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I earned my PhD years ago. It was a very traumatic experience. I have been through therapy, but I still have not moved past the anxiety and terror of my PhD experience. I am in a new field, and have the opportunity to write again. I am working on 3 projects, one of them triggers my PhD PTSD. I can’t write this paper, this person makes me EXTREMELY anxious. I have figured out where the trigger comes from, but I can’t get past it.

Anyone else with similar experiences, care to share your story? How are you coping, what are your strategies?

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Trauma Emphasis

Put your phd to work with trauma survivors.

Combat veterans. Mass casualty events. Domestic violence. Child abuse. The potential long-term – and immediate – psychological costs of trauma exposure can be catastrophic.

Patients need a fully trauma-informed support team across every healthcare specialty, and the demand for compassionate experts in treating trauma-related psychological issues has always been high.

When you choose an emphasis in Trauma at Palo Alto University, you’ll work alongside researchers, teacher, policy makers, and clinicians to treat patients in crisis and address the growing public health needs.

Trauma Emphasis Objectives

You will receive specialized education and training in evidence-based assessment and treatment approaches in trauma psychology.

Our prerequisites and trauma-specific courses fulfill the didactive education criteria identified in the New Haven Trauma Competencies.

And your education won’t stop after you earn your degree. You will be expected to demonstrate expertise in this specialty in your commitment to lifelong learning at the post-doctoral level.

New Haven Trauma Competencies

The learning objectives of PAU’s Trauma Area of Emphasis are aligned with the New Haven Core Competencies (Cook & Newman, 2014). These competencies broadly include foundational knowledge, a range of functional skills, and professional attitudes.

Specifically, five areas are important to the specialized education and training needed by clinicians who work with trauma survivors:

• Scientific knowledge about trauma
• Psychosocial trauma-related assessment
• Trauma-focused psychosocial intervention
• Trauma-informed professionalism
• Trauma-informed relational and systems

The Trauma Area of Emphasis uses a series of benchmarks to identify and to assess successful attainment of trauma competencies.

Learn More about the New Haven Core Competencies

Risk and Resilience Research Lab Webinar

Course Requirements

Among mental health professionals, the potential long-term psychological costs of exposure to trauma has long been recognized. Adverse consequences have been well documented by researchers who study combat veterans, people who have experienced mass casualty events (e.g., disasters and terrorist attacks), domestic violence, and adult survivors of genocide, sexual assault, childhood abuse, or car accidents.

In response to the growing scientific literature, there is national support for developing a trauma-informed workforce across all healthcare domains, as evidenced by initiatives undertaken by the Substance Abuse and Mental Health Services Administration and the Joint Commission.

Recent natural disasters, terrorist attacks, and international conflicts have hastened demand for clinicians with competence in assessing and treating trauma survivors. Alongside clinicians, trauma researchers, teachers, and policy makers who possess the knowledge, skills, and attitudes necessary to meet growing public health needs are greatly needed.

The Trauma Area of Emphasis provides students with a theoretical, research, and clinical foundation necessary for developing competency in working with traumatized adults, children, adolescents, and their families.

Core Coursework

You must complete the core coursework required of all clinical students. In addition, you must complete a series of three required courses (9 units) that focus on trauma psychology.

Trauma core coursework must be completed over the course of two years, [2nd and 3rd] or [3rd and 4th] of the PhD program.

Students should plan their schedules carefully as successful completion of the perquisite CBT course are required for enrolling in the advanced courses. 

Prerequisites:

To enroll in the Assessment and Treatment of Trauma courses, you must complete CBT and the Foundations of Clinical Trauma Psychology with a grade at or above an A-.

Child, Adolescent and Family Trauma Specialization

• Foundations of Clinical Trauma Psychology (required prerequisite for the Assessment and Treatment course)
• Assessment and Treatment of Trauma in Children and Adolescents
• Elective PAU course with a child or adolescent trauma component*

Although the focus of assessment of this specialization track is on children and adolescents, it also includes adult family members, such as parents and grandparents, who are integral members of the process and outcome.

Adult Trauma Specialization

• Assessment and Treatment of Trauma in Adults
• Elective PAU course with an adult trauma component

Students who elect to complete both the Child and Adolescent Trauma Specialization and the Adult Trauma Specialization may fulfill the elective requirement (i.e., #3 requirement listed above) by completing a single course (i.e., not two courses – one for each specialization track) if aspects of adult and child/adolescent trauma are addressed at some point during the course. No course approval for the selected elective course is needed from the Director of the Trauma Area of Emphasis.

*  Students can take CBT concurrently with Foundations of Clinical Trauma Psychology course, but not concurrently with the Assessment and Treatment of Trauma courses. CBT and Foundations of Clinical Trauma Psychology are prerequisite courses that need to be completed prior to taking the Assessment and Treatment of Trauma in Children and Assessment and Treatment of Trauma in Adults courses. 

Dr. Brown is a tenured Professor, Director of the Trauma Program, Director of the Risk and Resilience Research Lab at Palo Alto University, and faculty advisor for the Association of Traumatic Stress Studies. Her clinical and research focus is on trauma and resilience, global mental health, aging, and vulnerable populations.

Eligibility

All students may take the Assessment and Treatment trauma courses if the prerequisite courses are completed. No exceptions will be made for waiving CBT prerequisite course. 

Students can elect to complete one or both of the Trauma Area of Emphasis specializations in Child and Adolescent Trauma or in Adult Trauma. 

Students can only report completion of the Trauma Area of Emphasis if they have fulfilled all requirements of one or of both specialization tracks (i.e., required trauma courses, trauma focused practicum, dissertation).

With carefully planning, students can complete both specializations if desired.  

Additional Requirements

To be competitive for obtaining a top tier internship, you will need to demonstrate excellent writing and statistical skills.

You should be actively involved with a research group that is focused on trauma related projects, and strive to publish papers and give presentations on trauma related topics.

Professional Development

You will be expected to actively take part in professional activities. This includes student membership in the American Psychological Association, Division of Trauma Psychology (56) and regular attendance at the Palo Alto University Trauma Journal Club.

Dissertation

Students in the Trauma Area of Emphasis must complete a dissertation that makes a scientific contribution to the field of trauma psychology.

In your 3rd or 4th year, you must complete an official practicum placement (one year of full or supplemental training) in a setting that includes a caseload of patients with PTSD or other trauma-related disorders in which trauma is the primary treatment focus.

Students are required to complete an internship in a setting that includes a caseload of patients with PTSD or other trauma-related disorders in which trauma is the primary focus for at least 33% of the total internship hours.

Completion of the Trauma Area of Emphasis

Successful completion of the Trauma Area of Emphasis at Palo Alto University is only one component in the education and clinical training necessary to become a competent clinician. Further specialty preparation and development is expected at the pre-doctoral and post-doctoral level as part of a commitment to life-long learning in psychology.

Completion of the Trauma Area of Emphasis will be granted following the completion of all coursework requirements, completion or securement of a trauma focused practicum, fulfillment of internship requirements, and approval of the dissertation proposal by the dissertation committee.

Students who have successfully completed the Trauma Area of Emphasis may apply for a certificate of completion by clicking  here .

Asked what advice she would offer students today, Dr. White-Cooper says: "Figure out what you want, be intentional and stay focused on your micro-goals. In addition to schoolwork, get social support outside the classroom. This formula will take you on the path to self-discovery and rewarding career in helping others."

"I found a lot of support available to me during the MS program and during my own transition into the PhD."

PhD in Health Sciences – Trauma Informed Care Heal Hearts, Change Lives

Credit Hours

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100% online, 8-week courses

Transfer in up to 50% of the degree total

Prepare to Help People Overcome Trauma with Liberty’s PhD in Health Sciences – Trauma Informed Care

Trauma is more than a condition – it is a crippling, life-altering state of mind that can make the most common tasks impossible, damage relationships, and destroy one’s sense of self. Victims of trauma often find themselves in a pit of indescribable despair that seems impossible to climb out of. Fortunately, help and hope are available – and if you want to join the fight against trauma, Liberty University’s 100% online Doctor of Philosophy (PhD) in Health Sciences – Trauma Informed Care can equip you with the skills you need.

This degree program has been designed with the success of both you and your clients in mind. In this trauma psychology program, you will dive into curricula that cover a wide variety of topics – including ethical issues in the health sciences, crisis and first responder training, post-traumatic stress disorder (PTSD) and combat trauma, and much more. Our professors are experts with years of experience in education and trauma treatment – so you can feel confident in the quality of instruction you will receive.

The time has never been better to pursue an online trauma PhD program, and at Liberty University, it has never been simpler. Don’t put your career on hold any longer – partner with us, gain valuable skills, and take your career in the helping professions to new heights.

Ranked in the Top 10% of Niche.com’s Best Online Schools in America

• What Sets Us Apart?
• Private Nonprofit University
• 600+ Online Degrees
• No Standardized Testing for Admission
• Transfer in up to 75% of an Undergrad Degree
• Transfer in up to 50% of a Grad/Doctoral Degree

Why Choose Liberty’s Doctorate in Health Sciences – Trauma Informed Care Degree?

Liberty University has extensive experience developing distance degree programs – we’ve been pioneering nontraditional education since 1985. We don’t shortchange you when you pursue an online degree program – we empower you by harnessing the power of a world-class curriculum into a convenient format that you can access from anywhere in the world. This degree program is offered 100% online in mostly 8-week courses, so you can earn your PhD while remaining committed to your job, family, and community.

According to the U.S. Department of Veterans Affairs, about 60% of men and 50% of women experience at least 1 trauma in their lifetime.* In addition, 6 out of 100 Americans will have PTSD at some point in their life, and roughly 12 million American adults struggle with PTSD during a given year.* These troubling statistics demand action. By partnering with us for your trauma-informed care degree, you can help reverse the growing trend of trauma in the United States and abroad.

While some doctoral programs can take up to 5 years to complete, our doctorate in health sciences can be completed in as little as 3 years – so you won’t have to spend an extended amount of time earning your degree. While our health sciences and trauma PhD allows you to finish your studies in a reasonable amount of time, we do not sacrifice academic rigor for expediency. Liberty University is regionally accredited by the Southern Association of Colleges and Schools Commission on Colleges ( SACSCOC ) – so you can pursue your degree with confidence.

*PTSD: National Center for PTSD, U.S. Department of Veterans Affairs, at How Common Is PTSD in Adults? (viewed online Aug. 12, 2022).

What Will You Study in Our Trauma-Informed Care PhD Degree?

This degree program consists of 4 sections: core courses, research and statistics classes, the trauma-informed care specialization, and a dissertation sequence.

In the core courses, you will study ethical issues in health sciences, healthcare delivery systems, and cultural competency in health sciences. You will also study principles and theories of teaching in health professions, leadership in professional practices, risk management, and evidence-based practices in health sciences.

From there, this degree covers a review of health literature, qualitative research, and quantitative research. The trauma-informed care specialization teaches crisis and first responder training, the intricacies of PTSD and combat-related trauma, and effective community responses to mental health issues. Furthermore, you will explore assessment and testing in the treatment of trauma as well as empirically supported trauma treatments.

To round out your studies, you will complete a 4-step dissertation on a topic you’re passionate about. Each step of the dissertation is 1 semester long – giving you ample opportunity to think, research, write, and edit.

Potential Career Opportunities

Depending on your previously obtained certifications and licenses, some of the roles you could pursue with this degree include:

• Healthcare administrator
• Healthcare communications specialist
• Medical assistant
• Public health worker

Featured Courses

• CRIS 605 – Crisis and First Responder Training: Skills and Techniques
• CRIS 607 – PTSD and Combat-Related Trauma
• TRMA 820 – Disaster Mental Health and Community Response
• TRMA 840 – Empirically Supported Treatments for Trauma

Degree Information

• This program falls under the School of Health Sciences .
• View the Graduate Health Sciences Course Guides (login required) .

Degree Completion Plan

Not sure what to choose?

Speak to one of our admissions specialists to help you choose the program that best fits your needs.

