Post Traumatic Stress Disorder

What is PTSD?

Post-traumatic stress disorder (PTSD), triggered by ongoing frightening events such those experienced in combat, a single terrifying event such as a natural disaster, a serious accident, terrorist act, or violent personal assault, is recognized as a mental health condition. PTSD can also result from chronic high stress related to work, finances, or relationships. About 3.5 percent of American adults are affected; about one in eleven people will be diagnosed with PTSD during their lives.

Effect of PTSD

It is normal to have temporary difficulty adjusting to and coping with traumatic events. The chronic or extreme stresses which lead to PTSD cause “acute and chronic changes in neurochemical systems and specific brain regions which result in long-term changes in brain circuits, involved in the stress response.”1095 These give rise to symptoms that worsen and last for months or many years, and interfere with daily activities. In such cases PTSD is diagnosed. A person with PTSD may have trouble sleeping, experience nightmares and anxiety, or in severe cases may have flashbacks, panic attacks, uncontrollable thoughts, and extreme behavior that disrupt mental well-being, damage self-confidence, and impair relationships with others.

How the Brain Reacts to Trauma

The brain records traumatic events. An important role in PTSD is played by the hippocampus, amygdala, and medial prefrontal cortex. Two key neurotransmitters, cortisol and norepinephrine are critical in the stress response. Additional key players are the hypothalamic-pituitary-adrenal (HPA) axis and corticotropin-releasing factor (CRF).¹

Cortisol triggers neurochemical responses to stress, especially via the locus coeruleus in the brainstem. This center of neurons selects and catalogs “adaptive memories,” which are exciting or traumatic and which are important for survival1² so that we can avoid such events in the future. The locus coeruleus sends the neurotransmitter, norepinephrine,³ to most of the brain, including the prefrontal cortex, amygdala, hippocampus, thalamus, and anterior cingulate cortex. Norepinephrine controls arousal, memory, attention, and cognition. During a sharply exciting or frightening event the locus coeruleus amplifies neural input so that the resources for recording memories are prioritized, making “best” use of recording resources which are available at the time.⁴

But blurs memory details. Furthermore, in the case of PTSD, researchers are identifying impairment of the hippocampus-dependent associative learning ability, which reduces the victim's ability to recall exactly what happened.⁵

Brain Volume and Function

Chronic traumatic stress can actually change the shape of the brain’s regions. Patients with PTSD have smaller hippocampus and anterior cingulate cortex volumes. Amygdala activity increases, and anterior prefrontal/anterior cingulate function decreases.⁶ In adults with childhood maltreatment-related PTSD, the amygdala is shrunken in size:⁷ primarily the left amygdala, but not the hippocampus or prefrontal cortex.1105 Amygdala size can change (and recover). In one study life stress of “relatively short duration was associated with amygdala size … while temporally distant life stress was not, suggests that amygdala size changes may occur rapidly and reversibly…”⁸

Genetic Changes

Not only do chronic and acute stressors cause changes in volume and function in the amygdala, hippocampus, and other regions of the brain, but such stress modulates gene expression. Working with mice, researchers have learned that a history of stress can permanently alter gene expressions in the hippocampus and in the response to a new stress.

This may be the reason that severe PSTD can occur years later after an event. In terms of biophysiology, a smaller left hippocampus volume is linked with severe PSTD occurring years after the initial experience(s).

Symptoms of PTSD

Symptoms are both mental, experienced subjectively, and physiological, reflected in the brain structure.

• Increased depression, emotional numbness
• Anxiety, feeling jumpy, irritable
• Flashbacks or nightmares
• Intense negative thoughts and feelings
• Poor sleep
• Diminished cognitive ability
• Increased risk of substance abuse

Neurobiological Effects

Mast cell activation.⁹ Mast cells (mastocyte or labrocyte) are a kind of allergy-related cell derived from a stem cell that is part of the immune system. Mast cell activation refers to their releasing too many mediators and triggering allergic reactions, causing responses such as difficulty in breathing, severe diarrhea, or abnormally low blood pressure.

Neuroinflammation and oxidative stress in the prefrontal cortex and hippocampus. Inflammation affects not only the basal ganglia and cortex, but the amygdala, insula and anterior cingulate cortex leading to changes in glutamate and monoamines.

Reduced left amygdala and left hippocampal volumes.

