background Hypothermia is protective against brain injury after asphyxiation in animal models. However, the safety and effectiveness of hypothermia in term infants with encephalopathy is uncertain. methods We conducted a randomized trial of hypothermia in infants with a gestational age of at least 36 weeks who were admitted to the hospital at or before six hours of age with either severe acidosis or perinatal complications and resuscitation at birth and who had moderate or severe encephalopathy. Infants were randomly assigned to usual care (control group) or whole-body cooling to an esophageal temperature of 33.5°C for 72 hours, followed by slow rewarming (hypothermia group). Neurodevelopmental outcome was assessed at 18 to 22 months of age. The primary outcome was a combined end point of death or moderate or severe disability. results Of 239 eligible infants, 102 were assigned to the hypothermia group and 106 to the control group. Adverse events were similar in the two groups during the 72 hours of cooling. Primary outcome data were available for 205 infants. Death or moderate or severe disability occurred in 45 of 102 infants (44 percent) in the hypothermia group and 64 of 103 infants (62 percent) in the control group (risk ratio, 0.72; 95 percent confidence interval, 0.54 to 0.95; P=0.01). Twenty-four infants (24 percent) in the hypothermia group and 38 (37 percent) in the control group died (risk ratio, 0.68; 95 percent confidence interval, 0.44 to 1.05; P=0.08). There was no increase in major disability among survivors; the rate of cerebral palsy was 15 of 77 (19 percent) in the hypothermia group as compared with 19 of 64 (30 percent) in the control group (risk ratio, 0.68; 95 percent confidence interval, 0.38 to 1.22; P=0.20). conclusions Whole-body hypothermia reduces the risk of death or disability in infants with moderate or severe hypoxic–ischemic encephalopathy.

/pdf/whole-body-hypothermia-for-neonates-with-hypoxic-ischemic-15wd92xega.pdf

Whole-body hypothermia for neonates with hypoxic-ischemic encephalopathy.

More than 95 percent of infants who have neonatal stroke survive to adulthood, and many have residual motor or cognitive disabilities. This article makes the point that recognition of at-risk newborns by means of advanced methods of neuroimaging, combined with a plan for rational intervention, may result in the prevention or the reduction in the incidence of lifelong disabilities such as cerebral palsy, epilepsy, and behavioral and learning disorders.

https://www.nejm.org/doi/pdf/10.1056/NEJMra041996?articleTools=true

Neonatal brain injury.

The spectrum of leukomalacia using cranial ultrasound.

Intraventricular hemorrhage (IVH) is a major complication of prematurity. IVH typically initiates in the germinal matrix, which is a richly vascularized collection of neuronal-glial precursor cells in the developing brain. The etiology of IVH is multifactorial and is primarily attributed to the intrinsic fragility of the germinal matrix vasculature and the disturbance in the cerebral blood flow (CBF). Although this review broadly describes the pathogenesis of IVH, the main focus is on the recent development in molecular mechanisms that elucidates the fragility of the germinal matrix vasculature. The microvasculature of the germinal matrix is frail because of an abundance of angiogenic blood vessels that exhibit paucity of pericytes, immaturity of basal lamina, and deficiency of glial fibrillary acidic protein (GFAP) in the ensheathing astrocytes endfeet. High VEGF and angiopoietin-2 levels activate a rapid angiogenesis in the germinal matrix. The elevation of these growth factors may be ascribed to a relative hypoxia of the germinal matrix perhaps resulting from high metabolic activity and oxygen consumption of the neural progenitor cells. Hence, the rapid stabilization of the angiogenic vessels and the restoration of normal CBF on the first day of life are potential strategies to prevent IVH in premature infants.