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Your success is our success, which is why we are committed to providing quality academics at an affordable tuition rate. While other colleges are increasing their tuition, we have frozen tuition rates for the majority of our undergraduate, graduate, and doctoral programs for the past 9 years – and counting.

Eligible current and former military service members and their spouses may qualify for a special rate of $300/credit hour ( learn more ) .

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Admission Information for Liberty’s PhD in Health Sciences – Trauma Informed Care Degree

Admission requirements.

• A non-refundable, non-transferable $50 application fee will be posted on the current application upon enrollment (waived for qualifying service members, veterans, and military spouses – documentation verifying military status is required) .
• Send official college transcripts (mailed as sealed, unopened copies or sent via a direct electronic transcript system). A regionally or nationally accredited master’s degree with at least a 3.0 GPA is required for admission in good standing.
• Applicants whose native language is other than English must submit official scores for the Test of English as a Foreign Language (TOEFL) or an approved alternative assessment. For information on alternative assessments or TOEFL waivers, please call Admissions or view the official International Admissions policy .

Preliminary Acceptance

If you are sending in a preliminary transcript for acceptance, you must:

• Be in your final term and planning to start your doctoral degree after the last day of class for your master’s degree.
• Complete a Master’s Self-Certification Form confirming your completion date. You may download the form from the Forms and Downloads page or contact an admissions counselor to submit the form on your behalf.
• Submit an official transcript to confirm that you are in your final term. The preliminary transcript must show that you are within 6 credit hours of completion for a 30-48 credit hour master’s degree or within 9 credit hours of completion for a 49+ credit hour master’s degree.
• Send in an additional, final official transcript with a conferral date on it by the end of your first semester of enrollment in the new doctoral degree.

Transcript Policies

Official college transcript policy.

An acceptable official college transcript is one that has been issued directly from the institution and is in a sealed envelope. If you have one in your possession, it must meet the same requirements. If your previous institution offers electronic official transcript processing, they can send the document directly to [email protected] .

Admissions Office Contact Information

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Email for Questions

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Submit your application online or over the phone.

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Liberty University is dedicated to providing world-class educational experiences to military students across the globe.

Who May Qualify?

• Active Duty
• Reserve/National Guard
• Veterans/Retirees
• Spouses of Service Members and Veterans/Retirees

Military Tuition Discount

We want to help you find the doctoral degree you want – at a price you’ve earned. As a thank-you for your military service, Liberty University offers eligible current and former service members like you or your spouse multiple pathways to earn a doctoral degree for only $300/credit hour . Find out how you can take advantage of this unique opportunity as you work toward your goal of reaching the pinnacle of your profession – for less.

Frequently Asked Questions

Is liberty university accredited.

Liberty University is accredited by the Southern Association of Colleges and Schools Commission on Colleges ( SACSCOC ).

What resources will be available to me in this program?

You can access a wealth of resources through our top-notch library portal while pursuing your doctoral degree in health sciences.

Are there any networking opportunities in this degree?

As an online student, you’ll have the opportunity to network with leaders in health sciences from across the country.

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Clinical Psychology Ph.D. with Major Area of Study in Trauma

Psychology, ph.d., clinical psychology, major area of study in trauma psychology, application deadline.

The deadline for application to the Ph.D. program is November 15th.

Graduate Record Examination (GRE)

The GRE is not be required. This applies to all psychology graduate program applications: PhD, MA Clinical, and MA Psychological Science.

The applications for the Ph.D. Clinical Psychology – Geropsychology and Ph.D. Clinical Psychology – Trauma Psychology programs are the same. We utilize a holistic approach to our admissions process in our doctoral program such that each applicant receives a review that takes into consideration an applicant's range of qualifications, professional, and personal experiences.

ALL application materials (online graduate application, personal statement, vita or resume, four letters of recommendation, and all transcripts) are due on November 15 th for consideration of admission the following Fall.

Ph.D. Interview Day will be January 2025. If you are chosen to interview, attendance is required.

All applications are completed online at the UCCS Graduate School website .

Application requirements for the Ph.D. Clinical Psychology – Geropsychology and Ph.D. Clinical Psychology – Trauma Psychology are as follows:

• Complete the online graduate application and pay the application fee.
• Obtain three letters of recommendation from professors (or employers) through the online application.
• Attach a personal statement describing your interests, background (including your educational, personal, cultural, economic, or social experiences that shaped your academic journey), and your career aspirations in an increasingly culturally diverse world.
• Attach an up-to-date vita or resume.
• Attach unofficial transcripts or submit official transcripts (see below) from EVERY college or university attended. If you are admitted to the program, official transcripts will be required.

The FAFSA (Free Application for Federal Student Aid) is strongly recommended for all applicants. Applicants do not need to submit the original application to the department. Instead, have your results sent to UCCS at school code 004509.

How to Submit Official Transcripts

Electronic Submission: Official transcripts can be submitted electronically if the issuing institution is contracted with a secured server. Electronic transcripts should be sent directly to  [email protected] .

By Mail: Any application materials that need to be mailed in should be sent to the following address:

Office of Admissions & Records University of Colorado Colorado Springs 1420 Austin Bluffs Parkway Colorado Springs, CO 80918-3733

Millions of Americans are affected by trauma every year. The combination of being at war for over a decade, increased incidence of natural disasters, continuing challenges of interpersonal violence, and a high lifetime probability of traumatic accidents the need for mental health professionals trained in trauma psychology has never been greater. Approximately 70% of adults will report having major traumatic exposure and close to 3 out of 4 children will experience a significant trauma each year (Finkelhor, 2005). The extensive trauma exposure has real emotional, physical, and financial costs. Every year, 2.34 million women will experience domestic violence; 4.8 million women and 2.9 million men will suffer intimate partner rapes in the U.S. (Kazdin, 2011). The financial costs associated with interpersonal trauma is astounding with sexual assault economic costs estimated at $127 billion, domestic violence $5.8 billion, general assaults $93 billion. Non-mental health care utilization for trauma survivors is also significant. A recent study found veterans with mental health challenges utilized from 46% to 146% greater physical medical care (Cohn, 2007). Even more startling, those with untreated post-traumatic stress disorder sought physical health care 71% to 170% more often than those without mental health challenges.  Veteran and active duty military health and wellness is particularly important for UCCS due to our location and commitment to our service men and women. An estimated 85,000 to 100, 000 military members live in the Pikes Peak region with their families. Approximately 78,000 veterans live in El Paso County, comprising close to 20% of the County's population. The recent Operation Iraqi Freedom and Operation Enduring Freedom conflicts in Iraq and Afghanistan have required multiple deployments and unique blast injury warfare that has increased the behavioral health needs of these warriors. Many return with psychological and/or physical challenges that exceed previous conflicts. The level of suicides in the military has reached record levels. The Peak Military Care Network Assessment Report (2011) for the local area stated that behavioral health and social service needs were critical, immediate, and long term. They suggested that these needs were taxing the current service delivery systems: "There is a shortage of qualified providers and/or practitioners in the community. Professional providers are burning out."(page 13). With upcoming military downsizing, the veteran population in El Paso County will escalate and compound the already high need for specially trained mental health professionals in Trauma Psychology. Our curricular track in Trauma Psychology is dedicated to the scientist/practitioner model of training doctoral level psychologists.

The curriculum will require at least five years of post-baccalaureate work on site to accomplish requirements of the doctoral degree. Students complete 120 hours of required and elective courses, a comprehensive exam, a dissertation of original scholarship, clinical practica, and a clinical internship (off site). The clinical curriculum requires specific coursework, required for licensure and accreditation, and an off site internship year. The program is not available for distance learning access.  Students who enter the program with a B.A. or B.S. degree will earn an M.A. en route to the doctoral degree through the mechanism of the existing M.A. program.

Knowledge and skills in clinical psychology and basic scientific psychology are the foundations on which the trauma psychology focus is built. Students in this program are preparing to be clinical psychologists first and foremost, with a focus on trauma psychology as their curricular emphasis. Students entering this program are essentially agreeing to focus their work on trauma psychology rather than sampling the variety of populations and problems that might form the elective offerings in another program.

This program adheres to the scientist-practitioner model of training in clinical psychology, commonly referred to as the Boulder model. Under this model, professional psychologists are trained to be both scientists and practitioners with the goal of enhancing the interplay between science and practice. In an emerging field, such as trauma psychology, it is of utmost importance that practitioners add to the existing knowledge base regarding application strategies that are effective, and that scientists be informed of applied issues in shaping their pursuit of knowledge.

The curriculum will require at least five years of post-baccalaureate work to accomplish requirements of the doctoral degree. Students complete 101 hours of required and elective courses, a comprehensive exam, a dissertation of original scholarship, clinical practica, and a clinical internship (off site). The clinical curriculum requires specific coursework, required for licensure and accreditation, and an off-site internship year. Students who enter the program with a BA or BS degree will earn an MA en route to the doctoral degree through the mechanism of the existing MA program.

Timeline for program completion: Completion of the Clinical Psychology PhD program from the BA or BS starting point will typically take five years of residence on campus with the sixth year allocated for internship (students should expect this time frame as the general rule pending unusual exceptions).

Doctoral students are also advised that this is a 12-month program with clinical Practicum obligations during the summers and some limited Spring pre-term course requirements. Clinical and research work are continuous without regard to the semester structures and students are funded to participate year-round.

Successful completion of an APA-approved (or equivalent) one year (2000 hour) pre-doctoral internship is required for graduation.

This program values and promotes self-awareness as a significant component of training in clinical psychology. Students in this program engage in self-awareness exercises within their courses and practicum training, including assignments that promote growth in awareness of social structures that sustain privilege and oppression. Students are also strongly encouraged to engage in their own psychotherapy during their training.

Coursework: All students in the Ph.D. program in Clinical Psychology are required to complete 101 credit hours.

Required Coursework & Model Curriculum 

Be informed that doctoral training in clinical psychology requires a full-time clinical internship and typically includes community practicum placements in local agencies who partner with us for training opportunities. Many  of these institutions require a legal background check to ensure all employees and trainee meet current standards. In addition, licensure boards usually require applicants to report on their legal background. As such, certain types of criminal backgrounds will prevent applicants from being able to complete program requirements or to attain licensure as a psychologist in some states. Please disclose relevant background information accordingly.

The Ph.D. program is accredited by the Commission on Accreditation of the American Psychological Association through 2029.

UCCS APA Self-Study *Questions related to the program's accredited status should be directed to the Commission on Accreditation: Office of Program Consultation and Accreditation American Psychological Association 750 1st Street, NE Washington, DC 20002 Phone: (202) 336-5979 / Email:  [email protected] Web:  www.apa.org/ed/accreditation

Students will develop foundational skills in the science and practice of clinical psychology with an emphasis on trauma psychology. They will be prepared to provide diverse empirically based assessment and psychotherapeutic services, conduct research, educate, and provide leadership. Specifically, the 3 formal goals of the program (and the objectives for each goal) are:

Goal #1: Produce graduates who have the requisite knowledge and skills for entry into the professional practice of clinical psychology 

Objectives for Goal #1:

   1-A: Demonstrate knowledge and skill in clinical assessment    1-B: Demonstrate knowledge and skill in psychological and psychotherapeutic interventions    1-C: Demonstrate knowledge of the ethics of clinical practice, including ethical practice with diverse populations    1-D: Demonstrate knowledge of clinical supervision and consultation that is commensurate with level of training

Goal #2: Produce graduates who are capable of conducting, evaluating, and disseminating research

Objectives for Goal #2:

   2-A: Develop attitudes and skills essential for life-long learning and scholarly inquiry    2-B: Develop knowledge and skills to conduct empirical psychological research    2-C: Acquire knowledge and skills to disseminate research effectively to professional and lay audiences

Goal #3: Produce graduates who demonstrate competence in knowledge and skills in trauma psychology

Objectives for Goal #3:

   3-A: Demonstrate knowledge and skills in professional practice consistent with the New Haven competencies associated with graduate training in Trauma Psychology    3-B: Demonstrate knowledge and skills needed to conduct empirical research in Trauma Psychology

These Goals are consistent with training in health service psychology; we aim to provide foundational knowledge to students seeking scientist-practitioner careers and specialty training in Trauma Psychology.

