etiologies

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24 Terms

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Multiple Etiologies

Psychological disorders are caused by the interaction of various factors, including biological, cognitive, and sociocultural.

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Biological Etiology of PTSD

Focuses on brain abnormalities such as reduced hippocampal volume which is linked to PTSD symptoms.

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Hippocampus

A brain region implicated in PTSD, often showing reduced volume in individuals with the disorder.

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Ventromedial Prefrontal Cortex (vmPFC)

Brain area involved in emotion regulation, whose reduced activity is associated with PTSD.

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Amygdala

Brain region associated with fear responses, which can be affected by abnormalities in PTSD.

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Cognitive Appraisal

How individuals interpret traumatic experiences, influencing their emotional and psychological responses.

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Negative Cognitive Appraisals

Thought patterns that assess trauma and its effects pessimistically, linked to increased PTSD symptoms.

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Ehler and Clark's Cognitive Model of PTSD

Proposes that persistent PTSD results from negative appraisals combined with memory disturbances.

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Hitchcock et al. (2015) Study

Aim

To explore how survivors’ appraisals of their trauma (e.g., “I’m permanently damaged”) predict PTSD severity over time.

Methods

Participants: Assault survivors assessed 1 and 6 months post-trauma.
Measures: Self-report scales of negative appraisals, PTSD symptom checklists, and control for initial symptom levels.

Results

• Stronger negative appraisals at 1 month predicted higher PTSD symptoms at 6 months, even after controlling for initial symptom severity.

Conclusions

How people interpret their trauma—beyond the trauma itself—drives whether acute stress reactions evolve into chronic PTSD.

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Top-Down Processing

The brain mechanism where higher cognitive functions (like the vmPFC) regulate emotional responses.

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Socioeconomic Status (SES)

A significant sociocultural factor influencing PTSD risk; lower SES is correlated with increased vulnerability.

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Irish et al. (2011) Study

Aim (SOC)

To examine how gender and socioeconomic status (SES) jointly influence PTSD prevalence among motor-vehicle accident survivors.

Methods

Participants: 356 adult survivors of serious car crashes.
Design: Cross-sectional surveys assessed PTSD symptoms, demographic data (gender, income), and potential mediators (e.g., coping resources).

Results

• Women had about twice the PTSD rates of men.
• Lower-income survivors reported more severe PTSD symptoms.
• When controlling for SES, the gender gap narrowed—suggesting part of women’s higher risk stems from socioeconomic factors.

Conclusions

Both being female and having lower SES independently elevate PTSD risk; SES helps explain, but does not entirely account for, the gender difference.

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Garrison et al. (1995) Study

Aim (SOC)

To examine rates and correlates of posttraumatic stress disorder (PTSD) in adolescents exposed to Hurricane Andrew. PubMed

Methods

A random-digit-dial sample of 378 adolescent-parent pairs (158 Hispanic, 116 Black, 104 White) in high- and low-impact zones of Dade County, Florida, completed structured telephone interviews six months post-hurricane. Interviews assessed disaster experiences, emotional reactions, losses, lifetime trauma exposure, recent stressors, and psychiatric symptoms. PubMed

Results

PTSD prevalence: Only about 1 in 10 girls and 1 in 30 boys met full PTSD.

  • Nearly everyone had some stress: shaky nights, jumpy mornings, worries.

  • Kids dealing with loss—of home, school, or routine—struggled the most, even more than those who saw the worst of the storm itself.

Conclusions

While a relatively small percentage of adolescents developed full PTSD, most reported some posttraumatic symptoms. The findings highlight that post-disaster planning should address ongoing stressors (e.g., displacement, family upheaval) as key drivers of adolescent distress—often more so than direct disaster exposure.

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Correlational Studies

Research methods that examine relationships between variables, often used in PTSD research.

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Causation Limitations

Correlational studies cannot establish cause-and-effect relationships.

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Gilbertson et al. (2002) Study

Aim(BIO)

To determine whether smaller hippocampal volume is a pre-existing risk factor for PTSD, rather than a consequence of trauma exposure.

Methods

Participants: Vietnam-era monozygotic twin pairs (one combat-exposed twin, one non-exposed).
Design: MRI scans measured hippocampal volume in both exposed and unexposed twins; PTSD diagnosis was assessed via clinical interviews.

Results

• Combat-exposed twins with PTSD had significantly smaller hippocampi than exposed twins without PTSD.
• Crucially, their non-exposed co-twins also showed reduced hippocampal volume—despite never having trauma exposure.

Conclusions

Lower hippocampal volume appears to be a vulnerability marker for developing PTSD after trauma, not simply a result of it.

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Luby et al. (2013) Study

Aim(SOC)

To assess how childhood poverty and caregiving quality affect hippocampal development and later depression.

Methods

Participants: Socioeconomically diverse preschoolers followed longitudinally.
Assessments: MRI hippocampal volumes, observational measures of caregiver support, and later clinical interviews for depression.

Results

• Early caregiver support—but not poverty per se—predicted larger hippocampal volumes.
• Smaller hippocampi at school age were associated with higher depression rates in adolescence.

Conclusions

Supportive caregiving buffers the neurobiological impact of early stress; similar mechanisms may underlie resilience or vulnerability to PTSD after trauma.

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Survivor's Guilt

A negative cognitive appraisal where individuals feel guilt for surviving a traumatic event.

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Memory Disturbances

Cognitive deficits related to fear conditioning, significant in PTSD symptom maintenance.

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Urry et al. (2006) Study

Aim (COG/BIO)

To identify the neural mechanisms by which cognitive reappraisal reduces negative emotional responses.

Methods

Participants: Healthy adults in an fMRI scanner.
Procedure: Viewed aversive images under two conditions—“Attend” (just look) vs. “Reappraise” (reinterpret to feel less negative).

Results

• Reappraisal increased activation in prefrontal regions (dlPFC, vlPFC) and reduced amygdala response.
• Stronger PFC–amygdala coupling predicted greater success in down-regulating negative affect.

Conclusions

Top-down cognitive control networks can modulate emotion-generating circuits; deficits in this system may underlie vulnerability to PTSD.

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Cultural Beliefs in PTSD

Sociocultural factors like cultural beliefs can influence diagnosis and potential etiology of PTSD.

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Research Evaluation

Critical thinking involves identifying research limitations and considering alternative explanations.

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IB Psychology Paper 2 Structure

Include theory/etiology introduction, supporting studies, evaluations, and critical thinking.

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Vulnerability Marker

Indicates that certain biological characteristics, like reduced hippocampal volume, may increase PTSD risk.