lecture 21: Post-Traumatic Stress Disorder (PTSD)
Post-Traumatic Stress Disorder (PTSD)
Learning Objectives
Describe the acute stress response (SAM and HPA): Understanding the two systems activated during a stress response is crucial for recognizing how PTSD develops.
Discuss the negative consequences of chronic stress on brain structure: Chronic stress has significant impacts on brain regions important for emotional regulation.
List the primary symptoms required for a diagnosis of PTSD: Knowledge of symptoms aids in understanding the disorder.
Describe the process and neurobiology of extinction learning: Extinction learning is essential for understanding how fear responses can diminish over time.
Describe the 3 R’s of extinction memory: Exploring concepts related to fear and extinction memory can inform treatment approaches.
What are 3 ways extinguished fear can return? Recognizing triggers for the return of fear can help in therapy.
Draw parallels between fear memory and PTSD: Understanding the cognitive processes involved in PTSD through the lens of fear memory can enhance comprehension and intervention strategies.
Defining PTSD
PTSD as a Disorder: PTSD is categorized as a stress and learning disorder.
DSM-5 Classification: As per the Diagnostic and Statistical Manual of Mental Disorders, 5th edition (DSM-5), PTSD falls under the category of Trauma- and Stressor-related Disorders, which includes:
Post-Traumatic Stress Disorder (PTSD)
Acute Stress Disorder
Adjustment Disorders
Prolonged Grief Disorder
Traumatic Event Requirement: A qualifying event must have occurred for PTSD diagnosis, where symptoms notably affect memory.
Understanding Stress
Definition of Stress: Stress refers to any circumstance that disrupts the body's homeostatic balance, which may include:
Starvation
Fear
Severe insomnia
Social isolation
Parental neglect
Physical and emotional abuse
Exposure to toxins or microbial infections
Adaptive Responses: The brain develops systems to activate adaptive responses to stressors and ultimately restore homeostasis.
Acute Stress Response
SAM and HPA Systems:
Sympathetic-Adrenal-Medullary (SAM) System: Activates quickly.
Hypothalamic-Pituitary-Adrenal (HPA) Axis: Activates more slowly.
Amygdala's Role: It is a critical brain region in activating the stress response and managing emotional responses to fear-inducing stimuli.
Effects of Stress on Memory
Consolidation of Emotional Memories: Stress enhances memory consolidation regarding emotional events regardless of whether they are positive or negative.
Functions of the Amygdala:
Mobilizes the body's defensive systems in response to threat.
Contributes to fear learning.
HPA Axis: Plays a crucial role in stress regulation, and the hippocampus is vital for maintaining this regulation. A disrupted negative feedback loop in stress response is linked to neuropsychiatric disorders.
Chronic Stress and Its Consequences
Effects of Chronic Stress:
Chronic activation of the stress response leads to long-term physiological and psychological consequences.
Areas of the brain related to emotional regulation and recovery become altered due to elevated stress hormones.
Changes in Brain Structure:
Amygdala Neurons: Increase in size after prolonged stress (Vyas et al., 2002).
Prefrontal & Hippocampal Neurons: Shrinkage occurs with chronic stress (McEwen & Morrison, 2013).
PTSD Prevalence and Risk Factors
Prevalence of PTSD:
Approximately 8% of individuals will develop PTSD.
An estimated 30% of those who experience a traumatic event will develop PTSD:
This rate is about 30% among Vietnam veterans.
Ranges from 10% to 15% in Gulf War veterans.
Risk Factors: Factors that increase the likelihood of developing PTSD include:
Experiencing dangerous events and traumas, particularly repeatedly.
Suffering injuries or witnessing injury/death.
Childhood trauma exposure.
Feelings of horror or extreme fear.
Lack of social support post-event.
Experiencing additional stress after the event, such as the death of a loved one or job loss.
History of mental illness or substance abuse.
Diagnostic Criteria for PTSD (DSM-5)
Exposure to Trauma: Individuals must have experienced or been directly exposed to trauma.
Re-experiencing Symptoms: This includes:
Intrusive memories
Traumatic nightmares
Prolonged physiological responses to trauma reminders
Avoidance Symptoms: Behavioral avoidance related to reminders of trauma.
Negative Changes in Mood and Cognition:
Inability to recall important aspects of the trauma.
Persistent negative beliefs about oneself or the world (e.g., feelings of anger, guilt, alienation).
Depressive symptoms.
Changes in Arousal and Reactivity: Experiences may include hypervigilance, exaggerated startle response, sleep issues, difficulty concentrating, and irritability.
Insights from Fear Learning about PTSD
Fear Learning Mechanisms:
Includes classical conditioning: the pairing of an auditory conditioned stimulus (CS) with an unconditioned stimulus (UCS).
Contextual memory emphasizes the distinction between trauma (which is conditioned) and aversive scenarios (which are associated but not traumatic).
Persistent Memory Formation: Fear responses and avoidance behaviors can persist years after the original trauma, connecting back to the concepts of exaggerated fear response and poor control over fear.
Fear Extinction Process
Definition of Fear Extinction: Refers to the process of diminishing behavioral responses to threat-associated cues through repeated exposure without aversive stimuli (CS without UCS).
Competing Memories: Successful extinction creates new memories that compete with the original fear memory.
Return of Fear: The 3 R’s
Spontaneous Recovery: The re-emergence of fear after a period of time.
Renewal: The reinstatement of fear when the context changes from the extinction environment.
Reinstatement: The return of fear following reminders of the aversive experiences, such as a brief reminder of the trauma.
Neural Basis for Fear Extinction
Brain Regions Involved:
Prefrontal Cortex: Central to extinction learning, including top-down suppression of emotional reactions.
Hippocampus: Related to contextual learning, linked to the renewal of fear.
Amygdala: Involved in fear learning and extinction processes.
Characteristics of Extinction Memory
Extinction memory requires the prefrontal cortex for regulation and learning of context-specific responses.
Influence of Context: The conditions in which training occurs versus testing back might lead to differences in fear levels.
Broader Relevance of Extinction Learning
Extinction is not limited to fear: Associations can also be extinguished beyond just fear conditioning (CS-UCS to CS-no UCS).
Three R’s Applicability: Similar mechanisms apply across various forms of associative learning, leading to practical applications in drug addiction and other areas.
PTSD and Fear Memory Dynamics
Concerns about Control: Factors in PTSD share characteristics with fear memory behavior, showcasing poor control over fear as a common element.
Neurobiological Markers in PTSD
Prefrontal Cortex Activity: A decrease in activity has been observed in PTSD patients during tasks involving traumatic imagery (Arch Gen Psychiatry, 2004).
Amygdala and PFC Relationship: Evidence suggests disrupted interactions between the amygdala and prefrontal cortex.
Hippocampal Volume: Studies indicate reduced hippocampal volume may contribute to memory issues in PTSD, with genetic vulnerabilities further complicating these aspects.
Treatments for PTSD
Goal of Treatment: To mitigate arousal and stress-related symptoms.
Pharmacological Treatments:
Antidepressants such as SSRIs and SNRIs.
Psychotherapeutic Approaches:
Cognitive Behavioral Therapy (CBT) which includes:
Cognitive interventions challenging anxiety-inducing beliefs.
Behavioral components promoting exposure and extinction.
Challenges: Effective therapies must address the three R’s (spontaneous recovery, renewal, reinstatement) since extinction results in a new memory that co-exists with the original fear memory.
Future Directions of Research
Continued Investigation: There's a need for comprehensive research into complex PTSD formulations and the neurobiology underlying these experiences (Nees, Witt, & Flor, 2018).