To save content items to your account,
please confirm that you agree to abide by our usage policies.
If this is the first time you use this feature, you will be asked to authorise Cambridge Core to connect with your account.
Find out more about saving content to .
To save content items to your Kindle, first ensure firstname.lastname@example.org
is added to your Approved Personal Document E-mail List under your Personal Document Settings
on the Manage Your Content and Devices page of your Amazon account. Then enter the ‘name’ part
of your Kindle email address below.
Find out more about saving to your Kindle.
Note you can select to save to either the @free.kindle.com or @kindle.com variations.
‘@free.kindle.com’ emails are free but can only be saved to your device when it is connected to wi-fi.
‘@kindle.com’ emails can be delivered even when you are not connected to wi-fi, but note that service fees apply.
Secondary pharmacological interventions have shown promise at reducing the development of posttraumatic stress disorder symptoms (PTSS) in preclinical studies. The present study examined the preliminary efficacy of a 10-day low-dose (20 mg bid) course of hydrocortisone at preventing PTSS in traumatic injury victims.
Sixty-four traumatic injury patients (34% female) were randomly assigned in a double-blind protocol to receive either a 10-day course of hydrocortisone or placebo initiated within 12 hours of the trauma. One-month and 3-months posttrauma participants completed an interview to assess PTSS and self-report measures of depression and health-related quality of life.
Hydrocortisone recipients reported fewer PTSD and depression symptoms, and had greater improvements in health-related quality of life during the first 3 months posttrauma than did placebo recipients. Hydrocortisone recipients who had never received prior mental health treatment had the lowest PTSD scores.
Low-dose hydrocortisone may be a promising approach to the prevention of PTSD in acutely injured trauma patients, and may be particularly efficacious in acutely injured trauma victims without a history of significant psychopathology.
This chapter discusses the evidence for the role of genetic factors in the etiology of anxiety disorders, and summarizes the genetic study designs used in research on anxiety disorders. Molecular genetic study designs used to investigate the genetics of anxiety disorders include linkage analysis and candidate gene association studies. Twin studies support a heritability estimate between 30% and 40%. More recently, regulators of G-protein signaling have been investigated regarding anxiety-related phenotypes including panic disorder. Family studies suggest that risk of social anxiety disorder (SAD) to first-degree relatives of SAD probands ranges from 16% to 26%. Investigations of panic disorder, specific phobias, SAD, and obsessive-compulsive disorder (OCD) have produced some evidence of linkage to specific regions. Two exciting yet mostly unexplored areas in anxiety disorder research are gene-environment interaction and epigenetic studies. Epigenetic research examines the dynamic heritable changes in the function of a gene.
Email your librarian or administrator to recommend adding this to your organisation's collection.