21 days, critical growth period. Hypoxic-ischemic brain insults occurring during the perinatal period result in neuronal necrosis and permanent brain damage. To investigate the regulation of the action of IGF-I in response to such a hypoxic insult, we examined the gene expression of IGF-I and IGFBP-5 during the first 72 hr after hypoxic-ischemic injury in immature rat brain. METHODS:Ligation of the right carotid artery of 7-day-old rats was followed by 2 hour exposure to 8% oxygen to produce severe hypoxic brain damage. Using reverse transcriptase-polymerase chain reaction(RT-PCR), the expression of IGF-I mRNA and IGFBP-5 mRNA was determined in both hypoxic and control brains at post 1, 4, 12, 24, 48 hr and 72 hr after hypoxic-ischemic insult. RESULTS:The IGF-I mRNA and IGFBP-5 mRNA expression of hypoxic brain were not different from those of controls at 1 hr of recovery but IGF-I mRNA expression was decreased rapidly at post 4 hr, this decrease more pronounced at 12 hr of recovery. IGF-I mRNA and IGFBP-5 mRNA expression were increased at 48 hr and 24 hr of recovery, respectively and both IGF-I mRNA and IGFBP-5 mRNA expression showed similar level of controls at 72 hr of recovery. CONCLUSION: Out findings suggest that IGF-I play a important role in both neuronal loss and repair process following hypoxic-ischemic brain injury and IGFBP-5 is also strongly involved in the repair of damaged brain tissue by mediating IGF-I action. (J Korean Soc Pediatr Endocrinol 2003;8:56-63)
Animals ; Brain Injuries* ; Brain* ; Carotid Arteries ; Gene Expression ; Hypoxia, Brain ; Insulin-Like Growth Factor Binding Protein 5 ; Insulin-Like Growth Factor I ; Necrosis ; Negotiating ; Neurons ; Oxygen ; Rats* ; RNA, Messenger*