Etiology of Intermittent explosive disorder

Intermittent explosive disorder is associated with prefrontal cortex dysfunction, serotonin dysregulation, and early-life trauma.

  1. Brain Dysfunction & Aggression:
    The case of Phineas Gage highlights the role of the prefrontal cortex in impulse control and aggression.
    Studies show that frontal lobe damage, especially in the orbitofrontal region, is linked to increased aggression.
    fMRI studies in IED patients reveal abnormal activity in the dorsolateral prefrontal cortex, suggesting deficits in anger regulation.
  2. Serotonin & Impulsive Aggression:
    Reduced serotonin function is strongly linked to aggression in both animal and human studies.
    Lower levels of 5-HIAA (a serotonin metabolite) are associated with violent behavior and impulsivity, although some studies report mixed results.
    Tryptophan depletion studies show that reducing serotonin increases aggression in humans.
    Serotonin reuptake inhibitors (SSRIs) may help reduce impulsive aggression, but findings are inconsistent.
  3. Childhood Trauma & Environmental Factors:
    Childhood abuse, neglect, and exposure to violence significantly increase the risk of IED.
    Studies suggest a gene-environment interaction, where serotonin gene polymorphisms may increase vulnerability to impulsive aggression after early-life maltreatment.
    Interpersonal trauma in childhood is strongly associated with the development of IED

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