Anti-Social Behaviour and Psychopathy

How do we define anti-social behaviours? - the paradoxical nature of humans

Humans and non-human animals display prosocial behaviours but humans harm eachother intentionally sometimes

• likely the same pathways for prosocial behaviours are important for anti-social behaviours - a lot of shared neural areas

  • e.g. understadning others to lie and manipulate

  • causing harm = prosocial if defending the vulnerable, antisocial if unwarranted aggression

the importance of non-cooperation / compliance

sometimes we need people who think slightly differently as cooperation and compliance can be maladaptive due to

• pluralistic ignorance

• collective attribution biases

• bystander effect

• diffusion of responsibility

• tyranny of the majority

DEFINITION of antisocial behaviours

antisocial behaviours: behaviours that often yield a net negative effect for members within a group or against another group through undertaking behaviours that harm, disrupt or violate social norms (e.g., moral codes and conventions), established rules or laws

• behaviours that are difficult to justify

• but this definition may be too general for when we want to think about how social and affective neuroscience understands what causes antisocial behaviours

  • need to look beyond behaviours and think about the underlying processes - defensive behaviours

what do we need to understand about anti-social behaviour? - defensive behaviours and aggression

antisocial behaviours can be understood as an extension of defensive behaviours

defensive behaviours: associated with affective states like aggression, anxiety and disgust

• aggression is more approach than avoidance

• research often uses aggression and anger as key ways to study anti-social behaviour

the same brain systems underlie:

• prosocial behaviours (altruism)

• anti-social behaviours

→ so anti-social behaviours are not modular, to understand antisocial behaviours we need to look at defensive behaviours more broadly

• functioning well = prosocial behaviours

• disruptions and dysregulation = antisocial behaviour

proactive vs reactive aggression - reactive

reactive aggression: emotionally-driven, impulsive response to a perceived threat, provocation, or frustration. It's the "hot" anger response

• defensive aggression

• more intense and emotionally arousing

• e.g., road rage

• tend to show hostile attribution bias - misread neutral social cues as threatening

cognition and body markers:

• unplanned and spontaneous

• considered angry aggressive behaviour

• shorter-term goals / rewards

• higher physiological arousal

• proximal threat-related defensive circuitary

proactive aggression

proactive aggression: considered, instrumental and premeditated aggression. It's used as a tool to obtain something (dominance, resources, compliance) without emotional provocation. It's "cold" and calculated

• offensive aggression - trying to harm someone

• less intense and emotionally arousing

• Proactive aggressors show intact (sometimes superior) social cognition but use it instrumentally — they understand others' emotions well enough to exploit them

• e.g., emotional manipulation

cognition and body markers:

• deliberate and planned

• cognitive preparation (hiding intentions)

• longer term rewards / goals

• lower physiological arousal

• reduced cortisol levels and smaller amygdala volume

reactive and proactive aggression can occur within the same event - its adaptive, flexible and can be controlled

evolution of aggression

RA more readily observable across many species

• given there are fewer animals with PA, this could suggest PA evolved after RA

Wrangham’s theory proposes reactive aggression evolved first “as it is the one that is widespread across species,” then human self‑domestication occurred (reduction of reactive aggression and high proactive aggression over the last 300,000 years)

• humans show unusually low reactive aggression but high proactive aggression, especially in coalitionary violence, relative to other primates

primate aggression-type ratios

Core idea:

a way to understand the context in which anti-social behaviours arise is to look at the types of aggression in primates

Primates differ in their balance of:

• Reactive aggression (RA) = impulsive, defensive (“threat response”)

• Proactive aggression (PA) = planned, deliberate (“goal-directed”)

Species differences:

• Chimpanzees

  • Very high RA

  • Very high PA

• Bonobos

  • Intermediate RA

  • Low PA

  • → Slightly closer to humans overall

• Humans

  • Very low RA

  • Very high PA

  • → More planning and control

Key insight:

• Humans are less reactive but more strategic

• This suggests:

  • We share similar basic brain systems with other primates

  • BUT these systems are regulated differently by context

Why this matters:

• The RA : PA ratio helps explain anti-social behaviour

• To understand and predict behaviour, we must consider:

  • Type of aggression

  • Context!

  • Level of regulation (control vs impulse) - humans have strong regulatory capacity (larger PFC) but regulation ability is not fixed

social regulation and antisocial behaviours

Humans show greater control over arousal and aggression, shaping how anti-social behaviour is expressed.

