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Injuries to the scalp and cranium are often encountered in children who suffer abusive head trauma. Various imaging modalities, such as radiography, CT and MRI, contribute to accurately diagnosing these injuries and reliably differentiating them from normal variants. A significant challenge in both radiographic and clinical evaluations of skull fractures and extracranial soft tissue injuries is the resemblance between accidental and nonaccidental injuries. Thus, a comprehensive approach that combines imaging findings with the patient’s history, physical examination and laboratory results is essential in each case. This chapter presents vital information on the developmental anatomy of the cranium and scalp and how these relate to traumatic injuries. It also reviews the imaging features of typical abusive injuries, their association with specific mechanisms of trauma and the appropriateness of various imaging modalities.
Facial and orbital trauma are frequently seen in cases of child abuse, with certain patterns, such as specific types of retinal haemorrhage, being highly indicative of abusive head trauma. These injuries can be subtle on imaging and often lack a clear history. While some abusive injuries may resemble accidental ones, particular injury patterns or combinations of injuries, alongside additional clinical findings, raise concerns for abuse. Radiologists play a critical role in diagnosing these injuries by obtaining a thorough history and utilizing advanced imaging techniques like MRI and CT with three-dimensional reconstructions, which provide detailed views of soft tissue and bone. Recognizing subtle signs of trauma and correlating them with the clinical context is essential for accurate diagnosis and the child’s protection. Early detection and precise diagnosis by the radiologist enable the multidisciplinary team to intervene appropriately, ensuring the safety and well-being of vulnerable children.
This chapter provides a summary of longstanding and updated research for the accurate diagnosis of fractures of the clavicle, sternum and scapula in the setting of suspected physical abuse of infants and young children. Findings key to diagnosing fractures by radiographic skeletal survey, computed tomography, ultrasound and magnetic resonance imaging are demonstrated with numerous representative examples. A section for each of these anatomical regions includes a detailed review of anatomy and injury mechanisms in addition to characteristic imaging features. Considerations for differential diagnosis and pitfalls in interpretation are presented specific to each anatomic area. Attention to imaging technique and careful evaluation of findings are emphasized to promote proper diagnosis.
Abusive spinal injury is important to understand and recognize as it may be the only manifestation of child physical abuse and may result in significant morbidity and mortality if undetected. In this chapter, we review historical literature about spinal trauma in the era of radiography and skeletal surveys as well as the expanding literature, epidemiology and understanding of this manifestation of inflicted injury in the era of increased CT and MRI utilization. We highlight key anatomic considerations of developing infants and young children, which make them susceptible to specific types of inflicted spine trauma with emphasis placed on the craniocervical junction, which is particularly susceptible to injury. We provide many imaging case examples to help the reader understand and recognize the myriad and specific types of injuries that occur. Considering our increased understanding of abusive spinal trauma, we discuss implications to imaging evaluation, technique and screening if inflicted spinal injury is detected or suspected.
Visceral injuries are important manifestations of child abuse. This chapter reviews mechanisms, clinical presentation and imaging of inflicted injuries involving the neck, thorax, abdomen and pelvis. Because most visceral injuries can be plausibly explained as accidental, the significance of the injuries noted radiologically must be assessed in conjunction with the clinical context, including age and ambulatory status of the child, and other imaging findings, particularly skeletal findings that may be more specific for abuse.
This chapter, written by a team of radiologists, a pathologist and a child abuse pediatrician, focuses on extra-axial hemorrhage, i.e., epidural, subdural, subarachnoid and intraventricular hemorrhage, in relation to abusive head trauma. For each, an in-depth discussion of the hemorrhage and it’s clinical presentation in combination with imaging and neuropathological considerations is presented. In the section on subdural hematomas (SDHs), attention is also focused on birth-related SDHs and SDHs in children with benign enlargement of the subarachnoid space. Other types of subdural collections are presented, although with a more limited scope.
Given the relevance in child abuse investigations the authors also present data helpful in differentiating between accidental and nonaccidental causes of extra-axial hemorrhage and on the potential of imaging and neuropathologic examinations in dating the traumatic event leading to the extra-axial hemorrhage.
