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An aerostat-lofted, sonic anemometer was used to determine instantaneous 3 dimensional wind velocities at altitudes relevant to fire plume dispersion modeling. An integrated GPS, inertial measurement unit, and attitude heading and reference system cor rected the wind data for the rotational and translational motion of the anemometer and rotated wind vectors to a global North, West, Up coordinate system. Data were taken at rates of 10 and 20 Hz to adequately correct for motion of the aerostat. The method was applied during a prescribed forest burn. These data were averaged over 15 min intervals and used as inputs for subsequent dispersion modeling. The anemometer's orientation data are demonstrated to be robust for converting the wind vector from the internal anemometer reference system to the global reference system with an average bias between 5 and 7°. Lofted wind data are compared with sonic anemometer data acquired at 10m on a mast located near the tether point of the aerostat and with local meteorological data. [ABSTRACT FROM AUTHOR]

Severe, too many to count retinal hemorrhages (RH) in infants have been associated with abusive head trauma, but can occur in short falls. An 8-month-old male fell backward from a height of 26 cm, landing on his buttocks then hitting the back of his head on a vinyl floor. The fall was videotaped. Acute subdural hemorrhages were found along with extensive, too many to count intra-RH in both eyes. Falls from small heights on to the occiput can lead to extensive RH of the type often associated with abusive head trauma., Competing Interests: CB declares no conflicts of interest. WS has testified in court regarding SBS cases, both for the defense and the prosecution. JM has testified, unpaid, for the defense regarding SBS cases., (© 2024 The Author(s). Clinical Case Reports published by John Wiley & Sons Ltd.)

The shaken baby syndrome was originally proposed in the 1970s without any formal scientific basis. Once data generated by scientific research was available, the hypothesis became controversial. There developed essentially two sides in the debate. One side claimed that the clinical triad of subdural haemorrhage, retinal haemorrhage, and encephalopathy, or its components, is evidence that an infant has been shaken. The other side stated this is not a scientifically valid proposal and that alternative causes, such as low falls and natural diseases, should be considered. The controversy continues, but the contours have shifted. During the last 15 years, research has shown that the triad is not sufficient to infer shaking or abuse and the shaking hypothesis does not meet the standards of evidence-based medicine. This raises the issue of whether it is fit for either clinical practice or for the courtroom; evidence presented to the courts must be unassailable. WHAT THIS PAPER ADDS: There is insufficient scientific evidence to assume that an infant with the triad of subdural haemorrhage (SDH), retinal haemorrhage, and encephalopathy must have been shaken. Biomechanical and animal studies have failed to support the hypothesis that shaking can cause SDH and retinal haemorrhage. Patterns of retinal haemorrhage cannot distinguish abuse. Retinal haemorrhages are commonly associated with extracerebral fluid collections (including SDH) but not with shaking. Infants can develop SDH, retinal haemorrhage, and encephalopathy from natural diseases and falls as low as 1 foot. The shaking hypothesis and the literature on which it depends do not meet the standards of evidence-based medicine., (© 2023 Mac Keith Press.)

Maturation of the human fetal brain should follow precisely scheduled structural growth and folding of the cerebral cortex for optimal postnatal function 1 . We present a normative digital atlas of fetal brain maturation based on a prospective international cohort of healthy pregnant women 2 , selected using World Health Organization recommendations for growth standards 3 . Their fetuses were accurately dated in the first trimester, with satisfactory growth and neurodevelopment from early pregnancy to 2 years of age 4,5 . The atlas was produced using 1,059 optimal quality, three-dimensional ultrasound brain volumes from 899 of the fetuses and an automated analysis pipeline 6-8 . The atlas corresponds structurally to published magnetic resonance images 9 , but with finer anatomical details in deep grey matter. The between-study site variability represented less than 8.0% of the total variance of all brain measures, supporting pooling data from the eight study sites to produce patterns of normative maturation. We have thereby generated an average representation of each cerebral hemisphere between 14 and 31 weeks' gestation with quantification of intracranial volume variability and growth patterns. Emergent asymmetries were detectable from as early as 14 weeks, with peak asymmetries in regions associated with language development and functional lateralization between 20 and 26 weeks' gestation. These patterns were validated in 1,487 three-dimensional brain volumes from 1,295 different fetuses in the same cohort. We provide a unique spatiotemporal benchmark of fetal brain maturation from a large cohort with normative postnatal growth and neurodevelopment., (© 2023. The Author(s).)

