PTSD as a Memory Disorder

C. Robinson

University of Saskatchewan

                                       For Psych 255 with David Lane Nov 4^th 2020

Abstract

In this review we will be looking at PTSD as a Memory Disorder, and its impact on the Hippocampus, Amygdala and Pre-Frontal Cortex, and the neurobiological and psychological theories of PTSD. While PTSD is classified in the DSM5 as a “trauma and stress related disorder” I would argue that it is also a Memory Disorder caused by changes in the structures of the brain which result in deficits to Declarative and Non Declarative memory functions. I will also briefly discuss less commonly known risk factors for PTSD including ‘vicarious traumatization’ which is a relatively new phenomena, and we should all be aware of the impact it may have on our neurobiological structures and functions.

Keywords: PTSD, Hippocampal damage, Memory, memory deficit

What is PTSD ?

Studies have shown that approximately 70% of Canadians have experienced at least 1 traumatic event in their lifetime, of that 70%, approximately 8%will develop symptoms of Post-traumatic Stress Disorder which can persist anywhere from weeks or months, with 9.5% experiencing life-long prevalence. 1 PTSD was first added to the DSM in 1980, with the criteria having changed several times since due to advances in our understanding of this condition, resulting in updates in the DSM-5 which removed PTSD from ‘anxiety disorders’ to ‘trauma and stress related disorders’ however there are 4 core features of PTSD, with a 5^th being added in the updated DSM-5.2

1. Experiencing or witnessing a traumatic event.

2. Re-experiencing symptoms of the event that include nightmares and or flashbacks

3. Efforts to avoid situations, places, and people that are reminders of the traumatic event

4. Hyper arousal symptoms, such as irritability, concentration problems, and sleep disturbances

5. Negative alterations in cognitions and mood

There have also been major changes to the criteria for stressors which may trigger PTSD, with the criterion being exposure to ‘death, threatened death, actual or serious threatened injury, actual or threatened sexual violence’ 3

However, there are some other interesting risk factors which can also contribute to the development of PTSD symptoms which are not included in the above mentioned list, such as; medical trauma, or sudden onset of life threatening illness such as myocardial infarction, or heart attack may cause PTSD.4

More recent studies have also shown that viewing violent or traumatic events via social media can cause the viewer to experience symptoms very similar to PTSD, due to ‘vicarious exposure to trauma’. 5 In a study done by Dr. Pam Ramsden in May of 2015, approximately 189 participants with average age of 37 and a nearly even split in gender, showed that 22% of the participants were negatively affected by their vicarious exposure to coverage of violent events, such as 9/11, school shootings, terrorist attacks and bombing, resulting in high clinical scores consistent with PTSD, although the individuals themselves did not personally experience any of these events.

The study also indicated repeated exposure to the traumatic events via media and social media resulted in a higher rate of clinical symptoms, which I would hypothesize may indicate a possible increase of individuals at risk of experiencing symptoms of PTSD as social media usage continues to increase, with a heavy emphasis on violent, stress inducing and negative news stories continues to be a very prevalent part of daily life. This concept would be supported by Solomon and Beckerts TMT and Mortality Salience Theory.6

PTSD as a disorder of memory

In a study by B.M. Elzinger and J.D. Bremmer published in 2017, 7 PTSD was presented as a disorder of memory using psychological and neurobiological models and data.

There are typically two types of memory deficits experienced by persons who have been exposed to or experienced traumatic stress resulting in PTSD;8

1) Intrusive memories with high levels of arousal generated by a sensory modality response resulting in a behavior response, often experienced and described as a “flashback” - implicit memory process may automatically bring back memory of the event caused by underlying fear conditioned and re-experiencing response which is the result of a very strong memory encoded in the brain due to the sudden high level of fear experienced, and cortisol, adrenaline and glutamate released when the event occurred.