The curricular track in trauma psychology in our Clinical Psychology Ph.D. program directly addresses a local community need as well as a national challenge regarding a paucity of trained mental health professionals in the area of trauma psychology. UCCS has made a commitment to the training needs of our trauma students by opening the  Veterans Health & Trauma Clinic  at the Lane Center for Academic Health Sciences. With a 2 million dollar grant investment the clinic is a state of the art trauma care provider utilizing evidence-based interventions and cutting edge technology assisted approaches. This clinic provides students with a unique opportunity to focus their training on the specific challenges faced by traumatized veterans and their families. In addition to seeing veterans and their families, students in the trauma psychology track will work with survivors of other traumas. Possible clinical training opportunities at the Veterans Administration in Colorado Springs, the UCCS Counseling Center, and TESSA (domestic violence center) provide unique, focused clinical experiences and direct clinical services to our community.  A significant resource for training and research is the UCCS HealthCircle Veterans Health and Trauma Clinic (VHTC), a trauma-focused psychological services training and research center. The VHTC was established in February 2014, as part of the Lane Center for Academic Health Sciences and through a generous gift by Ms. Lyda Hill. The VHTC clinicians are experienced in trauma psychology and have strong relationships with the military and civilian communities in Colorado Springs. Client referrals come from Fort Carson, the Veterans Administration, other clinics within the Lane Center, physicians, other therapists, and other community agencies working with trauma survivors in the Pikes Peak region. Students choosing a trauma psychology emphasis will spend two years of their training at the VHTC and receive supervision from VHTC providers with many years of experience providing mental health services to military service members, veterans, their families, and civilian adults and adolescents. The VHTC also provides highly accessible research space that is dedicated for faculty and graduate students pursuing trauma psychology research. A state-of-the-art human computer interaction laboratory is available for monitoring real-time physiological reactions in response to trauma recovery websites and other web-based recovery tools. Research rooms are available at the Lane Center for other projects and a group room is available for focus groups and studies involving larger groups of participants. A trauma participant registry and a Lane Center-wide participant registry are being established to facilitate recruitment of research participants.

 Applicants should have the following credentials:

• A BS or BA degree or its equivalent from an accredited college or university.
• An overall average of 3.0 (“A” is equivalent to 4.0) or above in all undergraduate courses, and 3.5 or better on graduate coursework.
• Three letters of recommendation from professors, clinical supervisors, and/or employers.
• An adequate undergraduate program in psychology including college-level mathematics, statistics, experimental psychology, and some background in the biological, physical, and social sciences.
• Applicants should have career goals consistent with the program emphasis in trauma psychology and desire training consistent with the scientist-practitioner model of training.

Promising students who do not meet all of the requirements may be considered as applicants.  Graduate level courses completed prior to admission may be transferable into the program. Applicants with previous graduate coursework or degree may request a review of their transcript and related materials to determine whether specific courses or thesis requirements may be waived.

Faculty of the program and of the psychology department are strongly committed to respecting diversity in all of its forms. We strive to recruit and retain a diverse faculty and student body.

Program statistics such as   Student Admissions, Outcomes, and Other Data  is available.

Although not set as a firm limit (exceptions may arise), a typical cohort will consist of two to four students. Students may expect to be funded by research, teaching, or clinical assistantships and fellowships.

Faculty quality in trauma psychology is strong.

Dr. Charles Benight , Professor and Director of the  National Institute for Human Resilience  has research experience in trauma that has spanned over 20 years focusing on human adaptation and self-regulation along with more recent work on web-intervention systems for trauma recovery. 

Dr. Steven Bistricky , Assistant Professor, is a clinical psychologist whose research focusing on psychological vulnerability and resilience has been published in influential journals such as  Journal of Traumatic Stress, Journal of Affective Disorders,  and  Psychological Bulletin.  In addition to using traditional self-report methods, his research has also employed experimental information processing methods and clinical neuroscience.  

Dr. Heather Littleton , Associate Professor, has primary research interests in the role of social-cognitive factors in recovery from trauma, particularly sexual assault, as well as predictors of risk taking behaviors and re-victimization following sexual assault. In addition, she is interested in the use of technology and alternative interventions to address and prevent PTSD/trauma. Dr. Colin Mahoney , Assistant Professor, is a clinical psychologist whose research focuses on identifying risk, maintenance, and protective factors for the symptoms and diagnosis of posttraumatic stress disorder (PTSD) and substance use disorders (SUDs) among women following exposure to interpersonal violence (i.e., sexual violence, intimate partner violence [IPV], community violence) and among men following exposure to combat trauma through (1) experimental, (2) prospective, and (3) qualitative studies. 

Dr. Tom Pyszczynski , Distinguished Professor, is a social psychologist and a world leader in the area of Terror Management Theory. Dr. Pyszczynski recently published papers focusing on Anxiety Buffer Disruption Theory in order to understand the range of responses that traumatized individuals exhibit as they move forward in their lives. 

Faculty productivity in trauma research is high. It is also possible for students to work in a cross-disciplinary way through the with  National Institute for Human Resilience  faculty from geography and computer science. Faculty have generated well over 5 million dollars in external funding with grants from the National Science Foundation, the National Institute of Mental Health, the Department of Defense TATRC, and the Substance Abuse and Mental Health Services Administration.

Graduate psychology courses are taught by faculty who are actively involved in nationally recognized research programs. Most faculty are also engaged in community involvement and/or clinical service delivery. Clinical students also benefit from placements under local experts whose services exemplify the training goals of the program.

There are two forms of housing available for graduate student: off-campus housing in apartments and houses, and on-campus dormitories.

Off-campus housing  A housing survey of graduate and undergraduate honors students in psychology found that 50% of the students lived within 5 miles of campus (range = 1-12 miles) and that it took them 10 minutes or less to commute to campus (range 3 to 25 minutes). Several new apartment complexes are very close to campus. The average rent for an apartment in Colorado Springs i s $1,553. The cost of rent varies depending on several factors, including location, size, and quality.

On-campus housing  On-campus housing is available. See the  Housing Village  page for more information including information on the new apartment-style dorms.

The application deadline for Fall admission each year is November 15th. Virtual Ph.D. Interview Day will be on TBD for 2024.

Click  here  to see Application Materials and Procedures

The Comprehensive Examination Guidelines for the PhD Clinical Psychology Program with Curricular Emphasis in Trauma Forms are:

- Comprehensive Examination Portfolio Guidelines and Policy (GEROPSYCHOLOGY & TRAUMA) - Approval to Sit for the Comprehensive Examination 

These forms are located on the Graduate Downloads webpage . Students wishing to take the Comprehensive Examination must complete this form and submit it to the Director of Clinical Training for their signature by January 20th (for Spring Exam) or August 20th (for Fall Exam) of the year they wish to sit for the Examination.

Note: Students are expected to be engaged full-time in the program throughout the calendar year.

This handbook is designed to provide you with information about the program requirements, policies, and procedures. It supplements the information available on Graduate School website  and the UCCS Student Code of Conduct . In order to be fully informed of all important requirements, you should peruse the website and read the documents in their entirety. It is your responsibility to be informed of all relevant requirements and procedures. You are required to sign the written statement (at the end of this document) acknowledging that you have received, read, and agree to the policies and procedures detailed in this handbook. Please submit a signed version which will be sent to you electronically as soon as possible. An in-person orientation session is conducted for all entering students upon arrival on campus. 

PhD Handbook

The Director of Clinical Training, as well as appropriate accrediting bodies oversees all applied clinical training matters, including coordinating internal and external practica, overseeing students’ clinical evaluations and supervisors’ evaluations, tracking students’ internship preparation and applications, and coordinating students’ clinical professional development. The DCT also provides higher level oversight of applied clinical training.

Director of Clinical Training:  Dr. Leilani Feliciano Phone: (719) 255-4174 Email:  [email protected] Columbine Hall 4019

The Associate Director of Clinical Training is responsible for all aspects of the Clinical Psychology MA and PhD Trauma Psychology track including recruitment and admissions, curriculum, professional development, and assessment.

Associate Director:  Dr. Steven Bistricky Phone:  (719) 255-4150 E-Mail:  [email protected] Columbine Hall  4027

The Research Whisperer

Just like the thesis whisperer – but with more money, post-phd depression.

The author of this post has chosen to remain anonymous and they hope that sharing their post-PhD challenges will be helpful for others who may be going through the same things, or who are supporting those who are.

For those who mentor or manage Early Career Researchers, especially new postdocs, it may be useful to have this post’s perspective in the contextual mix.

———————

When I submitted my thesis, I was hit by post-submission blues, which I was already aware of. What I didn’t expect was that the cloud didn’t lift with completion and graduation. I pretended otherwise, but the moments of genuine excitement and happiness were fleeting. I felt confused and ashamed, compounding my emotions.

Wondering if anyone else had ever felt this way, I Googled it. It turns out that I’m not alone in experiencing post-PhD depression and it is a lot more common than I thought.

Alarmingly, I had never heard of it.

This post shines some light on post-PhD depression so that we can better prepare PhD candidates for life during and after completion and provide the best support that we can to graduates.

The PhD journey changes people

Even if your experience was overwhelmingly positive, a PhD changes people by virtue of its length and nature. Completion can trigger reflection on your experience. It takes time to understand and accept how you’ve changed; this can be confronting and surface as an identity crisis.

Sacrifices made might be a source of pride, grief, or both. You may struggle with poorer mental and/or physical health. Catching up with ‘normal life’ can be nice but also a constant reminder of what you missed.

Processing the emotional and mental impact of a PhD can be particularly confronting for those who faced trauma during their PhD (whether coincidentally and/or because of it). Candidates might have turned to coping mechanisms that have become unhealth, in hindsight. When life suddenly changes due to completion, trauma can surface, as can the reality of the mechanisms used to cope.

There’s a lot of good-byes

For most people, the lifestyle, environment, and relationships that are part of the PhD journey change significantly or come to an end along with the PhD itself. The loss of things you loved can be intense and overwhelming. It can take time to grieve and let go.

The future is uncertain

PhD candidates who submit and graduate are often asked, ‘What next?’.

The post-doctoral job market is highly competitive, and non-academic career pathways can be difficult to establish. Graduates – even if they know what they want to do next – can struggle to find a suitable position, especially if they are part of a marginalised group and/or are primary caregivers.

There can be a range of internal and external pressures shaping decisions. Graduates might apply for particular roles purely because they feel that is what is expected of them. They might suffer from imposter syndrome, and question whether their success was deserved, and whether they are capable of continuing to succeed (‘maybe I just got lucky’). Others might feel trapped in a particular pathway due to their life circumstances.

What can help

It can really help to know you’re not alone! Acknowledge and accept what you feel: your feelings are valid.

Be gentle with yourself. Adjusting to life post-PhD takes time and that’s ok. It can help to do other things that you enjoy, like hobbies and making the most of relationships with family and friends. Engage in ways that feel safe and are less triggering. Set goals to help give you the buzz of completing things but be aware that it’s normal to be underwhelmed by these when compared to a PhD thesis.

When you can, reflect on what you enjoyed most throughout your PhD and investigate how you can continue to do that. Perhaps you loved data analysis, writing, interviewing participants, or tutoring students. These are all skills which are used in other career pathways, such as business analytics and teaching – the specifics might be different, but the process is the same.

There will be a range of opportunities that might be available to you which aren’t immediately obvious – so don’t be afraid to ask people, from your personal and academic circles, to point them out.

Of course, that can all be easier said than done. Consider talking about what you are going through with trusted family and friends and seeking professional help where appropriate. It’s ok to ask for support.

How to help someone else struggling with post-PhD depression

It’s nice to congratulate people when they submit and complete their degree but be mindful that they might not be feeling excited. Allow this to inform how you interact with people throughout their PhD journey.