In infants, traumatic surface contusions of the brain are rare but subcortical clefts or cysts, variously labelled "contusional tears", "contusional clefts", "cortical tears" or "parenchymal lacerations" have been ascribed to trauma, and are even said to be characteristic of shaking and abuse. We describe the pathology of subcortical clefts or haemorrhages in seven infants. In none were the axonal swellings characteristic of traumatic axonal injury seen in relation to the clefts. Subpial bleeding was associated with clefts in all the cases of recent onset. We hypothesize that subcortical clefts are not due to direct mechanical forces of trauma but are part of a secondary cascade caused by impaired venous drainage which may or may not follow trauma. The finding of subcortical and subpial haemorrhages should prompt a search for CVT. We consider the term "contusion" is not accurate and is misleading., (Copyright © 2019 Elsevier B.V. All rights reserved.)

Objectives: To analyse subdural haemorrhage (SDH) during infancy in Sweden by incidence, SDH category, diagnostic distribution, age, co-morbidity, mortality, and maternal and perinatal risk factors; and its association with accidents and diagnosis of abuse., Methods: A Swedish population-based register study comprising infants born between 1997 and 2014, 0-1 years of age, diagnosed with SDH-diagnoses according to the (International Classification of Diseases, 10th version (ICD10), retrieved from the National Patient Register and linked to the Medical Birth Register and the Death Cause Register. Outcome measures were: 1) Incidence and distribution, 2) co-morbidity, 3) fall accidents by SDH category, 4) risk factors for all SDHs in the two age groups, 0-6 and 7-365 days, and for ICD10 SDH subgroups: S06.5 (traumatic SDH), I62.0 (acute nontraumatic), SDH and abuse diagnosis., Results: Incidence of SDH was 16·5 per 100 000 infants (n = 306). Median age was 2·5 months. For infants older than one week, the median age was 3·5 months. Case fatality was 6·5%. Male sex was overrepresented for all SDH subgroups. Accidental falls were reported in 1/3 of the cases. One-fourth occurred within 0-6 days, having a perinatal risk profile. For infants aged 7-365 days, acute nontraumatic SDH was associated with multiple birth, preterm birth, and small-for-gestational age. Fourteen percent also had an abuse diagnosis, having increased odds of being born preterm, and being small-for-gestational age., Conclusions: The incidence was in the range previously reported. SDH among newborns was associated with difficult birth and neonatal morbidity. Acute nontraumatic SDH and SDH with abuse diagnosis had similar perinatal risk profiles. The increased odds for acute nontraumatic SDH in twins, preterm births, neonatal convulsions or small-for-gestational age indicate a perinatal vulnerability for SDH beyond 1st week of life. The association between prematurity/small-for-gestational age and abuse diagnosis is intriguing and not easily understood., Competing Interests: The authors have declared that no competing interests exists.

The cause of death in infants who die suddenly and unexpectedly (sudden unexpected death in infancy [SUDI]) remains a diagnostic challenge. Some infants have identified diseases (explained SUDI); those without explanation are called sudden infant death syndrome (SIDS). Demographic data indicate subgroups among SUDI and SIDS cases, such as unsafe sleeping and apparent life-threatening events. Infants dying suddenly with retinal and dural bleeding are often classified as abused, but in many there is no evidence of trauma. Demographic features suggest that they may represent a further subgroup of SUDI. This review examines the neuropathological hypotheses to explain SIDS and highlights the interaction of infant oxygen-conserving reflexes with the brainstem networks considered responsible for SIDS. We consider sex- and age-specific vulnerabilities related to dural bleeding and how sensitization of the dural innervation by bleeding may influence these reflexes, potentially leading to collapse or even death after otherwise trivial insults., (© 2016 Mac Keith Press.)

Aim: Polymicrogyria (PMG) is one of the most common forms of cortical malformation yet the mechanism of its development remains unknown. This study describes the histopathological aspects of PMG in a large series including a significant proportion of fetal cases., Method: We have reviewed the neuropathology and medical records of 44 fetuses and 27 children and adults in whom the cortical architecture was focally or diffusely replaced by one or more festooning bands of neurons., Results: The pial surface of the brain overlying the polymicrogyric cortex was abnormal in almost 90% of cases irrespective of the aetiology. This accords with animal studies indicating the importance of the leptomeninges in cortical development. The aetiology of PMG was highly heterogeneous and there was no correlation between cortical layering patterns and aetiology. PMG was almost always associated with other brain malformations., Interpretation: The inclusion of many fetal cases has allowed us to examine the early developmental stages of PMG. The study indicates the significance of surface signals responsible for human corticogenesis and the complex interaction between genetic and environmental factors leading to this common endpoint of cortical maldevelopment., (© 2015 Mac Keith Press.)

