# 1 thing that all treatments mention is SAFETY
Followed by: coping skills/ support system/ regaining control/ reducing stress/ relaxation skills/ self nourishing
# 1 thing that all treatments mention is SAFETY
Followed by: coping skills/ support system/ regaining control/ reducing stress/ relaxation skills/ self nourishing
Overview of Post Traumatic Stress Disorder including diagnostic criteria from ICD-10 and DSM-5, prevalence, course, differential diagnosis, co-morbidity, assessment, risk, prognostic and protective factors, etiology and management.
Posttraumatic stress disorder (PTSD) is an anxiety disorder that a person may develop after experiencing or witnessing an extreme, overwhelming traumatic event during which they felt intense fear, helplessness, or horror.
Trauma & Stressor Related Disorders for NCMHCE StudyJohn R. Williams
Quick review of the essential points— DSM5 diagnosis criteria, assessments, treatments—of these disorders to better prepare for the National Clinical Mental Health Counseling Exam. This was informed by several exam prep programs, and can be used like flashcards or as a presentation.
PTSD is a disease first introduced into the diagnostic and statistical manual of mental disorders (DSM) in 1980
With the world experiencing an unprecedented onslaught of disasters and traumas, it is imperative that health workers are aware of the disease and the factors that affect it
primary care management of the returning veteran with PTSDgreytigyr
primary care management of the returning veteran with PTSD Overview on issues and approach in promary care to recognition and management of patients, veterans, and soldiers with PTSD and TBI.
Course Description (From www.PESI.com):
Attend this day of training and leave with a brand new toolkit of skills, interventions, and principles for rapid success with traumatized clients. Join Jamie Marich and learn the standard of care for treatment in the field of traumatic stress – and its key ingredients. Implement evidence-based treatment protocols and interventions for establishing safety, desensitizing and reprocessing trauma memories, metabolizing and resolving grief/loss and finally, assisting clients in reconnecting to lives full of hope, connection, and achievement.
Jamie is a certified EMDR Therapist and approved consultant through the EMDR International Association (EMDR). She is additionally a member of the American Academy of Experts in Traumatic Stress, the International Association of Trauma Professionals (IATP), and has earned Certification in Disaster Thanatology.
Jamie began her career in social services as a humanitarian aid worker in post-war Bosnia-Herzegovina opening her eyes to the widespread, horrific impact of traumatic stress and grief.
Objectives:
Describe the etiology and impact of traumatic stress on the client utilizing multiple assessment strategies.
Assess a client’s reaction to a traumatic event and make an appropriate diagnosis.
Explain how grief, bereavement, and mourning are accounted for in the new DSM-5®.
Implement interventions to assist a client in dealing with the biopsychosocial manifestations of trauma, PTSD, and traumatic grief/complicated mourning.
Utilize appropriate evidence-based interventions to assist a client in dealing with the biopsychosocial-spiritual manifestations of trauma.
Explain the effects of trauma on the structure and function of the brain.
Acute stress disorder (ASD) is a mental disorder that can occur in the first month following a trauma. The symptoms that define ASD overlap with those for PTSD. One difference, though, is that a PTSD diagnosis cannot be given until symptoms have lasted for one month. Also, compared to PTSD, ASD is more likely to involve feelings such as not knowing where you are, or feeling as if you are outside of your body.
How common is ASD?
Studies of ASD vary in terms of the tools used and the rates of ASD found. Overall, within one month of a trauma, survivors show rates of ASD ranging from 6% to 33%. Rates differ for different types of trauma. For example, survivors of accidents or disasters such as typhoons show lower rates of ASD. Survivors of violence such as robbery, assaults, and mass shootings show rates at the higher end of that range.
Overview of Post Traumatic Stress Disorder including diagnostic criteria from ICD-10 and DSM-5, prevalence, course, differential diagnosis, co-morbidity, assessment, risk, prognostic and protective factors, etiology and management.
Posttraumatic stress disorder (PTSD) is an anxiety disorder that a person may develop after experiencing or witnessing an extreme, overwhelming traumatic event during which they felt intense fear, helplessness, or horror.
