Anxiety disorders are highly debilitating illnesses that involve excessive worry, or an atypical fear response towards non-threatening stimuli. With estimates of lifetime prevalence at 29%, anxiety disorders are the most predominant form of mental illness, and about 90% of patients will also experience some other psychiatric problems in their lifetime[1] [2] . Due to high comorbidity with other psychiatric disorders such as depression, and bipolar disorder , substance abuse as well as physical ailments, the diagnosis of anxiety disorders can provide clinicians with more effective methods of treatment than to target the presenting illness alone[3] . Brain regions implicated in anxiety disorders are believed to be related to fear response and the limbic system, especially the amygdala, HPA-axis and the related structures of the prefrontal cortex, hippocampus, anterior cingulate cortex and insular cortex. For example, a number of abnormalities in the brain have been linked to GAD , including enlarged grey matter in the amygdala and dorsomedial prefrontal cortex[4] . Furthermore, it has been shown that multiple genetic polymorphisms as well as disruptions to certain neurotransmitter systems contribute to the onset of anxiety disorders. Among gene candidates are several single-nucleotide polymorphisms in fujimycin binding protein 5 interacting with childhood trauma predicting severity of adult PTSD , along with findings that suggest that SAD patients are more susceptible to a disruption of the serotonergic system, via carrying a short allele polymorphism in the serotonin transporter compared to the homozygous long allele found in healthy patients[5] [6] . Anxiety is often related to respiratory difficulties, and one of the initiators of anxiety is CO­2. Recent studies have found that the mechanism of the CO2 induced panic attacks might be correlated to the noradrenergic system/locus coeruleus system; in particular, elevated respiratory and cardiovascular response in anxiety disorder patients correlate to the NA/LC system[7] . Additionally, environmental effects such as traumatic events or childhood abuse are possible causal factors in combination with genetic effects, of anxiety disorders[8] . Current treatment options involve the pairing of psychotherapeutic interventions with anxiolytic drugs. The diagnosis of anxiety, along with the use of pharmaceuticals to treat its symptoms remains a controversial subject. As such, further research into the neurobiological basis of anxiety is increasingly important in order to develop more efficient and effective treatment for its many manifestations such as generalized anxiety disorder, panic disorder, post-traumatic stress disorder, and social anxiety disorder.

Generalized Anxiety Disorder (D. McKenna)
1.General Overview
  • 1.1. Characteristics and Diagnostic Criteria
  • 1.2. Controversies and the Possible Future of GAD
2.Neuroanatomy and Activity Associated with GAD
  • 2.1. Amygdala
  • 2.2. Prefrontal Cortex
  • 2.3. Anterior Cingulate Cortex
  • 2.4. Abnormal Connections Within the GAD Brain
3. The Immune system and GAD
  • 3.1. Th17, Inflammation and GAD
4. Treatment
  • 4.1. Pharmaceuticals
  • 4.2. Therapy

Panic Disorder (L. Tran)
1. General Overview
2. Etiology of Panic Disorder
  • 2.1 Genetics
  • 2.2 Neuroanatomical Correlates
    • 2.2.1 Amygdala
    • 2.2.2. Periaqueductal Gray
    • 2.2.3. Anterior Cingulate Cortex
    • 2.2.4. Cerebellum
  • 2.3 Neurotransmitters
    • 2.3.1. Serotonergic System
    • 2.3.2. GABA Dysfunction
    • 2.3.3. CCK System
    • 2.3.4. Orexin
  • 2.4 Environmental Factors
3. Treatment
  • 3.1. Psychotherapy
  • 3.2. Medications
  • 3.3. New Lines of Treatment

Post-Traumatic Stress Disorder (A. Sharma)
1.General Overview
  • 1.1. Symptoms
  • 1.2. Prevalence
2.Genetics
  • 2.1. Hereditary information
  • 2.2. FKBP5 SNPs
  • 2.3. Pituitary adenylate cyclase – activating polypeptide (PACAP) – PAC1 pathway
3. Neuroendocrinology
  • 3.1. Modulation of CRF concentrations
  • 3.2. Increased sensitivity in glucocorticoid receptors predicting abnormality in HPA axis
4. Areas in the brain
  • 4.1. Amygdala
  • 4.2. Hippocampus
5. Animal models
6. Treatments
  • 6.1. Psychotherapeutic interventions
  • 6.2. Medications

Social Anxiety Disorder (A. Slabiak)
1. Social anxiety causes
  • 1.1. Environmental causes
  • 1.2. Genetics and heredity
2. Brain regions
  • 2.1. Hyperactivity in the amygdala region
  • 2.2. Comparison of excitability of the amygdala region in response to facial expression in patients with social anxiety disorder versus healthy individuals
3. Serotonergic pathway
  • 3.1. short variation of 5’HTT promoter allele
4. Animal model
  • 4.1. 5’HTT promoter allele assessing social interaction
5. Treatments
  • 5.1. SSRI’s
  • 5.2. Challenges of Treatments

Carbon Dioxide and Anxiety (R. Huh)
1. Carbon Dioxide in the human brain
  • 1.1. Carbon Dioxide Sensitivie Cells in the Brain
2. Respiratory and Cardiovascular Response to Carbon Dioxide
  • 2.1. Regular Response
  • 2.2. Irregular Response i.e. Hyperventiliation
3. Prevalence of Carbon Dioxide Induced Panic Attacks in PD and PTSD
  • 3.1. Example of CO2 Induced Panic Attack
4. Mechanisms Of Carbon Dioxide Induced Panic Attacks

External Links


NIMH Fear/Safety, Anxiety, and Anxiety Disorders Interactive Guide
CAMHAnxiety Disorders
  1. ^ Kessler, R.C., Berglund, P., Demler, O., Jin, R., Merikangas, K.R., & Walters, E.E. Lifetime prevalence and age-of-onset distributions of DSM-IV Disorders in the National Comorbidity. Survey Replication. Arch Gen Psychiatry. 62, 593–602 (2005).
  2. ^ Kaufman, J., & Charney, D. Comorbidity of mood and anxiety disorders. Depression and Anxiety. 12(15), 69-76 (2000).
  3. ^ Sareen, J., Cox, B.J., Clara, I., Asmundson, & G.J.G . The relationship between anxiety disorders and physical disorders in the US National Comorbidity Survey. Depression and Anxiety. 21(4), 193-202 (2005).
  4. ^ Schienle, A., Ebner, F. and Schafer, A. Localized grey matter volume abnormalities in generalized anxiety disorder. Eur Arch Psychiatry Clin Neurosci. 261,303-307 (2011).
  5. ^ Shinozaki, G., Jowsey, S., Amer, H., Biernacka, J.M., Colby, C., Walker, D., Black, J., Rundell, J., Stegall, M., & Mrazek, D.A. Relationship between FKBP5 polymorhpisms and depression symptoms among kidney transplant recipients. Depress Anxiety. 28(12), 1111-8 (2011).
  6. ^ Furmark, T., Neurobiological Aspects of Social Anxiety Disorder. Israel Journal of Psychiatry and Related Sciences. 46(1), 5-12 (2009).
  7. ^ Eric, G., & Koen, S., Mechanisms of CO2 Challenges. J Psychopharmacol. 17(3), 260-262 (2003).
  8. ^ Hovens, J.G., Wiersma, J.E., Giltay, E.J., van Oppen, P., Spinhoven, P., Penninx, B.W., & Zitman F.G. Childhood life events and childhood trauma in adult patients with depressive, anxiety and comorbid disorders vs. controls. Acta Psychiatr Scand. 122(1), 66-74 (2009).