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Several neuroimaging studies on psychosis spectrum have been published in the last decades, most of them based on schizophrenia. In the context of neuroanatomical dysfunctions, clinical and prognosis implications have been reported. Nevertheless, only a few studies have been focused on delusional disorder (DD).
To present the case of a patient diagnosed with DD who suffered from two cerebrovascular events after the onset of the psychiatric disease. Our aim is to elucidate potential implications of those lesions on the course of DD. We also reviewed the literature to assess evidence for specific changes in DD on brain structures and functions.
Case report and non-systematic narrative review in PubMed (2000-2020).
Case report: A 66-year-old female with DD presenting, during the course of the disease, general atrophy and consecutive ischemic lesions on parietal, occipital and cerebellar areas. Clinical stabilization was achieved 12-16 months after risperidone 1.5mg/day treatment. Review: 19 studies were included: Structural brain data (n=15), Functional data (n=13). Most of the structural neuroimaging studies reported white and gray matter abnormalities, particularly in temporal, parietal and frontal lobes, and in limbic structures. Functional neuroimaging studies pointed to temporal and parietal lobes, as well as basal ganglia and limbic related structures.
Temporal, parietal, frontal, basal ganglia and limbic-related structures, as well as dysfunctions in other specific brain regions, may be implicated in the core symptoms of DD. These findings might be further investigated as potential neuroimaging markers of prognosis, such as partial or delayed response to antipsychotic treatment, as presented in our case.
Neuroimaging research regularly yields “incidental findings”: observations of potential clinical significance in healthy volunteers or patients, but which are unrelated to the purpose or variables of the study.
Fluorescence in vivo endomicroscopy (FIVE) is a state-of-the-art endoscopy technique used to image tissue interactions and molecular events in a cell. In Part 1 of this series, the history, types of confocal laser endomicroscopy (CLE), and limitations of the technology were discussed. In Part 2 of the series, we describe several applications of FIVE technology, including advances in cancer, gastrointestinal, liver, rectal mucosal barrier function, acute lung injury, and brain imaging. Future perspectives for the technology are also presented.
Spontaneous cerebrospinal fluid leak of the temporal bone is an emerging clinical entity for which prompt and accurate diagnosis is difficult given the subtle signs and symptoms that patients present with. This study sought to describe the key temporal bone abnormalities in patients with spontaneous cerebrospinal fluid leak.
A retrospective cohort study was conducted of adult patients with biochemically confirmed spontaneous cerebrospinal fluid leak. Demographics and radiological features identified on computed tomography imaging of the temporal bones and/or magnetic resonance imaging were analysed.
Sixty-one patients with spontaneous cerebrospinal fluid leak were identified. Fifty-four patients (88.5 per cent) underwent both temporal bone computed tomography and magnetic resonance imaging. Despite imaging revealing bilateral defects in over 75 per cent of the cohort, only two patients presented with bilateral spontaneous cerebrospinal fluid leaks. Anterior tegmen mastoideum defects were most common, with an average size of 2.5 mm (range, 1–10 mm).
Temporal bone computed tomography is sensitive for the identification of defects when suspicion exists. In the setting of an opacified middle ear and/or mastoid, close examination of the skull base is crucial given that this fluid is potentially cerebrospinal fluid.
The game of chess has provided a proper domain to study central psychophysiological mechanisms underlying basic psychological processes such as stress, emotion, or decision-making. This chapter describes the studies about the psychophysiology and brain functioning of chess players mostly involving the application of electroencephalography (EEG), functional magnetic resonance, or positron emission tomography, even though it reports about findings analyzing other issues such as cardiac and hormonal responses, and the topic of doping in chess. In addition, the chapter addresses three central themes in the study of the brain of chess players: the activation of cerebral cortex areas, the hemispheric specialization, and the anatomical changes.
