The prefrontal cortex, pathological anxiety, and anxiety disorders

Author(s):  
Margaux M. Kenwood ◽  
Ned H. Kalin ◽  
Helen Barbas
2021 ◽  
Vol 4 (1) ◽  
Author(s):  
Benjamin Suarez-Jimenez ◽  
Nicholas L. Balderston ◽  
James A. Bisby ◽  
Joseph Leshin ◽  
Abigail Hsiung ◽  
...  

AbstractAnxiety disorders are characterized by maladaptive defensive responses to distal or uncertain threats. Elucidating neural mechanisms of anxiety is essential to understand the development and maintenance of anxiety disorders. In fMRI, patients with pathological anxiety (ANX, n = 23) and healthy controls (HC, n = 28) completed a contextual threat learning paradigm in which they picked flowers in a virtual environment comprising a danger zone in which flowers were paired with shock and a safe zone (no shock). ANX compared with HC showed 1) decreased ventromedial prefrontal cortex and anterior hippocampus activation during the task, particularly in the safe zone, 2) increased insula and dorsomedial prefrontal cortex activation during the task, particularly in the danger zone, and 3) increased amygdala and midbrain/periaqueductal gray activation in the danger zone prior to potential shock delivery. Findings suggest that ANX engage brain areas differently to modulate context-appropriate emotional responses when learning to discriminate cues within an environment.


2002 ◽  
Vol 24 (suppl 1) ◽  
pp. 74-80 ◽  
Author(s):  
Gerard JA Byrne

Anxiety disorders decline in prevalence with advancing age but remain more common than depressive disorders. They are often of late-onset and there is frequent comorbidity with depressive disorders and physical illness. While anxiety disorders in older people are likely to respond to the same non-pharmacological interventions that have been shown to work in younger people, there is currently little formal evidence of this. Although there is some evidence that the non-benzodiazepine anxiolytic medication, buspirone, is effective against late life anxiety symptoms, clinical trials in older people with rigorously diagnosed anxiety disorders are needed. An anxiety scale with demonstrated reliability and validity in older people is needed for screening for pathological anxiety and for measuring change in older patients undergoing treatment for anxiety disorders.


Author(s):  
Vladan Starcevic, MD, PhD

Anxiety disorders can be defined as conditions characterized by pathological anxiety that has not been caused by physical illness, is not associated with substance use, and is not part of a psychotic illness. Therefore, the concept of anxiety disorders is largely based on exclusion of several causes of pathological anxiety–hardly a scientifically defensible position. Since pathological anxiety has been postulated as the sine qua non of anxiety disorders, it is important to first make a distinction between pathological and ‘‘normal’’ anxiety. For the sake of clarifying this matter, the terms anxiety and fear are used here interchangeably (as they both denote a response to a perceived threat), although there is also a prominent view that conceptual differences do exist between them (see also Table 2—21 and Barlow’s account of panic attacks in Chapter 2 for further discussion of this issue). There is broad agreement that pathological and normal anxiety can be distinguished on the basis of the criteria listed in Table 1—1. These criteria cut across all the components of anxiety: subjective, physiological (somatic), cognitive, and behavioral. Although the criteria may seem clear-cut, in practice it may be difficult to draw a precise boundary between pathological and normal anxiety. It is often assumed that normal anxiety has an adaptive role, because it serves as a signal that there is some danger and that measures need to be taken (e.g., a fight or flight response) to protect oneself against that danger; both the danger perceived and the measures taken are considered appropriate (i.e., not exaggerated) in normal anxiety. For example, a student who is anxious about failing the exam correctly judges herself to be well below the sufficient level of knowledge and doubles the effort to catch up with her studies and minimize the risk of failing. In contrast, pathological anxiety pertains to an inaccurate or excessive appraisal of danger; protective measures taken against this danger are way out of proportion to the real threat. Anxiety disorders were introduced in 1980 as a distinct nosological group in the Third Edition of the Diagnostic and Statistical Manual of Mental Disorders (DSM-III; American Psychiatric Association, 1980).


Author(s):  
Hans-Ulrich Wittchen ◽  
Katja Beesdo-Baum

This chapter describes the prevalence, onset, course, persistence, comorbidity, and outcome, as well as correlates and risk factors of anxiety disorders, namely separation anxiety disorder, specific phobia, social anxiety disorder, agoraphobia, panic disorder, and generalized anxiety disorder. The focus is laid upon the early years of life (childhood, adolescence, and young adulthood), given that most anxiety disorders have their onset at this time, typically persisting over the life course, and thus representing powerful risk factors for the onset of subsequent mental disorders such as depression and substance use disorders. Despite progress, continued research efforts are needed towards identifying which vulnerability and risk factors play a causal role for the onset and persistence of pathological anxiety. An improved understanding of the complex underlying biological and psychological mechanisms and interactions is crucial to facilitate more effective targeted prevention research and treatment.


Author(s):  
Ramon Tasan ◽  
Nicolas Singewald

Anxiety tests and models in rodents are useful tools to reveal neurochemical, cellular, and molecular underpinnings of normal and pathological anxiety-related behaviors, as well as novel treatment targets. While anxiety models are generated by various approaches such as selective breeding, anxiety tests most commonly involve unconditioned approach avoidance tasks and conditioned learning paradigms, both characterized by inherent advantages and limitations, in particular their predictive value for specific anxiety disorders. To further improve the validity and translatability of preclinical anxiety testing, it is promising that some anxiety-relevant endophenotypes have now been investigated using similar tests in rodents and humans and that the involved neural pathways and mechanisms overlap considerably in both species.


