Intermittent explosive disorder (IED) is regarded as a subtype of impulse control disorder characterized by impulsive, uncontrollable explosive outbursts of anger, aggression, and/or rage – sometimes accompanied by violence. To be considered intermittent explosive disorder, the explosive outbursts of anger must be triggered in situations and/or conditions in which such anger is unjustified. In other words, someone who explodes with anger after discovering that his/her wife was unfaithful – would not be considered to have intermittent explosive disorder.
Why? Because impulsive anger would be considered a normative, justified response in such a situation. As another hypothetical scenario, let’s consider someone who loses in a friendly pick-up game of basketball and lashes out with anger towards his/her teammates and/or opponents following the loss. In this case, intermittent explosive disorder may be the culprit for the outburst, but we cannot be absolutely certain based on a standalone occurrence.
Lashing out with anger after losing a pick-up game of basketball is usually unjustified, but it may have only occurred because the person was having a highly-stressful day – and the culmination of high-stress along with losing the game caused them reach the pinnacle level of stress they could tolerate, ultimately leading them to “snap.” Assuming this only occurs once, and the person doesn’t exhibit any further explosive episodes in the future – it’s not intermittent explosive disorder.
However, in the event that an individual always exploded with anger after a friendly pick-up game of basketball, as well as in other situations in which anger wasn’t justified, he/she may warrant evaluation for intermittent explosive disorder.
Intermittent Explosive Disorder (Diagnostic Criteria)
In the early editions of the DSM (Diagnostic and Statistical Manual of Mental Disorders), there was no formal diagnosis for “intermittent explosive disorder.” In the DSM-I, there was a disorder referred to as “passive-aggressive personality type” which was characterized as being: “over-responsive to environmental pressures” with “gross outbursts of rage or aggressiveness.” While this is similar to intermittent explosive disorder, the name passive-aggressive personality type is misleading.
Upon introduction of the DSM-III, psychologists introduced the specific diagnosis of “intermittent explosive disorder,” placing it under Axis I. Slight modifications were made to the IED classification in the DSM-IV, but many experts remained dissatisfied with its diagnostic criteria. Particularly, researchers disliked the fact that aggressive acts needed to be impulsive and distress was required to provoke the angry outbursts.
The DSM-5 classifies “intermittent explosive disorder” under the category of “Disruptive, Impulse Control, and Conduct Disorders.” When compared to the DSM-IV, the DSM-5 does not require the occurrence of “physical aggression” to meet diagnostic criteria for IED. The DSM-5 diagnostic criteria for IEDs is outlined below:
Criterion A: Recurrent impulsive outbursts characterized by either of the following…
- (Criterion A1): Verbal or physical aggression occurring at least 2 times per week for at least 3 months that does not lead to destruction of property nor infliction of physical harm. In other words, the aftermath of IEDs under the A1 subtype aren’t associated with physical nor material damages. Examples of A1 diagnoses would include: verbal arguments, tirades, and/or verbal assaults. Many individuals that fit A1 diagnostic criteria exhibit frequent, yet lower intensity outbursts (compared to A2).
- (Criterion A2): 3 or more outbursts involving injury or destruction within a 1-year term. Those that fit the A2 criterion tend to exhibit less frequent, but significantly more destructive outbursts than those fitting A1 criterion. Individuals with the A2 subtype tend to damage more property and/or inflict injury upon other people and/or animals. However, the frequency of the outbursts may only be a few times per year – compared to 2 times per week (as seen among those with A1 subtypes).
Criterion B: Aggressive behavior is grossly disproportionate to the magnitude of the psychosocial stressors. In other words, the aggression exhibited by the person isn’t justified in regards to their situational circumstances.
Criterion C: Outbursts are not premeditated and do not serve a premeditated purpose. In other words, someone with IED isn’t consciously planning their aggressive outburst towards someone else, it just happens impulsively or unconsciously akin to a “knee-jerk” reaction.
Criterion D: Outbursts cause distress or functional impairment, leading to deleterious financial, legal, and/or social ramifications. There are usually unwanted consequences for such unpredictable outbursts of anger and/or aggression. Examples of consequences include: relationship troubles (e.g. divorce), friendship losses, fines, and possible jail time (in the event that you inflict damage upon another person or property).
Criterion E: An individual must be at least 6 years of age. Someone under the age of 6 cannot be diagnosed with IED in part because angry outbursts are fairly common among children.
Criterion F: Recurrent explosive outbursts cannot be attributed to another neuropsychiatric disorder, medical condition, nor substance abuse. For example, an individual couldn’t be diagnosed with IED if he/she exhibited recurrent outbursts of anger as a result of cocaine abuse.
More specifics about IED…
Among those that fit diagnostic criteria for intermittent explosive disorder (IED), explosive outbursts occur unpredictably, with no forewarning. In most cases, each episode lasts less than 30 minutes in duration. It should also be noted that some individuals may exhibit a mix of A1 and A2 criteria and/or tendencies in that they may have infrequent, highly intense outbursts followed by frequent, lower intensity outbursts.
Self-reports collected from those with IEDs document outbursts as lasting less than an hour (on average). Outbursts are commonly accompanied by physical symptoms such as: chest tightness, heart palpitations, sweating, stuttering, and twitching. Additionally, those who act impulsively with anger tend to derive some immediate relief from their outbursts, but upon later reflection, feelings of remorse and/or guilt may emerge.
Many individuals with intermittent explosive disorder experience chronic anger, irritability, aggression, and impulsivity. Furthermore, it is often difficult to diagnose IEDs due to the fact that it is often presented with another distinct psychiatric disorder (e.g. ADHD, bipolar disorder, etc.). Diagnostic “Criterion F” explicitly states that symptoms of an IED cannot be explained by another mental disorder.