Trauma & Stressor Related Disorders for NCMHCE StudyJohn R. Williams
Quick review of the essential points— DSM5 diagnosis criteria, assessments, treatments—of these disorders to better prepare for the National Clinical Mental Health Counseling Exam. This was informed by several exam prep programs, and can be used like flashcards or as a presentation.
PTSD is a disease first introduced into the diagnostic and statistical manual of mental disorders (DSM) in 1980
With the world experiencing an unprecedented onslaught of disasters and traumas, it is imperative that health workers are aware of the disease and the factors that affect it
primary care management of the returning veteran with PTSDgreytigyr
primary care management of the returning veteran with PTSD Overview on issues and approach in promary care to recognition and management of patients, veterans, and soldiers with PTSD and TBI.
Course Description (From www.PESI.com):
Attend this day of training and leave with a brand new toolkit of skills, interventions, and principles for rapid success with traumatized clients. Join Jamie Marich and learn the standard of care for treatment in the field of traumatic stress – and its key ingredients. Implement evidence-based treatment protocols and interventions for establishing safety, desensitizing and reprocessing trauma memories, metabolizing and resolving grief/loss and finally, assisting clients in reconnecting to lives full of hope, connection, and achievement.
Jamie is a certified EMDR Therapist and approved consultant through the EMDR International Association (EMDR). She is additionally a member of the American Academy of Experts in Traumatic Stress, the International Association of Trauma Professionals (IATP), and has earned Certification in Disaster Thanatology.
Jamie began her career in social services as a humanitarian aid worker in post-war Bosnia-Herzegovina opening her eyes to the widespread, horrific impact of traumatic stress and grief.
Objectives:
Describe the etiology and impact of traumatic stress on the client utilizing multiple assessment strategies.
Assess a client’s reaction to a traumatic event and make an appropriate diagnosis.
Explain how grief, bereavement, and mourning are accounted for in the new DSM-5®.
Implement interventions to assist a client in dealing with the biopsychosocial manifestations of trauma, PTSD, and traumatic grief/complicated mourning.
Utilize appropriate evidence-based interventions to assist a client in dealing with the biopsychosocial-spiritual manifestations of trauma.
Explain the effects of trauma on the structure and function of the brain.
Acute stress disorder (ASD) is a mental disorder that can occur in the first month following a trauma. The symptoms that define ASD overlap with those for PTSD. One difference, though, is that a PTSD diagnosis cannot be given until symptoms have lasted for one month. Also, compared to PTSD, ASD is more likely to involve feelings such as not knowing where you are, or feeling as if you are outside of your body.
How common is ASD?
Studies of ASD vary in terms of the tools used and the rates of ASD found. Overall, within one month of a trauma, survivors show rates of ASD ranging from 6% to 33%. Rates differ for different types of trauma. For example, survivors of accidents or disasters such as typhoons show lower rates of ASD. Survivors of violence such as robbery, assaults, and mass shootings show rates at the higher end of that range.
Post Traumatic Stress Disorder is not a disease but a state of mind of patient. It comes in result of serious life event, threatening or worse nightmares. Post Traumatic Stress Disorder is developed slowly with time.
INTI2016 161124 Collective intelligence and territorial governance in Argenti...Territorial Intelligence
Présentation de Susana AZZOLINI, Hugo SIMKIN (Univ. Buenos Aires), "Collective intelligence and territorial governance in Argentina. Toward early intervention for post-traumatic stress disorder", dans l'Atelier 13 "Economie Sociale et Solidaire et Institutions" de la XVe Conférence Annuelle Internationale INTI « Économie Sociale et Solidaire dans les territoires », 22-25 novembre 2016, Charleroi et Liège, Belgique.
This a project for a high school AP Psychology course. This is a fictionalized account of having a psychological ailment. For questions about this blog project or its content please email the teacher, Laura Astorian: laura.astorian@cobbk12.org
Post-Traumatic Stress Disorder: New and Alternative Treatment MethodsRichard Stephens
A presentation on new and alternative treatment methods for Post-Traumatic Stress Disorder with a brief overview of Post-Traumatic Stress Disorder and treatment as usual.
