Abnormal fear circuitry in Attention Deficit Hyperactivity Disorder: A controlled magnetic resonance imaging study

Spencer, Andrea; Marin, Marie‐France; Milad, Mohammed R.; Spencer, Thomas; Bogucki, Olivia E.; Pope, Amanda; Plasencia, Natalie; Hughes, Brittany; Pace‐Schott, Edward F.; Fitzgerald, Maura; Uchida, Mai; Biederman, Joseph

doi:10.1016/j.pscychresns.2016.12.015

Cited by 17 publications

(11 citation statements)

References 34 publications

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“…Also, during reactive aggressive responses, ADHD adolescents showed abnormally reduced activation in ACC and temporo-parietal junction as well as in striato-limbic regions (Bubenzer-Busch et al, 2016 ). A recent study found abnormal activation in fronto-limbic regions during extinction learning and recall in adults with ADHD including hippocampus, insula (overactivated) and mACC and vmPFC (underactivated), suggesting medial frontal-limbic dysregulation similar to that observed in post-traumatic stress disorder (Spencer et al, 2017 ).…”

Section: Fmri Studies Of Hot Ef and Emotion Processing Tasksmentioning

confidence: 94%

Cognitive Neuroscience of Attention Deficit Hyperactivity Disorder (ADHD) and Its Clinical Translation

Rubia

2018

Front. Hum. Neurosci.

261

248

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This review focuses on the cognitive neuroscience of Attention Deficit Hyperactivity Disorder (ADHD) based on functional magnetic resonance imaging (fMRI) studies and on recent clinically relevant applications such as fMRI-based diagnostic classification or neuromodulation therapies targeting fMRI deficits with neurofeedback (NF) or brain stimulation. Meta-analyses of fMRI studies of executive functions (EFs) show that ADHD patients have cognitive-domain dissociated complex multisystem impairments in several right and left hemispheric dorsal, ventral and medial fronto-cingulo-striato-thalamic and fronto-parieto-cerebellar networks that mediate cognitive control, attention, timing and working memory (WM). There is furthermore emerging evidence for abnormalities in orbital and ventromedial prefrontal and limbic areas that mediate motivation and emotion control. In addition, poor deactivation of the default mode network (DMN) suggests an abnormal interrelationship between hypo-engaged task-positive and poorly “switched off” hyper-engaged task-negative networks, both of which are related to impaired cognition. Translational cognitive neuroscience in ADHD is still in its infancy. Pattern recognition analyses have attempted to provide diagnostic classification of ADHD using fMRI data with respectable classification accuracies of over 80%. Necessary replication studies, however, are still outstanding. Brain stimulation has been tested in heterogeneously designed, small numbered proof of concept studies targeting key frontal functional impairments in ADHD. Transcranial direct current stimulation (tDCS) appears to be promising to improve ADHD symptoms and cognitive functions based on some studies, but larger clinical trials of repeated stimulation with and without cognitive training are needed to test clinical efficacy and potential costs on non-targeted functions. Only three studies have piloted NF of fMRI-based frontal dysfunctions in ADHD using fMRI or near-infrared spectroscopy, with the two larger ones finding some improvements in cognition and symptoms, which, however, were not superior to the active control conditions, suggesting potential placebo effects. Neurotherapeutics seems attractive for ADHD due to their safety and potential longer-term neuroplastic effects, which drugs cannot offer. However, they need to be thoroughly tested for short- and longer-term clinical and cognitive efficacy and their potential for individualized treatment.

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Section: Fmri Studies Of Hot Ef and Emotion Processing Tasksmentioning

confidence: 94%

Cognitive Neuroscience of Attention Deficit Hyperactivity Disorder (ADHD) and Its Clinical Translation

Rubia

2018

Front. Hum. Neurosci.

261

248

View full text Add to dashboard Cite

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“…[89] for review). In this regard, we cannot discount the impact that the high magnetic field of the MR environment might have had on the skin conductance signal, despite following procedures used in several other studies in psychiatric patient populations under similar conditions [18,[21][22][23]97]. Fourth, given variability in scan start times (16:00-22:00) we cannot discount the potential impact of circadian factors and are limited by the absence of objective circadian markers.…”

Section: Limitationsmentioning

confidence: 96%

“…Extinction memory processing is abnormal in PTSD [2,[17][18][19][20] as well as in anxiety-related [21] and other psychiatric disorders [22,23]. For example, individuals with PTSD show poorer extinction memory than trauma-exposed, healthy controls [17,18].…”

Section: Introductionmentioning

confidence: 99%

Fear extinction memory is negatively associated with REM sleep in insomnia disorder