Post-mortem imaging is an indispensable tool in the investigation of suspicious childhood deaths, particularly for identifying fractures and intracranial hemorrhages. It offers significant logistical advantages over traditional autopsies, including cost-effectiveness and rapid image acquisition. However, its application requires close collaboration between radiologists, pathologists and forensic experts, and is rarely used as a standalone approach. This chapter delves into the role of post-mortem imaging, with a primary focus on post-mortem CT and some coverage of post-mortem MRI and novel techniques of micro-CT and linear slot scanning.
The chapter discusses key medicolegal considerations, imaging protocols, common findings and interpretation challenges and the importance of maintaining strict chain-of-custody protocols. As post-mortem imaging continues to gain traction, we underscore the need for standardized imaging protocols and enhanced support for multidisciplinary teams to safeguard the well-being of professionals conducting these sensitive examinations.
This chapter reviews the most common clinical presentations of abusive head trauma (AHT) and associated indications for imaging. The presentation of AHT is highly variable, and may include a history of accidental trauma, acute neurologic or constitutional symptoms, sentinel non-central nervous system (CNS) injuries, macrocephaly or chronic neurologic dysfunction or asymptomatic high-risk contacts of a child abuse victim. The indications for screening neuroimaging depend on clinical presentation and level of concern. Some patients warrant evaluation based on acute neurological presentation. In others the clinical history, physical examination, laboratory and non-CNS radiologic findings indicate the need for screening. This chapter reviews the available evidence and outlines an approach to screening neuroimaging followed by diagnostic evaluation. Cranial ultrasound, CT or MRI are used depending on presentation and clinical setting. If screening neuroimaging is suspicious for AHT then full diagnostic neuroimaging evaluation with brain and often spine MRI is essential. Strengths and limitations of the modalities used are discussed.
Abusive head trauma (AHT) is a leading cause of traumatic death in infants, often resulting in severe brain injuries with lifelong consequences. It can cause cognitive, sensory and behavioral impairments, which may not fully emerge until later in childhood. AHT injuries are typically classified as primary (direct mechanical damage, such as contusions and lacerations) or secondary (indirect effects like hypoxic-ischemic injury and cerebral edema).
Infants are particularly vulnerable due to factors like poor neck control, larger head size and incomplete brain development. Neuroimaging, especially MRI and diffusion-weighted imaging, is essential for diagnosing these injuries and tracking their evolution, as some manifestations develop over days or weeks. Mechanisms of cell death, including necrosis, apoptosis and autophagy, play a key role in the progression of brain damage.
Differentiating AHT from accidental trauma is challenging. Certain patterns, such as subdural hemorrhages with ischemic injury, strongly suggest abuse. Comprehensive imaging, clinical evaluation and follow-up are crucial for documenting injury progression and understanding its impact on the developing brain.
The habenula, a small brain structure involved in processing aversive stimuli, has been strongly implicated in the pathophysiology of mood disorders. While diminutions in hippocampal and medial prefrontal cortex volume have been demonstrated in individuals with a mood disorder, evidence for structural alterations in the habenula remains inconsistent. This set of meta-analyses examines whether individuals with a mood disorder show alterations in habenula volume compared to healthy controls. We conducted six meta-analyses. Two global analyses compared left and right habenula volumes between individuals with a mood disorder (MDD or BD) and healthy controls (HCs), each including 15 samples (left: 1,230 participants; right: 1,236). Four additional analyses compared MDD versus HCs and BD versus HCs for left and right volumes separately. Subgroup and meta-regression analyses tested the habenula segmentation method, medication status, and MRI resolution as moderators. The global meta-analyses pooling MDD and BD data showed small but significant volume reductions in the left (g = −0.1367, p = .0344) and right (g = −0.1562, p = .0409) habenula in mood disorder patients compared to controls. However, these effects did not survive correction for multiple comparisons. After correction, no significant group differences were found in the diagnosis-specific meta-analyses (MDD versus controls; BD versus controls), and no moderator analyses were significant. Current evidence points toward small habenula volume reductions in mood disorders, though findings did not withstand correction for multiple comparisons. Further high-resolution neuroimaging studies are needed to clarify habenula volume alterations in mood disorders.