Diagnostic Criteria:
exposure to actual or threatened death, serious, or sexual violence in one( or more) of the following ways:
1) Directly experiencing the traumatic events.
2) Witnessing in person
3) Learning that the traumatic event occur to close family member or friend.
4) Experiencing repeated or extreme exposure to aversive details of the traumatic events.
Dr. Cady presented this CME program on depression and TMS (Transcranial magnetic stimulation) to the medical staff of the Community Methodist Hospital in Henderson, KY on February 8, 2012. It reviews accurate diagnosis of depression, use of new medications, cautions on drug-drug interactions, and a review of the new development of TMS in the current treatments of 21st Century psychiatry.
Targeting abnormal neural circuits in mood and anxiety disorders:from the la...Kaan Y
My article presentation at the Journal Club on 22 January 2008
Targeting abnormal neural circuits in mood and anxiety disorders: from the laboratory to the clinic
Kerry J Ressler & Helen S Mayberg
VOLUME 10 NUMBER 9
SEPTEMBER 2007
1116-1124
NATURE NEUROSCIENCE
For a free full text of the article:
http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=2444035
This presentation explores neuropharmacology of TBI treatment. Including anatomical impacts of TBI, pharmacotherapy, implications for treatment and behavioral interventions.
Health Psychology Pharmacology - Biopsychosocial Approaches to Anxiety and De...Michael Changaris
This slide series explores pharmacotherapy for anxiety and depression in integrated health approaches to managing anxiety in primary care settings. the presentation offers an overview of common health co-morbidities and tools for treatment.
Magnets - Not Drugs: TMS IMMH San Antonio 2014Louis Cady, MD
In this talk, Dr. Cady covers a remarkable new treatment for depression: transcranial magnetic stimulation. The historical roots of this treatment are traced, followed by a review of the literature in terms of the proven efficacy of this treatment. A comparison with ECT shows that TMS has a very favorable profile, with remarkably fewer side effects and incredibly better tolerated side effects compared to ECT. Given that this was a "CME" talk, off-label uses of TMS were reviewed, including stepping stones for future avenues to explore
Running Head: DEPRESSION 1
DEPRESSION 3
Lana Eliot
Depression
Psychology 630
Professor Benton
August 25, 2018
Many people throughout the world experience some type of depression in their lives and it is one of the most common mental disorders. The current statistic show that depression is linked to genetic, environmental, biological and is also psychological. Depression can ben found with any age person. A small child or an adult may have to deal with the depression that is affecting them. Chemical imbalances in the brain is the leading cause for a person dealing with the depressive order. The neurotransmitter is the what we call the communicator between the brain and the limbic system. Researchers study the limbic system in the brain as this is where depression starts; especially for anxiety and stress. The 3 major neurotransmitters; serotonin, norepinephrine, and dopamine all have direct relations with a persons’ depression and anxiety.
Serotonin plays a crucial role in our brain. It is associated with many physical actions that we may portray. The actions associated with serotonin are mood altering, sleeping patterns, eating disorders, and aggression. If a persons’ serotonin levels decrease, they may experience these depressive symptoms. This can also make persons have a feeling of self-worth and suicidal feelings.
Another transmitter in the brain which is associated with the depressive disorder is dopamine. This is the part of the brain that deals with our motivation and how we gain the feeling of self-worth and self-pleasure. Early studies suggested that an existence of neurotransmitter norepinephrine deficiency in some certain areas of the brain resulted in depression. One main cause of depression is the reduction in the concentration of certain neurotransmitters in the brain, such as serotonin and dopamine. The decrease in the concentration of these neurotransmitters leads to disturbed neuronal signal processing which leads to alterations in the structure of the neuronal networks. These basic changes are accepted to be one of the fundamental purposes behind sorrow. The emergence of neuroimaging techniques, magnetic resonance imaging (MRI), positron emission tomography (PET) and functional fMRI, established the importance of the ‘neurocircuit of emotion’ which has been expanded to include other important brain areas and the prefrontal cortex (PFC). These brain sites and their connections, which have been widely studied, are responsible for maintaining emotional stability and their malfunction is considered central to the pathophysiology of depression (Palazidou, E., 2012).
