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Impulse Control Disorder (ICD): Causes, Symptoms, Treatment

Impulse control disorder (ICD) is an overarching classificatory label given to psychiatric disorders characterized by inability to resist impulses (or urges) that yield deleterious implications.  Examples of impulse control disorders include: compulsive gambling, incessant sexual encounters, and binge shopping.  If unrecognized and/or unaddressed for an extended duration, an impulse control disorder may ruin a person’s: health, friendships, finances, social relationships, and/or marriage.

To better understand impulse control disorders, it is necessary to elucidate specific diagnostic criteria and common diagnostic subtypes.  It may also help to learn about potential causes and/or risk factors that may increase susceptibility of developing an impulse control disorder.  For example, sometimes impulse control disorders are drug-induced as a result of a pharmaceutical intervention for a condition such as Parkinson’s disease – yet other times they occur organically with unknown etiology.

Mostly, it is of utmost importance to recognize common symptoms and signs of an impulse control disorder and encourage treatment for those afflicted.  Assuming an impulse control disorder can be identified quickly and managed with psychopharmacological and/or psychotherapeutic interventions, the punitive toll incurred can be kept to a minimum or possibly circumvented altogether.  If you have an impulse control disorder or suspect a friend or family struggles with ICD – consult a professional.

Impulse Control Disorder Symptoms & Diagnostic Criteria

Though the DSM (Diagnostic Statistical Manual of Mental Disorders) has diagnostic criteria for impulse control disorders (ICDs) based on the specific disorder, it does not have a generalized set of diagnostic criteria that can be applied to all ICDs. ICD literature emphasizes 4 necessary features required to be classified as an impulse control disorder.  Principal features of impulse control disorders include:

  1. Repetitive engagement in a behavior despite deleterious consequences

A person frequently engages in a specific behavior (e.g. sex) despite potentially disastrous consequences (e.g. contracting a disease, damaging a relationship, etc.).  The repetition of the behavior may be likely to occur as a result of neuroplasticity and/or changes in neural circuitry associated with the behavior.  The more a person engages in a particular act, the more neutrally “primed” he/she will be to continue the act in the future, irrespective of consequences.  This may be related to self-induced neuroplasticity.

  1. Inability to control or regulate the problematic behavior

The person is unable to decrease the problematic behavior, regardless of what they do.  For example, a person with intermittent explosive disorder may be aware of the fact that his/her aggressive outbursts are problematic, but even with self-taught coping strategies, the outbursts persist.  This could be due to lack of executive oversight from the prefrontal cortex while engaged in an impulsive act.

  1. Insatiable cravings prior to engagement in the problematic behavior

Before a person engages in a particular act associated with an ICD such as compulsive shopping, he/she experiences cravings.  Piggybacking off of the compulsive shopping example, the person will crave experience of purchasing novel items – despite their impracticality.  These cravings may be associated with increased activation of the reward center in the brain.

  1. Hedonic tone exhibited during engagement of the problematic behavior

As a person engages in the impulsive act (e.g. shoplifting), he/she tends to experience changes in affect and/or arousal.  The person may report a short rush of pleasure, likely facilitated by reward centers in the brain – possibly triggering bursts of dopamine.  This leads to positive valance associated with mood enhancement, increased energy, and heightened arousal. This pleasure is what tends to reinforce the impulsive behaviors.

Additional features…

In addition to the 4 predominant features of an impulse control disorder, most are understood to impair a person’s ability to function (in any area of life) and are often associated with negative emotion following the act.  Therefore, it is important to mention that functional interference and negative emotion may also be discovered as features of ICDs.

  • Interference with functionality: Impulse control disorders typically interfere with functioning in occupational, social, or familial settings. They may affect occupational productivity or the amount of work that you finish during a workday.  They may also affect social interactions or impair relationships with family members.  Moreover, they may detrimentally affect many aspects of functioning – possibly leading to social isolation.
  • Post-behavioral negative emotion: After engaging in a particular impulsive behavior, individuals may feel negative emotions such as anxiety, depression, guilt, or shame. These emotions may be a direct result of the particular act (e.g. guilt associated with an affair) or an indirect consequence of the behavior (e.g. depression after bankruptcy from compulsive shopping).  While not all individuals with impulse control disorders experience negative emotion after the particular problematic behavior, most present a dysphoric tone.

Types of Impulse Control Disorders (ICDs)

Although all impulse control disorders are characterized by inability to resist impulses, there are many specific subtypes of ICDs that are diagnosed.  Various subtypes of impulse control disorders include: pathological gambling, kleptomania, intermittent explosive disorder, pyromania, compulsive shopping, and compulsive sex.  It should be noted that while most individuals are diagnosed with a standalone ICD subtype, others may struggle with multiple simultaneous ICDs.

Hypersexuality (Compulsive sexual behavior)

Compulsive sexual behavior, also referred to as “hypersexuality,” is characterized by irresistible sexual urges that interfere with a person’s emotional, financial, social, and/or occupational function OR cause harm to others.  The compulsive behaviors may be nonparaphilic such as: masturbation, promiscuity, pornography, etc. – or paraphilic such as: exhibitionism, fetishes, voyeurism, etc.  Estimates suggest that between 3% and 6% of all adults in the United States engage in compulsive sexual behavior.