This does not mean that a person cannot be diagnosed with a condition such as bipolar disorder AND intermittent explosive disorder. Assuming the bipolar disorder is treated properly, yet criteria for an IED remains, it is possible that both could be diagnosed. Of course, to diagnose an IED after an initial diagnosis (e.g. bipolar disorder) would involve critical analysis by a skilled psychiatrist to make the distinction of two separate, yet simultaneously occurring conditions.
What causes intermittent explosive disorder?
Researchers haven’t been able to pinpoint the exact causes of intermittent explosive disorder. It is likely that in any particular individual diagnosed with the condition, numerous factors may play a role. Understand that an intermittent explosive disorder in one individual may be caused by a different unique blend of factors compared to another.
For example, one person may have severe intermittent explosive disorder as a result of his/her genetics, epigenetics, and environment. Another person may have intermittent explosive disorder as a result of lifelong substance abuse that altered his/her neurochemistry. Though the symptoms are similar, the exact cause(s) may not be the same for everyone diagnosed.
Environment: It is understood that a person’s environment can affect gene expression (via epigenetics), but it can alter brain activation and neurochemistry. Someone living in an impoverished environment may exhibit suboptimal brain development, altered densities of neurochemicals, and entirely different brain activation – than someone in an enriched environment. Those who are in poorer environments characterized by: violent crime, neurotoxins, fewer opportunities, and financial scarcity – may be at greater risk for intermittent explosive disorders.
- Childhood trauma: Any individuals that were traumatized by childhood experiences are more likely to develop intermittent explosive disorder. It could be that development of an IED is a survival mechanism or coping strategy that emerged from the trauma. Additionally, trauma tends to rewire the brain and alter developmental processes – perhaps short-circuiting optimal development of the prefrontal cortex to regulate limbic impulses.
- Familial separation: Research in groups of refugees suggest that separation and displacement of families may provoke intermittent explosive disorder. The psychological toll associated with familial separation is significant, likely manifesting in the form of anger and/or aggression.
- Ongoing stress: Another environmental factor that was shown to increase likelihood of intermittent explosive disorder is ongoing or chronic stress. If you’re in a highly stressful environment to the extent that you’re never able to relax or feel safe, intermittent explosive disorder is more likely to develop.
- Parental bonding: Research has shown a link between parental bonding and development of intermittent explosive disorder. Particularly, individuals who don’t receive proper parental care or form bonds with their parents tend to be at greatest risk for IEDs. In general, the lower the scores of bonding as measured by the Parental Bonding Inventory (PBI), the greater the likelihood that a child is to develop an intermittent explosive disorder.
- Poverty: Individuals living in extreme poverty are also more likely to develop intermittent explosive tendencies. This could be due to injustices associated with poverty in certain countries, poorer living conditions, and/or stress associated with low socioeconomic status.
- Violent behaviors: Children who are exposed to violent behaviors in their environment are more susceptible to develop intermittent explosive disorders. This could be due to a combination of acting similarly to the aggression frequently observed in the immediate environment. However, it could also be due to epigenetic, neurochemical, and changes that occur in the brain upon witnessing such environmental violence. Perhaps in this case, intermittent explosive anger is a stable coping strategy in response to a particular environment.
- Source: http://www.ncbi.nlm.nih.gov/pubmed/25064384
- Source: http://www.ncbi.nlm.nih.gov/pubmed/25754605
- Source: http://www.ncbi.nlm.nih.gov/pubmed/23950885
Genetics / Epigenetics: Your genetics are thought to play a role in determining your susceptibility to develop intermittent explosive disorder. If a family member has been diagnosed with intermittent explosive disorder (or an impulse control disorder), you may be at greater risk. There is likely a particular gene or polymorphism, that when inherited, could make you more prone to impulsive anger and/or aggressive behaviors.
Also consider that epigenetic changes such as those induced by your environment and experiences (of both you and your parents) may alter gene expression in such a way as to increase susceptibility to IED. Research has shown that abnormal copy number variants (CNVs) of genes may be associated with intermittent explosive disorder. Specifically, those with IEDs may have novel deletions of MBPs (myelin basic proteins) on certain chromosomes.
- Source: http://www.ncbi.nlm.nih.gov/pubmed/20488459
- Source: http://www.ncbi.nlm.nih.gov/pubmed/21812102
Neurochemistry: Extracellular concentrations of neurotransmitters such as serotonin, dopamine, and norepinephrine – as well as densities of receptors – may increase (or decrease) susceptibility to developing intermittent explosive disorder. Specifically, it is hypothesized that individuals with IED may exhibit deficits in serotonin and/or dopamine. Abnormalities in concentrations of norepinephrine, as well as various hormones such as cortisol may also be evident.
Serotonin: Many speculate that low serotonin in the synaptic cleft may be associated with development of impulse control disorders. Serotonin is understood to promote feelings of calmness and improves mood (among those with depression). A study published in 1993 discovered that individuals with fewer 5-HIAA metabolites were more likely to act impulsively aggressive under the influence of alcohol.
Later research would discover that among individuals with intermittent explosive disorder (specifically), there’s fewer 5-HT transporter binding sites compared to those without IED. Additional evidence suggests that 5-HT2A receptors are more abundant in the orbitofrontal cortex (OFC) of persons with impulsive aggression; perhaps another critical neurochemical biomarker of the disorder.
- Source: http://www.ncbi.nlm.nih.gov/pubmed/19767013
- Source: http://www.ncbi.nlm.nih.gov/pubmed/20434136
- Source: http://www.ncbi.nlm.nih.gov/pubmed/8410958
Dopamine: The role of dopamine in the development of intermittent explosive disorder is unclear. Many individuals with IED are thought to exhibit abnormally low dopamine production, perhaps increasing likelihood of impulsivity. Research has shown that abnormally low availability of D2 receptors is associated with impulsivity – particularly in the ventral striatum region.
Evidence indicates that dopamine has been implicated in the behavior of aggression. Among depressed patients, those with fewer D1 receptors are more likely to experience “anger attacks.” That said, dopaminergic dysfunction may not always be the direct culprit for the anger, but abnormal dopamine concentrations or density of a particular receptor subtype – may increase impulsivity, thereby leading to an unpredictable “explosion” of anger.
