Face Processing in the Chimpanzee Brain

SummaryHuman face recognition involves highly specialized cognitive and neural processes that enable the recognition of specific individuals [1–5]. Although comparative studies suggest that similar cognitive processes underlie face recognition in chimpanzees and humans ([6–8] and Supplemental Data), it remains unknown whether chimpanzees also show face-selective activity in ventral temporal cortex. This study is the first to examine regional cerebral glucose metabolism with 18F-flurodeoxyglucose positron emission tomography in chimpanzees after they performed computerized tasks matching conspecifics' faces and nonface objects (Supplemental Data). A whole-brain analysis comparing these two tasks in five chimpanzees revealed significant face-selective activity in regions known to comprise the distributed cortical face-processing network in humans, including superior temporal sulcus and orbitofrontal cortex [9–11]. In order to identify regions that were exclusively active during one task, but not the other, we subtracted a resting-state condition from each task and identified the activity exclusive to each. This revealed numerous distinct patches of face-selective activity in the fusiform gyrus that were interspersed within a large expanse of object-selective cortex. This pattern suggests similar object form topography in the ventral temporal cortex of chimpanzees and humans, in which faces may represent a special class of visual stimulus

Sleep‐disordered breathing is common among term and near term infants in the NICU

ObjectiveAmong older infants and children, sleep‐disordered breathing (SDB) has negative neurocognitive consequences. We evaluated the frequency and potential impact of SDB among newborns who require intensive care.Study DesignTerm and near‐term newborns at risk for seizures underwent 12‐h attended polysomnography in the neonatal intensive care unit (NICU). Bayley Scales of Infant Development, third edition (Bayley‐III) were administered at 18‐22 months.ResultThe 48 newborns (EGA 39.3 ± 1.6) had a median pediatric apnea‐hypopnea index (AHI) of 10.1 (3.3‐18.5) and most events were central (vs obstructive). Maternal and prenatal factors were not associated with AHI. Moreover, neonatal PSG results were not associated with Bayley‐III scores (P > 0.05).ConclusionSDB is common among term and near‐term newborns at risk for seizures. Follow‐up at ages when more nuanced testing can be performed may be necessary to establish whether neonatal SDB is associated with long‐term neurodevelopmental disability.Peer Reviewedhttps://deepblue.lib.umich.edu/bitstream/2027.42/149248/1/ppul24266.pdfhttps://deepblue.lib.umich.edu/bitstream/2027.42/149248/2/ppul24266_am.pd

Hypoxia-ischemia produces focal disruption of glutamate receptors in developing brain

We examined the impact of a perinatal hypoxic-ischemic insult on the distribution of glutamate receptors in developing brain. We used a well characterized rodent model for perinatal hypoxic-ischemic encephalopathy, unilateral carotid artery occlusion followed by exposure to 8% oxygen for 2.5 h in 7-day-old rat pups. This preparation results in focal neuronal damage in striatum, hippocampus, and cortex ipsilateral to ligation. Alterations in the regional distribution of glutamate binding in the first 24 h after the insult were assessed with quantitative in vitro [3H]glutamate autoradiography. In lesioned animals, we found progressive selective reductions in [3H]glutamate binding in forebrain ipsilateral to ligation in regions destined for neuronal damage. The earliest and most prominent unilateral reductions in binding were noted in the dentate gyrus of hippocampus (-45 +/- 9%, compared with contralateral hemisphere at 24 h). Acute reductions in specific glutamate binding appear to be a sensitive marker for hypoxic-ischemic neuronal damage in the immature brain. These observations suggest that neurons bearing glutamate receptors may be particularly susceptible to hypoxic-ischemic injury.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/26646/1/0000188.pd

Impact of hands‐on care on infant sleep in the neonatal intensive care unit

Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/135460/1/ppul23513_am.pdfhttp://deepblue.lib.umich.edu/bitstream/2027.42/135460/2/ppul23513.pd

Glutamate recognition sites in human fetal brain

We used in vitro autoradiography with [3H]glutamate to examine the distribution of glutamate recognition sites in 18 and 21 week gestation human fetal brains. We found a wide distribution of [3H]glutamate binding in both specimens, in a pattern distinct from that reported in adult brain using the same autoradiographic methods. In fetal brain, prominent [3H]glutamate binding was evident in hippocampal formation, caudate-putamen, globus pallidus, subthalamic nucleus, reticular nucleus of thalamus and substantia innominata.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/27426/1/0000464.pd

Weaning of Moderately Preterm Infants from the Incubator to the Crib: A Randomized Clinical Trial

OBJECTIVE: To assess whether length of hospital stay is decreased among moderately preterm infants weaned from incubator to crib at a lower vs higher weight. STUDY DESIGN: This trial was conducted in the Eunice Kennedy Shriver National Institute of Child Health and Human Development Neonatal Research Network. Infants with gestational ages 29-33 weeks, birthweight <1600 g, and in an incubator were randomly assigned to a weaning weight of 1600 or 1800 g. Within 60 to 100 g of weaning weight, the incubator temperature was decreased by 1.0°C to 1.5°C every 24 hours until 28.0°C. The infants were weaned to the crib following stable temperature at 36.5°C to 37.4°C for 8 to 12 hours. Clothing and bedcoverings were standardized. The primary outcome was length of hospital stay from birth to discharge; secondary outcomes included length of stay and growth velocity from weaning to discharge. Adverse events were monitored. RESULTS: Of 1565 infants screened, 885 were eligible, and 366 enrolled-187 to the 1600-g and 179 to the 1800-g group. Maternal and neonatal characteristics did not differ among weight groups. Length of hospital stay was a median of 43 days in the lower and 41 days in the higher weight group (P = .12). Growth velocity from completion of weaning to discharge was higher in the lower weight group, 13.7 g/kg/day vs 12.8 g/kg/day (P = .005). Groups did not differ in adverse events. CONCLUSIONS: Among moderately preterm neonates, weaning from incubator to crib at a lower weight did not decrease length of stay, but was safe and was accompanied by higher weight gain after weaning

