The Neurobiology The Neurobiology of Deliberate Self-of Deliberate Self-InjuryInjury

Sarah Swannell BSocSc(Hons)PsychSenior Research Technician

Discipline of PsychiatryThe University of Queensland

What is deliberate self-injury?

• Deliberate destruction or alteration of body tissue without suicidal intent (Favazza, 1989) & done to relieve an undesirable emotional or psychological state

• Low lethality & low intent to die • Repetitive • Borderline Personality Disorder• PTSD, depression, bi-polar disorder,

schizophrenia, antisocial personality disorder

Prevalence

• 60% of psychiatric patients

• 40% of high school students and university students

Why do people self-injure?

• to feel better–release tension

–stop dissociating–turning emotional pain into physical

pain which is easier to handle

–avoiding suicide

but how does self-injury make some people feel better?

• what happens in the brain when people self-injure?

The 5 phases of self-injury

1. Perception of threat unwanted negative emotion (desire to terminate it)

2. Choice of coping technique

3. Self-injury

4. Unknown mechanism of action

5. Objective and subjective tension relief

PHASE 1. Perception of ThreatImmediate reaction

Sensory cortex amygdala hypothalamus pituitary gland adrenal gland

Delayed reactionSensory cortex amygdala prefrontal cortex

Unwanted negative emotion

Vulnerabilities to experiencing unwanted negative emotion

• more intense negative emotions

• longer lasting negative emotions

• BPD & PTSD studies– the Hypothalamic-Pituitary-Adrenal Axis (HPA)

axis is more sensitive (Yehuda et al., 2001)– History of trauma

PHASE 2. Choice of coping technique

Serotonin system

Prefrontal cortex-limbic system connection

Prior learning

Beliefs

Serotonin System• Impulsivity & aggression

– Low levels of 5-HIAA in CSF of depressed suicide attempters (Asberg et al., 1976)

– Reduced levels of 5-HIAA in male borderlines (Brown et al., 1982)

– Low serotonin correlated with suicide attempts, assaultiveness, instability, aggression & impulsiveness (Coccaro et al., 1989; Markowitz et al., 1995)

– Self-mutilators had more personality pathology, greater lifetime aggression, more antisocial behaviour, and lower levels of serotonin activity (Simeon et al., 1992)

• Post-mortem studies of suicides found fewer presynaptic serotonin transporter sites in ventromedial prefrontal cortex, hypothalamus, occipital lobe, brainstem (Mann, 1998)

• Peer-reared monkeys have lower serotonergic activity in comparison to maternally raised monkeys (Higley et al., 1993)

• Adverse rearing sets serotonergic functioning at a lower level (Mann, 2003)

Prefrontal cortex-limbic system connection

• Emotion dysregulation via: dysfunctional transmission between prefrontal cortex and limbic system (amygdala/anterior cingulate are under inhibitory control of the prefrontal cortex)– dorsolateral prefrontal cortex (PFC) is implicated in

effortful regulation of affect – the orbitofrontal cortex, middle temporal gyrus,

cingulate cortex, and the caudate nucleus are implicated in the identification and production of affect (Ramel, 2005).

• The ventromedial prefrontal cortex has been widely implicated in impulse regulation (Potenza, Leung, Blumberg, Peterson, Fulbright, Lacadie, Skudlarski & Gore, 2003; Fukui, Murai, Fukuyama, Hayashi,& Hanakawa, 2005).

Prior Learning

• Observation, accident • Lack of physical pain

Beliefs • Action is needed to reduce unpleasant feelings• Self-injury is acceptable• My body and self is disgusting and deserving of

punishment• Overt action is needed to communicate feelings to

others• I must control my body and myself

PHASE 3. Self-injury• Noxious stimuli depolarize nociceptors & signals dorsal

root ganglia dorsal horns in spinal cord– a) projection neurons sensory info to brain– b) local excitatory & inhibitory interneurons to brain & regulate

flow of info to brain

• Noxious stimuli travel up the spinal cord via anterolateral pathways and transmitted contralaterally to the brain.

• Chemical signals arrive at thalamus, periaqueductal grey matter, primary sensory cortex and associated cortices, reticular formation, medulla, pons, midbrain, hypothalamus, and caudal anterior cingulate cortex (Ploghaus et al., 1999).

• normally this results in subjective pain

Endogenous opioid system

• Approx 60% feel no pain (Bohus et al., 2000; Russ et al., 1993)

• Abuse/neglect/trauma can alter EOS & reduce sensitivity to pain (Kirmayer et al., 1987; van der Kolk, 1989; Dubo et al., 1997; van der Kolk et al., 1991)

• Decrease in pain sensitivity following early traumatic experiences has been reported in both animal and human studies (Russ et al., 1993)

• In sample of BPD cutters, highest opioid levels correlated with recency and severity of cutting (Coid et al., 1983)

• Plasma opioid levels were higher in BPD patients who had SIB without pain compared to normals (Simeon et al., 2001).

PHASE 4. Unknown action

Noxious stimuli from tissue damage

Spinal cord

Sensory cortex

Limbic system (amygdala)

PHASE 5. Tension relief

• Objective (psychophysiological measures) & subjective tension relief (Haines et al., 1995; Brain et al., 1998)

– personalised imagery script – Finger pulse amplitude (FPA),

electrocardiograph (ECG), heart rate (HR), respiration (RESP)

– skin conductance level (SCL)

Implications for clinicians

• Something is going on in the brain when people self-injure

• Understand your clients

• Work within your client’s limitations

• Improve resilience, coping skills

• Reduce stress