The Neurobiology of Deliberate SelfInjury

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The Neurobiology of Deliberate Self-Injury

• Sarah Swannell BSocSc(Hons)Psych
• Senior Research Technician
• Discipline of Psychiatry
• The University of Queensland

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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

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Prevalence

• 60 of psychiatric patients
• 40 of high school students and university
  students

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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

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

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

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The 5 phases of self-injury

• Perception of threat ? unwanted negative emotion
  (desire to terminate it)
• Choice of coping technique
• Self-injury
• Unknown mechanism of action
• Objective and subjective tension relief

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PHASE 1. Perception of Threat

• Immediate reaction
• Sensory cortex ? amygdala ?hypothalamus
  ?pituitary gland ? adrenal gland
• Delayed reaction
• Sensory cortex ? amygdala ? prefrontal cortex
• ?
• Unwanted negative emotion

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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

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PHASE 2. Choice of coping technique

• Serotonin system
• Prefrontal cortex-limbic system connection
• Prior learning
• Beliefs

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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)

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• 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)

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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).

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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

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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

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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)

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• 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).

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PHASE 4. Unknown action
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(No Transcript)
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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)

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Implications for clinicians

• Something is going on in the brain when people
  self-injure
• Understand your clients
• Work within your clients limitations
• Improve resilience, coping skills
• Reduce stress