This review of neuroimaging studies in major depressive disorder reports that dysfunctional emotion regulation is associated with altered activity in brain systems involved in emotion processing and control. Across studies, findings implicate prefrontal regions and limbic areas, consistent with abnormal regulation of affect in depression.

This paper reports that anxiety and depression were associated with different patterns of abnormal activation in prefrontal and limbic regions. The findings support the idea that mood disorders involve altered activity in brain circuits related to emotion regulation and decision-making.

This systematic review reports that fMRI studies in psychiatric disorders commonly identify abnormal activity and connectivity in brain circuits linked to emotion processing, cognitive control, and reward. The review covers disorders including major depressive disorder, schizophrenia, bipolar disorder, anxiety disorders, PTSD, and obsessive-compulsive disorder, supporting the idea that neuroimaging can reveal disorder-associated brain-region differences.

The study found that emotion dysregulation was related to increased activation in dorsomedial prefrontal cortex and ventromedial prefrontal cortex in response to fearful stimuli. The authors note that dACC and dmPFC play central roles in fear expression and attention to emotional stimuli, and that these findings link psychiatric symptoms to altered activity in emotion-processing regions.

This review describes how psychiatric disorders are linked to abnormalities in neural systems that support decision-making, including prefrontal cortex and connected limbic regions. It notes that disturbances in these circuits are relevant to symptoms across multiple illnesses.

The meta-analysis found altered activation in regions including the amygdala, anterior cingulate cortex, prefrontal cortex, and related networks during tasks involving emotion and cognitive control. These brain regions are directly involved in fear, emotional regulation, and decision-making, which matches the claim’s described functional domains.

The review states that MRI and related neuroimaging methods have identified abnormal activity in prefrontal and limbic regions in mood disorders. It specifically discusses disrupted regulation of emotion and altered responses in circuits involving the amygdala and prefrontal cortex.

The review summarizes functional neuroimaging findings showing abnormal activity in the prefrontal cortex, anterior cingulate, amygdala, and related regions in depression. These regions are part of networks involved in emotional processing and regulation.

“In the past decade, neuroimaging research has identified key components in the neural system that underlies bipolar disorder (BD). The **ventral prefrontal cortex (vPFC)** and **amygdala** are the main structures in this system, with convergent evidence for **abnormal structure, function and connectivity** of these regions in adults with BD.” “Findings from functional magnetic resonance imaging (fMRI) studies suggest that BD is associated with **abnormal vPFC and amygdala activation** during emotion processing and regulation tasks, including **amygdala hyperactivation and vPFC hypoactivation** to emotional stimuli.” “These abnormalities in vPFC-amygdala circuits are hypothesized to underlie mood dysregulation and impaired decision-making in BD, particularly in the context of emotionally salient information.”

The article argues that evidence from neuroimaging is consistent with prefrontal cortex abnormalities across several psychiatric disorders. It links these abnormalities to deficits in executive control, emotion regulation, and other higher-order functions.

This meta-analysis found abnormal activation in prefrontal and other cortical and subcortical regions in schizophrenia. The affected circuitry is relevant to cognition, emotion, and behavioral control.

This meta-analysis found a common pattern of aberrant brain activation during emotional processing across schizophrenia, mood disorders, anxiety disorders, and substance use disorders. The aberrant pattern involved the amygdala, hippocampal and parahippocampal gyri, ventromedial prefrontal cortex, subgenual cingulate, anterior insula, and other regions associated with emotional reactivity and regulation.

The review explains that fMRI has been used to identify abnormal patterns of activation in brain regions such as the prefrontal cortex and amygdala in psychiatric illness. It emphasizes that these findings are not disease-specific but do support altered brain circuitry.

This review reports abnormal activity in prefrontal-striatal-limbic circuits in obsessive-compulsive disorder. The affected regions are involved in fear, emotional regulation, and decision-making.

The article describes converging imaging evidence for abnormal function in prefrontal and limbic circuits across psychiatric disorders. It links these circuits to emotion regulation, fear processing, and executive control.

This page explains that fMRI measures and maps brain activity and is being used in studies to understand how normal function is disrupted in disease. It also states that increased neural activity in a particular brain area is reflected by a small increase in the MR signal, the basis of the BOLD effect.

This systematic review and meta-analysis reports altered activation in prefrontal-limbic circuitry during emotion regulation tasks in posttraumatic stress disorder. The findings include abnormal responses in the amygdala, medial prefrontal cortex, anterior cingulate cortex, and insula, supporting a link between PTSD and disrupted neural control of fear and emotion.