Effect of Depth and Duration of Cooling on Death or Disability at Age 18 Months Among Neonates With Hypoxic-Ischemic Encephalopathy: A Randomized Clinical Trial

Importance Hypothermia for 72 hours at 33.5°C for neonatal hypoxic-ischemic encephalopathy reduces death or disability, but rates continue to be high. Objective To determine if cooling for 120 hours or to a temperature of 32.0°C reduces death or disability at age 18 months in infants with hypoxic-ischemic encephalopathy. Design, Setting, and Participants Randomized 2 × 2 factorial clinical trial in neonates (≥36 weeks’ gestation) with hypoxic-ischemic encephalopathy at 18 US centers in the Eunice Kennedy Shriver National Institute of Child Health and Human Development Neonatal Research Network between October 2010 and January 2016. Interventions A total of 364 neonates were randomly assigned to 4 hypothermia groups: 33.5°C for 72 hours (n = 95), 32.0°C for 72 hours (n = 90), 33.5°C for 120 hours (n = 96), or 32.0°C for 120 hours (n = 83). Main Outcomes and Measures The primary outcome was death or moderate or severe disability at 18 to 22 months of age adjusted for center and level of encephalopathy. Severe disability included any of Bayley Scales of Infant Development III cognitive score less than 70, Gross Motor Function Classification System (GMFCS) level of 3 to 5, or blindness or hearing loss despite amplification. Moderate disability was defined as a cognitive score of 70 to 84 and either GMFCS level 2, active seizures, or hearing with amplification. Results The trial was stopped for safety and futility in November 2013 after 364 of the planned 726 infants were enrolled. Among 347 infants (95%) with primary outcome data (mean age at follow-up, 20.7 [SD, 3.5] months; 42% female), death or disability occurred in 56 of 176 (31.8%) cooled for 72 hours and 54 of 171 (31.6%) cooled for 120 hours (adjusted risk ratio, 0.92 [95% CI, 0.68-1.25]; adjusted absolute risk difference, −1.0% [95% CI, −10.2% to 8.1%]) and in 59 of 185 (31.9%) cooled to 33.5°C and 51 of 162 (31.5%) cooled to 32.0°C (adjusted risk ratio, 0.92 [95% CI, 0.68-1.26]; adjusted absolute risk difference, −3.1% [95% CI, −12.3% to 6.1%]). A significant interaction between longer and deeper cooling was observed (P = .048), with primary outcome rates of 29.3% at 33.5°C for 72 hours, 34.5% at 32.0°C for 72 hours, 34.4% at 33.5°C for 120 hours, and 28.2% at 32.0°C for 120 hours. Conclusions and Relevance Among term neonates with moderate or severe hypoxic-ischemic encephalopathy, cooling for longer than 72 hours, cooling to lower than 33.5°C, or both did not reduce death or moderate or severe disability at 18 months of age. However, the trial may be underpowered, and an interaction was found between longer and deeper cooling. These results support the current regimen of cooling for 72 hours at 33.5°C

Long-Lasting Neural and Behavioral Effects of Iron Deficiency in Infancy

Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/72379/1/j.1753-4887.2006.tb00243.x.pd

Therapeutic hypothermia translates from ancient history in to practice

Acute postasphyxial encephalopathy around the time of birth remains a major cause of death and disability. The possibility that hypothermia may be able to prevent or lessen asphyxial brain injury is a “dream revisited”. In this review, a historical perspective is provided from the first reported use of therapeutic hypothermia for brain injuries in antiquity, to the present day. The first uncontrolled trials of cooling for resuscitation were reported more than 50 y ago. The seminal insight that led to the modern revival of studies of neuroprotection was that after profound asphyxia, many brain cells show initial recovery from the insult during a short “latent” phase, typically lasting ~6 h, only to die hours to days later during a “secondary” deterioration phase characterized by seizures, cytotoxic edema, and progressive failure of cerebral oxidative metabolism. Studies designed around this conceptual framework showed that mild hypothermia initiated as early as possible before the onset of secondary deterioration, and continued for a sufficient duration to allow the secondary deterioration to resolve, is associated with potent, long-lasting neuroprotection. There is now compelling evidence from randomized controlled trials that mild induced hypothermia significantly improves intact survival and neurodevelopmental outcomes to midchildhood

Recommendations for the design of therapeutic trials for neonatal seizures

Although seizures have a higher incidence in neonates than any other age group and are associated with significant mortality and neurodevelopmental disability, treatment is largely guided by physician preference and tradition, due to a lack of data from welldesigned clinical trials. There is increasing interest in conducting trials of novel drugs to treat neonatal seizures, but the unique characteristics of this disorder and patient population require special consideration with regard to trial design. The Critical Path Institute formed a global working group of experts and key stakeholders from academia, the pharmaceutical industry, regulatory agencies, neonatal nurse associations, and patient advocacy groups to develop consensus recommendations for design of clinical trials to treat neonatal seizures. The broad expertise and perspectives of this group were invaluable in developing recommendations addressing: (1) use of neonate-specific adaptive trial designs, (2) inclusion/exclusion criteria, (3) stratification and randomization, (4) statistical analysis, (5) safety monitoring, and (6) definitions of important outcomes. The guidelines are based on available literature and expert consensus, pharmacokinetic analyses, ethical considerations, and parental concerns. These recommendations will ultimately facilitate development of a Master Protocol and design of efficient and successful drug trials to improve the treatment and outcome for this highly vulnerable population