Recent follow up studies also shows that there is a group of individuals with a depression disorder who exhibit low levels of the chemical norepinephrine. In autopsy studies, it has been shown that in comparison,.
6. Amygdala
Group of nuclei within the
temporal lobe that are involved
in memory, decision making,
emotions, and other limbic
system functions.
Limbic – emotion, motivation,
behavior
Coronal MRI section of right
amygdala.
Shin, L. M., et al. (2006). "Amygdala, medial prefrontal
cortex, and hippocampal function in PTSD." Ann N Y Acad
Sci 1071: 67-79.
https://commons.wikimedia.org/wiki/File:MRI_Location_Am
ygdala_up.png
7. Hippocampus
Part of limbic system. Involved in
the consolidation of short-term
memory to long-term memory.
Located in medial temporal lobe.
Shin, L. M., et al. (2006). "Amygdala, medial prefrontal cortex, and hippocampal
function in PTSD." Ann N Y Acad Sci 1071: 67-79
https://commons.wikimedia.org/w/index.php?curid=9451294
https://commons.wikimedia.org/wiki/File:Gray739-emphasizing-hippocampus.png
8. Medial Prefrontal
Cortex
Cortex towards the
anterior of the frontal
lobe.
Planning of complex
behavior, personality,
decision making, social
behavior, executive
function, formation of
thoughts, internal
goals/motivation, and
specific forms of learning.
https://commons.wikimedia.org/wiki/File:Prefrontal_cortex_(left)_-
_medial_view.png
9. Definitions: Acute Stress Disorder
• Psychiatric disorder following traumatic experience.
• Acute symptoms occur between 3 days and 1 month (DSM V).
• Altered “fear-processing” pathway mediated by Amygdala and
prefrontal cortex hyperactivity.
Discovered through face-matching fMRI task.
Shin, L. M., et al. (2006). "Amygdala, medial prefrontal cortex, and hippocampal function in
PTSD." Ann N Y Acad Sci 1071: 67-79.
Reynaud, E., Guedj, E., Trousselard, M., El Khoury-Malhame, M., Zendjidjian, X., Fakra, E., . . .
Khalfa, S. (2015). Acute stress disorder modifies cerebral activity of amygdala and prefrontal
cortex. Cogn Neurosci, 6(1), 39-43. doi:10.1080/17588928.2014.996212
10. Face Matching Task
• Face matching –
comparing faces or
selecting one face, in a
different orientation,
that matches.
http://sitn.hms.harvard.edu/flash/2015/the-human-
microbiome-and-media-confusion/
11. Definitions: PTSD
• Symptoms persistent after a month following traumatic event
that is diagnosed at least 1 month after traumatic event (DSM
V).
Acute PTSD– 1-3 months
Chronic PTSD– 3 months or more
• At the time of the trauma, the Hippocampus is suppressed by
over-reactive adrenaline response.
Prevents proper “recording” of the memory.
Re-experiencing stimuli similar to trauma may induce a
flashback.
Medina, J. (2008). "Neurobiology of PTSD."
MOLECULES OF THE MIND: 29-33.
12. Definitions: PTSD
• Research in PTSD on specific populations.
Veterans/Traumatic Brain Injury (TBI)
Often comorbidity
• Currently, research on the neurobiology of PTSD returns mixed
results.
Sometimes, but not always, there is:
A heightened cortisol level
Atrophy
Hyper/Hypoactivation
Medina, J. (2008). "Neurobiology of PTSD."
MOLECULES OF THE MIND: 29-33.
13. Effects of Stress on Cognitive Functioning
• Cortisol – Steroid hormone released by the adrenal gland.