For example, consider avoiding directly asking what they’re doing next, as this can be triggering (even if well-intentioned). Instead, consider asking, ‘What are you looking forward to next?’ – it gives space for the graduate to answer however they are comfortable. If you have a closer relationship with the graduate, you could also ask, ‘What were the highlights of your journey?’ and ‘How can we support you during this next stage?’.

Consider being open about your own post-PhD experience, too. Even a casual remark can help de-stigmatise post-PhD depression. Something like ‘I realised after I finished that I actually really missed working in the laboratory, so much so that I decided to volunteer to do outreach in high schools’, for example.

If possible, don’t cut off support immediately, whether it’s at a personal, professional, or institutional level.

Most importantly, prevention is better than a cure. It helps to encourage a strong identity for doctoral researchers beyond academia, including maintaining connections with their family, friends, and hobbies. Supervisors and other doctoral support teams can help by openly discussing work-life balance and encouraging it for their researchers.

Take the time to learn about mental health and the PhD journey, and implement best practice for yourself, your colleagues, and for PhD candidates more generally. The ‘Managing you mental health during your PhD: A survival guide’ by Dr Zoë Ayres is a fantastic resource for candidates and academics (and it’s available through many university libraries for free).

A PhD is a life-changing journey culminating in an extraordinary accomplishment. Everyone’s journey is different, including completion and what life after may bring – and that’s ok. We can all benefit from learning to better support each other regardless of what our journeys and futures look like.

Other reading

• The post-PhD blues (blogpost by Mariam Dalhoumi)
• Loss of identity: Surviving post-PhD depression (blogpost by Amy Gaeta)
• Post-PhD depression: Simple steps to recovery (video by Andy Stapleton)

Support services

• Mental health support agencies around the world (list compiled by CheckPoint)
• Lifeline Australia  – 13 11 14
• Head to health  (Australian government mental health site)
• Beyond Blue (Australia) offers short, over-the-phone counselling and a number of other resources.

Share this:

I had a depression for a year and is only just lifting and that was following my Masters degree- is this at all possible.,The degree was pretty intense because it was partially during Covid but can’t have been by far as stressful as a PhD

Thanks, Sophie. I’m sorry that you had such a rough time, and I hope that you are doing OK now. Thanks for sharing this with us. We all need support to get through these things, and I hope that you have the support that you need.

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Post-traumatic growth in PhD students during the COVID-19 pandemic

Affiliations.

• 1 Harvard College, 86 Brattle Street, Cambridge, MA, 02138, USA.
• 2 Department of Global Health and Social Medicine, Harvard Medical School, 641 Huntington Avenue, Boston, MA, 02115, USA.
• 3 Department of Psychology, West Virginia University, West Virginia University, Morgantown, WV, 26506, USA.
• 4 Stanford University, School of Medicine, 291 Campus Drive, Stanford, CA, 94305, USA.
• 5 Harvard T.H. Chan School of Public Health, Massachusetts General Hospital, 677 Huntington Ave, Boston, MA, 02115, USA.
• 6 Massachusetts General Hospital, 55 Fruit St, Boston, MA, 02114, USA.
• 7 Massachusetts General Hospital, Harvard Medical School, 25 Shattuck St, Boston, MA, 02115, USA.
• 8 Department of Global Health and Population, Harvard T.H. Chan School of Public Health, 665 Huntington Avenue, Boston, MA, 02115, USA.
• 9 Office of the Provost and Harvard Medical School, Harvard University, Massachusetts Hall, Cambridge, MA, 02138, USA.
• 10 Departments of Pediatric Newborn Medicine and Psychiatry, Brigham and Women's Hospital, 75 Francis Street, Boston, MA, 02115, USA.
• 11 Harvard Medical School, 25 Shattuck St, Boston, MA, 02115, USA.
• PMID: 36743383
• PMCID: PMC9886426
• DOI: 10.1016/j.psycom.2023.100104

Throughout the COVID-19 pandemic, graduate students have faced increased risk of mental health challenges. Research suggests that experiencing adversity may induce positive psychological changes, called post-traumatic growth (PTG). These changes can include improved relationships with others, perceptions of oneself, and enjoyment of life. Few existing studies have explored this phenomenon among graduate students. This secondary data analysis of a survey conducted in November 2020 among graduate students at a private R1 University in the northeast United States examined graduate students' levels and correlates of PTG during the COVID-19 pandemic. Students had a low level of PTG, with a mean score of 10.31 out of 50. Linear regression models showed significant positive relationships between anxiety and PTG and between a measure of self-reported impact of the pandemic and PTG. Non-White minorities also had significantly greater PTG than White participants. Experiencing more negative impact due to the pandemic and ruminating about the pandemic were correlated with greater PTG. These findings advance research on the patterns of PTG during the COVID-19 pandemic and can inform future studies of graduate students' coping mechanisms and support efforts to promote pandemic recovery and resilience.

Keywords: Coping; Higher education; Resilience; School; Stress; Trauma; Young adults.

© 2023 The Authors.

PubMed Disclaimer

Conflict of interest statement

The authors declare the following financial interests/personal relationships which may be considered as potential competing interests: Vikram Patel reports financial support was provided by Massachusetts Consortium on Pathogen Readiness. Akshay Swaminathan reports a relationship with Cerebral, Inc that includes: employment.

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• COVID-19 pandemic-related posttraumatic growth in a small cohort of university students: A 1-year longitudinal study. Van der Hallen R, Godor BP. Van der Hallen R, et al. Psychiatry Res. 2022 Jun;312:114541. doi: 10.1016/j.psychres.2022.114541. Epub 2022 Apr 5. Psychiatry Res. 2022. PMID: 35429912 Free PMC article.
• Post-traumatic growth in people experiencing high post-traumatic stress during the COVID-19 pandemic: The protective role of psychological flexibility. Landi G, Pakenham KI, Mattioli E, Crocetti E, Agostini A, Grandi S, Tossani E. Landi G, et al. J Contextual Behav Sci. 2022 Oct;26:44-55. doi: 10.1016/j.jcbs.2022.08.008. Epub 2022 Aug 28. J Contextual Behav Sci. 2022. PMID: 36060527 Free PMC article.
• Factors associated with post-traumatic growth in response to the COVID-19 pandemic: Results from a national sample of U.S. military veterans. Na PJ, Tsai J, Southwick SM, Pietrzak RH. Na PJ, et al. Soc Sci Med. 2021 Nov;289:114409. doi: 10.1016/j.socscimed.2021.114409. Epub 2021 Sep 15. Soc Sci Med. 2021. PMID: 34537394 Free PMC article.
• Post-Traumatic Growth and Resilience in Adolescent and Young Adult Cancer Patients: An Overview. Greup SR, Kaal SEJ, Jansen R, Manten-Horst E, Thong MSY, van der Graaf WTA, Prins JB, Husson O. Greup SR, et al. J Adolesc Young Adult Oncol. 2018 Feb;7(1):1-14. doi: 10.1089/jayao.2017.0040. Epub 2017 Sep 8. J Adolesc Young Adult Oncol. 2018. PMID: 28885875 Review.
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• Aftyka A., Rozalska-Walaszek I., Rosa W., Rybojad B., Karakuła-Juchnowicz H. Post-traumatic growth in parents after infants' neonatal intensive care unit hospitalisation. J. Clin. Nurs. 2017;26:727–734. doi: 10.1111/jocn.13518. - DOI - PubMed
• Barskova T., Oesterreich R. Post-traumatic growth in people living with a serious medical condition and its relations to physical and mental health: a systematic review. Disabil. Rehabil. 2009 doi: 10.1080/09638280902738441. - DOI - PubMed
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• Cann A., Calhoun L.G., Tedeschi R.G., Taku K., Vishnevsky T., Triplett K.N., Danhauer S.C. A short form of the posttraumatic growth inventory. Hist. Philos. Logic. 2010;23:127–137. doi: 10.1080/10615800903094273. - DOI - PubMed
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Post-traumatic stress disorder: the neurobiological impact of psychological trauma

Trastomo por estrés postraumático: el impacto neurobiológico del trauma psiquico, État de stress post-traumatique: impact neurobiologique du traumatisme psychologique, jonathan e. sherin.

Department of Psychiatry and Behavioral Sciences, University of Miami, Leonard M. Miller School of Medicine, Miami, Florida, USA; Department of Mental Health and Behavioral Sciences, Miami VA Healthcare System, Miami, Florida, USA

Charles B. Nemeroff

Department of Psychiatry and Behavioral Sciences, University of Miami, Leonard M. Miller School of Medicine, Miami, Florida, USA

The classic fight-or-flight response to perceived threat is a reflexive nervous phenomenon thai has obvious survival advantages in evolutionary terms. However, the systems that organize the constellation of reflexive survival behaviors following exposure to perceived threat can under some circumstances become dysregulated in the process. Chronic dysregulation of these systems can lead to functional impairment in certain individuals who become “psychologically traumatized” and suffer from post-traumatic stress disorder (PTSD), A body of data accumulated over several decades has demonstrated neurobiological abnormalities in PTSD patients. Some of these findings offer insight into the pathophysiology of PTSD as well as the biological vulnerability of certain populations to develop PTSD, Several pathological features found in PTSD patients overlap with features found in patients with traumatic brain injury paralleling the shared signs and symptoms of these clinical syndromes.

La clâsica respuesta de ataque o huida ante la perceptión de una amenaza es un fenómeno nervioso reflejo que, obviamente en términos evolutivos, tiene ventajas para la supervivencia. Sin embargo, los sistemas que organizan la constelación de conductas reflejas de supervivencia que siguen a la exposición a la amenaza percibida en algunas circunstancias pueden constituirse en procesos mal regulados. La mala regulatión crónica de estos sistemas puede llevar a un deterioro funcional en ciertos individuos quienes pueden convertirse en “traumatizados psicológicamente” y presentar un trastorno por estrés postraumático (TEPT), Una gran cantidad de informatión acumulada en varias décadas ha demostrado alteraciones neurobiológicas en los patientes con TEPT, Algunos de estos hallazgos permiten adentrarse en la fisiopatologia asi como en la vulnerabilidad biológica de ciertas poblaciones que van a desarrollar un TEPT Algunas caracteristicas patológicas encontradas en patientes con TEPT se sobreponen con caracteristicas de patientes con daño cerebral traumático, estableciendo un paralelo de signos y sintomas compartidos entre estos sindromes clinicos.

La réponse classique de lutte ou de fuite à une menace perçue est un phénomène nerveux réflexe dont les avantages pour la survie sont évidents en termes d'évolution. Cependant, les systèmes organisés en constellation de comportements réflexes de survie après exposition à une menace perçue peuvent se déréguler dans certaines circonstances. Une dysregulation chronique de ces systèmes peut entraîner un déficit fonctionnel chez certains sujets qui deviennent « psychologiquement traumatisés » ef souffrent de l'état de stress posi-traumatique (ESPT), Des données recueillies pendant des dizaines d'années montrent des anomalies neurobiologiques chez les patients souffrant d'ESPT, ce qui permet de mieux comprendre la physiopathologie de l'ESPT ainsi que la vulnérabilité biologique de certaines populations à développer un ESPT, Certaines caractéristiques pathologiques de l'ESPT se superposent à celles trouvées chez des patients atteints de lésion cérébrale traumatique, en parallèle avec les signes et les symptômes partagés par ces deux syndromes.