/pdf/intraventricular-hemorrhage-in-premature-infants-mechanism-49pplhnfi4.pdf

Intraventricular hemorrhage in premature infants: Mechanism of disease

This randomized, controlled trial had as its goal to determine whether whole-body cooling, begun within 6 hours of birth and continuing for 72 hours, reduces disability and mortality in term infants with moderate or severe encephalopathy. Infants entered into the study had a gestational age of 36 weeks or longer, were admitted with either severe acidosis or perinatal complications, and required resuscitation at birth. They were randomized to usual care or whole-body cooling and were reassessed neurodevelopmentally at age 18 to 22 months. The 102 infants assigned to hypothermia were placed on a blanket precooled to 5°C and the esophageal temperature, measured with a probe, was reduced to 33.5°C. A second blanket then was attached to the cooling system decrease variability in esophageal temperature. A skin probe monitored the temperature of the abdominal-wall skin. At both sites, temperature was monitored continuously and recorded every 15 minutes for 4 hours and then hourly for 8 hours. After 72 hours, the set point of the automatic control on the cooling system was increased by 0.5°C per hour. After 6 hours, the esophageal probe was removed and warming continued until the set point of the warmer reached 36.5°C. The 106 control infants were exposed to an overhead radiant warmer to maintain an abdominal-wall skin temperature of 36.5°C to 37.0°C. The incidence of death or moderate/severe disability was 44% in treated infants and 62% of control infants (risk ratio [RR], 0.72; 95% confidence interval [CI], 0.54-0.95). Approximately one fourth of actively treated infants (24%) and 37% of control infants died (RR, 0.68; 95% CI, 0.44-1.05). No increase in major disability was observed in surviving infants. Cerebral palsy occurred in 19% of the hypothermia group and 30% of control infants (RR, 0.68; 95% CI, 0.38-1.22). These results suggest that whole-body cooling, or hypothermia, is a safe and effective means of limiting mortality and reducing disability in newborn infants with moderate or severe encephalopathy.

Whole-Body Hypothermia for Neonates With Hypoxic???Ischemic Encephalopathy

BACKGROUND AND PURPOSE: Although pathologic evidence of cerebellar injury due to birth asphyxia is well described, neuroimaging evidence is sparse. The primary purpose of this retrospective study was to evaluate the early and late imaging findings in the cerebellum of patients who had neonatal hypoxic-ischemic encephalopathy with thalamic edema shown by neonatal CT. The secondary aims were to validate thalamic edema shown by neonatal CT as a marker of thalamic injury and to assess the late cerebral cortical abnormalities associated with neonatal thalamic edema. METHODS: Fifty-five neonates with thalamic edema shown by CT performed when patients were 3 days old were identified from a cohort of full-term neonates with hypoxic-ischemic encephalopathy. Twenty-six of the 55 underwent follow-up neuroimaging. All sonograms, CT scans, and MR images of the brains of the 55 neonates were retrospectively reviewed by two pediatric neuroradiologists. The examinations were reviewed for evidence of hemorrhage, edema, atrophy, and CT attenuation or MR signal intensity abnormalities in the cerebellum, basal ganglia, and cerebral cortex. The neonatal autopsy findings in four cases were reviewed separately by a pediatric neuropathologist. RESULTS: Of the 55 neonates with thalamic edema shown by neonatal CT, 28 (51%) had thalamic edema with diffuse cerebral cortical edema, and 27 (49%) had thalamic edema without diffuse cortical edema. The cerebellar vermes appeared normal on all neonatal sonograms, CT scans, and MR images. However, atrophy of the cerebellar vermis was found in 12 (46%) of 26 patients by use of follow-up studies (95% CI, 27–65%). One of the 12 patients also had cerebellar hemispheric atrophy. Cerebellar vermian atrophy was shown at follow-up in eight (67%) of 12 patients who had neonatal thalamic edema with cortical sparing, compared with four (29%) of 14 patients who had thalamic edema with diffuse cortical edema. The difference did not reach statistical significance. The thalami appeared abnormal on follow-up neuroimages in 25 of 26 cases. Different patterns of cortical atrophy were observed on the images of patients who had thalamic edema with cortical sparing compared with those obtained in patients who had thalamic edema with cortical involvement. CONCLUSION: Cerebellar vermian atrophy is a frequent finding on follow-up images of patients in whom neonatal CT showed hypoxic-ischemic encephalopathy with abnormal thalami.

http://www.ajnr.org/content/ajnr/25/6/1008.full.pdf

Cerebellar vermian atrophy after neonatal hypoxic-ischemic encephalopathy.

Magnetic resonance imaging is presently the best modality for evaluating gray/white matter anatomy. However, this modality is expensive and not yet readily available in all countries. Most neuronal mi

Neuronal migration abnormalities can still be diagnosed by computed tomography

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Cerebellar vermian atrophy after neonatal hypoxic-ischemic encephalopathy.

Neuronal migration abnormalities can still be diagnosed by computed tomography