It’s a well understood fact among the psychological and psychiatric fields that people exposed to life-threatening traumatic situations are at high risk of developing Post-Traumatic Stress Disorder (PTSD). PTSD is characterized by persistent anxiety, several physiologic disturbances, and intrusive memories, which have been popularized by the “flashbacks” we tend to see in media portrayals of the condition. But the link between PTSD, memories, and the pathways that connect them have been the topic of conversation among mental health scholars for years.
To understand how stress and memory relate, it is important to understand the biologic stress response. One NIH manuscript published in 2014 outlines this response as the release of glucocorticoids, a type of steroids, through a brain pathway called the hypothalamic-pituitary-adrenocortical (HPA) axis and the release of chemicals called catecholamines, more commonly known as epinephrine and norepinephrine, or adrenaline and noradrenaline, which are neurotransmitters. These chemicals and pathways comprise what is known as the “fight or flight” response we’ve all learned about in science class. It’s what allows us and many other animals to not only adapt to new stresses but to also remember how to deal with these stressors if and when we next encounter them.
While moderate levels of stress can have a positive effect on memory and cognition, the opposite effect can result from extreme, traumatic, or chronic stress causing memory loss, cognitive impairments, and stress-related psychopathies, such as anxiety, depression, and PTSD. Experiments in rodents have demonstrated that glucocorticoids can induce PTSD-like memory impairments, such as the characteristic hypermnesia and the inability to restrict one’s fear response in a given context. This data suggest that there’s a disruption in the HPA axis involved in the pathophysiology of PTSD-associated memory impairment.
We must also try to grasp the physiologic and neuroscientific understanding of intact memory. In 1998, researchers at Harvard published a paper that asserted that most cognitive psychologists agree that there are two large categories of memory: explicit and implicit memory.
Explicit memory can be stated declaratively, can be recalled as an image or proposition, exists in a specific time frame, and is something of which most people, at least human adults, have conscious awareness. Examples you might recognize include the ability to recall specific events and things associated with them, places, and objects. It also allows us to see some aspect of ourselves in certain circumstances; for instance, perhaps you remember what you were doing when you learned that the World Trade Center towers were hit. That’s a form of explicit memory. Neural structures involved in explicit memory include the hippocampus, the rhinal cortex, and the parahippocampal gyrus.
Implicit memory typically reflects a combination of different subtypes of memory unrelated to explicit memory. Though varied, all forms are thought to be unconscious and may not reflect the self. Neural structures involved depend on the specific subtype of memory. Examples include conditioning, skilled motor learning, and artificial grammar learning.
How a particular stressor impacts memory and cognitive function is largely dependent on features of the stressor, such as its duration, chronicity, intensity, controllability, and predictability. Many studies have demonstrated that the intensity of a stressor and memory follow what’s called an inverted U-shaped relationship, such that our memories are the strongest when we experience intermediate degrees of stress, such as, perhaps, juggling a semester of classes and a couple extra curriculars or needing to remember what all of your nieces and nephews want for Christmas.
When it comes to stress- and trauma-induced conditions like PTSD, researchers have found that individuals with this condition can exhibit something called “fear conditioned responses.” This finding is based on the scientific observation that stress is a critical modulator of fear-learning and makes memory resistant to the fear extinction process. This extinction process involves a decline in fear-conditioned responses that occurs after a fear-inducing experience. Patients with anxiety disorders, including PTSD, who are exposed to extinction-like treatments tend to experience relapses in their symptoms. One major theory for why treatments that try to obliterate these memories fail is that stress hinders the dynamic remodeling of dendritic spines, which are structures on neurons that normally reshape brain networks during learning and memory processes.
New treatment modalities are on the forefront of treatment for PTSD and focus on the stress-induced brain remodeling effects on memory. These include eye movement desensitization and reprocessing (EMDR), an empirically-supported psychotherapy for the treatment of trauma, in which the person being treated is asked to recall distressing images while producing bilateral sensory input, like side-to-side eye movements or hand tapping. A meta-analysis of 87 studies of EMDR published last month demonstrated reasonable empiric support for the working memory hypothesis and for the physiologic changes associated with successful EMDR therapy. Another study published in 2013 found that the antidepressant tianeptine completely blocked the effects of psychosocial stress in a study of rats exposed to fear-inducing stressors.
These and other groundbreaking findings can make us hopeful that more effective and targeted treatment modalities can be used in the management of people struggling with the debilitating effects of psychological trauma.