Possible consequences:

  • Emotional distress
  • Poor productivity
  • Ruined relationships
  • Sexually transmitted diseases
  • Social isolation

It is unclear as to what causes hypersexuality, but researchers speculate that the condition is fueled by: pleasure seeking, anxiety reduction, or a combination (of both) factors.  Individuals with compulsive sexual behavior may experience frequent sexual thoughts that prompt irresistible urges to engage in sexual acts.  These sexual acts tend to negatively affect occupational performance, social relationships, and health.

If left untreated, individuals with compulsive sexual behavior may be more likely to: contract sexually transmitted infections (STIs), engage in extramarital affairs, or spend money on sex.  Even excessive self-stimulating sexual behavior (e.g. masturbation) may interfere with occupational productivity and lead to social isolation.  With psychotherapy and pharmacology, many individuals recover from compulsive sexual behavior.

Compulsive buying (shopping)

Compulsive shopping (or buying) is characterized as a preoccupation with shopping, usually resulting in the purchase of irresistible, impractical, and/or unnecessary items.  It may also be associated with shopping for a longer timespan than was originally intended.  To be classified as an impulse control disorder, the preoccupation with shopping necessitates simultaneous: emotional, financial, social, and/or occupational distress.

Possible consequences:

  • Bankruptcy
  • Credit card debt
  • Emotional distress
  • Foreclosure
  • Lost relationships

Some reports estimate that around 5% of adults in the United States engage in compulsive shopping.  For these individuals, the act of purchasing items is associated with feelings of intense pleasure.  However, once the items have been purchased, the reward associated with purchase ceases and emotions shift towards feelings of: embarrassment, guilt, and shame.

Thereafter, individuals tend to either: never use the items, give their purchases away, or return them to the store for a refund.  Perhaps most problematic is the fact that many compulsive shoppers purchase items without having sufficient funds in their bank account.  Compulsive shoppers often go into credit card debt and/or will borrow money to support their addiction.

Eventually, a compulsive shopper may need to declare bankruptcy, face property repossession, and possible foreclosure.  This can cause further emotional distress and affect the wellbeing of fellow family members.  Since compulsive shopping can quickly spiral out of control, intervention is recommended as soon as the condition is recognized.

Pathological gambling

Among the most common subtypes of impulse control disorders is pathological gambling.  This particular ICD subtype is identified by persistent and recurrent maladaptive patterns of gambling behavior.  Research suggests that it affects between 0.9% and 1.6% of individuals in the United States and males to a greater extent than females.

Possible consequences:

  • Bankruptcy
  • Divorce
  • Depression
  • Financial loss
  • Incarceration
  • Ruined relationships
  • Suicidal ideation

Pathological gambling (PG) is recognized as a chronic condition in which individuals frequently relapse and/or revert to gambling behavior.  They are unable to resist the urge to continuously gamble, and as a result, tend to lose a significant amount of money.  The loss of finances may lead to bankruptcy and compromise the financial well-being of family (and/or possibly friends).

Significant financial hardship stemming from pathological gambling may lead to theft, incarceration, or even suicide (17%).  One of the most common causes of suicide is financial distress related to unemployment.  Furthermore, since money is linked to happiness (to a certain extent), and gambling usually results in lost money, it can be inferred that pathological gamblers may end up experiencing severe depression and/or suicidal ideation.

Signs that individuals are struggling with pathological gambling include excessive: casino trips, online betting, sports betting, poker games, etc.  Statistical data reveals that 68% of pathological gamblers are males, whereas 32% are females.  Males tend to become pathological gamblers at a younger age than females, but pathology among females usually progresses at a faster rate.

Intermittent explosive disorder (IED)

Intermittent explosive disorder is an ICD recognized by recurrent, aggressive outbursts –sometimes leading to assaults or destruction of property.  Those diagnosed with intermittent explosive disorder are unable to resist the urge to act out pent up emotion of anger and/or aggression; hence they “explode” unpredictably.  These intermittent “explosions” involve an individual verbally or physically channeling their aggression towards other people or objects.

Possible consequences:

  • Abuse towards others
  • Jail or prison
  • Occupational distress
  • Ruined relationships

The outbursts of aggression exhibited by those with intermittent explosive disorder are usually of short duration (under 30 minutes), but frequently occurring.  Research estimates that around 1.4 million individuals living in the United States will suffer from transient IED, whereas up to 10 million individuals will struggle with inescapable, lifelong IED.  Although those afflicted with IED tend to realize that their behavior is problematic, they are often unable to properly manage it without professional help.

Unfortunately, a bulk of individuals with intermittent explosive disorder fail to seek help and/or don’t realize that it’s considered a psychiatric condition.  If left untreated, IED may lead to: assaults and/or outbursts that injure others, damage property, and yield lead to legal consequences (e.g. lawsuits, prison time, etc.).


