Understanding the neurobiology of comorbidity in anxiety disorders

CNS Spectr. 2006 Oct;11(10 Suppl 12):13-20. doi: 10.1017/s1092852900025803.

Abstract

Anxiety and depression are common disorders that frequently co-exist. Both disorders show good response to antidepressants, especially the selective serotonin reuptake inhibitors. Some suggest that these disorders are variants of the same underlying brain pathology. This review examines the similarities and differences between anxiety and depression in terms of the known neurobiological etiologic mechanisms as well as their biological underpinnings and response to treatment. Sufficient and significant differences between these disorders support the view that they are independent entities. Shared abnormalities in the 5HT1A receptor function, for example, may help explain some of the comorbidity.

Publication types

  • Review

MeSH terms

  • Anxiety Disorders / diagnosis
  • Anxiety Disorders / drug therapy
  • Anxiety Disorders / physiopathology*
  • Anxiety Disorders / psychology
  • Arousal / drug effects
  • Arousal / physiology
  • Brain / drug effects
  • Brain / physiopathology
  • Comorbidity
  • Depressive Disorder / diagnosis
  • Depressive Disorder / drug therapy
  • Depressive Disorder / physiopathology
  • Depressive Disorder / psychology
  • Humans
  • Mental Disorders / diagnosis
  • Mental Disorders / drug therapy
  • Mental Disorders / physiopathology*
  • Mental Disorders / psychology
  • Nerve Net / drug effects
  • Nerve Net / physiopathology
  • Receptor, Serotonin, 5-HT1A / drug effects
  • Receptor, Serotonin, 5-HT1A / physiology
  • Receptors, GABA / drug effects
  • Receptors, GABA / physiology
  • Selective Serotonin Reuptake Inhibitors / therapeutic use
  • Tomography, Emission-Computed, Single-Photon

Substances

  • Receptors, GABA
  • Serotonin Uptake Inhibitors
  • Receptor, Serotonin, 5-HT1A