2021 ◽  
Vol 34 (4) ◽  
pp. e100411
Author(s):  
Shuqi Xie ◽  
Xiaochen Zhang ◽  
Wenhong Cheng ◽  
Zhi Yang

Adolescence is the peak period for the incidence of anxiety disorders. Recent findings have revealed the immaturity of neural networks underlying emotional regulation in this population. Brain vulnerability to anxiety in adolescence is related to the unsynchronised development of anxiety-relevant brain functional systems. However, our current knowledge on brain deficits in adolescent anxiety is mainly borrowed from studies on adults. Understanding adolescent-specific brain deficits is essential for developing biomarkers and brain-based therapies targeting adolescent anxiety. This article reviews and compares recent neuroimaging literature on anxiety-related brain structural and functional deficits between adolescent and adult populations, and proposes a model highlighting the differences between adolescence and adulthood in anxiety-related brain networks. This model emphasises that in adolescence the emotional control system tends to be hypoactivated, the fear conditioning system is immature, and the reward and stress response systems are hypersensitive. Furthermore, the striatum’s functional links to the amygdala and the prefrontal cortex are strengthened, while the link between the prefrontal cortex and the amygdala is weakened in adolescence. This model helps to explain why adolescents are vulnerable to anxiety disorders and provides insights into potential brain-based approaches to intervene in adolescent anxiety disorders.


2021 ◽  
Vol 43 (2) ◽  
pp. 215-230
Author(s):  
Dietmar Hansch

Abstract Nicht zu Unrecht gilt die Behandlung von Angsterkrankungen als die Paradedisziplin der Verhaltenstherapie (VT). Hier wie auch generell zeigt sich die VT dabei aber als zersplittert in eine Vielzahl von Einzelmethoden: Verschiedene Lernformen – Einsichtslernen, Konditionierungslernen und Habituationslernen - werden in ihrem Beitrag zu Angsterkrankungen isoliert voneinander konzipiert. Entsprechend stehen auch auf diesen Lernformen basierende Therapiemethoden für sich. Dadurch werden wichtige Synergiepotenziale verschenkt. Menschliches Lernen, auch und gerade das Lernen und Verlernen von pathologischer Angst, ist aber immer ein ganzheitlicher Prozess. Der Artikel skizziert eine ganzheitliche Psycho-Logik der Eskalation und Chronifizierung pathologischer Angst unter integrierendem Einbezug der o.g. Lernformen. Hieraus leitet sich eine verfahrensintegrierende VT ab, die die etablierten Behandlungsmethoden so kombiniert, dass Synergiegewinne entstehen, was an einem Fallbeispiel verdeutlicht wird. Den theoretischen Hintergrund bildet die Theorie der Selbstorganisation komplexer Systeme, insbesondere die Synergetik – ein Feld, in dem wichtige Aspekte der Gestalttheorie aufgehoben sind. It is not without reason that the treatment of anxiety disorders is considered the showpiece of behavioral therapy (BT). Here as well as in general, however, the BT shows itself fragmented into a multitude of individual methods: Different forms of learning - insight learning, conditioning learning and habituation learning - are designed in isolation from each other in their contribution to anxiety disorders. Correspondingly, treatment methods based on these forms of learning stand for themselves. This gives away important synergy potential. Human learning, also and especially learning and unlearning of pathological anxiety, is always a holistic process. The paper outlines a holistic psycho-logic of the escalation and chronification of pathological anxiety, integrating the above mentioned forms of learning. This leads to the derivation of a method-integrating BT, which combines the established treatment methods in such a way that synergy gains are achieved, as illustrated by a case study. The theoretical background is formed by the theory of the self-organization of complex systems, in particular synergetics - a field in which important aspects of gestalt theory are implied.


2006 ◽  
Vol 8 (3) ◽  
pp. 323-333 ◽  

An impressive number of animal models to assess depression and anxiety are available today. However, the relationship between these models and the clinical syndromes of depression and anxiety is not always clear. Since human anxiety disorders represent a multifactorial phenomenon frequently comorbid with major depression and/or other psychiatric problems, the chance of creating animal models which consistently reflect the human situation is quite poor. When using experimental models to understand homologies between animal and human behavior, we have to consider the context in which an animal is investigated, and both the functional significance and relevance of the behavioral parameters that are quantified. Moreover, gender and interindividual and interspecies variabilities in behavioral responses to the test situation and in the sensitivity to pharmacological treatments are potential sources for confounding results. In the past, these aspects have been often neglected in preclinical approaches to behavioral pharmacology and psychopharmacology. A pragmatic approach of combined preclinical and clinical efforts is necessary to imitate one or more aspects relevant to pathological anxiety disorders and depression. The resulting models may identify central nervous processes regulating defined behavioral output, with the potential to develop more effective treatments.


Author(s):  
Bronwyn M. Graham ◽  
Mohammed R. Milad

The ability to appropriately regulate fear and anxiety is considered a top-down process involving higher-level cortical structures. Here, we review evidence that the prefrontal cortex (PFC) is critically involved in many laboratory emotion regulation tasks in both rodents and humans, including behavioral or experiential forms of regulation like fear extinction, and cognitive forms of regulation like reappraisal. We also discuss research demonstrating that failures in emotion regulation, as observed in many psychiatric conditions like anxiety disorders, are associated with PFC structural abnormalities and/or aberrant PFC functional activity. We conclude that the PFC may act as a common gateway between higher-level cortical structures and limbic/brainstem areas to mediate the appropriate control of emotions, irrespective of the regulation strategy (i.e., behavioral or cognitive) employed.


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