Another type of impulse control disorder is defined as uncontrollable, repeated shoplifting of items, most of which are deemed unnecessary for personal usage.  Those suffering from kleptomania tend to steal things that they don’t really need, sometimes for the psychological thrill derived from the act.  Most individuals with kleptomania initially engage in kleptomanic behaviors as adolescents or young adults.

Possible consequences:

  • Emotional guilt and shame
  • Jail or prison
  • Ruined reputation

In some cases, kleptomanic tendencies may emerge during childhood and if left untreated, may remain throughout a person’s entire lifespan.  Kleptomania is an ICD that often remains undiagnosed and undetected – usually because the thief is careful to avoid getting caught in the act (and sentenced to jail or prison).  Researchers estimate that between 64% and 87% of individuals with kleptomania have been caught in the act (by security or police).

Following the act of shoplifting, the stolen items are commonly: stowed away, hoarded, disposed (in the trash), or returned to the store.  Additionally, those struggling with kleptomania tend to report emotions of guilt and shame after stealing.  If untreated and/or unidentified for a long-term, a person with kleptomania may accrue significant jail or prison time.


Pyromania is another subtype of impulse control disorder in which individuals are unable to resist the urge to deliberately start fires.  Among those with pyromania, the starting of fires tends to alter physiological arousal and emotional state.  Individuals with pyromania also frequently derive pleasure and/or gratification from fire starting, particularly when witnessing or participating in the aftermath.

Possible consequences:

  • Damage to others (physical and emotional)
  • Legal penalization (jail or prison)
  • Property destruction

Some research estimates that between 2.5% and 3.5% of people in the United States are afflicted with pyromania.  Those suffering from pyromania do not always commit arson; this is important to distinguish.  However, individuals with pyromania may be more likely to commit arson, and for this reason, it is beneficial to treat the condition as soon as it is clinically identified.

Should an individual with pyromania engage in arson, the incurred damages may be significant.  Not only may the damages be in the form of lost property of victims, but victims may end up with severe burns, health complications, or even death (e.g. inside a burning house).  If caught in the act of arson, an individual with pyromania will be sentenced to legal penalization (e.g. prison).

  • Source: http://www.ncbi.nlm.nih.gov/pubmed/21556272

What causes impulse control disorders? (Possibilities)

It is difficult to pinpoint the specific causes of impulse control disorders.  Even among those with the same diagnostic subtype (e.g. compulsive shopping), causes are subject to significant interindividual variation.  In other words, one compulsive shopper may have developed the ICD during treatment with a drug that affects neurotransmission, yet another person may have developed the ICD as a result of genetics and epigenetics.

The overt symptoms of an ICD may be similar among those diagnosed, but the causative factors may differ significantly.  Furthermore, the cause of an ICD may not always be chalked up to a single, lone factor.  It may be a result of numerous factors in some sort of equipotent blend (e.g. 50% epigenetics / 50% medication) or hierarchical medley (e.g. 75% genetics, 15% brain injury, 10% drug use).

Research has attempted to elucidate the etiology of impulse control disorders, and has discovered a variety of causative factors including: pharmaceutical drugs, genetics, neural activation and/or connectivity, and neurotransmitter dysregulation.  Perhaps most prominent is a link between striatal dysfunction, particularly the ventral area, and impulse control disorders.  Other potential causes include: autonomic nervous system dysfunction, epigenetics, and neuroplasticity (as a result of learned behaviors).

Pharmaceutical Drugs

Many pharmaceutical drugs, particularly dopaminergic agents, are understood to provoke impulse control disorder as a side effect.  Impulse control disorders are relatively common among Parkinson’s patients taking dopamine receptor agonists (DAs) such as Mirapex and Requip.  However, they can occur among individuals taking agents such as dopamine precursors (e.g. levodopa) and in rare cases, among those using certain: antipsychotics, antidepressants, and hormonal modulators.

Dopamine agonists (DAs): Around 10% (1 out of 10) individuals taking dopamine agonists for the treatment of Parkinson’s disease will develop an impulse control disorder.  The most commonly reported impulse control disorder is pathological gambling, but others have been reported as well.  Dopamine agonists act upon D3, D2, and D4 receptors – which improves motor symptoms, but can also amplify activation within the reward center of the brain.

  • Mirapex (Pramipexole)
  • Permax (Pergolide)
  • Requip (Ropinirole)

Furthermore, dopamine agonists may also decrease regulatory top-down oversight from the prefrontal cortex over regions such as the nucleus accumbens.  This may lead individuals to engage in risky gambling or sexual pursuits.  Patients taking dopamine agonists should be monitored regularly for behavioral changes that may signify an ICD.

Statistics suggest that pathological gambling and compulsive buying are the two most common forms of impulse control disorder to occur among those being treated with dopamine agonists.  One study suggested that pathological gambling occurs in around 5% of users, whereas compulsive buying occurs in around 5.7% of users.  To a less significant extent, 4.3% of users engage in binge eating during treatment, whereas 3.5% engage in compulsive sexual behaviors.