Overview of psychological trauma, post-traumatic stress disorder, and biological markers

Psychological trauma can result from witnessing an event that is perceived to be life-threatening or to pose the potential of serious bodily injury to self or others. Such experiences, which are often accompanied by intense fear, horror, and helplessness, can lead to the development of, and are required for the diagnosis of, post-traumatic stress disorder (PTSD). 1 It was originallythought that PTSD represented a normative response, at the extreme end of a response continuum, the severity of which related primarily to trauma/stressor intensity. However, it has become clear over time that the response of an individual to trauma depends not only on stressor characteristics, but also on factors specific to the individual. 2 For the vast majority of the population, the psychological trauma brought about by the experience of profound threat is limited to an acute, transient disturbance. Though transient, such reactions can be quite unpleasant and are typically characterized by phenomena that can be grouped for the most part into three primary domains: (i) reminders of the exposure (including flashbacks, intrusive thoughts, nightmares); (ii) activation (including hyperarousal, insomnia, agitation, irritability, impulsivity and anger); and (iii) deactivation (including numbing, avoidance, withdrawal, confusion, derealization, dissociation, and depression). As these reactions are self-limiting by definition, in general they provoke minimal functional impairment over time. On the other hand, for a significant minority of the population, the psychological trauma brought about by the experience of profound threat leads to a longer-term syndrome that has been defined, validated, and termed PTSD in the clinical literature. PTSD is often accompanied by devastating functional impairment.

PTSD is characterized by the presence of signs and symptoms in the three primary domains described above for a period extending beyond 1 month (such periods can in some cases occur long after the original, precipitating traumatic exposure). The signs and symptoms of PTSD, therefore, appear to reflect a persistent, abnormal adaptation of neurobiological systems to the stress of witnessed trauma. The neurobiological systems that regulate stress responses include certain endocrine and neurotransmitter pathways as well as a network of brain regions known to regulate fear behavior at both conscious and unconscious levels. Not surprisingly, much research has consequently focused on exploring these systems in more detail as well as attempting to elucidate the pathological changes that occur in patients who develop PTSD. More specifically, there have been and continue to be ongoing efforts to link neurobiological changes identified in patients who suffer from PTSD to the specific clinical features that constitute PTSD, including altered learning/extinction, heightened arousal, and intermittent dissociative behavior as examples relevant to each of the three primary domains. Efforts to identify neurobiological markers for PTSD originally presumed that abnormalities were acquired “downstream” from an exposure, as a consequence of traumatic experience. It could be, however, that certain abnormalities in the patient with PTSD simply represent pre-existing or “upstream” pathology that is functionally dormant until released by trauma exposure and detected thereafter upon investigation. Along these lines, recent interest has focused on factors that seem to modulate outcome variation in neurobiological systems following trauma exposure including genetic susceptibility factors, female gender, prior trauma, early developmental stage at the time of traumatic exposure, and physical injury (including traumatic brain injury - TBI) at the time of psychological trauma; these parameters likely contribute to vulnerability for, versus resilience against, developing PTSD.

Although the biological, psychological, and social ramifications of PTSD have been under scientific scrutiny for some time now, and treatment has improved dramatically, much remains unknown about this condition and controversy persists in both the neuroscientific as well as the clinical/treatment literature. In this text, we review the neurobiological impact of psychological trauma from the perspective that genetic, developmental, and experiential factors predispose certain individuals to the development of PTSD. More specifically, we review the current database as pertains to biological markers of PTSD and the possibility that some biological markers may not be acquired but, rather, may in fact predate trauma until functionally “unmasked” by stress. Where relevant, we also make note of similarities between PTSD and TBI, which extend beyond wellknown signs and symptoms (such as irritability and social withdrawal) to include abnormalities in the same neurobiological systems. Lastly, the article includes a short section on basic considerations for future direction. Ideas put forth in this communication are done so in the interest of developing a consistent model for conceptual purposes. It is recognized at the outset that numerous inconsistencies can be found in the literature that highlight the multifactorial and complex nature of this field.

The biology of PTSD

There are a number of factors that must be considered in contemplating the interplay between adverse environmental stimulation, stress responses/reactions, and pathology. In this section, basic findings are reviewed from endocrinology, neurochemistry, and brain circuitry research conducted on patients with a diagnosis of PTSD (Table I).

Endocrine factors

Core endocrine features of PTSD include abnormal regulation of Cortisol and thyroid hormones, though there is some disagreement about these findings in the literature. Of note, endocrine dysregulation is also found in patients diagnosed with TBI as a result of damage to the pituitary stalk.

The hypothalamic-pituitary-adrenal axis

The hypothalamic-pituitary-adrenal (HPA) axis is the central coordinator of the mammalian neuroendocrine stress response systems, and as such, it has been a major focus of scrutiny in patients with PTSD ( Figure 1 . ) In short, the HPA axis is made up of endocrine hypothalamic components, including the anterior pituitary, as well as an effector organ, the adrenal glands. Upon exposure to stress, neurons in the hypothalamic paraventricular nucleus (PVN) secrete corticotropin-releasing hormone (CRH) from nerve terminals in the median eminence into the hypothalamo-hypophyscal portal circulation, which stimulates the production and release of adrenocorticotropin (ACTH) from the anterior pituitary. ACTH in turn stimulates the release of glucocorticoids from the adrenal cortex. Glucocorticoids modulate metabolism as well as immune and brain function, thereby orchestrating physiological and organismal behavior to manage stressors. At the same time, several brain pathways modulate HPA axis activity. In particular, the hippocampus and prefrontal cortex (PFC) inhibit, whereas the amygdala and aminergic brain stem neurons stimulate, CRH neurons in the PVN. In addition, glucocorticoids exert negative feedback control of the HPA axis by regulating hippocampal and PVN neurons. Sustained glucocorticoid exposure has adverse effects on hippocampal neurons, including reduction in dendritic branching, loss of dendritic spines, and impairment of neurogenesis. 3 - 5

Although stressors as a general rule activate the HPA axis, studies in combat veterans with PTSD demonstrate decreases in Cortisol concentrations, as detected in urine or blood, compared with healthy controls and other com parator groups. This surprising finding, though replicated in PTSD patients from other populations including Holocaust survivors, refugees, and abused persons, is not consistent across all studies. 6 It has been suggested that inconsistent findings may result from differences in the severity and timing of psychological trauma, the patterns of signs/symptoms, comorbid conditions, personality, and genetic makeup. 7 Studies using low-dose dexamethasone suppression testing suggest that hypocortisolism in PTSD occurs due to increased negative feedback sensitivity of the HPA axis. Sensitized negative feedback inhibition is supported by findings of increased glucocorticoid receptor binding and function in patients with PTSD. 6 Further, sustained increases of CRH concentrations have been measured in cerebrospinal fluid (CSF) of patients with PTSD. As such, blunted ACTH responses to CRH stimulation implicate a role for the downregulation of pituitary CRH receptors in patients with PTSD. 6 In addition, reduced volume of the hippocampus, the major brain region inhibiting the HPA axis, is a cardinal feature of PTSD. 8 Taken as a whole, these neuroendocrine findings in PTSD reflect dysregulation of the HPA axis to stressors. 6

In the context of the above discussion, prospective studies suggest that low Cortisol levels at the time of exposure to psychological trauma may predict the development of PTSD. 9 , 10 Therefore, hypocortisolism might be a risk factor for maladaptive stress responses and predispose to future PTSD. This hypothesis is supported in principle by the finding that exogenously administered hydrocortisone shortly after exposure to psychological trauma can prevent PTSD. 11 , 12 In addition, it has been shown that simulation of a normal circadian Cortisol rhythm using exogenously introduced hydrocortisone is effective in the treatment of PTSD. 13 In sum, it may be that decreased availability of Cortisol, as a result of or in combination with abnormal regulation of the HPA axis, may promote abnormal stress reactivity and perhaps fear processing in general. That said, it should be noted that glucocorticoids interfere with the retrieval of traumatic memories, an effect that may independently prevent or reduce symptoms of PTSD. 14

The hypothalamic-pituitary-thyroid axis

The hypothalamic-pituitary-thyroid (HPT) axis is involved in regulating metabolic versus anabolic states and other homeostatic functions, which it does by controlling the blood level of thyroid hormones. A possible role for the HPT axis in stress-related syndromes has been suspected for some time because it is known that trauma can trigger thyroid abnormalities. To date, however, there has not been a significant research effort targeting the relationship between the HPT axis and PTSD. Studies have been conducted, however, on Vietnam Veterans with PTSD who were found to have elevated baseline levels of both tri-iodothyronine (T3) and thyroxine (T4). Of note, the level of '13 in these subjects was disproportionately elevated relative to T4, implicating an increase in the peripheral deiodinization process. 15 , 16

These findings were replicated for the most part in a study of WWII Veterans with more longstanding PTSD diagnoses. In these individuals, isolated T3 levels were elevated whereas T4 levels were normal. 17 Taken together, these studies suggest that over time the impact of trauma on T4 levels may abate. The authors suggest that elevated T3 may relate to subjective anxiety in these individuals with PTSD.

Neurochemical factors

Core neurochemical features of PTSD include abnormal regulation of catecholamine, serotonin, amino acid, peptide, and opioid neurotransmitters, each of which is found in brain circuits that regulate/integrate stress and fear responses. Of note, catecholamine and serotonin (as well as acetylcholine) dysregulation is also found in patients diagnosed with TBI, presumably as a result of diffuse axonal injury.

The catecholamines

the catecholamine family of neurotransmitters, including dopamine (DA) and norepinephrine (NE), derive from the amino acid tyrosine. Increased urinary excretion of DA and its metabolite has been reported in patients with PTSD. Further, mesolimbic DA has been implicated in fear conditioning. There is evidence in humans that exposure to stressors induces mesolimbic DA release, which in turn could modulate HPA axis responses. Whether or not DA metabolism is altered in PTSD remains unclear, though genetic variations in the DA system have been implicated in moderating risk for PTSD (see below). NE, on the other hand, is one of the principal mediators of autonomic stress responses through both central and peripheral mechanisms. The majority of CNS NE is derived from neurons of the locus ceruleus (LC) that project to various brain regions involved in the stress response, including the prefrontal cortex, amygdala, hippocampus, hypothalamus, periaqueductal grey, and thalamus. In addition, there is evidence for a feed-forward circuit connecting the amygdala and hypothalamus with the LC, in which CRH and NE interact to increase fear conditioning and encoding of emotional memories, enhance arousal and vigilance, and integrate endocrine and autonomic responses to stress. Like other stress pathways, this cascade is inhibited by glucocorticoids, 18 which serve as a “brake” for the system. In the periphery, stress-induced sympathetic nervous system activation results in the release of NE and epinephrine from the adrenal medulla, increased release of NE from sympathetic nerve endings, and changes in blood flow to a variety of organs as needed for fight-or-flight behavior. The NE effects arc mediated via postsynaptic α 1 β 1 , and β 2 , receptors, whereas another NE-activated receptor, the α 2 receptor serves as a presynaptic autoreceptor inhibiting NE release. Because of its multiple roles in regulating arousal and autonomic stress responses, as well as promoting the encoding of emotional memories, NE has been a central focus of many studies investigating the pathophysiology of PTSD.