2) Impoverished memory function due to diminished encoding or impaired retrieval abilities, resulting in difficulties with declarative memory- they are constantly forgetting things, autobiographical memory – their memories about themselves may be fragmented there could be gaps, memories of the traumatic event may be fuzzy, or they may experience trauma related amnesia resulting in the loss of memory of the event completely which can last from minutes to day and is not ‘ordinary forgetting’ .

They may also experience general declarative and short term memory deficits in areas unrelated to the traumatic event, general memory impairment for neutral information, significant decrease in retention of previously presented material following exposure to an intervening word list, and general impairment in cognitive functioning when compared to individuals without PTSD

Information Processing Theory & Cognitive Model

Due to the distortion of neutral information experienced by PTSD patients, information processing theory looks at the how traumatic information is represented and processed cognitively. Emotional memory networks are central to this theory, which is comprised of; stimulus, response and meaning units. 9

When there is stimulus which matches something that’s encoded in your emotional memory, (for instance a firework being set off), may result in an automatic encoded emotional effect activating a distorted meaning to that stimuli, (someone is shooting at me) resulting in verbal, behavioral or physiological response and a recall of declarative or semantic knowledge which may trigger an experiencing of sensations, physiological arousal, intrusive memories and strong emotional reactions.

Cognitive models also assume that trauma introduces salient information that does not fit into our pre-existing schema of how the world works, when a person is able to recover from this shock, they have successfully processed the event, however, if they cannot successfully process the event, this may lead to activation of a trauma network producing excessive arousal levels. 10 The dual representation model looks at the conscious and nonconscious response, where accessible memories containing sensory information related to the traumatic response, eliciting the emotional and physiological responses, and the perceived meaning associated with this response and the event, result in highly detailed and repetitive memories, indicating selective attention and memory processing trauma related information is given priority over neutral information.

Neurobiology of Memory & PTSD

Studies done on the effect of stress on brain structures which mediate memory have added to the models for memory deficits or information distortions related to PTSD.

Stress is regulated by the hypothalamus-pituitary-adrenal axis (cortisol) and the noradrenergic system, which are inter-regulating systems which play mutually important roles in stress regulation.

Cortisol and (nor)adrenaline act on the brain structures associated with memory and PTSD which are the Hippocampus, the Amygdala, the Pre-Frontal Cortex, and other areas of the brain related to memory function. 11

Noradrenaline and the Amygdala Noradrenaline, which is produced by the noradrenergic system during a startle response or flight or fight response, has a short term effect which strengthens memory traces related to emotional events, when a higher dose of noradrenaline is released, a stronger connection is created to that emotional memory. 12 The enhanced encoding of this emotional memory trace is due to the noradrenergic system and the affect that adrenaline has on structures of the limbic system, particularly the amygdala, which is responsible for assessing threats in our environment and rapidly processing information. When this emotional memory is retrieved accompanied by adrenaline release, the encoding of the traumatic memory trace becomes stronger, which can result in deeply engraved memories experienced as intrusive and unwanted flashbacks. 13

The amygdala plays an important role in fear conditioning, studies have shown that in patients with whom fear has been conditioned as response, present with heightened activity in the amygdala via fMRI indicating that amygdala dysfunction due to increased fear conditioning may be the cause of the increase in startle response and physiological responses to stimuli that triggers traumatic reminders, suggesting that the amygdala play an important role in non-declarative, implicit emotional processing .14 15

Prefrontal cortex

The PCF plays an important role and acts as the “executive” processing incoming information from the amygdala, and regulating our response via inhibition of inappropriate responses. One of my professors explained it this way; “the amygdala sees a bulky image in a dark room and immediately assumes it’s a bear, about to attack, the PCF turns on the lights and says “this isn’t a bear, it’s a chair covered in dirty laundry’” this interaction between amygdala and the PCF happens very quickly, allowing for the planning and executing of organized and appropriate behavior.16