Approximately 3.9% of all dopamine agonist users experience 2 or more impulse control disorders (ICDs).  Patients taking dopamine agonists are at nearly 2.5-fold the risk of developing an impulse control during treatment compared to those utilizing a different agent.  Likelihood of developing an impulse control disorder during treatment with a dopamine agonist appears similar regardless of the drug. (Read: Requip Side Effects / Mirapex Side Effects).

Note: It’s understood that there’s a dose-dependent relationship in regards to ICD development from a dopamine agonist.  The greater the dose an individual takes, the more likely he/she will experience difficulty resisting problematic impulses.

  • Source: http://www.ncbi.nlm.nih.gov/pubmed/19127573
  • Source: http://www.ncbi.nlm.nih.gov/pubmed/24219002
  • Source: http://www.ncbi.nlm.nih.gov/pubmed/20457959

Levodopa: Although levodopa monotherapy is less likely to provoke impulse control disorders than dopamine agonists, it can still cause impulse control disorders in around 7-8% of users. (Read: Sinemet (Carbidopa-Levodopa) Side Effects).  The mechanism by which levodopa-based pharmacological preparations induce impulse control disorders isn’t fully elucidated.  Many speculate that levodopa causes dopaminergic dysregulation within the mesolimbic pathway of the brain, thereby giving rise to impulsive tendencies.

It could also be that the specific pathology of Parkinson’s disease in a subset of patients reacts to levodopa in such a way that the reward center becomes overactive and/or prefrontal cortex is underactive.  This combination of heightened reward center connectivity, decreased prefrontal activation, and dopaminergic abnormalities in the mesolimbic pathway could cause an ICD.

  • Source: http://www.ncbi.nlm.nih.gov/pubmed/3256388

Rasagiline: Another agent that is sometimes used for the treatment of Parkinson’s disease is the second-generation MAO-B inhibitor known as rasagiline.  Rasagiline was engineered to be the successor of Selegiline, a similar-acting agent.  There is some evidence that it may slow the progression of Parkinson’s disease and it is often regarded as a neuroprotective agent.  In some cases, patients with Parkinson’s disease taking Rasagiline may develop ICDs.

  • Source: http://www.ncbi.nlm.nih.gov/pubmed/24055209

Other drugs that may cause ICDs…

Dopamine agonists are most associated with development of drug-induced impulse control disorders.  However, other agents such as atypical antipsychotics, antidepressants, and even hormonal therapies have potential to cause drug-induced ICDs.  Keep in mind that drug-induced ICDs only occur in a small-percentage of patients being treated with these medications.

Atypical antipsychotics

There are numerous case reports of individuals taking atypical antipsychotics who experience drug-induced impulse control disorders.  Most reports of antipsychotic-induced ICDs are isolated to the usage of Abilify (Aripiprazole) and Risperdal (Risperidone).

Abilify: Many lawsuits have been filed against the makers of Abilify specifically for the fact that it can cause impulse control disorders in a subset of users.  Most common of the impulse control disorders associated with Abilify is pathological gambling.  Several cases of pathological gambling among Abilify users have been reported, and in each case, none of the patients had a prior history of gambling.

Another case has been documented of Abilify-induced hypersexuality among a 24-year old female.  She reported incessant urges to masturbate and a high sex drive after treatment with Abilify.  Researchers speculate that those with schizophrenia and/or schizoaffective disorder may be most prone to Abilify-induced ICDs due to abnormal dopaminergic tone.

Dopaminergic modulation as induced by Abilify is understood to affect sexual function, and could also increase urge to gamble.  Abilify’s partial D2 receptor agonism, agonism of dopaminergic activity in the mesolimbic circuit (especially in the nucleus accumbens), and possibly effects upon 5-HT1A or 5-HT2A receptors may give rise to ICDs.  In all cases of Abilify-induced impulse control disorders, urges subsided upon discontinuation of Abilify.

  • Source: http://www.ncbi.nlm.nih.gov/pubmed/21241242
  • Source: http://www.ncbi.nlm.nih.gov/pubmed/18794655

Risperdal: Several cases of Risperdal-induced hypersexuality have been reported.  In all 3 cases, individuals were taking Risperdal for the treatment of schizophrenia.  One patient, referred to as “Mrs. X” was 71 years of age, and widowed for 20 years.  She had been receiving Risperdal intramuscularly three times per week.  The treatment caused her to masturbate 2-3x per day and upon discontinuation of Risperdal, hypersexuality subsided.

Another couple cases were documented, including of a 53-year old male and 23-year old male.  In the first case, the 53-year old became preoccupied with masturbation and needing a sexual partner.  The case of the 23-year old, he reportedly engaged in exhibitionism, propositioning, and sexually disinhibited speech.  For both patients, discontinuation of Risperdal resulted in complete recovery from hypersexuality.

Researchers speculate that Risperdal may induce impulse control disorders, particularly hypersexuality, via antagonism of 5-HT2A receptors.  This antagonism enhances dopamine release in the prefrontal cortex.  Alpha-2 adrenergic receptor antagonism may also play a role in hypersexuality due to the fact that it can affect genital stimulation.