Aim: To determine specific cell types and pathways involved in calcification of the developing brain., Method: We examined the detailed histopathology of samples from 28 autopsied brains aged from 22 weeks' gestation to 14 years. The samples were selected because they showed calcification associated with a range of different diseases. Samples were examined with routine stains as well as stains to show calcification and specific markers for endothelium and macrophages., Results: Our observations indicate that calcification develops via two main pathways: dystrophic and vascular. Dystrophic calcification results from membrane disruption and uncontrolled calcium entry into necrotic (dead) cells in ischaemia and infections. Vascular calcification appears to be initiated in protein globules, sometimes intracellular, but outside the endothelium of small vessels. One case with mutation of the occludin gene, implicating impaired endothelial integrity, showed this pattern, but identical vascular calcification was seen in other conditions, including Sturge-Weber syndrome. Another form of vascular calcification involved the adventitia of arteries; the endothelium was always spared., Interpretation: Calcification in the developing brain that is not associated with tissue necrosis is initiated in cells associated with blood vessels. Calcium incrustation of blood vessels imposes rigidity, reduced vascular compliance, and altered permeability. This would explain associated atrophy, gliosis, and (in the developing brain) malformations of the cortex. Our findings suggest that pericytes initiate non-dystrophic brain calcification, but further studies are needed to explore this possibility., (© 2014 Mac Keith Press.)

Polymicrogyria (PMG) is a complex cortical malformation which has so far defied any mechanistic or genetic explanation. Adopting a broad definition of an abnormally folded or festooned cerebral cortical neuronal ribbon, this review addresses the literature on PMG and the mechanisms of its development, as derived from the neuropathological study of many cases of human PMG, a large proportion in fetal life. This reveals the several processes which appear to be involved in the early stages of formation of polymicrogyric cortex. The most consistent feature of developing PMG is disruption of the brain surface with pial defects, over-migration of cells, thickening and reduplication of the pial collagen layers and increased leptomeningeal vascularity. Evidence from animal models is consistent with our observations and supports the notion that disturbance in the formation of the leptomeninges or loss of their normal signalling functions are potent contributors to cortical malformation. Other mechanisms which may lead to PMG include premature folding of the neuronal band, abnormal fusion of adjacent gyri and laminar necrosis of the developing cortex. The observation of PMG in association with other and better understood forms of brain malformation, such as cobblestone cortex, suggests mechanistic pathways for some forms of PMG. The role of altered physical properties of the thickened leptomeninges in exerting mechanical constraints on the developing cortex is also considered.

This review presents an overview of human cortical malformation based on the insights gained from examination of human fetal brains. Examination at early stages of fetal brain development allows the identification of the specific pathways which are disrupted in human cortical malformation. Detailed examination of human fetal brains in parallel with studies of genetics and animal models is leading to new concepts of cortical malformations. Here we review a range of human cortical malformations based on a simple classification according to the developmental process thought to be disrupted: neuroblast proliferation, undermigration, overmigration, cortical maturation and destructive lesions. A single case example of a dated intrauterine injury illustrates the spectrum of malformations which may result at a single period in development. The recommended methods of examination of human fetal brain are described together with some of their pitfalls. Detailed neuropathological observations indicate the need for caution in the classification of malformations; radiological findings and pathology of the mature brain do not reflect the specific disruptive pathways of cortical malformations. While many insults may lead to the same pattern of malformation, a single insult can lead to multiple patterns of malformation. Our detailed studies of the human fetal brain suggest that the interface between the meninges and the radial glial end feet may be an intriguing new focus of interest in understanding cortical development., (© 2010 The Authors. Journal of Anatomy © 2010 Anatomical Society of Great Britain and Ireland.)

Band-like calcification with simplified gyration and polymicrogyria (BLC-PMG) is a rare autosomal-recessive neurological disorder showing highly characteristic clinical and neuroradiological features. Affected individuals demonstrate early-onset seizures, severe microcephaly, and developmental arrest with bilateral, symmetrical polymicrogyria (PMG) and a band of gray matter calcification on brain imaging; as such, the disorder can be considered as a "pseudo-TORCH" syndrome. By using autozygosity mapping and copy number analysis we identified intragenic deletions and mutations in OCLN in nine patients from six families with BLC-PMG. The OCLN gene encodes occludin, an integral component of tight junctions. Neuropathological analysis of an affected individual showed similarity to the mouse model of occludin deficiency with calcification predominantly associated with blood vessels. Both intracranial calcification and PMG are heterogeneous in etiology. Neuropathological and clinical studies of PMG have suggested that in utero ischemic or vascular insults may contribute to this common cortical abnormality. Tight junctions are functional in cerebral blood vessels early in fetal development and continue to play a vital role in maintenance of the blood-brain barrier during postnatal life. We provide evidence that the tight junction protein occludin (encoded by the OCLN gene) is involved in the pathogenesis of malformations of cortical development., (2010 The American Society of Human Genetics. Published by Elsevier Inc. All rights reserved.)

