Our original article examining chronic PTSD as a permanent life altering injury generated extensive inquiries. As we reviewed and answered these questions certian themes emerged. They are:(a) research describing the permanent effects on the brain;
(b) levels of recovery through therapy;
(c) research articles that describe PTSD as a physical injury, and
(d) the lifelong effects of PTSD on social-emotional functioning (i.e. family, friends, work, parenting, and social interactions).
In order to further assist trial lawyers working on these cases and because of the amount of inquiries, Lītigāre has compiled a list of research studies, in a pseudo-annotated bibliographic style, supporting the facts that chronic PTSD is a permanent life altering injury.
These studies were carefully chosen as a starting framework for validating the permanence of chronic PTSD as a life altering injury. The following research validates the MRI as the appropriate and correct tool of measurement to identify and track the permanent changes in brain structure, the areas of the brain that are permanently affected, and that PTSD is being considered in the medical and psychological world as a physical illness resulting from the traumatic event.
We reiterate that the current DSM diagnosis of acute and chronic PTSD is contingent upon the individual’s perception of the life threat, in other words how the person responded to the event or events.
I. Alterations in cerebral perfusion in post-traumatic stress disorder patients without re-exposure to accident-related stimuli.
For Your Case:
This study indicates that the negative effects of PTSD, problematic social-emotional functioning, are a direct result of alterations in the brain that occurred because of the traumatic event; this is just like a physical blow to the head or damage resulting from a stroke. The effects are just as damaging and just as permanent. Furthermore, the negative effects (problematic social-emotional functioning) are not elicited because of event related stimuli; the negative effects are the end result of the changes in brain structure (brain damage).
Current research has proven, through functional neuroimaging studies, that individuals with PTSD show abnormalities in the limbic region when re-experiencing a trauma. This is caused by cognitive activations during moments of re-exposure. This research study posited that the functional neuroimaging studies will show abnormalities in the limbic region when individuals with PTSD are not experiencing re-exposure to a traumatic event. The functional neuroimaging studies were compared with similar individuals without PTSD.
In the absence of re-exposure and cognitive activation individuals with PTSD showed marked differences in how the limbic and temporal regions functioned when compared to similar individuals without PTSD. “This result indicates that PTSD patients have alterations in cerebral perfusion of limbic regions and the frontal and temporal cortex without re-exposure to accident-related stimuli.” This study indicates that the negative effects of PTSD, problematic social-emotional functioning, actually come from the alterations in the brain that are a direct result of the traumatic event.
Chung, Y.A., Kim, S.H., Chung, S.K., Chae, J.H., Yang, D.W., Sohn, H.S., & Jeong, J. (2006). Alterations in cerebral perfusion in posttraumatic stress disorder patients without re-exposure to accident-related stimuli. Clinical Neurophysiology: Official Journal Of The International Federation Of Clinical Neurophysiology. Vol. 117 (3), pp. 637-42.
Update Code: 20121129
II. The zone of danger, physical impact, and PTSD.
For Your Case:
This article indicates that neurobiological research designates PTSD as a physical injury, which provides for you a foundation that PTSD is a permanent physical brain injury.
This journal article focused on insurance coverage and specifically coverage exemptions for psychological trauma that includes a threat of imminent direct physical peril. The authors described PTSD and refer to neurobiological research conducted on the effects of PTSD. They also made recommendations for revising coverage exemptions.
“Neurobiological research demonstrates that PTSD is associated with changes in brain imaging studies and neuroendocrinology, supporting the stance that PTSD is, in part, a physical illness.”.
Keram, E.A. (2006) The zone of danger, physical impact, and PTSD. The Journal Of The American Academy Of Psychiatry And The Law. Vol. 34 (2), pp. 200-3.
Author Address: email@example.com
III. Asymmetry of limbic structure (hippocampal formation and amygdaloidal complex) at PTSD
For Your Case:
The findings in this research established the validity and reliability of the MRI as the medical standard in corroborating changes in brain structure with a PTSD diagnosis.
This research evaluates the use of MRI and specific techniques of measuring changes in brain structure for PTSD suffers. The researchers were looking at the asymmetry of the limbic structures specifically the hippocampus and amygdaloidal complex.
This research supports the findings of other research studies on the use of the MRI as an effective and valid tool for the measurement the changes in brain structure of individuals with PTSD.
Sarac-Hadzihalilović, A. & Dilberović, F. (2003). Asymmetry of limbic structure (hippocampal formation and amygdaloidal complex) at ptsd. Bosnian Journal Of Basic Medical Sciences. Vol. 3 (2), pp. 17-24.
IV. Gray matter density in limbic and paralimbic cortices is associated with trauma load and EMDR outcome in PTSD patients.
For Your Case:
The results from this research study confirm that brain tissue (gray matter) in the limbic system shrinks as a direct result of chronic PTSD. Grey matter shrinking causes memory loss, issues with perception, negatively alters the sense of self, and affects levels of consciousness (all of which are dissociative disturbances).
The study hypothesized that the intensity level of a trauma would directly affect the density of gray matter (GM) specifically in the limbic system. MRI (Magnetic Resonance Imaging) was utilized to measure the GM densities.
There is a direct correlation between gray matter density in the limbic and paralimbic cortices and the level of trauma. Furthermore, trauma load affected GM densities which illustrated the symptoms of memory loss and dissociative disturbances.
Nardo, D. Hogberg, G., Looi, JC., Larsson, S., Hallstrom, T., & Pagani, M. (2010). Gray matter density in limbic and paralimbic cortices is associated with trauma load and EMDR outcome in PTSD patients. Journal of Pscyhiatric Research. Vol. 44 (7), pp. 477-85.
Author Address: firstname.lastname@example.org
V. An fMRI study of the brain responses of traumatized mothers to viewing their toddlers during separation and play.
For Your Case:
This study verifies the impact on ability to parent when confronted with the issues of PTSD. PTSD can severely impact present and future parenting skills. The alterations in perceptions about safety cause undue emotional distress on parent and child.
This research compared mothers with and without PTSD who, at the time of the study, were parenting young children. The reactions of the research subjects were recorded as they were watching their own children and unknown children play. The research posited that the increases in limbic system activity and decreases in frontocortical activity for women with PTSD would affect how they viewed the children at play.
As posited, mothers with PTSD showed increased levels of stress watching both their own and unknown children at play. The researches specified that the stress response is directly caused by the increased functioning in the limbic system and decreased frontocortical activity. The implications of this study are numerous.
Schechter, D.S., Moser, D.A., Wang, Z., Marsh, R., Hao, X., Duan, Y., Yu, S., Gunter, B., Murphy, D., McCaw, J., Kangarlu, A. ; Willheim E., Myers, M.M., Hofer, M.A. & Peterson. B.S. (2012). An fMRI study of the brain responses of traumatized mothers to viewing their toddlers during separation and play. Social Cognitive And Affective Neuroscience Vol. 7 (8), pp. 969-79.
Author Address: email@example.com
PubMed Central ID: PMC3501701