  • Source: http://www.ncbi.nlm.nih.gov/pubmed/23999483


Risk of developing an ICD from antidepressants is relatively low.  In fact, antidepressants are among the most common treatments for non-drug-induced impulse control disorders.  That said, there are case reports of individuals that developed ICDs during antidepressant treatment.

Flupentixol: This is an antidepressant and antipsychotic approved in countries outside the United States.  At low doses it can be used as an antidepressant, and at high doses, it acts as an antipsychotic by inhibiting the D1 and D2 receptors.  A case report suggests that flupentixol (at 7 mg) induced pathological online gambling. Discontinuation of this medication reduced excessive tendencies to gamble.

  • Source: http://www.ncbi.nlm.nih.gov/pubmed/24356928

Moclobemide: Research indicates that among individuals who’ve experienced a stroke or Parkinson’s disease, treatment with the atypical antidepressant moclobemide may cause hypersexuality.  In all cases, moclobemide-induced hypersexuality ceases upon discontinuation of treatment.  It is unclear as to whether ICDs such as hypersexuality occur among non-stroke and non-Parkinson’s patients.

  • Source: http://www.ncbi.nlm.nih.gov/pubmed/9704167

Selegiline: This is an MAOI or inhibitor of the enzyme monoamine oxidase that is utilized as an antidepressant, as well as an anti-Parkinson medication.  Although hypersexuality and paraphilia are understood to be side effects, they occur on an infrequent basis.  That said, a report documents both paraphilia and hypersexual behavior upon initiation of Selegiline treatment among two individuals with early-onset Parkinson’s disease.

  • Source: http://www.ncbi.nlm.nih.gov/pubmed/16730214

Zoloft: In rare cases, individuals taking Zoloft (Sertraline) may experience impulse control disorders.  One documented case of a 55-year old man referred to as “Mr. A” notes onset of high sexual desire and increased demands of sexual intercourse with his wife; this lead to marital conflict.  Although he had been taking Wellbutrin (Bupropion), it wasn’t until Zoloft was added as an adjunct that he exhibited the heightened sexual desire.

Upon discontinuation of Zoloft, hypersexuality resolved within a 1-month term.  Researchers speculate that Zoloft may have induced hypersexuality via numerous mechanisms including action on: serotonin (5-HT2 / 5-HT3) receptors, dopamine receptors (and levels in the nucleus accumbens), and norepinephrine receptors.  Decreased metabolism of Wellbutrin by Zoloft via CYP2D6 isoenzymes may also have given rise to hypersexuality among this patient.

  • Source: http://www.ncbi.nlm.nih.gov/pubmed/22943020

Miscellaneous agents

There appear to be drugs used to treat menstrual problems, growth hormone overproduction, type 2 diabetes and pituitary tumors – that may cause impulse control disorders.  The most common example of such a drug is bromocriptine, marketed under the brand names “Parlodel” and “Cyloset.”  While most users of these agents will not experience impulse control disorders, cases have been reported.

Bromocriptine: Several cases of individuals taking bromocriptine for the treatment of macroprolactinoma (hormone-secreting tumors in the pituitary gland) have reported drug-induced ICDs.  Usually the cases of ICDs occur after a long-term of treatment with agents like bromocriptine.  A young patient who develops pathological gambling after long-term administration of bromocriptine is cited in scientific literature.

  • Source: http://www.ncbi.nlm.nih.gov/pubmed/24045609

Neural activation & connectivity

Many individuals with impulse control disorders are thought to exhibit abnormal neural activation and/or connectivity.  Regions of the brain that have been speculated to influence development and severity of impulse control disorders include the: right ventral striatum, right ventromedial prefrontal cortex, and various other subsections within the prefrontal cortex.  The combination of underactivity in certain regions and poor connectivity makes it difficulty to resist impulsive (animalistic or libidinal) urges, leading to ongoing ICDs.

Right ventral striatum: Research indicates that among individuals with impulse control disorders associated with Parkinson’s disease, neural activation is substantially altered.  Comparative neuroimaging analyses reveal that during risk-taking activities, patients with impulse control disorders exhibit significantly reduced activation of the right ventral striatum.  Furthermore, those with ICDs [associated with Parkinson’s] appear to have significantly decreased cerebral blood flow to the right ventral striatum.

  • Reduced cerebral blood flow to right ventral striatum
  • Decreased activation of the right ventral striatum during risk-taking

Those with Parkinson’s, yet without ICDs, tend to activate the mesocorticolimbic pathways of the brain during risk-taking activities.  These individuals do not appear to exhibit deficits in cerebral blood flow to the right ventral striatum nor does right ventral striatal activity decrease during risk-taking activities.  Researchers hypothesize that neural underpinnings of ICDs associated with Parkinson’s disease may be similar to those of non-Parkinson’s ICDs.

In other words, it is likely that all individuals with impulse control disorders exhibit deficits in blood flow and activation of the right ventral striatum.  Treatments that attempt to enhance striatal blood flow and activation during risk taking may prove therapeutic.  Moreover, interventions for those with ICDs may be of similar efficacy regardless of whether an individual is diagnosed with Parkinson’s disease.

