Anxiety Disorders and Anxiety Medication

Anxiety Disorders

Role of Research in Improving the Understanding and Treatment of Anxiety Disorders

NIMH supports research into the causes, diagnosis, prevention, and treatment of anxiety disorders and other mental illnesses. Studies examine the genetic and environmental risks for major anxiety disorders, their course—both alone and when they occur along with other diseases such as depression—and their treatment. The ultimate goal is to be able to cure, and perhaps even to prevent, anxiety disorders.

NIMH is harnessing the most sophisticated scientific tools available to determine the causes of anxiety disorders. Like heart disease and diabetes, these brain disorders are complex and probably result from a combination of genetic, behavioral, developmental, and other factors.

Several parts of the brain are key actors in a highly dynamic interplay that gives rise to fear and anxiety.¹⁴ Using brain imaging technologies and neurochemical techniques, scientists are finding that a network of interacting structures is responsible for these emotions. Much research centers on the amygdala, an almond-shaped structure deep within the brain. The amygdala is believed to serve as a communications hub between the parts of the brain that process incoming sensory signals and the parts that interpret them. It can signal that a threat is present, and trigger a fear response or anxiety. It appears that emotional memories stored in the central part of the amygdala may play a role in disorders involving very distinct fears, like phobias, while different parts may be involved in other forms of anxiety.

Other research focuses on the hippocampus, another brain structure that is responsible for processing threatening or traumatic stimuli. The hippocampus plays a key role in the brain by helping to encode information into memories. Studies have shown that the hippocampus appears to be smaller in people who have undergone severe stress because of child abuse or military combat.¹⁵^,¹⁶ This reduced size could help explain why individuals with PTSD have flashbacks, deficits in explicit memory, and fragmented memory for details of the traumatic event.

Also, research indicates that other brain parts called the basal ganglia and striatum are involved in obsessive-compulsive disorder.¹⁷

By learning more about brain circuitry involved in fear and anxiety, scientists may be able to devise new and more specific treatments for anxiety disorders. For example, it someday may be possible to increase the influence of the thinking parts of the brain on the amygdala, thus placing the fear and anxiety response under conscious control. In addition, with new findings about neurogenesis (birth of new brain cells) throughout life,¹⁸ perhaps a method will be found to stimulate growth of new neurons in the hippocampus in people with PTSD.

NIMH-supported studies of twins and families suggest that genes play a role in the origin of anxiety disorders. But heredity alone can't explain what goes awry. Experience also plays a part. In PTSD, for example, trauma triggers the anxiety disorder; but genetic factors may explain why only certain individuals exposed to similar traumatic events develop full-blown PTSD. Researchers are attempting to learn how genetics and experience interact in each of the anxiety disorders—information they hope will yield clues to prevention and treatment.

Scientists supported by NIMH are also conducting clinical trials to find the most effective ways of treating anxiety disorders. For example, one trial is examining how well medication and behavioral therapies work together and separately in the treatment of OCD. Another trial is assessing the safety and efficacy of medication treatments for anxiety disorders in children and adolescents with co-occurring attention deficit hyperactivity disorder (ADHD). For more information about these and other clinical trials, visit the NIMH clinical trials web page, www.nimh.nih.gov/studies/index.cfm, or the National Library of Medicine's clinical trials database, www.clinicaltrials.gov.

References

¹Narrow WE, Rae DS, Regier DA. NIMH epidemiology note: prevalence of anxiety disorders. One-year prevalence best estimates calculated from ECA and NCS data. Population estimates based on U.S. Census estimated residential population age 18 to 54 on July 1, 1998. Unpublished.

²Robins LN, Regier DA, eds. Psychiatric disorders in America: the Epidemiologic Catchment Area Study. New York: The Free Press, 1991.

³The NIMH Genetics Workgroup. Genetics and mental disorders. NIH Publication No. 98-4268. Rockville, MD: National Institute of Mental Health, 1998.

