PTSD flashcards

Serotonin

A neurotransmitter that regulates mood, anxiety and stress responses; lower serotonin is associated with PTSD vulnerability.

Neurotransmission and SSRIs

Serotonin is released into the synapse, binds to receptors and is normally reabsorbed; SSRIs block reuptake, leaving serotonin in the synaptic gap longer.

SSRIs

Selective serotonin reuptake inhibitors block serotonin reuptake, increasing serotonin availability and helping reduce PTSD symptoms such as hypervigilance and fear responses.

Biological reductionism

Breaking PTSD into simpler biological components such as neurotransmitters or genes; useful for isolating variables and targeted treatment but risks oversimplifying a complex disorder.

Why can reductionism be a problem in PTSD?

PTSD is also influenced by trauma severity, coping, cognition, individual differences and sociocultural factors, which cannot be fully explained by serotonin alone.

Genetic inheritance

Genetic factors contribute to PTSD vulnerability, but PTSD is not simply inherited; environmental trauma and gene

Gene-environment interaction

Genetic vulnerability can interact with environmental stress, meaning the same trauma may produce different outcomes in different individuals.

Working Memory Model

Baddeley and Hitch’s model contains the central executive, phonological loop, visuospatial sketchpad and episodic buffer.

Central executive

Controls and allocates limited attentional resources within working memory.

PTSD and working memory

Trauma-related thoughts can consume limited working-memory resources, especially executive attention, contributing to intrusive memories and cognitive impairment.

Individualism

A cultural orientation emphasising personal autonomy, self-expression and the individual.

Collectivism

A cultural orientation emphasising social cohesion, interdependence, family/community support and group harmony.

Individualism vs Collectivism and PTSD

Individualistic cultures may encourage direct emotional disclosure and professional treatment, whereas collectivist cultures may favour collective processing and community support.

Uncertainty Avoidance

High-UA cultures emphasise structure, predictability and control; low-UA cultures emphasise flexibility, adaptability and tolerance of ambiguity.

High Uncertainty Avoidance and PTSD

Greater intolerance of uncertainty may increase distress when trauma disrupts predictability and control.

Alternative explanations for PTSD prevalence across cultures

Observed differences may reflect genuine differences but also stigma, help-seeking, social support, healthcare access, diagnostic practices and measurement bias.

Cultural bias in PTSD diagnosis

Western diagnostic frameworks may not fully capture culturally specific ways of experiencing or expressing distress.

Classical conditioning in PTSD

Trauma acts as the UCS, fear is the UCR, and previously neutral trauma-linked cues can become CSs that later trigger CRs of fear.

UCS in PTSD

The traumatic event that naturally produces fear.

UCR in PTSD

The natural fear response produced by the traumatic event.

CS in PTSD

A previously neutral cue associated with the trauma that later triggers fear.

CR in PTSD

The learned fear response triggered by the conditioned cue.

Extinction

Repeated exposure to a feared stimulus without the traumatic outcome weakens the conditioned fear response.

Counterconditioning

Pairing a feared stimulus with a new incompatible response, such as relaxation, so fear is replaced by a calmer response.

Operant conditioning in PTSD

Avoidance produces immediate relief, negatively reinforcing avoidance and making the avoidance behaviour more likely.

Negative reinforcement in PTSD

A behaviour increases because it removes an unpleasant experience, such as anxiety after avoiding a feared situation.

Why can avoidance maintain PTSD?

Immediate relief reinforces avoidance, preventing corrective experiences and maintaining the fear response.

Flooding

Prolonged or intense exposure to the feared stimulus, aiming to weaken conditioned fear through extinction.

Systematic desensitisation

Gradual exposure to feared situations while using relaxation, relying on counterconditioning.

Triangulation

Combining self-report, clinician assessment and biological/physiological evidence to obtain a more comprehensive measurement of PTSD.

Responsibility in animal research

Researchers must balance potential scientific/human benefits against animal suffering and minimise unnecessary harm.

Value of animal research

Animal models allow controlled manipulation of biological and environmental variables and testing of mechanisms or treatments that may be unethical or impossible in humans.

Limitation of animal research

Animal models cannot fully reproduce human cognition, emotion, trauma meaning and sociocultural context, limiting generalisation.

Duncan et al. (2017)

GWAS of ~20,000 people found that common genetic differences explained about 29% of PTSD risk in European-American women, but not clearly in men. Shows that genetic vulnerability to PTSD may vary by sex and ancestry.

True et al. (1993)

Among 4,042 male Vietnam-era twin pairs, genetic factors accounted for approximately 30% of the variance in PTSD risk; monozygotic twins had higher concordance. The sample limits generalisation.

Binder et al. (2008)

FKBP5 genetic variants interacted with childhood-abuse severity in predicting adult PTSD symptoms, supporting the diathesis-stress model.

Schweizer & Dalgleish (2011)

People with PTSD showed poorer recall of neutral words while processing trauma-related material, supporting working-memory interference from trauma-related processing.

Yeomans et al. (2010)

Trauma was more likely to be processed collectively in collectivist cultures, while Western psychological interventions could sometimes reinforce the expectation that trauma is debilitating.

Duckers et al. (2016)

Compared PTSD prevalence across cultures and found lower PTSD prevalence in collectivist cultures, possibly because stronger social-support networks help people manage trauma. Shows that culture and social support may influence PTSD prevalence.

Oglesby et al. (2017)

Intolerance of uncertainty was significantly associated with increased post-traumatic stress symptoms (PTSS), supporting the Uncertainty Avoidance explanation.

Davidson et al. (2001)

In 96 PTSD patients treated for 28 weeks, relapse was 5% with sertraline compared with 26% with placebo, supporting SSRI effectiveness.

Sengupta et al. (2017)

Rodent research showed that pharmacologically increasing serotonin reduced fear responses, supporting serotonin’s role in fear learning and the biological basis of PTSD, although animal findings have limited generalisability.

Homberg & Lesch (2011)

Serotonin-transporter/genetic variation was linked to PTSD susceptibility. In rodents, serotonin-transporter deficiencies were associated with exaggerated stress responses and increased anxiety-like behaviour, particularly after early-life stress.

Boudewyns & Hyer (1990)

Flooding/implosive therapy reduced PTSD symptoms in Vietnam veterans, although some participants experienced heightened distress before improvement.