  • Source: http://www.ncbi.nlm.nih.gov/pubmed/20589879

Nucleus Accumbens: A region within the striatum known as the nucleus accumbens is thought to contribute heavily to impulse control disorders.  Among patients with Parkinson’s who develop ICDs during treatment with dopamine agonists, there appears to be decreased frontostriatal connectivity, specifically between the nucleus accumbens and prefrontal cortex.

This is simultaneously accompanied by an increase in signaling between the nucleus accumbens and anterior insula, thereby bolstering likelihood that someone will engage in a gambling task; even with no prior gambling history.  Cessation of dopamine agonist treatment reverses or normalizes signaling between the prefrontal cortex and nucleus accumbens, as well as between the nucleus accumbens and anterior insula.  There is ample evidence to indicate that the nucleus accumbens, particularly the “core” and “shell” influence cortico-limbic-striatal circuitry that promotes impulse control disorders.

Research in rats suggests that deactivation of the nucleus accumbens core and/or shell increases impulsive choice as demonstrated by reduced waiting capacity.  That said, the nucleus accumbens core is more involved in motivational and motor aspects of impulse control – when compared to the shell.  Dysfunction in the nucleus accumbens (core and/or shell) may explain certain aspects of impulse control disorders in humans.

  • Source: http://www.ncbi.nlm.nih.gov/pubmed/24810333

Prefronal cortex & subregions: Those with impulse control disorders often appear to have suboptimal executive function as mediated by the prefrontal cortex.  Most speculate that the prefrontal cortex isn’t fully developed until the mid-20s to early 30s, hence a major reason as to why teenagers and young adults are likely to engage in risky behavior.  Lack of prefrontal activation and/or poor connectivity to other regions (e.g. nucleus accumbens) may increase odds of poor impulse control – possibly to the extent of an ICD.

  • Dorsolateral prefrontal cortex
  • Dorsomedial prefrontal cortex
  • Medial prefrontal cortex
  • Orbitofrontal cortex
  • Ventrolateral prefrontal cortex

Interestingly, a systematic review was conducted among those diagnosed with ADHD and bipolar disorder – two neuropsychiatric conditions often associated with impulsivity.  The purpose for this review was to elucidate how prefrontal dysfunction facilitated impulsive decisions.  Findings indicated that although both disorders exhibited prefrontal dysfunction, the prefrontal correlates associated with impulsivity were contingent upon the disorder.

In other words, those with ADHD were prone to increased impulsivity as a result of dysfunction within the ventrolateral and medial prefrontal cortex.  On the other hand, those with bipolar disorder exhibited impulsivity as a result of orbitofrontal, dorsomedial, and dorsolateral prefrontal cortex dysfunction.  This research indicates that the neural mechanisms of impulse control disorders may be subject to interindividual variation, especially among those with neuropsychiatric comorbidities.

  • Source: http://www.ncbi.nlm.nih.gov/pubmed/25232313

Other research in adolescents attempted to elucidate the neural underpinnings of risky sexual behaviors.  In one study, researchers collected fMRI neuroimaging scans from 20 sexually active adolescents and simultaneously assessed the riskiness of their sexual behavior.  Riskiness was assessed based on self-reports from each of the 20 participants.

  • Insula
  • Right inferior frontal gyrus

After the fMRI scans were collected and riskiness was assessed, researchers interpreted the results.  It was discovered that among the adolescents who engaged in risky sexual pursuits (e.g. unprotected intercourse), there was reduced activation of the prefrontal cortex.  Among those who didn’t engage in risky sexual acts, the prefrontal cortex was more active.

Since this study was conducted on adolescents, it is possible that neural development may occur at a quicker or slower pace based on the particular individual.  Those who experienced faster development of the prefrontal cortex may be less inclined to engage in risky sex.  It would be interesting if researchers conducted a follow-up study with the same sample of individuals to determine if results held up as adults.

It is possible that the underdeveloped “risk” takers may have simply been late-neural developers (“bloomers”) – and upon full development of the prefrontal cortex, risky behaviors may be reduced.  That said, a notable takeaway from this study is that there’s an inverse correlation between activity in the prefrontal cortex and risky sexual behavior, particularly in the insula and right inferior frontal gyrus.  Deficits in these regions lead to reduced attention and engagement (insula) and poorer behavioral inhibition (right inferior frontal gyrus).

Like sexually risky adolescents, it is plausible to consider that reduced activation of the insula and right inferior frontal gyrus may be associated with the impulse control disorder of hypersexuality (or “compulsive sex”).  Perhaps future research attempting to elucidate the distinct neural differences among those with hypersexuality will document similar dysfunction within prefrontal areas.

  • Source: http://www.scn.ucla.edu/pdf/Goldenberg(2013)DCN.pdf

Ventromedial prefrontal cortex: The ventromedial prefrontal cortex (vmPFC) is associated with risk assessment, fear, inhibition of emotional reactions, and aids in decision making.  Individuals with damage to the ventromedial prefrontal cortex often have difficulties making decisions in personal or social settings.  Although the ventromedial prefrontal cortex doesn’t affect one’s intellect, individuals with poor activation of this region often struggle to make a definitive decision.

