Citation

McFarlane AC. Psychol. Inj. Law 2010; 3(2): 100-110.

Copyright

(Copyright © 2010, Holtzbrinck Springer Nature Publishing Group)

DOI

10.1007/s12207-010-9074-z

PMID

unavailable

Abstract

Delayed onset posttraumatic stress disorder has been a challenging issue in medico-legal settings. Prospective studies have done much to characterise the validity of this construct and the prevalence in various populations. The delayed impact of these events places significant challenges on a plaintiff in establishing a causal link to some distal exposure. Furthermore, the literature highlights that depression is a frequent independent outcome from posttraumatic events, independent of the frequent comorbidity for posttraumatic stress disorder. To date, there has been little examination of the commonality of the underlying mechanisms of aetiology between depression and posttraumatic stress disorder. The concepts of sensitisation and kindling have been extensively discussed as underlying mechanisms relevant to a range of psychiatric disorders. This idea of increasing sensitisation of individuals who have multiple traumatic stress exposures is of critical importance to understanding the shared aetiology of major depressive disorder and posttraumatic stress disorder. Furthermore, the neural circuitry involved in these conditions particularly involves the amygdala, medial prefrontal cortex and anterior cingulate. Given the shared aetiological mechanisms, it is probable that the delays in treatment which have been demonstrated to be important factors for decreasing the probability of a full treatment response in depression are equally relevant to posttraumatic stress disorder. This raises important issues about the liability of employers particularly in the emergency services for vetting individuals where there is a foreseeable risk. A further challenge in litigation settings is the increasing body of evidence linking posttraumatic stress disorder and depression to cardiovascular disease and hypertension.