The role of negativity bias in emotional and cognitive dysregulation

Negativity bias is the tendency to focus more on negative experiences than positive ones.

In anxiety disorders, this bias can amplify perceived threats, fuel excessive worry, and distort emotional responses, making it harder to regulate fear and stress.

As a result, it contributes to heightened anxiety, emotional instability, and cognitive difficulties.

Norris, S., Salgado, F., Murray, S., Amen, D., & Keator, D. B. (2025). The Role of Negativity Bias in Emotional and Cognitive Dysregulation: A Neuroimaging Study in Anxiety Disorders. Depression and Anxiety, 2025(1), 2739947. https://doi.org/10.1155/da/2739947

Key Points

• Focus: This study explores how conscious negativity bias affects brain function, emotional regulation, and cognitive performance in individuals with anxiety disorders.
• Method: A retrospective analysis of 1,990 patients with anxiety disorders used neuroimaging (SPECT scans) and cognitive assessments from the Total Brain platform, alongside self-report symptom checklists.
• Findings: Greater negativity bias was associated with hypoperfusion in brain regions linked to cognitive control and emotional regulation, and hyperperfusion in cerebellar regions. Patients showed more depressive and anxiety symptoms, cognitive deficits, and reduced resilience.
• Implications: Targeting negativity bias in therapeutic interventions could improve emotional regulation and cognitive outcomes in anxiety disorders.

Rationale

Negativity bias refers to the cognitive tendency to give greater weight to negative stimuli over positive ones, even when both are of equal intensity.

This bias influences attention, memory, decision-making, and emotional regulation.

Previous research has linked negativity bias to increased sensitivity to threat and negative emotion, which contributes to the onset and maintenance of anxiety and depression.

Neuroimaging studies have demonstrated that this bias is encoded in brain regions such as the amygdala, prefrontal cortex, and insula.

However, most studies focus on general associations rather than examining negativity bias specifically in individuals with anxiety disorders.

Moreover, while functional MRI has identified relevant regions, few studies have assessed how brain function, symptoms, and cognitive performance interact within a clinical sample using multimodal assessments.

This study aimed to bridge that gap by examining how negativity bias correlates with brain function and patient-reported symptoms.

By using SPECT imaging and a large dataset of patients with anxiety, the researchers sought to clarify the neural correlates of negativity bias and understand how this bias may contribute to emotional and cognitive dysregulation.

Understanding these links could inform interventions that specifically target negativity bias in treatment.

Method

A retrospective analysis was conducted using clinical data from 1,990 anxiety disorder patients evaluated at Amen Clinics. Patients underwent:

• SPECT brain scans during resting state
• A 300-item DSM-based symptom checklist
• The Total Brain cognitive and emotional assessment battery

Neuroimaging data were preprocessed and registered to MNI space using ANTs and analyzed with voxel-based multiple regression models in SPM12.

Negativity bias was assessed via the Total Brain platform and linked to symptom and cognitive data using regression models in R.

Procedure

1. Patient recruitment: Retrospective data collection from 11 Amen Clinics.
2. Inclusion: Diagnosed anxiety disorder without certain comorbidities (e.g., epilepsy, substance use).
3. SPECT scan: Injection of tracer, followed by a resting-state brain scan.
4. Symptom checklist: 300 self-report questions (Likert scale).
5. Cognitive testing: Total Brain assessment on emotional regulation, cognition, and memory.
6. Data analysis:
   • Neuroimaging processed and aligned to MNI space.
   • Multiple regressions tested associations between negativity bias and symptoms, cognition, and brain function.
   • FDR correction was applied to control for multiple comparisons.