Researchers discovered that among boys ages 7 to 17, activation of the right ventromedial prefrontal cortex was predictive of impulse control abilities.  Specifically, among boys with compromised impulse control, the right ventromedial prefrontal cortex appeared of reduced volume (especially within the medial sector).  Boys with normative impulse control didn’t exhibit deficits in right vmPFC activation.

These findings have lead many to speculate that the ventromedial prefrontal cortex could predict susceptibility to impulse control disorders.  Since this research was conducted among “boys” without fully developed brains, it is unclear as to whether similar findings apply to adults.  That said, it is evident that decreased volume in the vmPFC leads to impulsive decision-making.

Studies in rodents also support the idea that the ventromedial prefrontal cortex plays a significant role in impulse control.  When the vmPFC was temporarily inactivated in the brains of rats, they performed significantly worse on an impulse control task compared to when it was normally activated.  Based on these findings, one would surmise that similar hypoactivation of the vmPFC in humans could contribute to an impulse control disorder.

  • Source: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2656876/
  • Source: http://www.ncbi.nlm.nih.gov/pubmed/24556205

Dorsolateral prefrontal cortex: The dorsolateral prefrontal cortex has been implicated in impulse control, particularly among those going on diets.  A study among obese patients revealed that long-term dietary success was contingent upon activation of the dorsolateral prefrontal cortex.  Particularly, obese patients that were able to successfully adhere to a specific diet for a long-term exhibited greater activity within the dorsolateral prefrontal cortex (DLPFC) compared to those who failed.

More evidence to support the role of the DLPFC in mediation of impulsivity comes from a study involving patients with borderline personality disorder.  It was noted that grey matter volume in the prefrontal cortex of those with borderline personality disorder was negatively correlated with impulsivity.  In other words, reduced overall dorsolateral prefrontal cortex volume may give rise to impulsive (possibly aggressive behaviors); similar findings may be evident among those with intermittent explosive disorder – a specific ICD subtype.

  • Source: http://www.ncbi.nlm.nih.gov/pubmed/25576647
  • Source: http://www.ncbi.nlm.nih.gov/pubmed/21211852

Orbitofrontal cortex: It has been historically documented that among individuals with damage to the OFC (orbitofrontal cortex), impulsivity is a predominant trait.  Perhaps the most historic example of the OFC’s impact in mediating impulsivity has been described in the case of Phineas Gage – a railway worker who suffered damage to the OFC [as a result of an iron rod penetrating his skull during an explosion].  After damage to his OFC, Gage acted increasingly impulsive – a significant behavioral contrast from his pre-OFC-damaged self.

Scientific literature indicates that the OFC is implicated when we make decisions and select responses.  It is also known to modulate goal-directed behavior via a synergism of thoughts, emotions, and motor responses.  Without proper function in the OFC, individuals are unable to shape their behavior to match predictable outcomes and/or consequences of actions.

It is important to highlight that the OFC does not directly inhibit impulsive behaviors.  Rather, it affects our ability to predict outcomes resulting from certain behaviors.  Those with poor OFC function are unable to foresee the potential deleterious consequences resulting form a particular act of impulsivity.

Researchers also speculate that the OFC plays a role in assessment and valuing outcomes under changing conditions.  In other words, those with poorer OFC function may find it difficult to alter their impulsive behaviors, even if there is greater reward OR less punishment for doing so.  It could be hypothesized that a subset of individuals with ICDs may exhibit deficits in OFC activity.

  • Source: http://psycnet.apa.org/psycinfo/2008-00661-007
  • Source: http://www.ncbi.nlm.nih.gov/pubmed/14985269/

Neurotransmitters & Receptors

Abnormal neurotransmission is associated with the development of impulse control disorder.  Specifically, many individuals diagnosed with ICDs tend to exhibit abnormal neurotransmission of dopamine.  In addition to dopaminergic systems affecting pathology of ICDs, the neurotransmission of: GABA, glutamate, norepinephrine, serotonin, and endorphins may also play critical roles.

Dopamine dysfunction: It is thought that dysregulation of dopamine in striatal regions such as the nucleus accumbens may impair impulse control.  Since many impulse control disorders involve reward-seeking / gratification, dopaminergic dysfunction likely plays the most critical role in ICD development.  Researchers have discovered that among cocaine abusers, D2 dopamine receptor densities are severely reduced and that repeated self-administration of cocaine in monkeys is associated with lower D2 receptor counts.

Deficient D2 receptors can lead to impaired metabolism of dopamine within the orbitofrontal cortex (OFC), which increases likelihood of impulsive, immediately-gratifying behaviors.  Striatal D2 receptor density is predictive of impulsivity in rats – the rats with fewer D2 receptors act more impulsively and are more susceptible to addiction.  In humans, dopamine is understood to modulate the rewards and reinforcement associated with gambling tasks.

