UNASSIGNED: The white cerebellum sign (WCS) is a classical but rare radiological finding usually associated with irreversible diffuse hypoxic-ischemic cerebral injury. Very few cases exist in the literature globally, especially from the West African region, as a potential hallmark of poor prognostic outcome. We describe the white cerebellum sign in a Nigerian pediatric patient, managed for severe head injury.
UNASSIGNED: A fourteen-year old boy presented to our emergency department with loss of consciousness following a pedestrian road traffic accident. Physical examination revealed a critically ill boy with fever, hypotension, tachycardia, gasping respiration, GCS 3, bilateral dilated unreactive pupils, absent corneal, gag and oculocephalic reflexes. He was thus diagnosed of severe traumatic brain injury and brainstem dysfunction. He had endotracheal intubation, ventilatory and inotropic support. Cranial computerized tomography scan of the patient showed radiological features in keeping with the WCS. His clinical status remained poor until he suffered a cardiac arrest about twelve hours after admission.
UNASSIGNED: WCS has been reported in relation to child abuse, anoxic-ischemic brain injury, inflammatory and metabolic brain disorders and trauma. It is a classical radiological description of diffuse cerebral edema alongside relatively normal cerebellar hemispheres and brainstem. Management of this pathology is symptomatic, and aims to ameliorate the associated raised intracranial pressure, control seizures and prevent cerebral infarction. The index patient, who presented 24 hours after severe head injury with associated early post-traumatic seizures, respiratory failure and brainstem dysfunction, had an unfavourable outcome consistent with previous reports of WCS. We have reported the rare but classical white cerebellum sign. It remains a grave prognosticator of cerebral injury and should be sought for in the neuroimaging of patients with acute brain insults.

BACKGROUND: Peripartum asphyxia is one of the main causes of neonatal morbidity and mortality. In moderate and severe cases of asphyxia, a condition called hypoxic-ischemic encephalopathy (HIE) and associated permanent neurological morbidities may follow. Due to the multifactorial etiology of asphyxia, it may be difficult prevent, but in term neonates, therapeutic cooling can be used to prevent or reduce permanent brain damage. The aim of this study was to assess the significance of different antenatal and delivery related risk factors for moderate and severe HIE and the need for therapeutic hypothermia.
METHODS: We conducted a retrospective matched case-control study in Helsinki University area hospitals during 2013-2017. Newborn singletons with moderate or severe HIE and the need for therapeutic hypothermia were included. They were identified from the hospital database using ICD-codes P91.00, P91.01 and P91.02. For every newborn with the need for therapeutic hypothermia the consecutive term singleton newborn matched by gender, fetal presentation, delivery hospital, and the mode of delivery was selected as a control. Odds ratios (OR) between obstetric and delivery risk factors and the development of HIE were calculated.
RESULTS: Eighty-eight cases with matched controls met the inclusion criteria during the study period. Maternal and infant characteristics among cases and controls were similar, but smoking was more common among cases (aOR 1.46, CI 1.14-1.64, p = 0.003). The incidence of preeclampsia, diabetes and intrauterine growth restriction in groups was equal. Induction of labour (aOR 3.08, CI 1.18-8.05, p = 0.02) and obstetric emergencies (aOR 3.51, CI 1.28-9.60, p = 0.015) were more common in the case group. No difference was detected in the duration of the second stage of labour or the delivery analgesia.
CONCLUSIONS: Smoking, induction of labour and any obstetric emergency, especially shoulder dystocia, increase the risk for HIE and need for therapeutic hypothermia. The decisions upon induction of labour need to be carefully weighed, since maternal smoking and obstetric emergencies can hardly be controlled by the clinician.

BACKGROUND: We present a severe neonatal consequence due to the unexpected and crucial inversion of the fetal position after sudden termination of tocolysis during early labor of a woman with congenital uterine anomaly. It has been reported that congenital uterine anomalies latently affect the fetal position. The clinical pitfalls in childbirth with uterine anomalies are discussed here on the basis of clinical evidence.
METHODS: At a perinatal medical center in Japan, a 29-year-old Japanese mother who had a history of bicornuate uterus, received tocolysis to prolong her pregnancy for 5 days during the late preterm period after preterm-premature rupture of the membrane. She gave birth to a 2304 g male neonate of the gestational age of 35 weeks and 5 days with severe asphyxia by means of crash cesarean section for fetal sustained bradycardia after sudden termination of tocolysis. We found the fetal position to reverse from cephalic to breech position during early labor. He ended up having severe cerebral palsy after brain cooling against hypoxic-ischemic encephalopathy for 3 days. The mechanism of inversion from cephalic to breech position without amnionic fluid remains unclear, although women with a known diagnosis of a uterine anomaly have higher risk of adverse outcomes such as malpresentation.
CONCLUSIONS: When considering the clinical course of this case on the basis of the medical reports, we suspected that uterine anomalies and changes in intrauterine pressure could cause fetal malpresentation and adverse neonatal outcomes.