NIMH describes PTSD as involving changes in brain areas that process fear and stress, including the amygdala, hippocampus, and prefrontal cortex. The agency explains that these brain systems are involved in fear responses, memory, and regulation of emotional reactions.

NIMH notes that depression is associated with changes in brain circuits that regulate mood, thinking, sleep, appetite, and behavior. The resource specifically discusses altered function in brain regions involved in emotion and decision-making, including prefrontal systems and limbic structures.

In general, these studies have reported **relatively heightened amygdala activation** in response to disorder-relevant stimuli in **post-traumatic stress disorder, social phobia, and specific phobia**. Activation in the **insular cortex appears to be heightened in many of the anxiety disorders**. Unlike other anxiety disorders, **post-traumatic stress disorder is associated with diminished responsivity in the rostral anterior cingulate cortex and adjacent ventral medial prefrontal cortex**. Key components of fear circuitry including the **amygdala**, **hippocampus**, **ventromedial hypothalamus**, **periaqueductal gray**, thalamic nuclei, **insular cortex**, and some **prefrontal regions** have been identified in these studies.

“Major depressive disorder (MDD) is characterized by **emotional dysregulation**, implicating abnormalities of **frontal-limbic neural circuits** involved in emotional processing as the core feature.” “Convergent studies provide consistent evidence for **functional and structural abnormalities in the prefrontal cortex (PFC) and amygdala**, the key components of frontal-limbic neural circuits in adult MDD.” “Dysfunction of amygdala-prefrontal circuits has been implicated in MDD through functional magnetic resonance imaging (fMRI). **Hyperactivation of amygdala and hypoactivation of PFC** were shown in task-related fMRI studies within adult MDD, as well as adolescent MDD.” “In this adolescent sample, we observed **decreased functional connectivity between left amygdala and left ventral PFC**, suggesting that abnormalities of the amygdala-prefrontal circuit are present early in the course of MDD.”

This review states that anxiety disorders have been associated with abnormal function in fear-related neural circuitry, especially the amygdala, insula, and medial prefrontal cortex. It synthesizes MRI and fMRI evidence showing exaggerated responses to threat and impaired top-down regulation.

Considerable evidence shows that **PTSD results from a dysfunction in highly conserved brain systems involved in regulating stress, anxiety, fear, and reward**. The neural disruptions shared by PTSD include **white matter tract abnormalities and gray matter changes in the prefrontal cortex (PFC), hippocampus, and basolateral amygdala (BLA)**. Previous studies have characterized a **fear learning and memory network centered on the PFC, hippocampus, and amygdala that plays a key role in the pathology of PTSD**. Several neuroimaging studies have identified **brain circuits including the hippocampus, amygdala, and PFC that contribute to the behavioral and molecular abnormalities in PTSD**; this triad is also central to the **brain circuit implicated in fear and safety learning**.

Clinical observations and psychophysiological assessments have characterized **PTSD as a disorder of fear responses and hyperarousal, emotion processing, and decreased regulation of emotions and unwanted reminders of the trauma**. Research on the pathophysiology of PTSD has provided **strong evidence for PTSD-related impairments in emotion processing and prefrontal regulation regions, both structurally and functionally, and showed reduced functional and structural connectivity suggesting impaired prefrontal control over subcortical emotion processing**. Milad et al. (2009) showed **less activation of the hippocampus and ventromedial prefrontal cortex (vmPFC), but greater activation of the dorsal anterior cingulate cortex (dACC) during recall of fear extinction in participants with PTSD compared to trauma-exposed controls**. Several studies demonstrated **greater amygdala reactivity in PTSD patients compared with controls and lower control by the vmPFC**.

“Findings from **functional neuroimaging** studies indicate **abnormalities in adults with bipolar disorder in prefrontal cortical–amygdala-centered emotion regulation networks**.” “Studies of adults with BD have consistently demonstrated **amygdala hyperactivation** and abnormalities in ventral prefrontal regions during emotional processing tasks, suggesting disrupted **emotion regulation circuitry**.” “These data support a model in which **dysfunction within prefrontal–amygdala networks** may contribute to the **emotion dysregulation** that characterizes bipolar disorder and may also influence decision-making in emotionally salient contexts.”

