Trauma and Related Disorders Quiz

Trauma and Related Disorders

• Trauma- and stressor-related disorders, as defined in DSM 5, are characterized by an explicit exposure to a traumatic or stressful event as the diagnostic criterion.

Introduction

• Post-traumatic stress disorder (PTSD) is a type of trauma-related disorder.

History of Post-Traumatic Stress Disorder (PTSD)

• Early recognition of PTSD-like symptoms included "soldier's heart" (American Civil War), "shell shock" (WWI), combat fatigue (WWII), and delayed stress (Vietnam War).
• PTSD was formally recognized as a distinct diagnostic entity in 1980 (DSM-III).
• Initially, the recognition of PTSD was met with hesitancy, but current understanding emphasizes the importance of biomarkers in diagnosis, and PTSD is now classified as an anxiety disorder.

Clinical Features of PTSD

• The core feature of PTSD is the development of characteristic symptoms following exposure to one or more traumatic events.
• Traumatic events can include war experiences (civilian or combatant), threatened or actual physical assault, and threatened or actual sexual violence.
• Clinical presentations of PTSD can vary from fear/anxiety to anhedonic/dysphoria, arousal/reactivity, or dissociative symptoms or a combination of these.

PTSD Diagnostic Features

• A. Confirmed experience of trauma: Exposure to actual or threatened death, serious injury, or sexual violence through direct experience, witnessing, or learning about it from a close friend or family member. In first responders, this can manifest as repeated or extreme exposure.
• B. Presence of intrusion symptoms: These persistent and reemerging symptoms include recurrent, involuntary, intrusive distressing memories or dreams; dissociative reactions (e.g., flashbacks); intense, prolonged psychological distress and physiologic response to trauma-related cues.

PTSD Diagnostic Features (2)

• C. Persistent avoidance of stimuli: Avoidance of trauma-related stimuli (people, places, conversations, activities, objects, situations, thoughts, or feelings).
• D. Negative alterations in cognitions and mood: Negative beliefs about self, expectations, and feelings of detachment from others, inability to remember key components of the traumatic event, etc.
• F. Marked alterations in arousal and reactivity: Increased irritability, angry outbursts, reckless/self-destructive behaviors, hypervigilance, exaggerated startle response, and sleep disturbances. These symptoms must have significantly impacted psychological well-being for at least 1 month.

PTSD Epidemiology

• The projected lifetime risk of PTSD in the US at age 75 is 8.7%.
• 12-month prevalence is approximately 3.5%.
• Canada's projected lifetime risk is 9.2%, while the current 1-month rate is 2.4% (2008).
• Females show higher rates of PTSD across the lifespan compared to males, often experiencing longer durations of the disease. This difference could be associated with greater trauma exposure, such as rape.
• PTSD is associated with a higher risk of suicidality.

What is the Neural Basis of PTSD?

• The fear circuitry involves the amygdala, medial prefrontal cortex (mPFC), and hippocampus/hypothalamus.

Fear Circuitry: Traumatic Events

• The amygdala becomes hyper-sensitive, and prefrontal cortex activity is reduced, leading to an ineffective inhibition of amygdala response.
• The impact of this is hypervigilance, intrusive symptoms, avoidance of trauma-related stimuli, and cognitive distortion.

Structural Anatomical Findings

• Reduced volume of hippocampus and ventral medial prefrontal cortex (vmPFC).
• This could be a result of pre-existing conditions.
• Hippocampal dysfunction impedes context-based safety cues.
• vmPFC fails to extinguish conditioned fearful responses.
• Reduced cortical capacity to control fear and negative emotions is observed.

Gene x Environment Interactions

• Risk for PTSD varies based on the interplay between genetic predisposition and environmental factors. Individuals with a genetic predisposition and significant trauma exposure are more susceptible to developing PTSD, whereas less vulnerable individuals may experience little to no impact.

Functional Anatomical Differences

• Exaggerated amygdala activation occurs in response to trauma-related and generic stimuli.
• Traumatic events can become unconditioned stimuli, leading to fear responses from exposure to associated stimuli (such as noises or scents).
• This heightened response is frequently paired with decreased mPFC activity.

Different Symptoms of PTSD Correlate with Distinct Circuits

• Symptoms and correlates, such as avoidance, cognition, mood disorders, arousal and stress, are associated with particular anatomical brain circuits.

Neurobiological Differences

• PTSD patients typically experience heightened stress responses in both the sympathetic (SAM) and hypothalamic-pituitary-adrenal (HPA) axes.
• Dysregulated adrenaline, noradrenaline, and cortisol levels are common.
• Elevated noradrenaline signaling is a potential marker for PTSD.

PTSD Pharmacological Treatment

• Propranolol, a beta-receptor antagonist, can be used to prevent noradrenaline binding. It appears to be effective in preventing the consolidation of traumatic memories within the first 20 hours following trauma. Timing is vital, as its efficacy is reduced when administered after memory formation.
• Though early data suggests efficacy, findings have been inconsistent and are actively being studied.

Treatment (2): PTSD and Cannabis Use

• Cannabis use is associated with a higher risk in PTSD patients.
• Reduced endocannabinoids and increased Cannabinoid Receptors in these individuals can suggest possible self-medication or dysregulation of the endocannabinoid system.
• However, smoking cannabis exacerbates rather than alleviates the affliction.
• Cannabidiol (CBD) may reduce some symptoms.
• Enhancing eCB activity offers promising treatment, possibly replacing cannabis use.