Released as a response to stress and low blood sugar.
• High Affinity Receptors – Easily binds molecules (low
concentrations of molecules).
• Low Affinity Receptors – More difficult to bind molecules
(increased concentration).
Medina, J. (2008). "Neurobiology of PTSD."
MOLECULES OF THE MIND: 29-33.
14. Effects of Stress on Cognitive Functioning
• Moderate stress -> Cortisol binds to high affinity receptors ->
Hippocampus activated and subjects performed better on tasks.
• Severe/Chronic Stress -> Cortisol binds to both low and high
affinity receptors -> Hippocampus inhibited; subjects perform
worse on tasks. (Since only high levels of cortisol can
significantly activate low affinity receptors).
Medina, J. (2008). "Neurobiology of PTSD."
MOLECULES OF THE MIND: 29-33.
15. Hypothalamic-Pituitary-Adrenal Axis
(HPAAxis)
• Hypothalamus – Synthesis and secretion of
hormones which stimulate/inhibit pituitary from
secreting hormones.
• Pituitary gland – Regulation of stress via
hormone secretion.
• Adrenal cortex – Production of glucocorticoids
(steroid hormone) such as cortisol. Glands
located above kidneys
16. Hypothalamic-
Pituitary-
Adrenal Axis
1. Chronic stress.
2. Increases in
glucocorticoids.
3. Cellular changes in
the hippocampus.
4. Decreased regulation
of cortisol.
http://www.biology.ucr.edu/people/faculty/Garland/HPA_axis.jpg
Pariante, C. M. and S. L. Lightman (2008). "The HPA axis in
major depression: classical theories and new developments."
Trends Neurosci 31(9): 464-468.
17. What brain region, given your
pre-class readings and lecture
material, do you think is most
significantly affected in
PTSD/chronic stress?
19. Hippocampus
• Vietnam combat
veterans.
• Brain Imaging (MRI)
• Combat Veterans found
to have 8% reduction in
right hippocampal
volume.
• No significant
differences in any other
region.
• Measurable loss of
neurons due to
neurotoxicity (cortisol)
J. Douglas Bremner, M. D. (2000). "The Invisible Epidemic: Post-Traumatic
Stress Disorder, Memory and the Brain."
20. Current Treatment Options
• Critical Incident Stress Management (CISM) (First Responders)
• Cognitive Behavioral Therapy
Psychosocial intervention that teaches improved coping
strategies and removing unwanted behaviors and emotions.
• Interpersonal psychotherapy
Support groups with other persons with PTSD or Acute Stress
Disorder.
Burkle, F. M., Jr. (1996). "Acute-phase mental health consequences of disasters: implications
for triage and emergency medical services." Ann Emerg Med 28(2): 119-128.
Wee, D. F., et al. (1999). "The effects of critical incident stress debriefing (CISD) on emergency
medical services personnel following the Los Angeles Civil Disturbance." Int J Emerg Ment
Health 1(1): 33-37.
21. Current Treatment Options
• Most accepted method is behavioral + psychotherapeutics
• Psychotherapeutics
SSRIs – Antidepressant
Serotonin – Neurotransmitter associated with feeling of well-being
Comorbidity with Depression.
Promotes neurogenesis (growth of neurons) in hippocampus.
Benzodiazepines – Anxiolytics (anxiety reducing)
Cannabinoids – Research pending
Burkle, F. M., Jr. (1996). "Acute-phase mental health consequences of disasters: implications
for triage and emergency medical services." Ann Emerg Med 28(2): 119-128.
Wee, D. F., et al. (1999). "The effects of critical incident stress debriefing (CISD) on emergency
medical services personnel following the Los Angeles Civil Disturbance." Int J Emerg Ment
Health 1(1): 33-37.
Bremner, J. D. (2006). "Traumatic stress: effects on the brain." Dialogues Clin Neurosci 8(4):
445-461.
22. The Future
• Oculus Rift
• Immersive Cognitive
Behavioral Therapy
• Potential involvement of
Virtual Reality Re-
exposure to the incident
May allow for
psychological
debriefing and
reprocessing of the
event within the
hippocampus.