- Source: http://www.ncbi.nlm.nih.gov/pubmed/18346997
Norepinephrine: Heightened concentrations of norepinephrine is associated with outwardly directed aggression. Studies of depressed patients indicate that those with high noradrenergic activity are more likely to act aggressively than those with low noradrenergic activity. Since norepinephrine production is closely tied with activation of the sympathetic nervous system (“freeze-fight-flight” response) – it may be that individuals with IEDs are more prone to experiencing a fight-flight response that triggers their impulsive, unconscious expression of anger.
There is often an inverse relationship of norepinephrine concentrations and those of serotonin. For this reason, it would make sense that an individual with IED may have high circulating norepinephrine and deficits in serotonin levels. The norepinephrine makes the individual hypersensitive and/or hyper-reactive to environmental stimuli without calming intervention via serotonin.
- Source: http://www.ncbi.nlm.nih.gov/pubmed/18346997
Acetylcholine: Some evidence indicates that abnormal transmission of acetylcholine may lead to dysphoria and/or irritability, which may lead to aggressive behaviors. Administration of the chemical physostigmine, an acetylcholinesterase inhibitor (blocker of the enzymatic metabolism of acetylcholine), increases depression scores among those with underlying neuropsychiatric disorders. The increased depressive mood, accompanied by emotional instability could contribute to the onset of IED in certain cases.
- Source: http://www.ncbi.nlm.nih.gov/pubmed/18346997
GABA / Glutamate: GABA (gamma-aminobutyric-acid) and glutamate are understood to be inhibitory and excitatory neurotransmitters, respectively. Individuals with sufficient concentrations of GABA are thought to be calmer and less anxious than those with insufficient GABA. This may be due to the fact that they are less reactive to unpleasant stimuli as a result of increased internal calmness.
Administration of drugs that increase concentrations of GABA in the synaptic cleft such as Tiagabine are understood to decrease aggression. On the other hand, individuals with low activity at GABA receptor sites tend to experience heightened aggression. Assuming the GABA receptors remain understimulated, an individual may exhibit heightened reactivity to unpleasant stimuli – possibly causing intermittent explosive disorder.
When glutamate concentrations are high, individuals also tend to behave aggressively. This is perhaps best evidenced by research among humans noting that cerebrospinal fluid concentrations of glutamate directly correlate with simultaneous aggression and impulsivity. In other words, those who are both aggressive and impulsive tend to have higher-than-average peripheral glutamic acid; possibly an important biomarker to examine among those with IEDs.
- Source: http://www.ncbi.nlm.nih.gov/pubmed/18346997
- Source: http://www.ncbi.nlm.nih.gov/pubmed/23791397
Vasopressin: Neuropeptides such as vasopressin are understood to influence aggressive behaviors. Studies have shown that individuals with a life history of aggressive behaviors tend to exhibit higher concentrations of vasopressin in cerebrospinal fluid. Furthermore, animals that contain greater levels of vasopressin in neurons within the anterior hypothalamus tend to exhibit more aggression than those with less. When vasopressin receptor densities are manipulated such as in “knock-out mice” by scientists, aggressive behavior decreases.
- Source: http://www.ncbi.nlm.nih.gov/pubmed/18346997
Oxytocin: Sufficient concentrations of oxytocin are associated with bonding, harmonious relationships, trust, and reduced aggression. For this reason, some speculate that among individuals with intermittent explosive tendencies, oxytocin concentrations may be deficient. Research from mice studies suggest that when oxytocin is depleted, aggressive behaviors are abnormally high. In humans, there appears to be an inverse relationship between cerebrospinal oxytocin levels and aggression.
- Source: http://www.ncbi.nlm.nih.gov/pubmed/18346997
Cortisol: Individuals with intermittent explosive disorder tend to exhibit decreased cortisol reactivity compared to those without the condition. Peak cortisol responses and prolactin appear to be reduced among those diagnosed with IEDs. Other research documents that low cortisol concentrations are discovered among those with high aggression, disruptive behavior, and criminal behaviors. Cortisol irregularities may stem from dysfunction or chronic imbalance of the autonomic nervous system.
- Source: http://www.ncbi.nlm.nih.gov/pubmed/16123761
Neural activation & connectivity: It is likely that neural activation and/or connectivity contributes to the development and maintenance of intermittent explosive disorder. Particularly, reduced functionality and/or blood flow to various subregions within the prefrontal cortex has been thought to increase impulsive tendencies and anger. Damage or compromised neural function of regions responsible for emotional regulation and/or modulation may lead to heightened aggression, hostility, and/or anger – and ultimately an IED.
Ventromedial prefrontal cortex (vmPFC): Among humans that are impulsively aggressive, the ventromedial prefrontal cortex often plays a role. Specifically, those with low activation of the vmPFC tend to act impulsively aggressive more frequently than those with normative activation. Studies utilizing neuroimaging have discovered that anger outbursts are associated with poorer cerebral blood flow in the left ventromedial prefrontal cortex.
- Source: http://www.ncbi.nlm.nih.gov/pubmed/15289278/
Dorsolateral prefrontal cortex (DLPFC): The dorsolateral prefrontal cortex (DLPFC) is involved in cognitive control during the completion of tasks. Studies of individuals with intermittent explosive disorder reveal heightened error-related activity in subregions of the dorsolateral prefrontal cortex. In other words, error-processing centers within the DLPFC were hyperactive among those with IED – particularly in the superior frontal gyrus.
Among those without IED, greater activity is exhibited in the supramarginal gyrus – a region implicated in attentional processes and top-down control. Perhaps the overactive superior frontal gyrus (among those with IEDs) reduces activity of the supramarginal gyrus. On the other hand, it could be that a hypoactive supramarginal gyrus leads to a hyperactive superior frontal gyrus.