Congenital uterine anomalies arise from an abnormality in the embryological development process. There can be defects in unification, canalisation or complete agenesis. Uterine anomalies are mnore common in those who experience miscaarriage compared with the general population. Patients with uterine anomalies are at higher risk of infertility, early and second trimester miscarriage, pre-term birth and malpresenatation at delivery.
Maternal hyperglycemia is associated with higher risk of metabolic diseases in offspring. Despite various hypotheses, the exact mechanisms remain unclear and the neural implication is yet to be fully investigated. The hypothalamus plays a critical role in energy regulation. In utero exposure to maternal hyperglycemia might selectively affect the developing hypothalamus. To test this hypothesis, we investigated associations between in utero exposure to maternal hyperglycemia and hypothalamic volume at 10–12 years of age. We included 82 mother–child pairs from the Gen3G prospective birth cohort, followed up 10–12 years after birth. Women underwent a 75g Oral Glucose Tolerance Test (OGTT) at 24–30 weeks of gestation, and we calculated the area-under-the-curve of glucose (AUCgluc) from maternal glucose measurements at fasting, 1h and 2h during OGTT to reflect prenatal hyperglycemia exposure. During the follow-up visit at 10–12 years of age, a subsample of children (n = 82) completed 3 T brain magnetic resonance imaging (MRI) to quantify brain volumes with FreeSurfer 7. We used Pearson correlations and partial correlations with adjustments to test associations between the AUCgluc and offspring hypothalamic brain volumes. We found that higher maternal AUCgluc was associated with greater total offspring hypothalamic volume (r = 0.30; p = 0.006). In comparison, no other brain region was significantly correlated with the maternal AUCgluc. Correlations remain significant when adjusted for maternal or offspring’s variables. Overall, we found that higher maternal glycemic response following OGTT in pregnancy appears associated with larger offspring hypothalamic volume. Our results suggest that prenatal exposure to hyperglycemia may lead to hypothalamic programming.
Anorexia nervosa (AN) is an eating disorder that is mediated by psychological and metabolic factors, yet it is unclear how these factors interact. The NAMA trial objective is to clarify the metabo–psychiatric interaction and identify how it affects AN patients’ behaviour. This randomised trial will recruit thirty-six treatment-naïve female AN patients, 13–18 years of age, and thirty-six matched healthy controls. Participants will undergo psychiatric assessments followed by 12-h overnight fasting. The next morning, baseline assessments of outcomes will be performed. Patients will be randomly allocated 1:1 to receive a mixture with calories or receive a mixture without calories. Healthy controls will also be allocated to receive mixtures with/without calories. Mixtures will be standardised for taste and appearance, and allocation will be masked. The primary outcome measure is resting-state functional MRI 60 min post-consumption of the mixture. Secondary outcomes include (1) blood samples to study markers reflecting metabolic states, hunger/satiety and stress responses, (2) psychometric evaluations of subjective experiences and (3) assessment, in a second meal 3 h later, of the effects of previous calorie intake on subsequent food consumption. This article describes the study protocol, including the analysis plan, for a randomised controlled trial to comprehensively evaluate the effects of calorie intake in AN. The trial will distinguish psychological and metabolic neuronal networks associated with food intake and uncover how their integration affects food intake and other hallmark symptoms in AN. The aim is to accelerate treatment development by identifying brain mechanisms that drive AN.
Considerable effort has been devoted to investigate the neuroimaging correlates and predictors of antidepressant response to ketamine, yet inconsistency in the location and nature of the regional brain effects makes it difficult to unify this research. Despite the revolutionary notion that psychiatric therapeutics show network-level brain representations, investigations into network localization of brain functional effects of ketamine treatment are still lacking.
Methods
We initially identified the locations of longitudinal brain functional alterations (increase and decrease separately) induced by ketamine treatment from 16 published studies with 508 depressed patients. By integrating these affected brain locations with large-scale functional MRI datasets from 1113 healthy and 255 depressed individuals, we then leveraged a novel functional connectivity network mapping approach to construct ketamine-induced hyper-functional and hypo-functional networks respectively.
Results
The hyper-functional network mainly involved the subcortical (caudate nucleus and thalamus) and default (medial prefrontal cortex) networks, while its hypo-functional counterpart predominantly implicated the limbic (temporal pole), subcortical (hippocampus and amygdala), and default (lateral temporal cortex) networks.