BACKGROUND: Hypoxic-ischemic encephalopathy (HIE) appears in neurological conditions where some brain areas are likely to be injured, such as deep grey matter, basal ganglia area, and white matter subcortical periventricular áreas. Moreover, modeling these brain areas in a newborn is challenging due to significant variability in the intensities associated with HIE conditions. This paper aims to evaluate functional measurements and 3D machine learning models of a given HIE case by correlating the affected brain areas with the pathophysiology and clinical neurodevelopmental.
METHODS: A comprehensive analysis of a term infant with perinatal asphyxia using longitudinal 3D brain information from Machine Learning Models is presented. The clinical analysis revealed the perinatal asphyxia diagnosis with APGAR <5 at 5 and 10 minutes, umbilical arterial pH of 7.0 BE of -21.2 mmol / L), neonatal seizures, and invasive ventilation mechanics. Therapeutic interventions: physical, occupational, and language neurodevelopmental therapies. Epilepsy treatment: vagus nerve stimulation, levetiracetam, and phenobarbital. Furthermore, the 3D analysis showed how the volume decreases due to age, exhibiting an increasing asymmetry between hemispheres. The results of the basal ganglia area showed that thalamus asymmetry, caudate, and putamen increase over time while globus pallidus decreases.
RESULTS: spastic cerebral palsy, microcephaly, treatment-refractory epilepsy.
CONCLUSIONS: Slight changes in the basal ganglia and cerebellum require 3D volumetry for detection, as standard MRI examinations cannot fully reveal their complex shape variations. Quantifying these subtle neurodevelopmental changes helps in understanding their clinical implications. Besides, neurophysiological evaluations can boost neuroplasticity in children with neurological sequelae by stimulating new neuronal connections.

UNASSIGNED: Hypoxic-ischemic encephalopathy (HIE) is one of severe neonatal brain injuries, resulting from inflammation and the immune response after perinatal hypoxia and ischemia. IgG N-glycosylation plays a crucial role in various inflammatory diseases through mediating the balance between anti-inflammatory and pro-inflammatory responses. This study aimed to explore the effect of IgG N-glycosylation on the development of HIE.
UNASSIGNED: This case-control study included 53 HIE patients and 57 control neonates. An ultrahigh-performance liquid chromatography (UPLC) method was used to determine the features of the plasma IgG N-glycans, by which 24 initial glycan peaks (GPs) were quantified. Multivariate logistic regression was used to examine the association between initial glycans and HIE, by which the significant parameters were used to develop a diagnostic model. Though receiver operating characteristic (ROC) curves, area under the curve (AUC) and 95% confidence interval (CI) were calculated to assess the performance of the diagnostic model.
UNASSIGNED: There were significant differences in 11 initial glycans between the patient and control groups. The levels of fucosylated and galactosylated glycans were significantly lower in HIE patients than in control individuals, while sialylated glycans were higher in HIE patients (p < 0.05). A prediction model was developed using three initial IgG N-glycans and fetal distress, low birth weight, and globulin. The ROC analysis showed that this model was able to discriminate between HIE patients and healthy individuals [AUC = 0.798, 95% CI: (0.716-0.880)].
UNASSIGNED: IgG N-glycosylation may play a role in the pathogenesis of HIE. Plasma IgG N-glycans are potential noninvasive biomarkers for screening individuals at high risk of HIE.

Carbon monoxide (CO) poisoning during pregnancy is a rare occurrence, associated with high maternal and fetal mortality rates. As CO can cross the placenta, leading to intrauterine hypoxia, CO intoxication can result in neurological sequelae and neurologic complications in fetuses who survive. We report a case of a preterm newborn acutely exposed to CO in-utero and delivered by emergent cesarean section at the 31st week of gestation due to the severe burns suffered by the mother following an indoor boiler explosion. As CO has serious adverse effects both on the mother and fetus, it is important to recognize and treat poisoning in a timely manner. Despite maternal blood CO levels, CO intoxication at critical stage of central nervous system development can lead to hypoxic-ischemic lesions, thus interdisciplinary care and follow up for these patients are mandatory.