Bottary

Seo

Daffre

et al. 2020

Sleep

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Study Objectives Formation and maintenance of fear-extinction memories are disrupted in post-traumatic stress disorder (PTSD) and anxiety disorders. Sleep contributes to emotional memory consolidation and emotion regulation. Insomnia disorder (ID) is characterized by persistent sleep disturbance as well as rapid eye movement (REM) sleep abnormalities and often precedes or develops in parallel with PTSD and anxiety disorders. Here, we explore the impact of chronic poor sleep and sleep immediately following fear conditioning and extinction learning on preservation of extinction memories. Methods Twenty-four ID age- and sex-matched to 24 healthy, good sleeper controls (GS) completed up to 2 weeks of habitual sleep monitoring with daily sleep–wake diaries and actigraphy, and then participated in a two-session fear conditioning, extinction learning and extinction recall procedure. Fear Conditioning and Extinction Learning occurred during session 1, followed by Extinction Recall approximately 24 hours later. Skin-conductance responses (SCR) and shock expectancies were recorded throughout all experimental phases to evaluate associative learning and memory. Overnight sleep between sessions 1 and 2 was recorded using ambulatory polysomnography. Results ID showed greater physiological reactivity during Fear Conditioning. REM sleep physiology was associated with poorer extinction memory in ID but better extinction memory in GS. Conclusion REM sleep physiology may differentially support emotional memory retention and expression in ID and GS. In the former, REM may enhance retention of fear memories, while in the later, REM may enhance the expression of extinction memories.

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“… 98 Recently, fear circuits' abnormalities during extinction learning and recall have been reported in medication-naïve, non-traumatized subjects with ADHD. 99 …”

Section: Orx-s Dysfunction and Main Symptom Domain Of Essence Within ...mentioning

confidence: 99%

Orexin/Hypocretin System Dysfunction in ESSENCE (Early Symptomatic Syndromes Eliciting Neurodevelopmental Clinical Examinations)

Knez¹,

Stevanović²,

Fernell³

et al. 2022

NDT

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Early Symptomatic Syndromes Eliciting Neurodevelopmental Clinical Examinations (ESSENCE) is an umbrella term covering a wide range of neurodevelopmental difficulties and disorders. Thus, ESSENCE includes attention-deficit/hyperactivity disorder (ADHD), autism spectrum disorder (ASD), and other neurodevelopmental disorders (NDDs) and difficulties, with a variety of symptoms in cognitive, motor, sensory, social, arousal, regulatory, emotional, and behavioral developmental domains, frequently co-occurring and likely having partly common neurobiological substrates. The ESSENCE concept is a clinical paradigm that promotes organizing NDDs in everyday clinical practice according to their coexistence, symptom dimensions overlapping, and treatment possibilities. Despite increased knowledge regarding NDDs, the neurobiological mechanisms that underlie them and other ESSENCE-related problems, are not well understood. With its wide range of neural circuits and interactions with numerous neurotransmitters, the orexin/hypocretin system (Orx-S) is possibly associated with a variety of neurocognitive, psychobiological, neuroendocrine, and physiological functions and behaviors. Dysfunction of Orx-S has been implicated in various psychiatric and neurological disorders. This article provides an overview of Orx-S dysfunctions' possible involvement in the development, presentation, and maintenance of ESSENCE. We provide a focused review of current research evidence linking orexin neuropeptides with specific clinical NDDs symptoms, mostly in ADHD and ASD, within the Research Domain Criteria (RDoC) framework. We propose that Orx-S dysfunction might have an important role in some of these neurodevelopmental symptom domains, such as arousal, wakefulness, sleep, motor and sensory processing, mood and emotional regulation, fear processing, reward, feeding, attention, executive functions, and sociability. Our perspective is presented from a clinical point of view. Further, more thorough systematic reviews are needed as well as planning of extensive new research into the Orx-S’s role in ESSENCE, especially considering RDoC elements.

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Abnormal fear circuitry in Attention Deficit Hyperactivity Disorder: A controlled magnetic resonance imaging study

Cited by 17 publications

References 34 publications

Cognitive Neuroscience of Attention Deficit Hyperactivity Disorder (ADHD) and Its Clinical Translation

Cognitive Neuroscience of Attention Deficit Hyperactivity Disorder (ADHD) and Its Clinical Translation

Fear extinction memory is negatively associated with REM sleep in insomnia disorder

Orexin/Hypocretin System Dysfunction in ESSENCE (Early Symptomatic Syndromes Eliciting Neurodevelopmental Clinical Examinations)

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