“In healthy subjects, the **ventrolateral prefrontal cortex (VLPFC)** has been shown to **negatively modulate amygdala response** when subjects cognitively evaluate an emotional face by identifying and labeling the emotion expressed.” “Patients with **bipolar disorder** showed **greater amygdala activation** to fearful faces and **reduced VLPFC activation** relative to healthy subjects during this task.” “These findings provide evidence for **deficient modulation of amygdala response by prefrontal cortex** in bipolar disorder and implicate disruption of this **emotion regulation circuit** in the pathophysiology of the illness.”

Using fMRI, **limbic and paralimbic regions such as the amygdala, hippocampus, dorsal anterior cingulate cortex (dACC), and ventromedial prefrontal cortex (vmPFC), as well as the insula and thalamus, have been repeatedly demonstrated to subserve fear conditioning and extinction in healthy individuals**. A meta-analysis of 26 functional neuroimaging studies of **PTSD** found that the **dACC and amygdala were the most strongly activated regions in PTSD**, whereas the **vmPFC and inferior frontal gyri were the most strongly deactivated regions**. Results revealed that across anxiety disorders, **patients showed hyperactivity in the amygdala and insula**, analogous to fear conditioning in healthy subjects. However, **only PTSD further showed hypoactivity in the ventro- and dorsomedial prefrontal cortex, anterior hippocampus, and parahippocampal gyrus**, indicating disorder‑specific alterations in fear and regulation circuits.

An abundance of research suggests that the **prefrontal cortex is central to fear processing—that is, how fears are acquired and strategies to regulate or diminish fear**. The **amygdala is critical for detecting threat and generating fear responses**, while **prefrontal regions (including ventromedial and dorsolateral PFC) support regulation of these responses and decision-making under threat**. Neuroimaging studies in anxiety disorders consistently show **heightened amygdala activation to threat cues** and **altered prefrontal recruitment during emotion regulation tasks**, indicating abnormalities in **threat processing and regulatory circuits**.

This review concludes that affective and anxiety disorders involve altered recruitment of brain systems supporting emotion regulation. The paper highlights the prefrontal cortex, anterior cingulate cortex, amygdala, and striatum as key regions whose activity differs from healthy controls during regulation tasks.

Neuroimaging studies in humans show that **fear and anxiety engage overlapping networks involving the amygdala, bed nucleus of the stria terminalis, hippocampus, insula, and medial prefrontal cortex**. Clinical neuroimaging of anxiety disorders indicates **persistent hyper-responsivity of the amygdala and insula to threat and altered activity in medial prefrontal and anterior cingulate regions that normally regulate fear responses and guide decisions under threat**. These data support models in which **specific mental disorders are associated with characteristic patterns of abnormal activation in fear and regulation circuits**.

Using **functional MRI**, the researchers detected **unusual activity in several regions of the brain when people with PTSD were shown images that were only vaguely similar to the trauma underlying the disorder**. People with PTSD showed **heightened brain activity when they saw the most fearful face and associated it with the electric shock**, even though similar faces were not paired with shock. The study reported **heightened activity in response to the most frightened expression in brain regions such as the fusiform gyrus, insula, primary visual cortex, locus coeruleus and thalamus**, indicating that **specific brain regions involved in processing fear and emotional salience respond abnormally in PTSD**.

Functional neuroimaging studies of **anxiety disorders** have consistently shown **abnormal activation of the amygdala, insula, and anterior cingulate cortex in response to disorder-relevant and generic threat stimuli**. In addition, **altered recruitment of medial and lateral prefrontal regions during tasks involving emotion regulation, cognitive control, and decision-making under threat** has been observed, suggesting disturbances in **circuits mediating fear, emotional regulation, and higher-order control**. These abnormalities appear across several anxiety disorders, including generalized anxiety disorder, social anxiety disorder, and specific phobias.

Describing fMRI work in PTSD, the lab notes: “Our research suggests that the **amygdala and dorsal anterior cingulate cortex are hyper-responsive** while the **ventral medial prefrontal cortex is hypo-responsive** in individuals with this disorder.” “The general goal of our research is to assess the function of brain structures such as the **amygdala, medial prefrontal cortex, and hippocampus in PTSD**… Evidence thus far suggests that hypermetabolism and hyperactivity of the dorsal anterior cingulate cortex may be familial vulnerability factors.” “Pre-treatment neuroimaging measures of **amygdala and medial prefrontal cortex function** can predict response to treatment with behavioral therapy, indicating that activity in these fear and emotion-regulation regions is closely linked to PTSD symptoms and their improvement.”

The prefrontal cortex helps with attention, emotions, self-control and decision-making. Cleveland Clinic also notes that conditions such as ADHD, bipolar disorder, depression, OCD, and schizophrenia can affect this brain region.