Economic globalization brings increasing demands and opportunities for intercultural training and education that produce novel consequences on people’s mind, behavior, and life quality. Why and how do intercultural training and education change mind and behavior? This chapter aims to address these issues from a cultural neuroscience perspective. By reviewing recent brain imaging findings of East Asian/Western cultural differences in neural underpinnings of cognition and emotion, we discuss the neural basis for understanding intercultural training and education by examining changes of functional brain activity underlying cognitive and affective processes. We propose a theoretical analysis of intercultural training and education based on the culture-behavior-brain loop model of human development. Future issues related to intercultural training and education are discussed.
Catatonia is a frequent, complex and severe identifiable syndrome of motor dysregulation. However, its pathophysiology is poorly understood.
We aimed to provide a systematic review of all brain imaging studies (both structural and functional) in catatonia.
We identified 137 case reports and 18 group studies representing 186 individual patients with catatonia. Catatonia is often associated with brain imaging abnormalities (in more than 75% of cases). The majority of the case reports show diffuse lesions of white matter, in a wide range of brain regions. Most of the case reports of functional imaging usually show frontal, temporal, or basal ganglia hypoperfusion. These abnormalities appear to be alleviated after successful treatment of clinical symptoms. Structural brain magnetic resonance imaging studies are very scarce in the catatonia literature, mostly showing diffuse cerebral atrophy. Group studies assessing functional brain imaging after catatonic episodes show that emotional dysregulation is related to the GABAergic system, with hypoactivation of orbitofrontal cortex, hyperactivation of median prefrontal cortex, and dysconnectivity between frontal and motor areas.
In catatonia, brain imaging is abnormal in the majority of cases, and abnormalities more frequently diffuse than localised. Brain imaging studies published so far suffer from serious limitations and for now the different models presented in the literature do not explain most of the cases. There is an important need for further studies including a better clinical characterisation of patients with catatonia, functional imaging with concurrent catatonic symptoms and the use of novel brain imaging techniques.
To provide a review of the available literature about the functional neuroimaging of anorexia nervosa, and to summarize the possible role of neurobiological factors in its pathogenesis.
A systematic review of the literature was performed using PubMed and Medline electronic database (1950–September 2009). Eligible studies were restricted to those involving the main parameters of cerebral activity and functional neuroimaging techniques. Findings of the reviewed studies have been grouped on a diagnostic subtype basis, and their comparison has been interpreted in terms of concordance.
We found a high level of concordance among available studies with regard to the presence of frontal, parietal and cingulate functional disturbances in both anorexia nervosa restricting and binge/purging subtypes. Concordance among studies conducted regardless of the anorexia nervosa subtypes suggests an alteration in temporal and parietal functions and striatal metabolism.
The most consistent alterations in anorexia nervosa cerebral activity seem to involve the dorsolateral prefrontal cortex, the inferior parietal lobule, the anterior cingulate cortex and the caudate nucleus. They may affect different neural systems such as the frontal visual system, the attention network, the arousal and emotional processing systems, the reward processing network, and the network for the body schema.
Structural neuroimaging studies have revealed a consistent pattern of volumetric reductions in both the hippocampus and the anterior cingulate cortex (ACC) of individuals with a major depressive episode (MDE). This study investigated hippocampal and ACC volume differences in the elderly comparing currently depressed individuals and individuals with a past lifetime history of MDE versus healthy controls.
We studied non-demented individuals from a cohort of community-dwelling people aged 65 and over (ESPRIT study). T1-weighted magnetic resonance images were used to acquire anatomical scans from 150 currently depressed individuals, 79 individuals with at least one past MDE, and 310 healthy controls. We derived quantitative regional estimates of subcortical volume of hippocampus and ACC using FreeSurfer Software (automated method). Concerning hippocampus, we also used a manual method of measurement. General Linear Model was used to study brain volumes in current and past depression adjusting for gender, age, education level, total brain volume, and anxiety disorder comorbidity.
After adjustment, current depression was associated with a lower left posterior hippocampal volume (F = 10.38, P = 0.001) using manual estimation of volume. No other significant differences were observed. A positive correlation was found between time since the last MDE and left posterior hippocampal volume.
The finding of left posterior hippocampal volume reduction in currently depressed individuals but not in those with a past MDE compared to healthy controls could be related to brain neuroplasticity. Additionally, our results suggest manual measures to be more sensitive than automated methods.