Trait anger expression is associated with alterations in the DLPFC, regardless of whether a person has IED. However, IED diagnoses may result in more persistent dysfunction and/or suboptimal activation of the supramarginal gyrus and superior frontal gyrus. Further research is warranted to elucidate the DLPFC correlates of IEDs.
- Source: http://www.ncbi.nlm.nih.gov/pubmed/25106072
Anterior cingulate cortex (ACC): Feelings angry has been directly linked to activation of the dorsal anterior cingulate cortex. The greater the activity in this particular region, the angrier someone is likely to feel. Research has shown that when a person is insulted, the dorsal anterior cingulate cortex lights up with activity, thereby causing anger. Other neural correlates that may be increase in activation during an intermittent explosive episode include the: medial prefrontal cortex, hippocampus, and insula.
- Source: http://www.ncbi.nlm.nih.gov/pubmed/18578600
Orbital / Medial prefrontal cortex: Individuals with damage to the orbital/medial prefrontal cortex and connecting areas tend to exhibit impulsive aggression. As a result of increased impulsive aggression among those with lesions to the orbital/medial PFC, researchers speculated that dysfunction in these regions may occur among those with impulse control disorders. Researchers discovered that during tasks such as the Iowa Gambling Task, facial emotion recognition task, odor identification tasks, and working memory tasks – those with IED reacted differently.
Results indicates that patients with IED made suboptimal decisions during the gambling task compared to the control groups. Additionally, IED patients had difficulties recognizing emotions such as anger, disgust, and surprise on facial recognition tasks. What’s more is that those with IED labeled neutral faces with emotions such as “fear” and “disgust” more often.
Although neuroimaging was not conducted, performance by patients with IEDs is similar to that exhibited by patients with lesions to the orbital / medial PFC. This suggests that the impulsive aggression that occurs among patients with IEDs may be related to dysfunction within the orbital and/or medial prefrontal cortices. Further research is warranted to confirm these suspected neural correlates to IED.
- Source: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC123087/
Amygdala: Research comparing individuals with IED to healthy controls revealed differences in amygdala reactivity. Specifically, individuals diagnosed with IED exhibited exaggerated amygdala reactivity and reduced orbitofrontal cortex (OFC) activation when presented with angry faces. In healthy controls, the amygdala reactivity was considered normative and orbitofrontal cortex function wasn’t diminished when presented with angry faces.
Not only do individuals with intermittent explosive disorder appear to have dysfunctional amygdala activity, but they also appear to exhibit hypoactivity of the orbitofrontal cortex. Researchers also speculate that IED may be associated with impaired connectivity and/or signaling between the amygdala and orbitofrontal cortex. There is a clear link between cortico-limbic network abnormalities and aggression.
- Source: http://www.ncbi.nlm.nih.gov/pubmed/17210136
Autonomic nervous system: Dysfunction of the autonomic nervous system is not frequently discussed among IED researchers. Researchers are mostly focused on genetic and neurochemical correlates associated with the disorder. However, it should be suspected that dysfunction within the autonomic nervous system may exist prior to both epigenetic, neurochemical, and activation abnormalities.
- Hypoactive parasympathetic branch
- Hyperactive sympathetic branch
In cases of intermittent explosive disorder, it may be that chronic stress leads to underactivity within the parasympathetic branch and overactivity within the sympathetic branch. Overactivity in the sympathetic branch, especially from a young age, may impaired balance between the two branches. Individuals with sympathetic dominance tend to have low serotonin, high norepinephrine, and dopamine dysregulation.
When maintained for a long-term, sympathetic tone may downregulate activity in the prefrontal cortex and lead to heightened limbic activation. This could increase emotional sensitivity and reactivity to aversive stimuli. The combination of epigenetic, neurochemical/neuropeptide, hormonal, neural activation, and physiological changes induced by autonomic nervous system dysfunction may directly induce an intermittent explosive disorder.
Intermittent Explosive Disorder Symptoms & Signs (List)
To better understand impulse control disorder, it may be helpful to examine common symptoms associated with the condition. Realize that although many of these symptoms may indicate that a person has IED, symptoms alone cannot be used for diagnosis. Many of these symptoms also occur in an array of neuropsychiatric conditions. Therefore, to legitimately know whether a person has IED, he/she would necessitate DSM-5 diagnostic evaluation (as outlined above).
- Aggression: Among the most common symptoms of intermittent explosive disorder is aggression. Individuals with this condition will act aggressively towards others on a whim. The aggression may be physical, verbal, or a combination of both. Unfortunately, the inability to restrain this aggression is what often leads to physical injuries and/or property damage.
- Anger: Nearly all individuals with IED experience a combination of anger and aggression. The anger may be triggered unpredictably and could result in a temper tantrum, tirade, and may be characterized as “rage.” Since the anger emerges unpredictably and is overwhelming, an individual has a difficult time resisting the urge to express it. Among those with IED, the outward expression of anger generally inflicts psychological or physical pain upon others.
- Anxiety: Those with IED may simultaneously experience some anxiety along with the anger. While not all individuals with IED will feel anxious during times of anger, the anxiety may be activated by the fight-flight response that accompanies sympathetic activation during an outburst. Some individuals may notice low-grade anxiety such as feelings of nervousness, while others many report feeling highly anxious during and after their explosive episode.
- Chest tightness: A common physical symptom associated with IED is tightness of chest. When a person is about to explode with anger, significant changes in their physiology have taken place. Specifically, activity in the sympathetic nervous system spikes to an abnormally high level, overriding the relaxation response provided by the parasympathetic. This alters blood flow, heart function, increases muscle tension – leading to chest tightness.
- Emotional detachment: Many people with IED reportedly detach from emotions during the explosive attack. Transient emotional detachment makes sense due to the fact that hormones and neurochemicals such as epinephrine and norepinephrine flood the body during times of anger. These essentially alter our ability to feel normative emotions, possibly leading to detachment and/or depersonalization during an outburst. Only after the outburst of anger does a person with IED realize that they were detached from their normative range of emotions.
