OBJECTIVE: To study the relationship between the degree of white matter damage and changes in brain function in premature infants early after birth according to amplitude-integrated electroencephalogram (aEEG) and raw EEG (with burst-suppression patterns). METHODS: Thirty-eight premature infants of less than 32 weeks′ gestational age and with white matter damage, including 20 cases of mild white matter damage and 18 cases of severe white matter damage, were included in the study. Forty-two premature infants without white matter damage were selected as a control group. After birth, they were examined using aEEG and brain ultrasound once a week until four weeks after birth or a corrected gestational age of 32 weeks. The white matter damage and control groups were compared in terms of aEEG patterns and amplitudes and burst suppression ratio (BSR) on EEG. RESULTS: The white matter damage and control groups had highly discontinuous patterns and had no complete sleep cycles. The lower amplitude was significantly smaller in the severe white matter damage subgroup than in the mild white matter damage subgroup and control group. There was alternating burst-suppression activity on the raw EEG in the white matter damage and control groups; and the severe white matter damage subgroup had a significantly longer suppression time and a significantly higher BSR on EEG compared with the mild white matter damage subgroup and control group. CONCLUSIONS: Brain function monitoring should be performed in premature infants with white matter damage early after birth so as to detect cases of severe white matter damage in time.
OBJECTIVE: To observe the therapeutic effect of Ommaya reservoir implantation on hydrocephalus in premature infants following intraventricular hemorrhage (IVH) and to investigate factors influencing the therapeutic effect. METHODS: An ambispective cohort study was conducted on the clinical and follow-up data of 20 premature infants (gestational age <32 weeks, birth weight <1500 g) who received Ommaya reservoir implantation because of hydrocephalus following IVH. The therapeutic effect of Ommaya reservoir implantation was observed. These patients were divided into cure and treatment failure groups according to their treatment outcomes. The factors influencing therapeutic effects were investigated by univariate analysis. RESULTS: Hydrocephalus was relieved significantly at 30 days after Ommaya reservoir implantation. However, some patients showed significantly decreased therapeutic effects since 3 months after operation: during 3-6 months after operation, 7 cases underwent ventriculoperitoneal shunt, 4 cases discontinued treatment because of economic reasons, and 1 case underwent endoscopic third ventriculostomy due to scalp hematoma with skin necrosis. The ventricles of the remaining 8 cases returned to normal size at 12-18 months after operation. As for postoperative complications, secondary IVH was seen in 8 cases, intracranial infection in 2 cases, and scalp hematoma with skin necrosis in 1 case. The univariate analysis revealed significant differences in gestational age, birth weight and duration of hydrocephalus before Ommaya reservoir implantation between the cure and the treatment failure groups (P<0.05). CONCLUSIONS: Ommaya reservoir implantation has a remarkable short-term therapeutic effect on hydrocephalus in premature infants following IVH, but later the effect decreases in some patients. Low gestational age, low birth weight and long duration of hydrocephalus may be the main factors influencing therapeutic effects of Ommaya reservoir implantation.
OBJECTIVE: To explore the role of spinal MAPK-ERK signal pathway in myocardial ischemia-reperfusion (I/R) injury. METHODS: Sixty male Sprague-Dawley(SD) rats (80-100 g) were randomly divided into 3 groups: sham (n=10), PD98059 (n=25) and I/R groups (n=25). Three days after successful intrathecal implantation, 5 μg DMSO was injected intrathecally into the sham group, and then the left coronary arteries were separated without being tied. Rats in the I/R and PD98059 groups were injected with 5 μL DMSO and PD98059 (5 μg) 30 minutes before thoractomy respectively. Then the left coronary artery was tied for 30 minutes followed by 120 minutes of reperfusion. After the experiments, the ERK phosphorylation condition of T1-T4 spinal cord segments was detected with immunofluorescence; the myocardiac apoptosic index and infarct size were measured. RESULTS: Expression of p-ERK in the I/R group was significantly higher than in the sham and PD98059 groups (P<0.05). Myocardial apoptotic index and infarct size in the PD98059 group were significantly lower than in the I/R group (P<0.05), but higher in the PD98059 group than in the sham group (P<0.05). CONCLUSIONS: The MAPK-ERK pathway in the superior thorathic spinal cord can be activated by myocardial ischemia-reperfusion and inhibition of the pathway can play a protective role in myocardial ischemiareperfusion injury.
Periventricular white matter damage is one of the characteristics of brain damage in preterm infants, and it is the most important type of encephalopathy. The pathological changes including the white matter of coagulation necrosis, oligodendrocyte damage, myelin damage, axonal injury and reactive gliosis and microglia infiltration in necrotic areas. All of these lesions are closely related to the nervous system sequelae in later-neonatal period. The pathogenesis of periventricular leukomalacia in premature infants are mainly cause by its immature brain vascular, and precursor oligodendrocytes of the attack of hypoxia, ischemia, infection, oxygen free radicals, inflammatory cytokines, increasing glutamate, and other high-risk factors. In this paper, an overview of progress in the study of the pathogenesis of periventricular white matter damage in premature infants through literature review to provide a theoretical support for clinical prevention, diagnosis and treatment.