Disclosure of interest
The authors have not supplied their declaration of competing interest.
The essence of the neurobiology of suicidal behavior is that a specific vulnerability to suicidal behavior is mediated by an underlying genetic predisposition interacting with environmental stressors and probable epigenetic factors throughout the lifespan to modify the function of neuronal circuits, thus rendering an individual more likely to engage in a suicidal act.
This chapter will introduce the methods by which the behaviors and models discussed in the previous two chapters are studied. This chapter will thus provide the reader with a foundation of neuroscience techniques from which they can build upon with information in the remainder of the book. These techniques address (epi-)genetics and functional neuro-anatomy.
Neuroscience approaches to the study and understanding of suicidal behavior may differ somewhat from those targeting other behavioral issues. As suicide appears to be a unique human behavior, there is a lack of animal models. However, much information is available from postmortem studies of brain tissue, in which brain characteristics of suicide victims are compared to those of individuals who died from other causes. Postmortem studies are sometimes accompanied by psychological autopsies, which are standardized interviews with individuals who were in close contact with the deceased, covering a wide range of health- and personality-related issues.
Neuropolitics is the intersection of neuroscience and political science, and it has the interdisciplinary goal of transforming both disciplines. This article reviews the past 20 years of work in the field, identifying its roots, some overarching themes—reactions to political attitudinal questions and candidates faces, identification of political ideology based on brain structure or reactivity to nonpolitical stimuli, and racial attitudes—and obstacles to its progress. I then explore the methodological and analytical advances that point the way forward for the future of neuropolitics. Although the field has been slow to develop compared with neurolaw and neuroeconomics, innovations look ripe for dramatically improving our ability to model political behaviors and attitudes in individuals and predict political choices in mass publics. The coming advancements, however, pose risks to our current norms of democratic deliberation, and academics need to anticipate and mitigate these risks.
A large proportion of the persons who join terrorist groups as well as lone-acting terrorists have a history of violent behavior or mental disorder that predated their becoming terrorists. This suggests that brain alterations found to occur in violent perpetrators may also be present in a significant percentage of terrorists. After a short delineation of phylogenetically old neuronal networks that are important for the generation of aggressive behavior in inconspicuous brains, this review summarizes structural and functional brain-imaging studies in violent offenders published over the last 10 years. Depending on the subtype of violence (impulsive or instrumental), deviations in structure or function were mainly found in the prefrontal, orbitofrontal, and insular cortex, as well as in temporolimbic structures (e.g., the amygdala, hippocampus, and parahippocampus). These brain areas are essentially responsible for the control of the archaic neuronal generators of aggression located in the hypothalamus and limbic system. This regional distribution of brain alterations also shows a remarkable overlap with those brain regions that are crucial for such prosocial traits as empathy and compassion. Feelings of superiority, dominance, and satisfaction gained by performing violent and terroristic attacks suggest that a hedonistic component via an activation of brain reward systems plays an additional role. In our current debate about the causes of terrorism, aspects of brain dysfunction should receive more attention.
In the face of shifting demographics and an increase in human longevity, it is important to examine carefully what is known about cognitive ageing, and to identify and promote possibly malleable lifestyle and health-related factors that might mitigate age-associated cognitive decline. The Lothian Birth Cohorts of 1921 (LBC1921, n = 550) and 1936 (LBC1936, n = 1091) are longitudinal studies of cognitive and brain ageing based in Scotland. Childhood IQ data are available for these participants, who were recruited in later life and then followed up regularly. This overview summarises some of the main LBC findings to date, illustrating the possible genetic and environmental contributions to cognitive function (level and change) and brain imaging biomarkers in later life. Key associations include genetic variation, health and fitness, psychosocial and lifestyle factors, and aspects of the brain's structure. It addresses some key methodological issues such as confounding by early-life intelligence and social factors and emphasises areas requiring further investigation. Overall, the findings that have emerged from the LBC studies highlight that there are multiple correlates of cognitive ability level in later life, many of which have small effects, that there are as yet few reliable predictors of cognitive change, and that not all of the correlates have independent additive associations. The concept of marginal gains, whereby there might be a cumulative effect of small incremental improvements across a wide range of lifestyle and health-related factors, may offer a useful way to think about and promote a multivariate recipe for healthy cognitive and brain ageing.