- Guilt: Though not all individuals with IED feel guilty about the damage they’ve inflicted upon others during their explosive episodes of anger – many end up feeling guilty in the aftermath. In other words, once the aggression/anger is expressed, a person may realize that he/she simply took things too far and regrets it. The guilt likely stems from the cumulative toll of emotional, physical, and/or property damages caused by the IED.
- Frustration: Those with intermittent explosive disorder usually have a low tolerance for frustration. Little things that most people can simply “put up with” even when bothersome may be perceived as a huge deal to someone with IED. For example, someone cutting you off in traffic may provoke some frustration, but you can likely forget about it and continue on with your day. Those with intermittent explosive disorder may explode with anger yelling curses, making gestures, and possibly tracking the person down to damage his/her vehicle or start a fight.
- Headaches: It is common for many people diagnosed with IED to experience headaches. The headaches may be mild, but they could also be extreme – nearly to the extent of migraines. When someone is emotionally distraught and full of anger – the sympathetic nervous system provokes vasoconstriction via norepinephrine acting upon adrenergic receptors. This excessive vasoconstriction is understood to cause headaches, some of which could be severe. Usually when the outburst of anger subsides, the headache will dissipate.
- Increased energy: If you suffer from IED, you may notice transient surges in energy during your outbursts. The sudden emergence of an emotion such as anger is understood to rev up activity in your sympathetic nervous system, altering levels of hormones and neurotransmitters. Those with IED essentially get a jolt of endogenous stimulants each time they have an outburst, which provides them with heightened energy. Some individuals may notice an energy “crash” several hours after the outburst and/or feel the need to rest and recover.
- Irritability: A common symptom of intermittent explosive disorder is irritability. Triggers of stress that wouldn’t irritate most individuals seem to sent those with IED into a tailspin of fury. Understand that while irritability may provoke an explosive outburst, those with IED may be more irritable than usual all the time. It is this constant irritability that may accumulate, and once a certain threshold is reached, explosive outbursts may ensue.
- Palpitations: Those with intermittent explosive disorder often report heart palpitations or sensations that the heart is beating abnormally, loudly, fluttering, or skipping a beat. This may cause the person to feel concerned over his/her health. Palpitations are a cornerstone physical symptom of anxiety and a sign that the sympathetic nervous system is highly active. In most cases, assuming the individual with IED doesn’t anxiously ruminate over the palpitations – they’ll subside within hours (possibly days) of the outburst.
- Racing thoughts: Prior, during, and after explosive outbursts – individuals with IED may experience racing, uncontrollable thoughts. These thoughts may be highly negative and filled with hate towards others. Essentially, these thoughts are unconscious and triggered as a survival mechanism by evolutionarily primitive regions of the brain. Although the person with IED wishes he/she could stop the racing thoughts, they cannot be controlled.
- Rage: Rage is characterized by violent, uncontrollable bouts of anger. While those diagnosed with IED are not always violent, sometimes the anger may escalate to violence. The rage could occur at any time throughout the day, but may be most likely to occur while commuting in a motor vehicle (e.g. driving to work). Driving is a stressful experience for most humans, but for those with IED, any mistake by another driver may be perceived as a personal affront which causes road rage.
- Shame: In the aftermath of an explosive outburst, many people experience the emotion of shame. They feel ashamed that they verbally or physically attacked or abused another person. They may also have been shamed by others for engaging in such explosive behavior. Shame is a normal emotion to experience following an outburst, but it is necessary to realize that not everyone with IED will feel ashamed.
- Shortness of breath: Sometimes a person with intermittent explosive disorder will exhibit shortness of breath. This shortness of breath is directly associated with the physiological changes that occur during emotions of anger and/or rage. The heart beats quicker, breathing speeds up, and the individual may notice a surge of adrenaline coursing through his/her body. In some cases, the shortness of breath could lead to hyperventilation.
- Stuttering: Another symptom of intermittent explosive disorder is stuttering. Stuttering can occur during bouts of extreme anger and emotional distress for several reasons. When primed during anger, the sympathetic nervous system triggers release of neurochemicals (e.g. norepinephrine) and hormones (e.g. cortisol) that increase tension. Our thoughts become uncontrollable and extremely fast. The incoherent thinking accompanied by physical tension leads some people with IED to stutter.
- Tension: If you’ve been angry in the past, you’ve likely experienced increased muscle tension. This muscle tension can cause tightness in the chest, but also throughout the entire body. Some individuals with IED may experience such extreme muscular constriction that they end up with transient weakness and/or pain. In most cases, the tension significantly decreases several hours after the outburst. That said, some individuals with IED may be inherently “high-strung” and experience constant tension – regardless of whether they’re having an outburst.
- Tingling: Those with IED have reported tingling sensations throughout their body during outbursts. Like many of these symptoms, the tingling is likely fueled by changes in sympathetic nervous system activity. Heightened activity in the sympathetic nervous system alters sweat, blood flow, etc. – which affects electrodermal activity and causes tingling.
- Tremors: Another common symptom of IED is tremors or shakiness. The shakes will most likely occur during an outburst and for a brief term after the outburst. Shakiness can be fueled by a hyperactive sympathetic nervous system which facilitates the release of adrenaline, norepinephrine, and other stimulatory chemicals throughout the body. As a result, we become so physiologically aroused – that shaking occurs.
Note: Not all individuals with intermittent explosive disorder will experience every single symptom listed above. Although most will experience anger and aggression, not all individuals will experience guilt/shame, palpitations, stuttering, and/or tremors. In addition to specific symptoms varying based on the individual, severity of symptoms is also likely to differ.
Intermittent Explosive Disorder Treatment
An array of treatments are available for individuals suffering from intermittent explosive disorder. Most professionals recommend treating the condition with a combination of psychotherapeutic (therapy) and pharmacologic interventions (medications). That said, the efficacy of these approaches may be subject to interindividual variation based on the specific causative underpinnings of IED.