Sample

• N = 1,990
• Mean age: 38.8 years (SD = 14.8)
• Sex: 806 males, 1,184 females
• Ethnicity: 74.3% Caucasian, 2.8% Black, 2.7% Asian, 4.2% Multiracial, 15.8% Unknown
• Comorbidities: Mean = 4.9 per patient
• Negativity bias: Mean z-score = -1.1 (higher negative thinking)

Measures

• SPECT Imaging: Measures resting-state brain perfusion.
• Total Brain Platform:
  • Negativity Bias: Ability to recognize/respond to negative emotions.
  • Feeling Domain: Stress, anxiety, and mood control.
  • Resilience: Coping and recovery from adversity.
  • Verbal Memory Recognition: Immediate and delayed recall.
  • Thinking Domain: Attention, planning, and memory tasks.
• 300-item DSM Checklist: Measures depression, anxiety, motivation, suicidal ideation, etc.

Statistical Measures

• Voxel-based multiple regression models (SPM12)
• Whole-brain FDR correction (p < 0.05)
• Ordinal regression for symptom severity (R software)
• Multiple regression for cognitive associations (Holm correction for multiple comparisons)

Results

• Brain Function:
  • Hypoperfusion in bilateral frontal, temporal, and parietal lobes and insula.
  • Hyperperfusion in cerebellar lobules IV–VI and hypothalamic regions.
• Symptoms:
  • Strong links between negativity bias and depressive symptoms (sadness, helplessness, guilt).
  • High anxiety symptoms: excessive worry, catastrophizing.
  • Repetitive thoughts, reduced motivation, and suicidal ideation.
  • Increased emotional instability and social withdrawal.
• Cognitive Associations:
  • Poorer emotion and mood regulation
  • Lower resilience and stress control
  • Impaired verbal memory (both immediate and delayed recall)
  • Reduced cognitive flexibility and attention

Insight

This study offers compelling evidence that negativity bias is not just a psychological trait but is underpinned by measurable neural dysfunction.

Patients with high negativity bias showed reduced function in areas vital for emotion regulation and decision-making and increased activity in regions related to stress response.

These findings illuminate how distorted emotional processing may worsen anxiety and depressive symptoms.

By integrating neural, cognitive, and symptom data, the study reveals the mechanisms by which cognitive biases perpetuate psychiatric distress and supports the view that negativity bias should be a therapeutic target.

Clinical Implications

• Therapeutic Target: Negativity bias may be an actionable treatment focus in anxiety disorders.
• Neurofeedback & TMS: Can stimulate underactive regions (e.g., DLPFC) to improve emotion regulation.
• CBT: Should address repetitive negative thinking and build cognitive flexibility.
• Mindfulness & Breathing Techniques: May help modulate HPA axis and reduce autonomic arousal.
• Tailored Interventions: Combining behavioral and biological insights can lead to more personalized treatment plans for anxiety.

Strengths

This study had several methodological strengths, including:

• Large, well-characterized clinical sample (N = 1,990)
• Integration of neuroimaging, cognitive, and symptom data
• Use of validated tools (SPM12, Total Brain platform)
• Whole-brain voxel-based analysis with FDR correction
• Multimodal approach supports robust conclusions about brain-behavior links

Limitations

This study also had several limitations, including:

• Use of retrospective data limits causal inference.
• Comorbidities may confound the associations despite statistical controls.
• SPECT resolution is lower than fMRI (~6.5 mm voxel), limiting fine-grained interpretations.
• Clinical diagnoses were based on chart review and DSM criteria, possibly introducing diagnostic variability.
• Neuroimaging findings are correlational and require replication with prospective designs.

Socratic Questions

1. How might we distinguish between conscious and unconscious negativity bias in clinical assessments?
2. In what ways could comorbid conditions (e.g., depression) distort the associations seen here?
3. What alternative explanations could account for the observed brain perfusion patterns?
4. How could we test whether reducing negativity bias improves emotional and cognitive regulation?
5. Should therapies targeting negativity bias differ by patient age, gender, or symptom profile?
6. Could similar neural patterns be observed in disorders characterized by rumination, such as OCD?
7. How does negativity bias interact with cultural or environmental factors in shaping emotion processing?
8. What are the implications for designing school or workplace interventions to promote resilience?
9. How might these findings guide future neuroimaging studies of cognitive bias?
10. What are the ethical considerations in using brain imaging for clinical decisions about bias and emotion?