Key points:

• Humans have:

  • Lower reactive (impulsive) aggression

  • Higher proactive (planned) aggression
    → Behaviour is more controlled and deliberate

• Raw emotions (e.g. aggression) are:

  • Filtered and regulated before action

Role of social complexity:

• Humans live in highly complex social systems

• Behaviour depends on understanding:

  • Social rules

  • Norms

  • Context

• Individuals with delayed social development:

  • Struggle to understand these rules

  • → More likely to show anti-social behaviour

Evolutionary insight:

• Human brains have evolved to:

  • Be more socially driven

  • Rely more on planning and control (PA)

• Anti-social behaviour is therefore:

  • More considered

  • Shaped by context and social pressures

Key takeaway:
Anti-social behaviour in humans reflects controlled, context-dependent aggression, shaped by our complex social world

why does socical regulation differ cross species?

humans have bigger PFC and increased frontal lobe connections compared to non-human primates (Barrett et al, 2020)

• larger PFC volume may explain why we express anti-social behaviours in more proactive forms of aggression

  • reason: PFC linked to executive functioning (higher order processes that enable individuals to control psychological processes and behaviours to achieve goals)

  • e.g., inhibition, updating and shifting focus (part of the frontoparietal network)

Larger PFC volume → stronger executive control → ability to suppress reactive impulses and plan deliberate actions → aggression becomes proactive rather than reactive

the importance of the PFC and brain networks

the PFC is connected to other regions to support executive functioning so human anti-social behaviour cannot be reduced to a single brain region → it emerges from atypical connectivity and disrupted feedback loops shaping how context is processed and behaviour is regulated

core idea:

• it’s not just about size, it’s about the connectivity

• humans have more connectivity than non-human primates which may explain why human antisocial behaviour tends to be more planned and context-sensitive

• critical to remember the feedback loops which helps us learn new things and update information - links to predictive coding and reinforcement learning

PFC → Amygdala	Controls/dampens emotional/threat responses
Amygdala → PFC	Flags emotional significance of a situation
Memory regions → PFC	Informs decisions with past experience
PFC → Action	Produces regulated, goal-directed behaviour

why is the PFC so important to understanding antisocial behaviour? - functional connectivity

Core idea:
Optimal functioning requires flexibility—the ability to switch between brain networks

Key networks:

• DMN (default mode network) → self-related thinking (internal focus)

• FPN (frontoparietal network) → cognitive control (external tasks)

• SN (salience network) → switches between DMN & FPN

Why switching matters:

• Helps cope with ever-changing environmental demands

• Allows appropriate responses to:

  • internal thoughts

  • external tasks

When connectivity is LOW:

• Reduced flexibility in switching

• Linked to:

  • Mood disorders (depression, anxiety)

  • Developmental & learning difficulties

  • Learning disabilities

Key takeaway:
Healthy brain function = flexible switching between networks
Poor connectivity = rigid, less adaptive behaviour

how does the brain ensure efficient functioning? (this is some random information i fear)

Mohr et al (2016)

Core idea:
The brain balances integration (communication) and segregation (specialisation) for efficient functioning

Integration (early learning):

• High communication between regions

• High FPN activity (focus, control)

• Used when tasks are new or difficult

Segregation (late learning):

• Regions become more independent

• Reduced FPN activity but enhanced communication between cingulo-opercular network (CON) and dorsal attention network (DAN)

• Tasks become automatic → less attention needed

• Helps save energy

Connectivity is flexible:

• Changes depending on task demands

Key takeaway:
Early learning = high effort + integration
Skilled performance = low effort + segregation

atypical PFC activity

violent offenders struggle with emotion regulation

• emotional dysregulation

• aggression

• impulsiveness

• risky behaviours

why?- my research on the forensic application

forensic populations (e.g. individuals with psychopathy, persistent violent offenders) serve as examples of atypical feedback loops — where the usual PFC ↔ Amygdala communication is disrupted, reducing emotional learning and impulse regulation

example:

• In prisoners, weaker vmPFC–striatal (NAcc) connectivity disrupts regulation of reward signals, relates to impulsive, short‑term choices, and predicts more criminal convictions (Penagos-Corzo et al, 2022)

• the disrupted feedback loop undermines fear‑based learning, empathy, moral evaluation, and control of emotional actions, providing a mechanistic account of persistent violent and antisocial behaviour in these populations.

Loop element	Typical function	Disruption in forensic psychopathy
Amygdala → vmPFC	Convey emotional value of outcomes	Impaired stimulus–reinforcement learning, reduced fear conditioning and emotional responses
vmPFC → Amygdala	Regulate emotional reactivity, guide choices	Reduced functional connectivity; weaker top‑down control
PFC control of action	Inhibit maladaptive emotional actions	Less anterior PFC activity and PFC–amygdala coupling during tasks requiring control of emotional actions in psychopathic offenders

study to show PFC irregularities in violent offenders

da Cunha-bang et al (2017)

• violent and non-violent male offenders

• had to keep pressing a button and after a certain amount of times there was money, every few seconds another opponent (computerised) would steal points and the participant was given different options

  • ignore

  • retaliate (steal points)