Boggio, P. S., et al. (2010). "Noninvasive brain stimulation with high-frequency and
low-intensity repetitive transcranial magnetic stimulation treatment for
posttraumatic stress disorder." J Clin Psychiatry 71(8): 992-999.
http://www.kotaku.com.au/2016/10/how-to-play-virtual-reality-games-on-a-budget/
23. The Future: Treatment Options being
Explored
• Fear Response Extinction Learning with MDMA
MDMA (ecstasy) - Entering Phase III clinical trials in April
2017.
Cognitive Behavioral Therapy in conjunction with MDMA may
allow patients to reprocess the event without becoming
emotionally overwhelmed. MDMA has been shown to decrease
fear response (biochemical process).
Philipps, D. (2016). "F.D.A. Agrees to New Trials for Ecstasy as Relief for PTSD Patients." New York Times.
Boggio, P. S., et al. (2010). "Noninvasive brain stimulation with high-frequency and low-intensity repetitive
transcranial magnetic stimulation treatment for posttraumatic stress disorder." J Clin Psychiatry 71(8): 992-
999.
24. The Future: Treatment Options being
Explored
• Research on psychoactive compounds to decrease hyperactivity in
the Amygdala and prefrontal cortex.
• Noninvasive Brain Stimulation with High and Low-Frequency
Intensity Repetitive Transcranial Magnetic Stimulation
Treatment.
Double blind experiment; placebo-controlled phase II trial.
Wechsler Memory Scale
Led to a significant decrease in manifestation of symptoms as
shown by the PTSD Checklist and Treatment Outcome PTSD
Scale and significant improvement in mood/anxiety.
Results long lasting; results significant at 3-month follow up.
Gilbert, D. L. (2007). "Low and high-frequency repetitive transcranial magnetic
stimulation for the treatment of spasticity." Dev Med Child Neurol 49(7): 486.
25. Transcranial
Magnetic
Stimulation (TMS)
• High (10-20 Hz) and low
(1-5 Hz) frequency
repetive TMS
• Frequency dependent
opposite effect
• If one frequency inhibits,
the other promotes
• Used mostly in
depression
• Faraday’s law
• Magnetic field interacts
with an electric force
https://c.o0bg.com/rf/image_960w/Boston/2011-
2020/2016/03/15/BostonGlobe.com/Lifestyle/Images/160314_KD
B_TMS_THERAPY_006.jpg
26. References:
• Berlim, M. T., Van den Eynde, F., & Jeff Daskalakis, Z. (2013). Clinically meaningful efficacy and acceptability of low-frequency
repetitive transcranial magnetic stimulation (rTMS) for treating primary major depression: a meta-analysis of randomized, double-
blind and sham-controlled trials. Neuropsychopharmacology, 38(4), 543-551. doi:10.1038/npp.2012.237
• Boggio, P. S., Rocha, M., Oliveira, M. O., Fecteau, S., Cohen, R. B., Campanha, C., . . . Fregni, F. (2010). Noninvasive brain
stimulation with high-frequency and low-intensity repetitive transcranial magnetic stimulation treatment for posttraumatic stress
disorder. J Clin Psychiatry, 71(8), 992-999. doi:10.4088/JCP.08m04638blu
• Bremner, J. D. (2006). "Traumatic stress: effects on the brain." Dialogues Clin Neurosci 8(4): 445-461.
• Bremner, J. D., et al. (1995). "MRI-based measurement of hippocampal volume in patients with combat-related posttraumatic stress
disorder." Am J Psychiatry 152(7): 973-981.
• Burkle, F. M., Jr. (1996). Acute-phase mental health consequences of disasters: implications for triage and emergency medical
services. Ann Emerg Med, 28(2), 119-128.