Purpose: Doublecortin (DCX) is a microtubule-associated protein with regulatory roles in radial and tangential migration of neurons during cortical development. In normal adult cortex there is restricted expression, and DCX is widely used as a marker of neurogenesis. Imperfect corticogenesis is thought to underpin many focal cortical pathologies in epilepsy surgical series, including focal cortical dysplasia (FCD). The aim was to study DCX expression patterns in such lesions compared to normal developing and mature cortex., Method: Cases of FCD types Ia (13) and IIb (4), pediatric hippocampal sclerosis (HS) (5), temporal lobe sclerosis (5), glioneuronal tumors (5), gray matter heterotopia (3), and control tissues (16) from a wide age range [20 gestational weeks (GW) to 85 years] were studied using immunohistochemistry to DCX., Results: In controls and all epilepsy cases, perinuclear labeling of small round cells (SRCs) and satellite perineuronal cells was observed in both postmortem and surgical tissues. In FCD Ia up to the age of 4 years, prominent DCX-positive (DCX(+)), immature cells were present along the junction of layers I and II, with processes extending into the molecular layer. These cell types were not a significant feature in other pathologies, which showed multipolar DCX(+) cells or labeling of dysmorphic cells throughout the cortex., Discussion: Persistent cellular DCX expression is confirmed in normal adult cortex. Characteristic expression patterns in layer II of FCD Ia could indicate delayed or abnormal cortical maturation rather than ongoing cytogenesis. This could be indicative of enhanced local cortical plasticity as well as a potential diagnostic feature of this type of pathology.

Subdural haemorrhage (SDH) in the infant has a different pattern from that seen in the older child and adult. It is usually a widespread, bilateral, thin film, unlike the thick, space-occupying and often unilateral clot seen in older children and adults after trauma. Whether both arise by the same mechanism is unknown, but it seems unlikely. Most SDH is said to be due to trauma but in infants there are other, atraumatic causes. Birth is also important; recent MRI studies show an incidence of almost 50% in asymptomatic neonates. Traumatic SDH is said to result from rupture of bridging veins but new insights into the anatomy of infant dura suggest a dural origin for thin film subdural bleeding in young babies. Acute SDH usually rapidly resolves, but sometimes develops into a chronic fluid collection. Healing of SDH is by formation of a granulating membrane which may confer vulnerability to rebleeding, either spontaneously or after an otherwise innocuous event. SDH has a particular significance as one of the features of the triad (together with retinal haemorrhage and encephalopathy) associated with non-accidental injury. As the possibility of non-accidental injury is often first raised by a radiologic report of subdural bleeding, it becomes critically important in the interpretation of the scan appearances to understand the unique physiology and anatomy of the infant dura.

Background and Purpose: Sturge-Weber syndrome (SWS) is frequently associated with neurologic complications such as seizures, so diagnosing this condition has important implications for patient management. The purpose of this study was to report unusual neuroimaging findings in patients with facial port-wine stain (PWS) and clinically suspected SWS., Materials and Methods: Cranial MR imaging was reviewed for all children with facial port-wine stain (PWS) involving the upper face and eyelids who were referred to Great Ormond Street Hospital between 2003 and 2007 for investigation of suspected SWS. Patients were excluded from further analysis if the imaging findings were normal on initial and subsequent scans and the subject remained free of neurologic disease, or if the imaging showed the well-recognized pattern of exclusively supratentorial pial enhancement representing the pial angioma of SWS. For the remaining patients, the neurologic, dermatologic, and ophthalmologic records were examined and all available imaging was reviewed by a neuroradiologist. We documented the presence and distribution of pial enhancement; corroborative features of SWS, such as atrophy, calcification, choroid plexus changes, and ocular abnormalities; and all other intracranial abnormalities., Results: Of the 62 patients referred for assessment, imaging findings were considered typical of SWS in 32 (52%) and were normal or showed abnormalities attributable to an unrelated pathology in 20 (32%). Of the remaining 10 patients, in 7 (11%), there was evidence of a pial angioma in an unusual distribution involving infratentorial structures, with the angioma in 1 patient being diagnosed at postmortem only; in 2 (3%), there were imaging abnormalities with some features in common with typical SWS, such as subcortical calcification, but with no evidence of pial enhancement; in 1 (1.6%), the initial MR imaging finding was normal, but repeat imaging subsequently revealed pial enhancement., Conclusions: Involvement of infratentorial structures is common but may be relatively subtle and should be actively sought. Cases in which there are certain patterns of imaging abnormalities but an apparent absence of supratentorial pial enhancement on MR imaging may represent formes frustes of SWS; visualization of pial angiomatosis may also be delayed until later in childhood than expected.