Conclusion
Our findings may shed light on the neurobiological effects of ketamine from a network perspective, which might represent a crucial step toward fostering the clinical application of ketamine in antidepressant treatment.
People with schizophrenia develop more chronic diseases at a younger age and die younger than people in the general population. It has been hypothesized that this excess morbidity and mortality could be partially due to accelerated aging in schizophrenia. If true, this would motivate the development of ‘gero-protective’ interventions to reduce chronic disease burden in schizophrenia. However, it has been difficult to test this hypothesis, in part, due to the limited ability to measure aging in samples of people with schizophrenia.
Methods
We utilized a novel neuroimaging biomarker of the longitudinal pace of aging, DunedinPACNI, to test for accelerated whole-body aging in schizophrenia across four neuroimaging datasets (total N = 2,096, 48% female) accessed through the Lieber Institute for Brain Development, the University of Bari Aldo Moro, and the North American Prodrome Longitudinal Study – 3.
Results
We found consistent evidence of faster DunedinPACNI in schizophrenia compared with controls. In contrast, youth at clinical-high risk for psychosis did not have faster DunedinPACNI compared to controls. Unaffected siblings of patients also did not have faster DunedinPACNI than controls. Faster DunedinPACNI in schizophrenia was not explained by tobacco smoking or antipsychotic medication use.
Conclusions
The results support the hypothesis that schizophrenia is accompanied by accelerated aging. Results were inconsistent with some of the most obvious explanations for accelerated aging in schizophrenia (familial risk, smoking, and iatrogenic medication effects). Research should aim to uncover why people who have schizophrenia age rapidly, as well as the utility of early disease-risk monitoring and anti-aging interventions in schizophrenia.
Right atrial appendage aneurysm, or giant right atrial appendage, is extremely rare, with very few cases reported in scientific literature. We sought to systematically review the published cases of right atrial appendage aneurysm in terms of age, sex, clinical presentation, electrocardiography, imaging (chest X-ray, echocardiography, CT/cardiac magnetic resonance), and outcome.
Methodology:
An electronic search for case reports, case series, and related articles published until March 2025 was carried out, and clinical data were extracted and analysed.
Results:
Forty-four cases of right atrial appendage aneurysm were identified with a clear male prevalence (68.2%) and commonly presenting in the third decade of life. Palpitation (27.3%) and dyspnoea (18.2%) were the most common clinical presentations, whereas 40.9% of right atrial appendage aneurysm patients were asymptomatic. Electrocardiography was done in 77.3% of the sample. It displayed an atrial arrhythmia (atrial fibrillation or flutter, atrial tachycardia, supraventricular tachycardia) in 31.8%. A chest X-ray was done in 65.9%. Echocardiography was the most common diagnostic modality (93.2%). Right atrial appendage aneurysm diagnosis was confirmed on CT and/or MRI in 79.5%. The mean size of the right atrial appendage aneurysm was 93 × 70 mm. In 12 patients (27.3%), an associated congenital cardiac abnormality was found, mostly in the form of an atrial septal defect/patent foramen ovale (22.7%). Half of the patients (50.0%) were treated surgically, whilst 47.8% were treated medically with close follow-up. One patient experienced right atrial appendage aneurysm reduction in size after atrial septal defect device closure. One death (2.3%) was reported also.
Conclusion:
Although very uncommon, right atrial appendage aneurysm can be linked to considerable morbidity. Surgical removal is recommended for patients who are symptomatic.
Early diagnosis of amyotrophic lateral sclerosis (ALS) is essential for treatment initiation and symptom management, yet it remains challenging due to nonspecific symptoms and the lack of reliable diagnostic biomarkers. Although conventional MRI sequences such as T2* weighted and fluid-attenuated inversion recovery (FLAIR) have shown potential in identifying upper motor neuron abnormalities, their diagnostic utility in ALS is not well established. This study aimed to evaluate the sensitivity and specificity of brain T2* weighted and FLAIR MRI sequences in diagnosing ALS using prospectively collected data and to assess associations with disease severity.