The review states: “Evidence from **neuroimaging studies is consistent with metabolic abnormalities in prefrontal cortex or in the top-down connections diminishing its influence in almost all psychiatric disorders**.” “**Diminished metabolic activity in prefrontal cortex** has been shown in **schizophrenia, depression, bipolar disorder, addictive behavior, obsessive-compulsive disorder, chronic pain**… Reduced functional connectivity within cortical–limbic loop has been shown in obsessive compulsive disorder and depression.” “Remission from depression normalizes **hypo-functioning in frontal, prefrontal and orbitofrontal regions** while it reduces activity in paralimbic, parietal-temporal regions including the **amygdala, hippocampus and parahippocampal gyrus**… In general it appears that there is no psychiatric illness without any decline of prefrontal cortex function or influence.”

The APA article describes neuroimaging findings that link psychiatric disorders to altered function in circuits involved in emotion regulation, reward, and executive control. It also notes that these patterns are informative for research even though they are not sufficient as a general diagnostic tool.

“Results indicate that **greater structural connectivity of the uncinate fasciculus predicts reduced amygdala activation to sad and happy faces**… These results provide important insights into brain structure–function relationships during adolescence, and suggest that greater structural connectivity of the uncinate fasciculus may facilitate regulation of the amygdala, particularly during early adolescence.” “Further, **decreased amygdala activation to sad faces predicts lower internalizing symptoms**. These findings also have implications for understanding the relation between brain structure, function, and the development of **emotion regulation difficulties, such as internalizing symptoms**.” “Studies conducted in adults that have combined DTI and functional MRI (fMRI) suggest that structural connectivity of the uncinate fasciculus is related to activation as well as connectivity within **prefrontal cortex–amygdala circuitry**, which is central to emotion regulation.”

This review of fMRI studies reports that “a number of **neuroimaging studies in anxiety disorders and major depression** have demonstrated **abnormal activation in limbic and paralimbic regions (including the amygdala, insula, and anterior cingulate cortex)** in response to emotional stimuli.” “Patients with **anxiety disorders often exhibit amygdala hyperactivation** to threat-related cues, while those with major depression may show both **increased amygdala responses** to negative stimuli and **reduced activation in prefrontal regions** involved in emotion regulation.” “Altered patterns of activation within these circuits are thought to underlie key symptoms related to **fear, negative affect, and impaired regulation of emotion** in anxiety and depressive disorders.”

This meta-analysis “examined functional neuroimaging studies of **decision-making in mood and anxiety disorders**.” It found that “across studies, patients showed **abnormal activation in the ventromedial prefrontal cortex, dorsolateral prefrontal cortex, anterior cingulate cortex, and striatum** during decision-making tasks.” “Individuals with these disorders often exhibited **reduced activation in ventromedial prefrontal regions** and **altered recruitment of dorsal prefrontal and cingulate areas** when evaluating rewards, punishments, and risk, suggesting disrupted neural processing of value and control during decision-making.” “The authors conclude that these **prefrontal and cingulate abnormalities** may represent a shared neural substrate for **decision-making deficits** observed in mood and anxiety disorders.”

Reviewing animal and human imaging work, the authors state: “**Fear extinction** depends critically on the **ventromedial prefrontal cortex (vmPFC)** and **hippocampus**, which inhibit fear responses mediated by the **amygdala**.” “Human **fMRI studies** of fear conditioning and extinction have shown that failure to recruit vmPFC and hippocampus, combined with **persistent amygdala activation**, is associated with **pathological fear** and may underlie symptoms in anxiety disorders such as PTSD.” “These data support a model in which **abnormal activity within a vmPFC–amygdala–hippocampal circuit** contributes to impaired regulation of fear and persistent anxiety in clinical populations.”

Across contemporary cognitive neuroscience, there is broad consensus that many **psychiatric disorders** (including anxiety disorders, major depression, bipolar disorder, PTSD, and others) involve **abnormal activity and connectivity in circuits linking the amygdala, prefrontal cortex, anterior cingulate, and related regions**. Functional MRI studies repeatedly show **amygdala hyperactivation to threat or negative emotion**, together with **hypoactivation or dysregulated activation in medial and lateral prefrontal regions** that normally support **emotion regulation and decision-making**. This consensus is reflected in multiple reviews and meta-analyses that interpret these findings as core to the neurobiology of fear, emotional dysregulation, and altered decision-making in mental illness.