Reduced brain reserve. Reduced ability to tolerate age-related change

Endocrine system changes. Hypocortisolism in the hypothalamic-pituitary-adrenal axis causes abnormal stress encoding

Neurochemical patterns changes of dopamine, norepinephrine, serotonin, amino acids, and peptides.

Anatomical changes: hippocampus volume and activity decreases, amygdala activity increases, and there is a reduced prefrontal cortex, anterior cingulate cortexes, and decreased medial prefrontal activation.

Risk Factors

Certain risk factors make one more vulnerable to PTSD. These include existing mental health conditions, genetics, previous trauma, lack of support, or chronic stress in life such as in the areas of love, work, or finances. A history of having suffered abuse or maltreatment as a child increases the risk of PTSD after a later traumatic event.¹⁰

Women are more likely to develop PTSD than men (10-12 percent for women, and 4-5 percent among men). Traumatic stress affects girls and boys at different ages, and in different parts of the brain.¹¹ Researchers estimate that in women about one third of the risk is due to genetic factors, much higher than for men.¹²

There is some evidence that certain genetic structures increase vulnerability to PTSD and anxiety disorders.¹³ A gene, 5HTTLPR, with a long and a short form (5HTTLPR/short), is linked to the stress response. About forty percent of the population carries the short form and are clearly more vulnerable to all sorts of anxious behavior, including PTSD.¹⁴

Next: PTSD Support

Footnotes

Note: additional sources of the above information are available in our guide to brain care, Natural Brain Care, or upon request.

1. Bremner JD. (2006). Traumatic stress: effects on the brain. Dialogues Clin Neurosci. Dec;8(4):445-461.
2. Newcomb B. (2018). How your brain records the memory of a stressful experience. Retrieved Sep 25 2019 from https://news.usc.edu/136280/in-a-stressful-situation-this-part-of-the-brain-helps-you-turn-that-experience-into-a-vivid-memory/.
3. Schwarz LA, Luo L. (2015). Organization of the locus coeruleus-norepinephrine system. Curr Biol. Nov 2;25(21):R1051-R1056.
4. Clewett DV, Huang R, Valasco R, Lee TH, Mather M. (2018). Locus Coeruleus Activity Strengthens Prioritized Memories Under Arousal. J Neurosci. Feb7;38(6):1558-1574.
5. Lambert HK, McLaughlin KA. (2019). Impaired Hippocampus-Dependent Associative Learning as a Mechanism Underlying PTSD: a Meta-Analysis. Neurosci Biobehav Rev. Sep 20:S0149-763(19)30138-1.
6. Ibid. Bremner. (2006). 7. Ahmed-Leitao F, Spies G, van den Heuvel L, Seedat S. (2016). Hippocampal and amygdala volumes in adults with posttraumatic stress disorder secondary to childhood abuse or maltreatment: A systematic review. Psychiatry Red Neuroimaging. Oct30;256:33-43.
8. Sublette ME, Galfalvy HC, Oquendo MA, Bart CP, Schneck N, et al. (2016). Relationship of recent stress to amygdala volume in depression and healthy adults. J Affect Disord. Oct;203:136-142.
9. Kempuraj D, Selvakumar GP, Thangavel R, Ahmed ME, Zaheer S, et al. (2017). Mast Cell Activation in Brain Injury, Stress, and Post-traumatic Stress Disorder and Alzheimer's Disease Pathogenesis. Front Neurosci. Dec 12;11:703.
10. Danniowski U, Stuhrmann A, Beutelmann V, Zwanger P, Lenzen T, et al. (2012). Limbic scars: long-term consequences of childhood maltreatment revealed by functional and structural magnetic resonance imaging. Biol Psychiatry. Feb 15;71(4):286-93.
11. Olff M. (2017). Sex and gender differences in post-traumatic stress disorder: an update. Psychotraumatology in Greece: Abstracts of the First Greek Psychotraumatology Conference. Jul 27:13351204.
12. Tull M. (2019). Causes and Risk Factors of PTSD. Retrieved Sep 27 2019 from https://www.verywellmind.com/ptsd-causes-and-riskfactors-2797397.
13. Van der Merwe C, Jahanshad N, Cheung JW, Mufford M, Groenewold NA, et al. (2019). Concordance of genetic variation that increases risk for anxiety disorders and posttraumatic stress disorders and that influence their underlying neurocircuitry. J Affect Disord. Feb 15;245:885-896.
14. Mukherjee, S. (2016). The Gene. (p. 459). New York, Simon & Shuster, Inc.