A cardinal feature of patients with PTSD is sustained hyperactivity of the autonomic sympathetic branch of the autonomic nervous system, as evidenced by elevations in heart rate, blood pressure, skin conductance, and other psychophysiological measures. Accordingly, increased urinary excretion of catecholamines, and their metabolites, has been documented in combat veterans, abused women, and children with PTSD. In addition, patients with PTSD exhibit increased heart rate, blood pressure, and NE responses to traumatic reminders. Decreased platelet α 2 receptor binding further suggests NE hyperactivity in PTSD. 19 , 20 Administration of the α 2 receptor antagonist yohimbine, which increases NE release, induces flashbacks and increased autonomic responses in patients with PTSD. 21 Serial sampling revealed sustained increases in CSF NE concentrations and increased CSF NE responses to psychological stressors in PTSD: 22 , 23 Taken together, there is an abundance of evidence that NF, accounts for certain classic aspects of PTSD symptomatology, including hyperarousal, heightened startle, and increased encoding of fear memories. 20

Interestingly, prospective studies have shown that increased heart rate and peripheral epinephrine excretion at the time of exposure to trauma predict subsequent development of PTSD. 10 Further, administration of the centrally acting β-adrenergic receptor antagonist propranolol shortly after exposure to psychological trauma has been reported to reduce PTSD symptom severity and reactivity to trauma cues. 24 Although propranolol administration in this study did not prevent the development of PTSD, it may have blocked traumatic memory consolidation, 25 and therefore may reduce the severity and/or chronicity of PTSD. It is important to note, however, that this finding contradicts those from an earlier study. 26 Various antiadrenergic agents have been tested for their therapeutic efficacy in the treatment of PTSD in open-label trials; there is a paucity of controlled trials. 20

Serotonin (5HT), is a monoamine neurotransmitter synthesized from the amino acid tryptophan. Neurons containing 5HT originate in the dorsal and median raphe nuclei in the brain stem and project to multiple forebrain regions, including the amygdala, bed nucleus of the stria terminalis, hippocampus, hypothalamus, and prefrontal cortex. 5HT has roles in regulating sleep, appetite, sexual behavior, aggression/impulsivity, motor function, analgesia, and neuroendocrine funtion. Not surprisingly, given its connectivity and broad homeostatic role, 5HT has been implicated in the modulation of affective and stress responses, as well as a role in PTSD. Although the mechanisms are not entirely clear, the effects of 5HT on affective and stress responses vary according to stressor intensity, brain region, and receptor type. It is believed that 5HT neurons of the dorsal raphe mediate anxiogenic effects via 5HT 2 receptors through projections to the amygdala and hippocampus. In contrast, 5HT neurons from the median raphe are thought to mediate anxiolytic effects, facilitate extinction and suppress encoding of learned associations via 5HT 1A receptors. Chronic exposure to stressors induces upregulation of 5HT 2 and downregulation of 5HT 1A receptors in animal models. Further, 5HT 1A knockouts exhibit increased stress responses.

The 5HT system interacts with the CRH and NE systems in coordinating affective and stress responses. 19 , 27 Indirect evidence suggests a role for 5HT in PTSDrelated behaviors including impulsivity, hostility, aggression, depression, and suicidally. In addition, 5HT presumably mediates the therapeutic effects of the selective serotonin reuptake inhibitors (SSRIs). A recent small and controversial study suggests that the street drug 3,4-Methylenedioxymetharnphetamine (also known as .MDMA or “ecstasy”), which alters central serotonin transmission, has therapeutic potential in the treatment of PTSD. 28 Other evidence for altered 5 HT neurotransmission in PTSD includes decreased serum concentrations of 5HT, decreased density of platelet 5HT uptake sites, and altered responsiveness to CNS serotonergic challenge in patients diagnosed with PTSD. 19 , 27 However, no differences in CNS 5HT 1A receptor binding were detected in patients with PTSD compared with controls using PET imaging. 28 Taken together, altered 5HT transmission may contribute to symptoms of PTSD including hypervigilance, increased startle, impulsivity, and intrusive memories, though the exact roles and mechanisms remain uncertain.

Amino acids

γ-Aminobutyric acid (GABA) is the principal inhibitory neurotransmitter in the brain. GABA has profound anxiolytic effects and dampens behavioral and physiological responses to stressors, in part by inhibiting the CRH/NE circuits involved in mediating fear and stress responses. GABA's effects are mediated by GABA A receptors, which are colocalized with benzodiazepine receptors that potentiate the inhibitory effects of GABA on postsynaptic elements. Uncontrollable stress leads to alterations of the GABA/benzodiazepine receptor complex such that patients with PTSD exhibit decreased peripheral benzodiazepine binding sites. 29 Further, SPECT and PET imaging studies have revealed decreased binding of radiolabeled benzodiazepine receptor ligands in the cortex, hippocampus, and thalamus of patients with PTSD, suggesting that decreased density or receptor affinity may play a role in PTSD. 30 - 31 However, treatment with benzodiazepines after exposure to psychological trauma does not prevent PTSD. 32 - 33 Further, a recent study suggests that traumatic exposure at times of intoxication actually facilitates the development of PTSD. 34 Although perhaps counterintuitive, the authors suggest that the contextual misperceptions which commonly accompany alcohol intoxication may serve to make stressful experiences more difficult to incorporate intellectually, thereby exacerbating fear. Taken together, while there are multiple studies strongly implicating the GABA/bcnzodiazepine receptor system in anxiety disorders, studies in PTSD are relatively sparse and conclusive statements would be premature. 19

Glutamate is the primary excitatory neurotransmitter in the brain. Exposure to stressors and the release of, or administration of, glucocorticoids activates glutamate release in the brain. Among a number of receptor subtypes, glutamate binds to N -methyl D -aspartate (NMDA) receptors that are localized throughout the brain. The NMDA receptor system has been implicated in synaptic plasticity, as well as learning and memory, thereby contributing in all likelihood to consolidation of trauma memories in PTSD. The NMDA receptor system is also believed to play a central role in the derealization phenomena and dissocation associated with illicit and medical uses of the anesthetic ketamine. In addition to its role in learning and memory, overexposure of neurons to glutamate is known to be excitotoxic, and may contribute to the loss of neurons and/ or neuronal integrity in the hippocampus and prefrontal cortex of patients with PTSD. Of additional note, elevated glucocorticoids increase the expression and/or sensitivity of NMDA receptors, which may render the brain generally more vulnerable to excitoxic insults at times of stress.

CRH neurons in the hypothalamic PVN integrate information relevant to stress and thereby serve as a major component of the HPA axis. CRH neurons are also found in widespread circuitry throughout the brain, including the prefrontal and cingulate cortices, central nucleus of the amygdala, the bed nucleus of the stria terminais, hippocampus, nucleus accumbens, periaqueductal gray, and locus coeruleus (LC) as well as both dorsal and median raphe. Direct injection of CRH into the brain of laboratory animals produces physiological stress responses and anxiety-like behavior, including neophobia (fear of new things or experiences), enhanced startle, and facilitated fear conditioning. Anxiety -like behaviors have been specifically linked with increased activity of amygdalar CRH-containing neurons that project to the LC. Of note, glucocorticoids inhibit CRH-induced activation of LC noradrenergic neurons, providing a potential mechanism by which low Cortisol may facilitate sustained central stress and fear responses. The effects of CRH are mediated primarily through two CRH receptor subtypes, CRH 2 ., and CRH 2 . In animal experiments, both exogenous administration of a CRH 1 , receptor antagonist, and experimental knockout of the CRH 1 receptor, produce attenuated stress responses and reduced anxiety. A recent experiment demonstrated that CRHj receptor blockade impacted not only gastrointestinal measures of chronic stress, but also prevented stress-induced hair loss in rodents. 35 Thus, CRH] receptor stimulation may be involved in facilitating stress responses and anxiety. By contrast, CRH 7 knockout mice demonstrate stress sensitization and increased anxiety, suggesting a role for CRH 2 receptor activation in reducing stress reactivity. 3 Given the central effects of CRH, as described in animal models, increased CNS CRH activity may promote certain of the cardinal features of PTSD, such as conditioned fear responses, increased startle reactivity, sensitization to stressor exposure, and hyperarousal. These results suggest that CRH] receptor antagonists and/or CRH, agonists might have important therapeutic potential in the treatment of PTSD.

Neuropeptide Y (NPY) may well be protective against the development of PTSD in that it has anxiolytic and stress-buffering properties. NPY has been shown to inhibit CRH/NE circuits involved in stress and fear responses and to reduce the release of NE from sympathetic neurons. As such, a lack of NPY may promote maladaptive stress responses and contribute to the development of PTSD. Indeed, patients with PTSD have been reported to exhibit decreased plasma NPY concentrations and blunted NPY responses to yohimbine challenge, compared with controls. Together, these findings suggest that decreased NPY activity may contribute to noradrenergic hyperactivity in PTSD. 36 Moreover, it has been suggested that NPY may be involved in promoting recovery from, or perhaps resilience to PTSD, given that combat veterans without PTSD have been shown to exhibit elevated NPY levels compared with veterans with PTSD. 6

Endogenous opioid peptides including the endorphins and enkephalins act upon the same CNS receptors activated by exogenous opioid molecules such as morphine or heroin. Endogenous opioids exert inhibitory influences on the HPA axis. Naloxone, an opioid receptor antagonist, increases HPA axis activation as evidenced by exaggerated HPA axis response to naloxone. PTSD patients exhibit increased CSF p-endorphin levels, suggesting increased activation of the endogenous opioid system. Alterations in endogenous opioids may be involved in certain PTSD symptoms such as numbing, stress-induced analgesia, and dissociation. Of additional interest, the nonselective opioid receptor antagonist, naltrexone, appears to be effective in treating symptoms of dissociation and flashbacks in traumatized persons. 19 , 37 Further, the administration of morphine has been reported to prevent PTSD. 38 Of note, an experiment investigating the hypothesis that PTSD may play an ctiologic role in fostering opioid addiction in an opioiddependent group of subjects rendered negative results. 39

Brain circuitry

Characteristic changes in brain structure and function have been identified in patients with PTSD using brainimaging methods. 40 - 42 Brain regions that arc altered in patients with PTSD include the hippocampus and amygdala as well as cortical regions including the anterior cingulate, insula, and orbitofrontal region. These areas interconnect to form a neural circuit that mediates, among other functions, adaptation to stress and fear conditioning. Changes in these circuits have been proposed to have a direct link to the development of PTSD. 40 Recent work raises the question as to which CNS elements are involved in circuit changes resulting from stress, and suggests a critical role for myelin. 43 Similar to PTSD, brain areas most impacted by TBI include inferior frontal and temporal lobes, and it is likely that myelinated circuits are subject to damage broadly as a result of shear forces.

Hippocampus

A hallmark feature of PTSD is reduced hippocampal volume. The hippocampus is implicated in the control of stress responses, declarative memory, and contextual aspects of fear conditioning. Not surprisingly, the hippocampus is one of the most plastic regions in the brain. As mentioned above, prolonged exposure to stress and high levels of glucocorticoids in laboratory animals damages the hippocampus, leading to reduction in dendritic branching, loss of dendritic spines, and impairment of neurogenesis. 4 Initial magnetic resonance imaging (M.RI) studies demonstrated smaller hippocampal volumes in Vietnam Veterans with PTSD and patients with abuse-related PTSD compared with controls. 44 - 47 Small hippocampal volumes were associated with the severity of trauma and memory impairments in these studies. These findings were generally replicated in most but not all subsequent work. Studies using proton magnetic resonance spectroscopy further observed reduced levels of N-acctyl aspartate (NAA), a marker of neuronal integrity, in the hippocampus of adult patients with PTSD. 40 Of note, NAA reductions were correlated with Cortisol levels. 48 Interestingly, reduced hippocampal volume has been observed in depressed women with a history of early life trauma 49 but not in children with PTSD. 50

Hippocampal volume reduction in PTSD may reflect the accumulated toxic effects of repeated exposure to increased glucocorticoid levels or increased glucocorticoid sensitivity, though recent evidence also suggests that decreased hippocampal volumes might be a pre-existing vulnerability factor for developing PTSD. 24 Indeed, hippocampal deficits may promote activation of and failure to terminate stress responses, and may also contribute to impaired extinction of conditioned fear as well as deficits in discriminating between safe and unsafe environmental contexts. Studies using functional neuroimaging have further shown that PTSD patients have deficits in hippocampal activation during a verbal declarative memory task. 51 Both hippocampal atrophy and functional deficits reverse to a considerable extent after treatment with SSRIs, 52 which have been demonstrated to increase neurotrophic factors and neurogenesis in some preclinical studies, 5 but not others. 53

The amygdala is a limbic structure involved in emotional processing and is critical for the acquisition of fear responses. The functional role of the amygdala in mediating both stress responses and emotional learning implicate its role in the pathophysiology of PTSD. Although there is no clear evidence for structural alterations of the amygdala in PTSD, functional imaging studies have revealed hyper-responsiveness in PTSD during the presentation of stressful scripts, cues, and/or trauma reminders. 41 PTSD patients further show increased amygdala responses to general emotional stimuli that are not trauma-associated, such as emotional faces. 41 The amygdala also seems to be sensitized to the presentation of subliminally threatening cues in patients with PTSD, 54 - 56 and increased activation of the amygdala has been reported in PTSD patients during fear acquisition in a conditioning experiment. 57 Given that increased amygdala reactivity has been linked to genetic traits which moderate risk for PTSD, 58 , 59 increased amygdala reactivity may represent a biological risk factor for developing PTSD.