For example, someone experiencing IED primarily as a result of abnormalities in the serotonin system may necessitate treatment with a serotonergic medication (e.g. SSRIs). Another individual may simply have an overactive sympathetic nervous system and would benefit more from cognitive behavioral therapy and self-awareness training (e.g. mindfulness). There’s no universally effective drug or therapy for all individuals with IED.
CBT: Cognitive behavioral therapy (CBT) is a form of psychotherapy originally engineered to treat depression. It is now commonly used for an array of other conditions, including intermittent explosive disorder. This form of psychotherapy aims to correct maladaptive thoughts and behaviors that lead to the explosive tendencies.
CBT involves analyzing a person’s IED and how it’s causing harm, as well as developing new skills to prevent future outbursts of anger. A psychotherapist utilizing CBT will work with a client and teach him/her ways to minimize likelihood of an explosive outburst in the future. The goal will be for the patient to eventually hone these new thought/behavioral skills to decrease outburst occurrences.
Though many patients with IED have successfully learned to overcome or manage the condition with skills acquired in CBT, the clinical efficacy of CBT hasn’t been elucidated. Some research published in 2008 documented the efficacy of psychotherapy for IED in a 12-week pilot study among 45 patients (that had been diagnosed with IED). Aggression, anger, and other symptoms were assessed at pre-CBT baseline, halfway through treatment, and after a 3-month post-treatment follow-up.
The study implemented a specific type of CBT known as CRCST (Cognitive Relaxation and Coping Skills Therapy) in both individual and group settings. The CRCST therapy involves several sessions of relaxation training, teaching patients to decrease physiological arousal with specific techniques. After the relaxation is learned, thoughts are restructured with “cognitive restructuring” and finally, patients are exposed to IED triggers in therapy and guided through how to resist aggressive urges and prevent them from arising.
Results indicated that after 12 sessions, both the group and individual forms of CRCST therapy effectively reduced anger, aggression, hostile thinking and depressive symptoms – compared to a “wait-list” control group. What’s more is that the symptoms remained significantly improved at the 3-month post-treatment follow-up assessment – indicating sustained benefit from CBT.
- Source: http://www.ncbi.nlm.nih.gov/pubmed/18837604
Antidepressants: Since many individuals with IED are thought to exhibit poor serotonergic turnover, they are commonly treated with SSRI or tricyclic antidepressants. These drugs function by increasing extracellular concentrations of serotonin within the synapse, thereby improving serotonergic signaling. Not all antidepressants may help individuals with IED, hence the reason SSRIs and TCAs are commonly preferred.
SSRIs: Treatment of IED with an SSRI may provide benefit in that it improves signaling of serotonin within the brain. This improvement in serotonin signaling may enhance mood, decrease irritability, and reduce overall anger/aggression towards others. One study documented that Prozac (Fluoxetine) significantly reduced symptoms of impulsive aggression and irritability – compared to a placebo.
This study was conducted for a duration of 14-weeks and incorporated 100 individuals diagnosed with IED. Although their impulsive aggression significantly decreased from baseline after 14-weeks of ongoing Prozac treatment, only 29% of participants were in complete remission from IED by the end of the study. While it appears as though SSRIs are an effective first-line intervention for some individuals with IED, efficacy is clearly not universal.
Other SSRIs that may be effective for the treatment of IED include Prozac, Lexapro, and Luvox. These medications are thought to bolster activity in the left temporal parietal junction (TPJ) of the brain, thereby improving social-cognitive processes among those with IED. That said, it should be considered that SSRIs may worsen symptoms of aggression and/or anger in a subset of users. Those being treated with such medications should be cautious as to avoid increases in occurrences of angry outbursts.
- Source: http://www.ncbi.nlm.nih.gov/pubmed/19389333/
- Source: http://www.ncbi.nlm.nih.gov/pubmed/10192598
- Source: http://www.ncbi.nlm.nih.gov/pubmed/26105140
TCAs: Older antidepressants known as tricyclics are also thought to provide benefit to a subset of individuals with IED. Though the side effects associated with tricyclic antidepressants may be more severe than those associated with SSRIs, they may provide benefit if an individual is unable to tolerate an SSRI. Like the SSRIs, tricyclic agents tend to improve serotonergic signaling, but may also affect norepinephrine.
The TCAs that enhance noradrenergic tone may be suboptimal for most individuals with IED due to the fact that noradrenaline is often associated with aggression and anger. Therefore, if a TCA is utilized, one that principally serves to increase serotonin should be preferred. Compared to SSRIs, it is unknown as to whether TCAs are more/less or equal in efficacy for IED.
- Source: http://www.ncbi.nlm.nih.gov/pubmed/21786470
Anxiolytics: Drugs engineered for the treatment of anxiety are often useful for reducing physiological triggers associated with outbursts. For example, administration of an anxiolytic generally decreases activation of the sympathetic nervous system, thereby allowing a person to remain physically calm. Additionally, many of these agents reduce uncontrolled, fast-paced thinking that leads to an outburst. Benzodiazepines, beta blockers, and even alternative agents such as gabapentin may be effective for IED.
Benzodiazepines: Drugs like Xanax, Ativan, Klonopin, and Valium act by binding to the gamma subunit of the GABAA receptors in your brain. Upon binding to this gamma subunit, it allows for increased endogenous binding of GABA to the GABAA receptors. This in turn leads to hyperpolarization of neurons via an influx of chloride ions, which decreases neuronal responses to excitatory postsynaptic potentials and reduces CNS activation.
A reduction in CNS activation is helpful for individuals with IEDs because many have overactive sympathetic function. Therefore, treatment with a benzodiazepine may provide significant benefit to some with IED. Since benzodiazepines have numerous risks such as fast onset tolerance and addiction – they may be less preferred over SSRIs for those with IED.