The relationship between the PCF and the amygdala can become complicated when the amygdala is operating at a persistent heightened state of vigilance due to fear conditioning and the subsequent releases the hormone adrenaline and the production of catecholamines, dopamine and noradrenaline.17The PCF is also responsible for assigning emotional valiance to memory, and the stronger the release of noradrenaline, the stronger the that valiance becomes.18 Noradrenaline acts on the alpa 1 and alpa 2 receptors, with opposing effects, noradrenaline acting on alpha 1 receptors can cause impaired PCF functions post synapse, while noradrenaline acting on alpa2 receptors can result in improved performance, with higher levels more likely to engage the alpha 1 receptors causing deficits in PCF functioning related to working memory and response inhibition.19

Elevated levels of Noradrenaline and dopamine have been shown to cause deficits in working memory, and can explain the issues experienced by individuals who have PTSD surrounding attention and ability to focus, as well as their inability to regulate their response to stress.20

Cortisol and the Hippocampus The hippocampus plays important roles in explicit or declarative memory and learning, it stores short term memory until it can be consolidated to long term memory stores, and it also organizes the retrieval of memory from various stores and brings them together to create a cohesive memory, needless to say, the hippocampus is integral to learning and memory processes.

In patients with damage to the hippocampal area, declarative memory is affected while procedural memory is unaffected.21 22 When a (traumatic) stress occurs, the adrenal gland also releases a hormone called cortisol or corticosterone, which is a part of the stress-regulating hypothalamic-pituitary-adrenal axis which causes a chain reaction releasing adrenocorticotropin releasing hormone (ACTH) from the pituitary, which is regulated by corticotropin releasing factor (CRF) which comes from the paraventricular nucleus of the hypothalamus, which inhibits further production of CRF and ACTH. 23

The hippocampus contains glucocor-ticoid (GC) receptor sites, which create regulatory feedback to keep cortisol levels within an appropriate range, making the hippocampus vulnerable to the impact of stress. When the amygdala is constantly sounding the alarm and producing elevated levels of adrenaline due to fear conditioning, it also causes the release of elevated cortisol and GC.24

Elevated levels of stress can also affect long term potentiation, impeding the synchronized and repeated activation of two neurons which is required for learning, and may reduce the ability to form new memory traces.25

Animal studies have shown that exposure to GC causes loss of neurons in the hippocampus, and can decrease dendritic branching causing changes to the synaptic terminal structure and inhibit neuronal regeneration.26 27 28

Studies of patients with Cushing’s Disease, which causes excessive release of cortisol, have verbal declarative memory deficits, and show a loss of volume via MRI, indicating just how damaging prolonged periods of stress and the subsequent release of catecholamines can be to the hippocampus and memory functions.29

The inability of the hippocampus to regulate GC levels appropriately can lead to elevated levels of GC and can cause GC-mediated hippocampal toxicity which over prolonged periods can lead to a reduction in volume and eventually atrophy of the hippocampus.

Reduction of volume in adults has also been observed in patients who suffered severe abuse as children, as well as veterans of the Vietnam war who presented with PTSD.30

Summery

In summary, I agree with the distinction of PTSD being a memory disorder, as the regions of the brain affected play important roles in memory function. PTSD can be acquired not only via personally experienced traumatic events, but also via vicarious traumatization caused by viewing violent or traumatic events on social media which increases cortisol less due to the heightened stress caused by mortality salience affect, which is also brought into play when an individual experiences a sudden severe illness, such as heart attack, which may threaten their mortality.

PTSD can affect both declarative and non-declarative memory, and can also be identified via fMRI and MRI scan, which show differences in brain activity in the amygdala and prefrontal cortex, as well as changes in volume in the hippocampus. Elevated catecholamine levels which can be observed via urinalysis, to confirm prolonged exposure to stress via elevated levels of noradrenaline and cortisol hormone.31

These neurobiological findings point towards PTSD as a neurological deficit or impairment, which affects memory function.

References

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