The medial prefrontal cortex (PFC) comprises the anterior cingulate cortex (ACC), subcallosal cortex, and the medial frontal gyrus. The medial PFC exerts inhibitory control over stress responses and emotional reactivity in part by its connections with the amygdala. It further mediates extinction of conditioned fear through active inhibition of acquired fear responses. 41 Patients with PTSD exhibit decreased volumes of the frontal cortex, 60 including reduced ACC volumes. 61 , 62 This reduction in ACC volume has been correlated with PTSD symptom severity in some studies. In addition, an abnormal shape of the ACC, 63 as well as a decrease of NAA levels in the ACC, 64 has been reported for PTSD patients. A recent twin study suggests that, unlike the hippocampus, volume loss in the ACC is secondary to the development of PTSD rather than a pre-existing risk factor. 65 Functional imaging studies have found decreased activation of the medial PFC in PTSD patients in response to stimuli, such as trauma scripts, 66 , 67 combat pictures and sounds, 68 trauma-unrelated negative narratives, 69 fearful faces, 70 emotional stroop, 71 and others, though there are also discordant findings. 41 Reduced activation of the medial PFC was associated with PTSD symptom severity in several studies and successful SSRI treatment has been shown to restore medial prefrontal cortical activation patterns. 41 Of note, in the abovementioned conditioning experiment, 57 extinction of conditioned fear was associated with decreased activation of the ACC, providing a biological correlate for imprinted traumatic memories in PTSD. Not surprisingly, given the connectivity between the amygdala and medial PFC, interactions in activation patterns between these regions have been reported in PTSD, though the direction of the relationship is inconsistent across studies. 41

The origin of neurobiological abnormalities in PTSD

A number of studies have investigated the fundamental question as to whether the neurobiological changes identified in patients with PTSD represent markers of neural risk to develop PTSD upon exposure to extreme stress as opposed to abnormalities acquired through traumatic exposure or, most likely, a combination of both. As an example, low Cortisol levels at the time of a trauma predict subsequent development of PTSD. Thus, low levels of Cortisol might be a pre-existing risk factor that engenders the development of PTSD; low levels of Cortisol could disinhibit CRH/NE circuits and thereby promote unopposed autonomic and neuroendocrine responses to stress, as well as augmented fear conditioning and traumatic memory consolidation. Similarly, the reduced size of the hippocampus in PTSD has remained an unresolved question for many years. There has been considerable debate as to whether this brain region shrinks as a result of trauma exposure, or whether the hippocampus of PTSD patients might be smaller prior to trauma exposure. Studies in twins discordant for trauma exposure have provided a means to address this question, though without complete resolution. Gilbertson and colleagues 72 studied 40 pairs of identical twins, including Vietnam Veterans who were exposed to combat trauma and their twins who did not serve in Vietnam, and measured hippocampal volumes in all subjects. As expected, among Vietnam Veterans, the hippocampus was smaller in those diagnosed with PTSD as compared with those without a diagnosis. However, this brain region was abnormally smaller in non-PTSD twins as well, despite the absence of trauma exposure and diagnosis. These findings suggest that a smaller hippocampus could be a pre-existing, potentially genetic, neurodevelopmental, and almost surely multifactorial vulnerability factor that predisposes to the development of PTSD (and perhaps other stress-spectrum disorders). Recent results from the same study group indicate, as above, that gray matter loss in the ACC seems on the contrary to be an acquired feature. 65 Studies are needed to identify the timing and/or etiology of other hallmark neurobiological features of PTSD.

Risk and resilience for developing PTSD

Individuals exposed to an event that either threatens serious injury/death, or is perceived as such, respond in different ways. Most will experience minimal (seconds) to brief (hours) to short-term (days/weeks) abnormalities while a smaller number will suffer from significant psychopathology over longer-term (months) and chronic (lifetime) time frames. In short, not all individuals who face potentially catastrophic trauma go on to develop PTSD. Why some individuals will develop PTSD following trauma, whereas others do not, is of paramount importance. Because the majority of trauma survivors do not go on to develop PTSD, it is crucial going forward to understand vulnerability and resiliency factors. In this section, the role of genetic factors, gender differences, and early developmental stress experiences in moderating risk for developing PTSD in response to psychological trauma are discussed as is the increased risk for developing PTSD in the context of co-occurring physical traumas (including TBI).

Genetic risk factors for PTSD

Studies on the genetics of PTSD have been hampered by a variety of factors, such as genetic heterogeneity (similar phenotypes develop from different genotypes) and incomplete phenotypic penetrance (a person with genetic risk for PTSD, who is not exposed to trauma, will not develop PTSD). Despite these confounds, there is accumulating evidence that risk for PTSD is heavily influenced by genetic factors. Evidence from family and twin studies has long suggested a heritable contribution to the development of PTSD. In addition, there is evidence for heritable contributions to some of the neurobiological endophenotypes of PTSD as discussed above, such as decreased hippocampal volume 72 or exaggerated amygdala reactivity. 58 Although it is beyond the scope of this review to comprehensively discuss the genetics of PTSD, it should be noted that there is an emerging literature on genetic variations in those neurobiological systems that drive responses to trauma and, consequently, risk versus resilience to develop PTSD. 73

One study has linked a polymorphism in the DA transporter gene to PTSD risk. In this study, PTSD patients were found to have an excess of the SLC6A39 repeat allele. This finding suggests that genetically determined features of DA transmission may contribute to the development of PTSD among trauma survivors. 74 Several studies have suggested polymorphisms in the D 2 receptor as possible elements of PTSD risk, though results have not been consistent. 73 In addition, there is evidence linking a low expression variant of the serotonin transporter to stress responsiveness and risk for developing depression in relation to life stress, particularly in the presence of low social support. 59 This finding is intriguing as the same polymorphism is associated with increased amygdala reactivity 58 as well as the trait of neuroticism, 75 which is another risk factor for PTSD. It must be noted, however, that these findings of genetic risk with regard to the serotonin transporter have recently been questioned. 76

Particularly exciting are findings that a genetic variation of the glucocorticoid receptor cochaperone protein, FKBP5, moderates risk of developing PTSD in relation to childhood abuse. 77 This study tested interactions of childhood abuse, adulthood trauma, and genetic polymorphisms in the FKBP5 gene in 900 nonpsychiatric, general internal medicine clinic patients. Childhood abuse and adulthood trauma each predicted PTSD symptoms and FKBP5 polymorphisms significantly interacted with childhood abuse to predict adult PTSD symptoms. The FKBP5 genotype was further linked to enhanced glucocorticoid receptor sensitivity, as reflected by dexamethasone hypersuppression, a hallmark feature of PTSD. 77 Most recently, Ressler and colleagues have demonstrated that a female-specific elevation of pituitary adenylate cyclase-activating peptide (PACAP) correlated not only with fear physiology and the diagnosis of PTSD 78 but also a specific single nucleotide repeat on an estrogen response element in the same subjects. These findings and this type of work may shed new light not only on the well-known differences in PTSD risk between men and women that are discussed in the next section, but on our mechanistic understanding of PTSD in general.

Gender differences and risk for PTSD

Women more frequently suffer from PTSD than men for reasons that are not entirely clear. Women and men are, in general, subjected to different types of trauma, though the differences in PTSD frequency (reportedly 2:1) arc unlikely to be explained solely on the basis of exposure type and/or severity alone. In addition to those findings by Ressler described above, a number of gender-related differences in the neurobiological response to trauma have been documented. 79 Rodent studies suggest that females generally exhibit greater magnitude and duration of HPA axis responses to stress than males, 80 though findings in humans are not entirely consistent. 81 Sex differences in neuroendocrine stress responses have been attributed to direct effects of circulating estrogen on CRH neurons. 82 Sex steroids also interact with other neurotransmitter systems involved in the stress response, such as the serotonin system. 83 Progesterone has been implicated in modulating these systems as well. 84 However, gender differences in HPA responses to stress have also been observed independent of acute gonadal steroid effects. 85

Factors that might determine gender differences in the stress response include genomic differences (as above) and/or devclopmentally programmed effects of gonadal steroids. 81 , 85 , 86 Of note, a very recent study of female Veterans demonstrated that pregnancy raises the risk of PTSD above that for nonpregnant females. 87 In addition, sex steroids play a role in structural plasticity across the lifespan of several brain regions, including areas involved in stress responsiveness such as the hippocampus and amygdala. 86 Functional imaging studies have identified gender differences in the brain's response to fear stimuli. 88 Over time our understanding of this constellation of processes may eventually converge to allow for a better description of the basis for gender differences and, specifically, how the consequences of trauma translate into differential risk for PTSD.

Early developmental factors and PTSD

Previous experience moderates risk for developing PTSD in response to trauma, particularly when exposure to stress occurs early in life. Thus, childhood adversity is associated with increased risk to develop PTSD in response to combat exposure in Vietnam Veterans. 51 There is a burgeoning literature documenting that early adverse experience, including prenatal stress and stress throughout childhood, has profound and long-lasting effects on the development of neurobiological systems, thereby “programming” subsequent stress reactivity and vulnerability to develop PTSD. 89 - 91 As an example, children with a history of date violence have recently been shown at risk of developing future PTSD. 92 Further, a study of child survivors from the Hurricane Katrina disaster indicates significantly increased risk of PTSD. 93 Along these lines, nonhuman primates exposed to a variable foraging demand condition, which causes unpredictable maternal care in the infant, leads to an adult phenotype with sensitization to fear cues, CRH hyperactivity and low Cortisol levels, a pattern of the classic features found in PTSD. 94 Consistent with these findings, adult women with childhood trauma histories exhibit sensitization of both neuroendocrine, and autonomic stress responses. 95 Studies are needed that identify particular sensitive periods for the effects of early stress, determine parameters for their reversal, and scrutinize the interactions of dispositional factors (genes, gender) with developmental features in determining neurobiological vulnerability to PTSD.

The influence of physical trauma (and TBI) on the development of PTSD

It has been known for some time that physical injury concomitant with psychological trauma increases risk for the development of PTSD. In studies of Vietnam Veterans, 96 , 97 and more recently in a study of Iraq and Afghanistan Veterans, 98 it was found that physical injury increased the risk of PTSD at least twofold. Similarly, a literature review of patients with documented TBI and program evaluation data from surveys of US Marines following blast exposures in Iraq 99 demonstrate that TBI presents an increased risk for the development of PTSD. Though differentiating the risk of developing PTSD in patients with TBI is complicated by the subjective and objective abnormalities common to both clinical entities, it is striking that each shares common endocrine, neurochemical, and circuit abnormalities (see above, The biology of PTSD ). As such, it would follow that the existence of both diagnoses in an individual patient might be additive if not multiplicative from a clinical standpoint. For example, in the context of TBI (with frontal lobe damage and behavioral disinhibition) it would be reasonable to expect a very high violence risk profile for a patient suffering from the irritability and anger characteristic of comorbid PTSD. Of additional note, the helplessness that accompanies certain physical injuries (perhaps most notably TBI) is certain to compound issues of limited self-efficacy (and the overall lost sense of agency) that characterize PTSD. The psychological challenges of TBI may thereby introduce an additional chronic risk for the victimization that fosters PTSD in those patients with a tendency to become increasingly dependent over time.

A basic model of PTSD neurobiology

The biological perturbations observed in patients suffering from PTSD are numerous, and likely reflect an enduring dysregulation of multiple stress-mediating systems that occurs as a result of a psychological “shock.” These pathophysiological perturbations presumably occur in patients with genetic, epigenetic, and experiential predispositions when exposed to certain extreme conditions. Presumably these changes signify an indelible sensory imprint of a maladaptively processed experience that co-opts an imbalanccd degree of emotional importance and thereafter releases (or restrains) behavioral reactions that focus on defending against future trauma via activation (or deactivation) in a losing effort to secure homeostasis.