To characterize the yearly incidence, diagnostic distribution, and neuro-radiologic findings in patients aged over 60 years, referred to psychiatric treatment with first episode psychosis (FEP).
A computerized search, including all patients referred to psychiatric treatment during 12 consecutive months with a de novo diagnosis of psychosis was performed in the Helsinki region catchment area with 1.2 million inhabitants. Diagnoses based on hospital records were made by a group of one neurologist and three psychiatrists. MRI- or CT scans performed as a part of routine clinical management were used when available.
107 patients (27 males and 80 females) with FEP were identified and categorized into four diagnostic groups: schizophrenia, delusional disorder, psychotic depression, and psychosis due to another medical condition. No patients with de novo onset mania were found. Psychosis due to another medical condition was the most common diagnosis. A high frequency of signs of cortical brain atrophy was seen in all diagnostic groups, while central atrophy was more frequent in patients with psychosis due to another medical condition than in the other groups.
Organic brain changes related to ageing or degenerative illnesses may be an etiologic factor in elderly patients with FEP.
Health nudge interventions to steer people into healthier lifestyles are increasingly applied by governments worldwide, and it is natural to look to such approaches to improve health by altering what people choose to eat. However, to produce policy recommendations that are likely to be effective, we need to be able to make valid predictions about the consequences of proposed interventions, and for this, we need a better understanding of the determinants of food choice. These determinants include dietary components (e.g. highly palatable foods and alcohol), but also diverse cultural and social pressures, cognitive-affective factors (perceived stress, health attitude, anxiety and depression), and familial, genetic and epigenetic influences on personality characteristics. In addition, our choices are influenced by an array of physiological mechanisms, including signals to the brain from the gastrointestinal tract and adipose tissue, which affect not only our hunger and satiety but also our motivation to eat particular nutrients, and the reward we experience from eating. Thus, to develop the evidence base necessary for effective policies, we need to build bridges across different levels of knowledge and understanding. This requires experimental models that can fill in the gaps in our understanding that are needed to inform policy, translational models that connect mechanistic understanding from laboratory studies to the real life human condition, and formal models that encapsulate scientific knowledge from diverse disciplines, and which embed understanding in a way that enables policy-relevant predictions to be made. Here we review recent developments in these areas.
The pathogenesis of bipolar disorder (BD) is to date not entirely clear. Classical genetic research showed that there is a contribution of genetic factors in BD, with high heritability. Twin studies, thanks to the fact that confounding factors as genetic background or family environment are shared, allow etiological inferences. In this work, we selected twin studies, which focus on the relationship between BD, genetic factors and brain structure, evaluated with magnetic resonance imaging. All the studies found differences in brain structure between BD patients and their co-twins, and also in respect to healthy controls. Genetic effects are predominant in white matter, except corpus callosum, while gray matter resulted more influenced by environment, or by the disease itself. All studies found no interactions between BD and shared environment between twins. Twin studies have been demonstrated to be useful in exploring BD pathogenesis and could be extremely effective at discriminating the neural mechanisms underlying BD.
In the contemporary debate on the use of the neurosciences in ethics and law, numerous arguments have been bandied about among scientists and philosophers looking to uphold or reject the reliability and validity of scientific findings obtained by brain imaging technologies. Among the most vexing questions is, Can we trust that technology? One point of disagreement is whether brain scans offer a window through which to observe the functioning of the mind, in such a way as to enable lawyers, judges, physicians, and lawmakers to detect anomalies in brain function that may account for criminal unconscious behavior. Those who stand behind brain imaging believe that this can indeed be achieved, whereas those in opposition stress that brain scans are highly open to interpretation and that the data they provide is insufficient to establish causal connections. The question essentially comes down to whether technology can reliably be used to determine the intentions of the individual, thus establishing mens rea, for example, and hence responsibility. This article focuses on the latter notion and explores whether we can rely on the neurosciences to shed light on a complex form of moral and legal reasoning, as well as the role of the neurosciences in reawakening a philosophical and legal interest in trying to set responsibility on an empirical basis.