Beta blockers: An abundance of scientific literature has highlighted the fact that using beta blockers for anxiety is often effective. This is because beta blockers decrease sympathetic nervous system function by acting as antagonists at beta adrenoreceptors. As a result, individuals using beta blockers tend to notice reductions in palpitations, shakiness, and sweating.
Clinical reports have discovered that beta blockers (e.g. Propranolol) may be useful for certain patients with intermittent explosive disorder as well. They may decrease physical triggers and/or arousal that leads to an explosive outburst. In particular, one report highlighted the usage of Metoprolol, a selective beta-1 adrenoreceptor blocker in 2 patients diagnosed with IED.
- Source: http://www.ncbi.nlm.nih.gov/pubmed/4025634
- Source: http://www.ncbi.nlm.nih.gov/pubmed/3546964
Mood stabilizers: Administration of mood stabilizers appears to improve symptoms of intermittent explosive disorder. Although mood stabilizers are typically reserved for the treatment of bipolar disorder, they may help decrease impulsive aggression among those with IED. Examples of some mood stabilizers that are thought to improve symptoms of IED include: Carbamazepine, Depakote, and Lithium.
Should traditional first-line pharmacological interventions with serotonergic antidepressants fail to attenuate IED symptoms, mood stabilizers may be tested. That said, most may want to test an anxiolytic prior to jumping immediately to a pharmaceutical-grade mood stabilizer. Moreover, some patients may derive maximal benefit from an antidepressant plus mood stabilizer.
Neuropeptides: Novel therapies involving administration of neuropeptidic agents that modulate oxytocin and/or vasopressin may be useful for those with IED. As was already discussed, it is clear that many individuals with IED tend to have abnormally low concentrations of oxytocin and high vasopressin. Some speculate that administration of oxytocin and/or vasopressin antagonists may be useful therapies for those with IED.
Oxytocin: Administration of intranasal oxytocin may be a viable treatment for intermittent explosive disorder. Although it hasn’t been formally investigated as a treatment for IED, there is emerging clinical evidence to suggest its efficacy in reducing anger and aggression, while simultaneously improving social bonds and social cognition. Theoretically, administration of the neuropeptide oxytocin on an “as-needed” basis may attenuate IED.
What’s more is that there appear to be epigenetic implications associated with oxytocin administration. The greater the level of OXTR methylation, the more active various regions of the brain such as the amygdala, fusiform, and insula are – all areas involves in emotional processing. It is possible that oxytocin administration may facilitate neuroplastic changes in the brain and epigenetic changes that decrease IED.
- Source: http://www.ncbi.nlm.nih.gov/pubmed/25675509
Vasopressin receptor antagonists: Clinical trials are being conducted for vasopressin antagonists for the treatment of IED. Individuals with intermittent explosive disorder are thought to exhibit heightened concentrations of vasopressin in the brain. Elevated vasopressin concentrations appear to increase activity within the temporal parietal junction (TPJ), anterior cingulate, putamen, and precuneus regions – leading to increased reactivity to angry faces.
Intranasal administration of the agent SRX246, a V1 receptor antagonist, appears to decrease activity in the aforestated regions, thereby reducing reactivity to angry faces. The cumulative neural effects of V1 receptor agonist SRX246 results in decreased reactivity in the amygdala. For this reason, many speculate that V1 antagonists may be useful for the treatment of IED.
- Source: http://www.ncbi.nlm.nih.gov/pubmed/24376401
Dietary supplements: The efficacy of dietary supplements have not been investigated for the treatment of intermittent explosive disorder. However, it is understood that nutritional deficiencies can cause neuropsychiatric symptoms such as irritability, anger, and compromised impulse control. Upon optimization of one’s diet as well as utilization of specific supplements, perhaps outbursts can be successfully managed. If you want to treat IED with supplements, be sure to confirm safety and hypothesized efficacy with a medical professional.
- Adaptogenic herbs: Some individuals may derive benefit from using adaptogenic herbs such as Rhodiola Rosea to alter neurotransmission and decrease likelihood of an explosive outburst. Adaptogens increase physiological stimulation when energy levels are low, but also decrease physiological stimulation when excessively high. They also act as low-grade enzymatic MAO inhibitors, leading to increases in serotonin, norepinephrine, and dopamine.
- Cannabidiol: There is evidence that CBD (cannabidiol) is neuroprotective within the brain. It doesn’t contain THC and therefore isn’t considered addictive nor illicit. Therapeutic effects of CBD include: increased physical relaxation, lower psychological stress, and improved mood. There is reason to hypothesize that CBD may improve outcomes among those with IED.
- Lithium orotate: This is a supplement akin to pharmaceutical-grade lithium with some differences. It hasn’t been as thoroughly researched, but is commonly used by individuals for its mood balancing effects. Some with IED may find that regular lithium orotate supplementation significantly decreases outbursts.
- L-Tryptophan: This is an amino acid precursor that converts to 5-HTP, which in turn converts to serotonin within the body. If you aren’t receiving enough L-tryptophan in your diet, supplementation may be useful for increasing central concentrations of serotonin. This intervention may be most helpful for those with suboptimal serotonin production.
- Omega-3 fatty acids: Insufficient omega-3 fatty acid intake could affect mood and lead to aggression, irritability, anger, and depression. Increasing dietary intake of fatty fish (e.g. wild-caught sockeye salmon) should help with omega-3 levels. You could also consider supplementing with high quality fish oil or krill oil to determine whether anger improves.
- Valerian root: This is an herb commonly used to increase relaxation and sedation. It acts similar to benzodiazepines by binding to a subunit of the GABAA receptor and allowing increased GABA binding. Some individuals with IEDs may find valerian root to be a useful dietary supplement in decreasing arousal and/or physical triggers of an outburst.
Autonomic Nervous System (ANS) Adjustments
Those with intermittent explosive disorder often have difficulty modulating function of the autonomic nervous system. The sympathetic branch seems to be hyper-reactive to aversive stimuli, thereby setting off an angry outburst at unpredictable moments. Though autonomic nervous system dysfunction may not be the standalone cause of IED, it may contribute.