• Classen, C., Koopman, C., Hales, R., & Spiegel, D. (1998). Acute stress disorder as a predictor of posttraumatic stress symptoms. Am
J Psychiatry, 155(5), 620-624. doi:10.1176/ajp.155.5.620
• Eche, J., Mondino, M., Haesebaert, F., Saoud, M., Poulet, E., & Brunelin, J. (2012). Low- vs High-Frequency Repetitive Transcranial
Magnetic Stimulation as an Add-On Treatment for Refractory Depression. Front Psychiatry, 3, 13. doi:10.3389/fpsyt.2012.00013
• Gilbert, D. L. (2007). "Low and high-frequency repetitive transcranial magnetic stimulation for the treatment of spasticity." Dev Med
Child Neurol 49(7): 486.
• J. Douglas Bremner, M. D. (2000). The Invisible Epidemic: Post-Traumatic Stress Disorder, Memory and the Brain.
• Jakupcak, M., Roberts, L. J., Martell, C., Mulick, P., Michael, S., Reed, R., . . . McFall, M. (2006). A pilot study of behavioral
activation for veterans with posttraumatic stress disorder. J Trauma Stress, 19(3), 387-391. doi:10.1002/jts.20125
• Kraft, D. (2012). Panic Disorder Without Agoraphobia. A Multi-Modal Approach: Solution-Focused Therapy, Hypnosis and
Psychodynamic Psychotherapy. Journal of Integrative Research, Counselling and Psychotherapy, 1(1), 4-15.
• Medina, J. (2008). Neurobiology of PTSD. MOLECULES OF THE MIND, 29-33.
• Mol, S. S., Arntz, A., Metsemakers, J. F., Dinant, G. J., Vilters-van Montfort, P. A., & Knottnerus, J. A. (2005). Symptoms of post-
traumatic stress disorder after non-traumatic events: evidence from an open population study. Br J Psychiatry, 186, 494-499.
doi:10.1192/bjp.186.6.494
27. References:
• Pariante, C. M., & Lightman, S. L. (2008). The HPA axis in major depression: classical theories and new developments.
Trends Neurosci, 31(9), 464-468. doi:10.1016/j.tins.2008.06.006
• Philipps, D. (2016). F.D.A. Agrees to New Trials for Ecstasy as Relief for PTSD Patients. New York Times.
• Reynaud, E., Guedj, E., Trousselard, M., El Khoury-Malhame, M., Zendjidjian, X., Fakra, E., . . . Khalfa, S. (2015). Acute
stress disorder modifies cerebral activity of amygdala and prefrontal cortex. Cogn Neurosci, 6(1), 39-43.
doi:10.1080/17588928.2014.996212
• Shin, L. M., Rauch, S. L., & Pitman, R. K. (2006). Amygdala, medial prefrontal cortex, and hippocampal function in PTSD.
Ann N Y Acad Sci, 1071, 67-79. doi:10.1196/annals.1364.007
• Speer, A. M., Kimbrell, T. A., Wassermann, E. M., J, D. R., Willis, M. W., Herscovitch, P., & Post, R. M. (2000). Opposite
effects of high and low frequency rTMS on regional brain activity in depressed patients. Biol Psychiatry, 48(12), 1133-1141.
• Valle, A. C., Dionisio, K., Pitskel, N. B., Pascual-Leone, A., Orsati, F., Ferreira, M. J., . . . Fregni, F. (2007). Low and high
frequency repetitive transcranial magnetic stimulation for the treatment of spasticity. Dev Med Child Neurol, 49(7), 534-
538. doi:10.1111/j.1469-8749.2007.00534.x
• Wee, D. F., Mills, D. M., & Koehler, G. (1999). The effects of critical incident stress debriefing (CISD) on emergency medical
services personnel following the Los Angeles Civil Disturbance. Int J Emerg Ment Health, 1(1), 33-37.
28. Contact Information and Acknowledgements
• John Caccaviello
• Jcaccavi@bu.edu
• I would like to acknowledge and thank:
Nina Shaafi Kabiri for letting me present in her course and for her mentorship
The Vesalius committee for their support and assistance.
Dr. Kevin Thomas and those in the laboratory for human neurobiology for
providing feedback at my practice sessions.