When children have marked problems with motor coordination, they often have problems with attention and impulse control. Here, we map the neuroanatomic substrate of motor coordination in childhood and ask whether this substrate differs in the presence of concurrent symptoms of attention-deficit/hyperactivity disorder (ADHD).
Participants were 226 children. All completed Diagnostic and Statistical Manual of Mental Disorders, fifth edition (DSM-5)-based assessment of ADHD symptoms and standardized tests of motor coordination skills assessing aiming/catching, manual dexterity and balance. Symptoms of developmental coordination disorder (DCD) were determined using parental questionnaires. Using 3 Tesla magnetic resonance data, four latent neuroanatomic variables (for the cerebral cortex, cerebellum, basal ganglia and thalamus) were extracted and mapped onto each motor coordination skill using partial least squares pathway modeling.
The motor coordination skill of aiming/catching was significantly linked to latent variables for both the cerebral cortex (t = 4.31, p < 0.0001) and the cerebellum (t = 2.31, p = 0.02). This effect was driven by the premotor/motor cortical regions and the superior cerebellar lobules. These links were not moderated by the severity of symptoms of inattention, hyperactivity and impulsivity. In categorical analyses, the DCD group showed atypical reduction in the volumes of these regions. However, the group with DCD alone did not differ significantly from those with DCD and co-morbid ADHD.
The superior cerebellar lobules and the premotor/motor cortex emerged as pivotal neural substrates of motor coordination in children. The dimensions of these motor coordination regions did not differ significantly between those who had DCD, with or without co-morbid ADHD.
One of the most exciting psychiatric conditions is the bizarre psychomotor syndrome called catatonia, which may present with a large number of different motor signs and even vegetative instability. Catatonia is potentially life threatening. The use of benzodiazepines and electroconvulsive therapy (ECT) has been efficient in the majority of patients. The rich clinical literature of the past has attempted to capture the nature of catatonia. But the lack of diagnostic clarity and operationalization has hampered research on catatonia for a long time. Within the last decades, it became clear that catatonia had to be separated from schizophrenia, which was finally accomplished in the Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition (DSM-5). In DSM-5, catatonia syndrome may be diagnosed as a specifier to major mood disorders, psychotic disorders, general medical conditions, and as catatonia not otherwise specified. This allows diagnosing the syndrome in a large variety of psychiatric disorders. Currently, the pathobiology remains widely unknown. Suspected neurotransmitter systems include gamma-aminobutyric acid (GABA) and glutamate. Neuroimaging reports pointed to reduced resting state activity and reduced task activation in motor areas of the frontal and parietal cortex. The new classification of catatonia will foster more clinical research and neuroscientific approaches by testing catatonia in various populations and applying stringent criteria. The scarce number of prospective trials will hopefully increase, as more trials will be encouraged within a more precise concept of catatonia.
Attention deficit hyperactivity disorder (ADHD) is a common, highly heritable psychiatric disorder. Additionally, environmental factors such as perinatal stress and early adversities contribute to the occurrence and severity of ADHD. Recently, DNA methylation has emerged as a mechanism that potentially mediates gene–environmental interaction effects in the aetiology and phenomenology of psychiatric disorders. Here, we investigated whether serotonin transporter gene (SLC6A4) methylation patterns were associated with clinical characteristics and regional cortical thickness in children with ADHD.
In 102 children with ADHD (age 6–15 years), the methylation status of the SLC6A4 promoter was measured. Brain magnetic resonance imaging was obtained and ADHD symptoms were evaluated.
A higher methylation status of the SLC6A4 promoter was significantly associated with worse clinical presentations (more hyperactive-impulsive symptoms and more commission errors). Additionally, a negative correlation was observed between SLC6A4 methylation levels and cortical thickness values in the right occipito-temproral regions.
Our results suggest that the SLC6A4 methylation status may be associated with certain symptoms of ADHD, such as behavioural disinhibition, and related brain changes. Future studies that use a larger sample size and a control group are required to corroborate these results.