- Brainwave entrainment: An intervention to correct neuroelectrical abnormalities that may cause IED is brainwave entrainment. A major benefit of brainwave entrainment is that you can increase brainwaves associated with psychological relaxation such as alpha waves. Individuals with anger are often locked into beta wave states and are unable to produce alpha to calm their thinking.
- Deep breathing: Breathing deeply is an effective way to ramp up physiological and psychological relaxation. When practiced consistently, deep breathing may yield effects similar to meditation such as: brain wave changes, increased parasympathetic tone, and heightened self-awareness.
- EmWave2: This is a biofeedback device that I personally use whenever I’m anxious, upset and/or angry. It measures HRV (heart-rate-variability) or the amount of time between heartbeats. The goal is to increase the amount of time between heartbeats by balancing the parasympathetic and sympathetic nervous system. Higher variability tends to yield positive emotions, reduced anger, and relaxation.
- Meditation: There are many types of meditation you could choose from if you have IED to alter neural activity and nervous system activation; different types of meditation affect the brain in unique ways – some may be better suited for correction of IED-related neural abnormalities. However, the type with the most scientific-support for the treatment of neuropsychiatric disorders is known as Mindfulness (or Vipassana). Mindfulness meditation (or simply mindfulness-CBT) may help with IED by increasing self-awareness and relaxation.
- Self-hypnosis: This is similar to meditation in that it involves self-reflection and relaxation. However, it also helps reprogram thought patterns that may prove useful if you feel angry. Although self-hypnosis with a specific recorded to treat IED could provide benefit, it may also be helpful to work with a licensed hypnotherapist.
How many people suffer from intermittent explosive disorder (IED)?
It appears as though intermittent explosive disorder is more common than was previously thought. Around 16 million Americans are thought to fit DSM-5 diagnostic criteria for intermittent explosive disorder. Additionally, it tends to have an early age of onset (14 years of age) and is often linked with concurrent appearance of other neuropsychiatric disorders and substance abuse problems.
Research estimates that lifetime prevalence of intermittent explosive disorder occurs in approximately 4% to 6% of the population. Among those that fit diagnostic criteria for the disorder, around 60% will end up receiving treatment for simultaneous emotional and/or substance abuse issues. However, less than 30% of those with IED will seek out treatment for their anger.
Scientific findings indicate that of Americans diagnosed with IED, over 67% had engaged in direct interpersonal aggression and over 11% had acted aggressively upon objects. Around 20% of those diagnosed have been documented as making threats of aggression to others. Estimates suggest that lifetime cumulative property damage by those with IED exceeds $1600.
- Source: https://www.ncbi.nlm.nih.gov/pubmed/16754840
- Source: https://www.ncbi.nlm.nih.gov/pubmed/16259534
- Source: http://www.kiis.com.ua/materials/articles/Bromet%20Ukr%20prev%202005.pdf
Risk factors for intermittent explosive disorder
There are several risk factors that may increase a person’s odds of developing intermittent explosive disorder. Examples of some common risk factors include: being bullied or abused, male (sex), and having a family history of IED. Keep in mind that correlation with these risk factors does NOT automatically indicate a person has IED.
- Bullying: Excessive bullying may also increase likelihood that someone develops IED. Bullying is known to affect epigenetic expression, neural activation, and create neuroplastic changes within the brain – some of which may lead to the onset of IED.
- Ethnicity: Some evidence indicates that individuals of Celtic descent are more likely to suffer from IED compared to those of Germanic descent. Due to the lack of research regarding ethnicity and IED, the risks associated with other ethnic groups isn’t clear.
- Family history: Anyone with a family history of IED should be considered to have increased risk for IED. If a parent or sibling has the disorder, you may have inherited certain genes/neurobiological features that make you more susceptible as well.
- Personality disorders: Various personality disorders such as antisocial and borderline are at increased risk of IED. That said, just because a person has a personality disorder such as APD or BPD – does not mean that they have IED; individual diagnoses are necessary.
- Male sex: Males appear to be at increased risk for IED compared to women. Though testosterone has not been linked to IED, it may be that men are inherently more aggressive or prone to anger. That said, it could also be that males with the disorder are more easily identified.
- Neuropsychiatric conditions: Psychiatric disorders such as ADHD, bipolar disorder, and oppositional defiant disorder may increase likelihood of IED.
- Physical abuse: If a person was physically abused as a child, this increases their odds of IED.
- Substance abuse: Individuals that abuse drugs are more likely to have IED. It is unclear as to whether the drug abuse creates neurochemical changes that make anger and aggression more likely OR if the anger/aggressive tendencies lead to the IED; for some individuals it may be a combination of both.
- Trauma: Past history of trauma increases likelihood that someone will develop IED. This could mean PTSD or simply a traumatic experience.
Have you been diagnosed with intermittent explosive disorder (IED)?
If you’ve been diagnosed with IED or know someone that has, feel free to share a comment below. Discuss the age at which you first noticed the onset of outbursts and how long it took before you were diagnosed with IED. Assuming you were formally diagnosed with IED, mention whether you’ve been diagnosed with any comorbid personality disorders and/or neuropsychiatric disorders.
To help others get a better understanding of your situation, mention whether you have more frequent outbursts of lower intensity OR infrequent outbursts of higher intensity. Also note whether you’ve ever physically harmed another person or inflicted damage upon property due to your uncontrollable anger/aggression. Since being diagnosed with IED, have you sought out psychotherapy and/or psychiatric treatment?
If so, what treatments have you found to be most effective in the management of outbursts? If you’d like to speculate and/or reflect upon the etiology of your IED, share possible causative factors (e.g. genetics, bullying, abuse, substance abuse, etc.) that may have contributed to its pathology. In your comment, feel free to share any additional tips or strategies that you think may be of benefit to others with this condition.