Hypoxic-ischemic encephalopathy (HIE) secondary to perinatal asphyxia occurs when the brain does not receive enough oxygen and blood. A surrogate marker for \"intact survival\" is necessary for the successful management of HIE. The severity of HIE can be classified based on clinical presentation, including the presence of seizures, using a clinical classification scale called Sarnat staging; however, Sarnat staging is subjective, and the score changes over time. Furthermore, seizures are difficult to detect clinically and are associated with a poor prognosis. Therefore, a tool for continuous monitoring on the cot side is necessary, for example, an electroencephalogram (EEG) that noninvasively measures the electrical activity of the brain from the scalp. Then, multimodal brain imaging, when combined with functional near-infrared spectroscopy (fNIRS), can capture the neurovascular coupling (NVC) status. In this study, we first tested the feasibility of a low-cost EEG-fNIRS imaging system to differentiate between normal, hypoxic, and ictal states in a perinatal ovine hypoxia model. Here, the objective was to evaluate a portable cot-side device and perform autoregressive with extra input (ARX) modeling to capture the perinatal ovine brain states during a simulated HIE injury. So, ARX parameters were tested with a linear classifier using a single differential channel EEG, with varying states of tissue oxygenation detected using fNIRS, to label simulated HIE states in the ovine model. Then, we showed the technical feasibility of the low-cost EEG-fNIRS device and ARX modeling with support vector machine classification for a human HIE case series with and without sepsis. The classifier trained with the ovine hypoxia data labeled ten severe HIE human cases (with and without sepsis) as the \"hypoxia\" group and the four moderate HIE human cases as the \"control\" group. Furthermore, we showed the feasibility of experimental modal analysis (EMA) based on the ARX model to investigate the NVC dynamics using EEG-fNIRS joint-imaging data that differentiated six severe HIE human cases without sepsis from four severe HIE human cases with sepsis. In conclusion, our study showed the technical feasibility of EEG-fNIRS imaging, ARX modeling of NVC for HIE classification, and EMA that may provide a biomarker of sepsis effects on the NVC in HIE.

UNASSIGNED: Perinatal asphyxia is a public health problem and the third major cause of death among children under 5 years.
UNASSIGNED: Two clinical cases of newborns with perinatal asphyxia submitted to therapeutic hypothermia and the follow-up of their motor development after hospital discharge have been reported.
UNASSIGNED: This retrospective case report study included two newborns with hypoxic-ischemic encephalopathy due to perinatal asphyxia who received a hypothermia protocol at the neonatal intensive care unit (NICU). The two newborns and their families were followed up at the outpatient clinic and assessed using the Hammersmith Child Neurological Examination, Alberta Child Motor Scale, and Denver Developmental Screening Test-II.
UNASSIGNED: The newborns were submitted to a 72-hour hypothermia protocol. One newborn remained for 13 days in the NICU, while the other remained for 22 days. According to the multidisciplinary team, both cases presented with typical motor development with no cerebral palsy during the follow-up.
UNASSIGNED: Both cases showed positive results and a good prognostic for motor development. Therapeutic hypothermia may be a strategy to prevent neurologic sequelae in newborns with perinatal asphyxia, including cerebral palsy.

Gastroschisis is a congenital, typically isolated, full-thickness abdominal wall defect in which the abdominal contents, usually only the small intestine, remain outside the abdominal cavity. It is commonly detected on fetal ultrasonography, and has generally excellent survival and outcomes, though these can be decreased in cases of complicated gastroschisis. We present the case of a female infant with a prenatal diagnosis of gastroschisis who required a prolonged and complex resuscitation after delivery. In addition to her gastroschisis, she presented with a history and physical examination consistent with severe hypoxic-ischemic encephalopathy and was treated with therapeutic hypothermia (TH) without further compromise to her bowel. In addition, careful consideration of neuroprotection, fluid status, bowel viability, and hemodynamics were undertaken in her care. She was discharged home on full enteral feeds, with only mild language and gross motor delays at 6 months of age. To our knowledge, there are no reports in the literature of the use of TH in the setting of unrepaired simple gastroschisis.

Neonatal hypoxic-ischemic encephalopathy is a clinical phenomenon that often results from perinatal asphyxia. To mitigate secondary neurologic injury, prompt initial assessment and diagnosis is needed to identify patients eligible for therapeutic hypothermia. However, occasionally neonates present with a clinical picture of hypoxic-ischemic encephalopathy without significant risk factors for perinatal asphyxia. We hypothesized that in patients with genetic abnormalities, the clinical manifestation of those abnormalities may overlap with hypoxic-ischemic encephalopathy criteria, potentially contributing to a causal misattribution. We reviewed 210 charts of infants meeting local protocol criteria for moderate to severe hypoxic-ischemic encephalopathy in neonatal intensive care units in Calgary, Alberta. All patients that met criteria for therapeutic hypothermia were eligible for the study. Data were collected surrounding pregnancy and birth histories, as well as any available genetic or metabolic testing including microarray, gene panels, whole-exome sequencing, and newborn metabolic screens. Twenty-eight patients had genetic testing such as microarray, whole-exome sequencing, or a gene panel, because of clinical suspicion. Ten of 28 patients had genetic mutations, including CDKL5, pyruvate dehydrogenase, CFTR, CYP21A2, ISY1, KIF1A, KCNQ2, SCN9A, MTFMT, and NPHP1. All patients lacked significant risk factors to support a moderate to severe hypoxic-ischemic encephalopathy diagnosis. Treatment was changed in 2 patients because of confirmed genetic etiology. This study demonstrates the importance of identifying genetic comorbidities as potential contributors to a hypoxic-ischemic encephalopathy phenotype in neonates. Early identification of clinical factors that support an alternate diagnosis should be considered when the patient\'s clinical picture is not typical of hypoxic-ischemic encephalopathy and could aid in both treatment decisions and outcome prognostication.