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The Neurobiology of Deliberate Self-Injury

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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
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 Threat
            Immediate reaction
 Sensory cortex  amygdala hypothalamus
        pituitary gland  adrenal gland


             Delayed reaction
Sensory 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

				
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