Methods:
Data were analyzed from 20 patients with ALS and 20 healthy controls enrolled at the Edmonton site of the Canadian ALS Neuroimaging Consortium 1 (CALSNIC-1) study. Single-slice 2D axial susceptibility-weighted echo planar imaging (SWEPI) and FLAIR images were independently rated by a blinded neurologist and radiologist for signs of corticospinal tract and motor cortex abnormalities. Sensitivity and specificity were calculated, and linear regression was used to examine associations with ALS Functional Rating Scale-Revised (ALSFRS-R) scores.
Results:
T2* weighted and FLAIR MRI sequences showed high specificity (0.95 and 0.85, respectively) but low sensitivity (both 0.25) for ALS diagnosis. No significant correlation was found between imaging abnormalities and ALSFRS-R scores. Inter-rater reliability was poor (κ = 0.25 for SWEPI; κ = 0.14 for FLAIR).
Conclusion:
While T2* weighted and FLAIR MRI sequences may have some specificity for ALS, our study suggests they are not sufficiently sensitive to be used as reliable diagnostic tools for ALS.
Understanding the neuroanatomical correlates of treatment response in schizophrenia is crucial for improving clinical stratification and clarifying underlying pathophysiological mechanisms.
Aims
To examine subcortical volumetric differences across clinically defined schizophrenia treatment-response subgroups.
Method
T1-weighted structural magnetic resonance imaging data were analysed from 109 participants, including 79 individuals with schizophrenia and 30 healthy controls. Patients were categorised into three distinct treatment response groups: ultra-treatment-resistant (UTR; n = 22), clozapine-responsive (n = 28) and first-line antipsychotic responsive (FLR; n = 29). Group differences were examined across 33 regions of interest, including subcortical, ventricular and hippocampal subfield regions.
Results
The UTR group had higher antipsychotic dosages and exhibited greater symptom severity than other patient groups. Across all schizophrenia subgroups, hippocampal and amygdala volumes were smaller relative to controls. Treatment-resistant patients (UTR and clozapine-responsive) also showed reduced nucleus accumbens volumes, whereas FLR patients demonstrated larger pallidal volumes. In addition, the UTR subgroup exhibited enlarged lateral ventricles. Hippocampal subfield analyses revealed widespread reductions in treatment-resistant patients, most prominently in the CA4/dentate gyrus, subiculum and stratum, whereas FLR patients showed more focal reductions in the CA4/dentate gyrus and left subiculum.
Conclusions
These results suggest that smaller hippocampal and amygdala volumes represent a shared neuroanatomical signature of schizophrenia, whereas reduced accumbens and enlarged pallidal volumes may differentiate treatment-resistant and treatment-responsive profiles, respectively. The findings underscore the heterogeneity of schizophrenia and highlight the need for longitudinal research to disentangle illness-related pathology from medication effects.
Half a century of neuroimaging has transformed our understanding of psychiatric disorders but not our clinical practice. This piece examines why that promise remains unfulfilled and argues that the future lies not in ever newer tools but in rigorous, mechanistically grounded and clinically embedded imaging approaches that bridge brains, behaviours and treatments.
Loss of signals from substantia nigra (SN) and locus coeruleus (LC) on neuromelanin (NM)-sensitive sequences of MRI is reported as a potential biomarker in patients with Parkinson’s disease (PD) and related diseases. This scoping review aims to consolidate current knowledge on MRI techniques to visualize and quantify these signals and their clinical applications in PD. Publicly available databases were searched for original studies using MRI to quantify NM in PD and other related disorders. Different studies were compared based on MRI sequence, quantification techniques and correlations with clinical scores. Furthermore, studies on genetic forms of PD and prodromal PD were also evaluated and compared. The most common MRI sequences used were T1-weighted sequences and gradient echo sequences. Different studies used different quantitative measures such as signal-to-noise ratio, contrast-to-noise ratio and contrast ratio. Morphometric evaluations such as volume and area of the SN and LC signals were also used. Most studies showed evidence of significant difference in the signals in different stages of PD compared to controls both at the SN and LC. There were significant correlations between the SN and LC signals and clinical scores. Hence, quantification of these signals may be reliable in diagnosis and disease monitoring in PD. The relative ease of signal quantification and widespread availability of MRI may make it a quantitative surrogate biomarker.