  • protect (protect points for a breif period of time)

findings:

Violent offenders – saw different levels of connectivity

• Reduced connectivity between A and PFC and S-PFC in violent offenders → increased amygdala and striatal activity

• Issues in regulating anger

• Reduced activity from PFC but hypoeractive A and S suggests there is less top-down control, feeling anger way more intense

another study on emotion regulation in violent offenders

Siep et al (2019)

Violent offenders show poor emotion regulation due to abnormal PFC–amygdala interaction

Study setup:

• 25 violent offenders (high reactive aggression)

• 24 controls

• Emotions induced using stories (anger, happy, neutral)

Medial PFC (control/regulation):

• Controls:

  • Before → low activity

  • After emotion → increased activity
    → PFC engages to regulate emotion

• Violent offenders:

  • Before → already high (baseline overactive)

  • After emotion → activity decreases
    → fails to regulate, becomes dysregulated

Amygdala (emotional reactivity):

• Controls:

  • Before → high activity

  • After emotion → decreases
    → PFC successfully downregulates emotion

• Violent offenders:

  • After emotion → amygdala increases
    → Emotion escalates instead of being controlled

Key takeaway:

Controls:
PFC ↑ → Amygdala ↓ → regulated emotion

Violent offenders:
PFC ↓ (when needed) → Amygdala ↑ → loss of control

but are the brains of people who commit murder-based violence different from non-murder-based violence?

criminal aggression is not alway the same

• non-violent crime → fraud, hacking

• violent crime → robbery, murder and manslaughter

Sajous-Turner et al (2020) → looked at whether there were grey matter volume differences between murderers and non-murderers

Key finding about homicide offenders’ brains

• Homicide offenders showed widespread reductions in gray matter compared with all non‑homicide offenders (both violent and non‑violent)

Which brain regions had reduced gray matter in homicide offenders?
(all reduced vs non‑homicide offenders):

• Prefrontal regions: ventromedial/orbitofrontal, dorsolateral, ventrolateral, dorsomedial prefrontal cortex

• Cingulate regions: dorsal anterior, mid‑cingulate, posterior cingulate/precuneus

• Temporal regions: anterior temporal cortex

• Insula and cerebellum, plus superior parietal areas

these functions are linked to emotional processing, behavioural control, executive function, social cognition (empathy, theory of mind), moral decision‑making, and regulation of one’s own emotions

summary: among incarcerated men, those who committed homicide can be reliably distinguished by more extensive gray matter deficits in control and social‑emotional brain networks than other serious violent or non‑violent offenders, though this does not mean brain scans can identify individual murderers or predict homicide

TBI evidence

• greater proportion of individuals with TBI in prison populations versus in the general population

• vulnerable brain regions affected by TBI include, frontal lobe, basal ganglia and temporal lobes

• personality changes (and mental health issues) are often observed in those who have with TBI, including chronic aggressive behaviours

Why do we find higher rates of TBI is prison populations?

• 40-60% of prisoners have TBI, compared to the 8-15% in general population

• TBI can cause impulsivity, aggression, poor judgment, and cognitive deficits, which are linked to violence, offending, and earlier entry into the justice system

  • however, may be bidirectional as behaviour that leads to crime may increase risk of getting injured

criminal responsibility and the brain

Core question:

• Did the person have control and intent during the crime?

Factors that can reduce responsibility:

• Genetics (e.g. MAOA, serotonin)

• Trauma (affecting brain function)

• Temporary impairment (e.g. drugs, illness)

• Mental health / intellectual disability

• Brain abnormalities (emotion or control systems)

Why it matters:
Reduced capacity = may influence jury decisions & sentencing

Using Neuroscience in Law (Caution)

Core idea:
Be careful using brain data in legal decisions

Why?

• Behaviour is multifactorial (not just the brain)

• Brain measures are not fully reliable yet

• Have limitations (timing + location of brain activity)

• Especially risky in serious cases (e.g. death penalty)

• need more reliable and robust biomarkers

One-line takeaway:

Brain factors can influence behaviour, but don’t fully determine responsibility - could use PFC to explain criminal behaviour but would have to be careful not to be reductionist

PSYCHOPATHY - associated behaviours and definition

psychopathy: personality trait characterised by atypical affective and social processing patterns that may increase the likelihood of antisocial or risk-taking behaviours. These patterns are often linked to persistent difficulties in empathising with others, alongside traits such as callousness, impulsivity, egocentricity, and boldness

• there are many theories about why it arises and need to think about it from a fear not aggression standpoint

associated behaviours:

• low empathy

• high attention seeking behaviour

• callousness

• greater recidivism rates

psychopathy theoretical approaches

1. low fear

2. executive dysregulation

3. low empathy

the low fear hypothesis - do elevated levels of psychopathy primarily reflect a reduction in fear?