⁴Regier DA, Rae DS, Narrow WE, et al. Prevalence of anxiety disorders and their comorbidity with mood and addictive disorders. British Journal of Psychiatry Supplement, 1998; (34): 24-8.

⁵Kushner MG, Sher KJ, Beitman BD. The relation between alcohol problems and the anxiety disorders. American Journal of Psychiatry, 1990; 147(6): 685-95.

⁶Wonderlich SA, Mitchell JE. Eating disorders and comorbidity: empirical, conceptual, and clinical implications. Psychopharmacology Bulletin, 1997; 33(3): 381-90.

⁷Davidson JR. Trauma: the impact of post-traumatic stress disorder. Journal of Psychopharmacology, 2000; 14(2 Suppl 1): S5-S12.

⁸Margolin G, Gordis EB. The effects of family and community violence on children. Annual Review of Psychology, 2000; 51: 445-79.

⁹Yehuda R. Biological factors associated with susceptibility to posttraumatic stress disorder. Canadian Journal of Psychiatry, 1999; 44(1): 34-9.

¹⁰Bourdon KH, Boyd JH, Rae DS, et al. Gender differences in phobias: results of the ECA community survey. Journal of Anxiety Disorders, 1988; 2: 227-41.

¹¹Kendler KS, Walters EE, Truett KR, et al. A twin-family study of self-report symptoms of panic-phobia and somatization. Behavior Genetics, 1995; 25(6): 499-515.

¹²Boyd JH, Rae DS, Thompson JW, et al. Phobia: prevalence and risk factors. Social Psychiatry and Psychiatric Epidemiology, 1990; 25(6): 314-23.

¹³Kendler KS, Neale MC, Kessler RC, et al. Generalized anxiety disorder in women. A population-based twin study. Archives of General Psychiatry, 1992; 49(4): 267-72.

¹⁴LeDoux J. Fear and the brain: where have we been, and where are we going? Biological Psychiatry, 1998; 44(12): 1229-38.

¹⁵Bremner JD, Randall P, Scott TM, et al. MRI-based measurement of hippocampal volume in combat-related posttraumatic stress disorder. American Journal of Psychiatry, 1995; 152: 973-81.

¹⁶Stein MB, Hanna C, Koverola C, et al. Structural brain changes in PTSD: does trauma alter neuroanatomy? In: Yehuda R, McFarlane AC, eds. Psychobiology of posttraumatic stress disorder. Annals of the New York Academy of Sciences, 821. New York: The New York Academy of Sciences, 1997.

¹⁷Rauch SL, Savage CR. Neuroimaging and neuropsychology of the striatum. Bridging basic science and clinical practice. Psychiatric Clinics of North America, 1997; 20(4): 741-68.

¹⁸Gould E, Reeves AJ, Fallah M, et al. Hippocampal neurogenesis in adult Old World primates. Proceedings of the National Academy of Sciences USA, 1999, 96(9): 5263-7.

¹⁹Hyman SE, Rudorfer MV. Anxiety disorders. In: Dale DC, Federman DD, eds. Scientific American® Medicine. Volume 3. New York: Healtheon/WebMD Corp., 2000, Sect. 13, Subsect. VIII.

This brochure is a revision by Mary Lynn Hendrix of an earlier version written by Marilyn Dickey.

Scientific information and/or review for this revision were provided by Steven E. Hyman, M.D., Richard Nakamura, Ph.D., Matthew Rudorfer, M.D., Linda Street, Ph.D., and Elaine Baldwin, all of NIMH, and Una McCann, M.D., now of The Johns Hopkins University. Editorial assistance was provided by Clarissa Wittenberg, Margaret Strock, and Melissa Spearing of NIMH.

All material in this publication is in the public domain and may be copied or reproduced without permission of the Institute. Citation of the source is appreciated.

NIH Publication No. 3879

Posted: 04/09/2004

This material can also be obtained as a pdf at the National Institute of Mental Health.

Sourced at: http://www.nimh.nih.gov/Publicat/anxiety.cfm