Considering neurobiological findings in PTSD patients with this overview in mind, a relative lack of baseline Cortisol at the time of a psychological trauma may facilitate overactivation of the central CRH-NE cascade, resulting in enhanced and prolonged stress responses. 6 , 95 This increased stress responsiveness may be further accentuated by inadequate regulatory effects of GABA, serotonin, and NPY. Additionally, altered norpinephrine and stress hormone activity may be critically involved in processes of learning and extinction, both of which are abnormal in PTSD; for example, norepinephrine enhances the encoding of fear memories and glucococorticoids block the retrieval of emotional memories. The constellation of elevated noradrenergic activity and relative hypocortisolism may lead to the enhanced encoding of traumatic memories and the lack of inhibition of memory retrieval both of which presumably trigger re-experiencing phenomena in PTSD. 12

Further, an abnormally functioning hippocampus may account for some of the cognitive symptoms of PTSD, such as declarative memory deficits. In addition, because the hippocampus is critical for context conditioning, an impaired hippocampus may facilitate generalization of learned fear in contexts unrelated to a previous traumatic exposure and impair the ability to discriminate between safe and unsafe stimuli. In combination with exaggerated amygdalar responses seen in patients with PTSD, a limited capacity for discerning threat due to hippocampal and amygdalar dysfunction may promote paranoia, hypervigilance, behavioral activation, exaggerated stress responses, and further acquisition of fear associations. Disrupted prefrontal cortical function may then serve to facilitate PTSD pathology further as a result of deficient suppression of stress responses, fear associations, and extinction.

Future directions

In this article, we have selected findings from a broad range of the PTSD literature to consider the impact of psychological trauma on neurobiological systems. As described, some neurobiological findings in patients with PTSD are controversial and need to be further examined. In addition, there are a number of understudied yet important topics in the field such as factors that impact resiliency and vulnerability. For example, stress-protective neurobiological factors such as activity in oxytocin and NPY-containing circuits could, in principle, be manipulated to promote resilience. In addition, there is a general need to explore further the molecular biology of PTSD; identifying interactions between dispositional factors (genetic and epigenetic) and trauma exposure is critical to understand PTSD risk, gauge illness course, and predict treatment response. The effects of trauma on neurotrophic factors (in the hippocampus), neural plasticity (CNS-wide), circuit remodeling (myelination patterns) and gene expression need to be assessed in detail across illness duration. Though difficult, such studies will necessitate accessing, assaying and following populations at risk for exposure to trauma before any exposure occurs (ideally, predeployment soldiers). Where possible, the distinction between PTSD and TBI must also be better understood. Though the presumed mechanism of injury from psychological trauma as opposed to brain trauma is overtly different, the etiologic abnormalities seem to involve similar neurobiological systems and produce overlapping clinical syndromes.

Acknowledgments

The authors would like to thank Ms Cynthia CriderVega, Ms Magaly Gomez, and Ms Carmen Alsina for their outstanding administrative assistance.

Selected abbreviations and acronyms

• Health, Fitness & Dieting
• Alternative Medicine

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Post-Traumatic Thriving: The Art, Science, & Stories of Resilience Paperback – January 1, 2021

• Print length 365 pages
• Language English
• Publisher Leadership Institute Press
• Publication date January 1, 2021
• Reading age 18 years and up
• Dimensions 6.25 x 1 x 8.25 inches
• ISBN-10 0996793178
• ISBN-13 978-0996793179
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About the author, excerpt. © reprinted by permission. all rights reserved., product details.

• Publisher ‏ : ‎ Leadership Institute Press (January 1, 2021)
• Language ‏ : ‎ English
• Paperback ‏ : ‎ 365 pages
• ISBN-10 ‏ : ‎ 0996793178
• ISBN-13 ‏ : ‎ 978-0996793179
• Reading age ‏ : ‎ 18 years and up
• Item Weight ‏ : ‎ 1.41 pounds
• Dimensions ‏ : ‎ 6.25 x 1 x 8.25 inches
• #1,160 in New Age Reference (Books)
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About the author

Randall bell phd.

Randall Bell, PhD, is a sociologist and economist who specializes in disaster recovery projects.

No stranger to how harsh the world is, Dr. Bell has consulted in more tragedies around the world than anyone. He was retained for the World Trade Center, Flight 93, Sandy Hook, BP Oil Spill, Hurricane Katrina, the Bikini Atoll Nuclear Test sites, the BP Oil spill, the Northridge earthquake, OJ Simpson, Jon Benet Ramsey, Heaven's Gate, and hundreds of other cases. He has been retained by the Federal Governments of the United States, Canada, and Australia to help resolve numerous crises, and his work has generated billions of dollars to rebuild damaged communities.

Dr. Bell’s investigations have taken him to 50 states, and seven continents. Having met with countless victims, he earned the nickname of Master of Disaster. In every case, Dr. Bell observed the emotional consequences and how some fared better than others. He was inspired to put his unique research skills to work and study the cycle of trauma.

A frequent guest of the media, Dr. Bell is the featured expert in Topic’s “Distressed Real Estate” documentary series directed by Jason Stefaniak. His career has been profiled by NBC's Today Show, Rolling Stone Magazine, The Wall Street Journal, People Magazine, ABC's 20/20, Hallmark’s Home & Family, and many others.

Dr. Bell is the author of MeWeDoBe and the founder of Core IQ, a non-profit educational foundation that provides free online training on life skills. He is certified through the Insight Prison Project to facilitate

group discussions with victims and offenders at San Quentin Prison. He has been active in jail ministries and a volunteer in homeless shelters.

In Post-Traumatic Thriving, Dr. Bell lays out the academic research and speaks freely about his trauma of being born with a congenital heart defect. Diagnosed with PTSD, he utilized these principles to heal from his childhood trauma and summit Africa's Mt. Kilimanjaro at 60.

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Customers find the book provides practical knowledge and steps toward healing from trauma. They also say it takes post-traumatic growth concepts and lays them out simply. Readers appreciate the detailed examples and interesting point of view. They say the book contains simple techniques that help when dealing with stress.

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Thema Bryant, PhD on Post-Traumatic Growth

11 comments.

When clients begin to heal from the pain of trauma, safety is often their priority.

But continually seeking safety can limit a client’s opportunities for growth and keep them stuck in survival mode.

So in the video below, Thema Bryant, PhD shares how she helps clients invite more fun and freedom into their lives – without compromising feelings of safety.

Take a look.

Howard Thurman, who’s a great theologian who’s no longer alive, he said, “We need more people who do the things that make them come alive because far too few of us are actually alive.” So that is when we are in survival mode. That is what rigidity is. Rigidity is living in survival mode and not yet fully living or thriving. So, to help clients to get from surviving to thriving requires an openness to new possibility. Because if I just keep doing what I have done to stay safe, then I am safe but unfulfilled. But when I start to think about, “I have been freed from and I have worked, it didn’t just happen, I worked to free myself from that mindset for what?” I work to get myself out of that house or out of that relationship. But what I often say to clients is trauma affects you, but it doesn’t define you. It is not the sum total of who you are.

So now that you are out of those cobwebs, even physically, and we’ve done the work emotionally and spiritually, now it is time for the creating of a life. The creating of the life requires coming out of those bars.

So once we want to shift that, two of the important things to use are play and art. When I say play, I don’t just mean for children, I mean for adults to explore their creativity, to discover new habits. And play can even be creating new relationships and friendships, going to different places. Being out in nature can be a form of play. But how do I do that when I am used to everything being controlled?

The first part of it can be planning my play. That’s a good middle place. For someone who’s used to being very rigid, and we’re trying to help them step out of it, is for them to start creating plans and opportunities to do things that are out of their norm. So, one of my clients who was very isolated, she works with numbers. She’s very good at finding the problem, solving it, and making sure everybody is on their Excel sheet where they’re supposed to be. But then on the weekends, what she would say is, “I like to be in my house reading.” She stays in the house all weekend reading, but a part of her desires more. Even though she loves to read, a part of her is unfulfilled.

We started with her being willing to go to a festival, a food festival. Online they have the map of like which booth is where. So, she could map out her whole Saturday of where she was going to be and where she was going to go. So she’s out of the box, but with a map. So, us being able to help people cultivate those spaces, create those spaces where I can try the new while also having my security blanket in some ways.

For more expert strategies to help foster post-traumatic growth, check out this course with Steven Hayes, PhD; Stephen Porges, PhD; Shelly Harrell, PhD; Marsha Linehan, PhD; Pat Ogden, PhD; and other leaders in the field.

Now, I’d like to hear from you. What strategies do you have for helping clients find freedom and fun? Leave a comment below.

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Helping them to reflect on what brings pleasure. Having discussions about photos, tapping into a sense of humour, observing behaviours that reflect changes and commenting on the observations.

Re: Strategies I’ve used for helping clients find freedom and fun I have used a Pleasant Events calendar which was introduced in a Psych training. It increases self awareness of pleasure, increasing presence during pleasure with awareness of sensation, emotion and thoughts.

Loved this presentation. It’s so timely for my work with current clients. Thanks for sharing

Persons who are in survivor mode will continue to seek safe & low risk options. It may be possible to break out of one’s safety zone by expanding the comfort zone in small incremental steps. Through well-designed practices, one may reaccess perceived risk and come to realize pursuing safety exposes them to even greater risk.

This is GREAT!

Heya Thema, What have you found most beneficial with clients who have disassociation and cant seem to re-associate with themselves?

I fully agree. And yes, do really live. Thank you.

My comment to Nora was meant for Thema, my bad. Best wishes to all.

Thought Field Therapy comment left by

I use Thought Field Therapy to relieve traumatic sequelae such as nightmares, depression, anxiety and phobias. It is effective in releasing these feelings, without having to discuss what the trauma was. This is a major positive facet of TFT. the results are felt immediately, and the negative states do not return. It is the most efficient therapy I have ever encountered. I use it with my patients who have disabilities and those who do not. There are no “negatives” in the use of the therapy. Its effects are felt during the session and persist over time. Powerful, gentle,easy to use. Developed by Dr. Roger Callahan. It can be used for non-verbal persons (infants, individuals with disabilities).

Thank you Nora. The “freedom to” is easily forgotten, and yet it is essential.

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Rebecca Adlington reveals she 'hated her body' after stillbirth trauma

The Nottinghamshire-born Olympic champion discovered her daughter had no heartbeat during a 20-week scan

• 15:44, 25 AUG 2024

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Nottinghamshire-born Olympian Rebecca Adlington has described how she could not help blaming herself for her stillbirth tragedy and how she "hated" her body afterwards. The 35-year-old former swimmer, from Mansfield , gave birth to her daughter Harper in October 2023 after a scan discovered that the baby had no heartbeat.

The stillbirth came after Rebecca suffered a miscarriage the previous year, with the Olympian saying she did not have the "strength of words" at the time to speak about the tragedy. Now speaking to The Sunday Times, Rebecca said: "I couldn't help blaming myself. You analyse everything, but I'd done everything by the book — sleeping on my left side, not lying on my back, not eating this and that, no alcohol — and then this still happened...

"Afterwards I hated my body because it couldn't keep Harper alive. I felt it had let me down and I didn't look after myself: I wasn't exercising and eating badly."

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Rebecca retired from competitive swimming at the age of 23 and after an initial marriage to Harry Needs ended in divorce, she found love again with Andy Parsons. Their first baby trauma came in 2022 when Rebecca endured a miscarriage at 12 weeks, an experience that necessitated emergency surgery and treatment for sepsis.

The loss of Harper the following year came when a 20-week scan found no heartbeat. In her Sunday Times interview about the tragedy, Rebecca added: "It was very hard for me to accept. I'm very logical so I wanted to find out why this had happened, but the post-mortem [in May] showed there was no reason; sometimes things just happen. I have to come to terms with that somehow and stop obsessing about it."

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