Among individuals classified as pathological gamblers, lower levels of DOPAC and HVA metabolites appear in the cerebrospinal fluid; this suggests low dopamine concentrations.  Evidence that dopamine plays a significant role in impulse control disorder comes from Parkinson’s patients being treated with dopamine receptor agonists.  Prior to receiving the dopamine receptor agonists, most patients have no difficulties with impulse control.

However, with repeated administration of a dopamine agonist, 10% of all patients will develop a drug-induced impulse control disorder.  Since impulse control disorder sometimes occurs among those treated with levodopa (~6% of patients), both the concentration and receptor stimulation of dopamine likely influence ICDs.  Dopamine receptors may play a more significant extent than extracellular concentrations of dopamine, but high dopamine may also lead to impulsivity.

  • Source: http://www.ncbi.nlm.nih.gov/pubmed/18278382

GABA and Glutamate: The inhibitory neurotransmitter GABA and excitatory neurotransmitter glutamate may play a role in the development of ICDs.  Though the role of GABA may not be direct, many speculate that GABA transmission affects dopaminergic processes which give rise to impulse control disorders.  Administration of GABAergic agents appear to demonstrate efficacy for the treatment of cocaine addiction and decrease impulsive tendencies.

The transmission of glutamate, particularly within the nucleus accumbens, is associated with reward-seeking behaviors.  Administration of agents that increase extracellular concentrations of glutamate while simultaneously decreasing synaptic release of glutamate – tend to improve pathological gambling and addiction.  Those diagnosed with ICDs may be deficient in GABA and appear to release abnormally large quantities of synaptic glutamate.

  • Source: http://www.ncbi.nlm.nih.gov/pubmed/18278382

Low Serotonin: The serotonin system is believed to play a major role in the development of impulse control disorders (ICDs).  A majority of those diagnosed with ICDs tend to exhibit low serotonin levels compared to those without ICDs.  For this reason, many impulse control disorders are successfully managed or treated with serotonergic antidepressants (SSRIs).

Neuroscience researchers have discovered that 5-HT (serotonin) neurons signal from the dorsal raphe nucleus throughout the brain to other regions such as the hippocampus, frontal cortex, and amygdala.  Depletion of serotonin in animal models results in impulsive decision making.  Conversely, stimulation of serotonin receptors with a 5-HT agonist, minimizes impulsive decision making.

Mice lacking certain serotonin receptors and depletion of tryptophan (an amino acid precursor) increases motor impulsivity.  Furthermore, among pathological gamblers, individuals with impulsive personality types, and animals who engage in risky behaviors – lower concentrations of 5-HIAA (serotonin metabolites) are exhibited; this signifies deficient serotonin.  Therefore, in many cases of those diagnosed with ICD, the serotonin system may be dysfunctional.

  • Source: http://www.ncbi.nlm.nih.gov/pubmed/18278382

High Norepinephrine: Norepinephrine is a neurotransmitter that mediates attention, arousal, vigilance, and cognition.  There are links between low norepinephrine and depression, ADHD, and fatigue.  Those who are pathological gamblers tend to exhibit heightened noradrenergic tone – thereby increasing readiness for risk-taking and gambling pursuits.

Among problem gamblers, elevations of norepinephrine concentrations and its metabolites have been discovered in cerebrospinal fluid – compared to those who were not problem gamblers.  This suggests that among those with the pathological gambling subtype of ICDs, overactive norepinephrine systems may be an important cause.  When a pathological gambler “wins” in a gambling task, norepinephrine production further skyrockets; possibly indicating that it reinforces the gambling behavior.

It is unclear as to whether a similar noradrenergic tone is evident among individuals with other forms of ICDs such as hypersexuality, compulsive buying, or kleptomania.  Possibly similar spikes in noradrenergic activity prior to, during, and/or immediately after an impulsive task lead to additional reinforcement in all cases.  The noradrenergic activity may be simultaneously accompanied by other monoaminergic alterations (e.g. dopamine increases and serotonin decreases) during the behavior associated with ICD.

  • Source: http://www.ncbi.nlm.nih.gov/pubmed/18278382

Beta-endorphin: Beta-endorphin functions as an agonist at opioid receptor sites, perhaps most notably at the mu-receptor.  Upon binding to the mu-opioid receptor, beta-endorphin is thought to elicit similar neurophysiological effects to morphine.  Individuals classified as pathological gamblers [in accordance with ICD criteria] tend to have abnormally high concentrations of beta-endorphin production during the gambling task.

This surge of beta-endorphin evokes a similar emotional response as is attained from opioidergic drugs.  Although the stimulation from endogenous beta-endorphin spikes is compared to those attained from exogenously administered opioids isn’t nearly as significant, the endogenous elevations reinforce the impulsive decision to engage in the gambling task.  In other words, pathological gamblers have a tough time resisting the urge to gamble, in part, because of the opioidergic response generated via beta-endorphin each time they play.

It is important to also consider the gestalt of the neurophysiological changes occurring among pathological gamblers each time they gamble.  The beta-endorphin surge not only elicits emotional changes itself, but it modulates the release of dopamine and GABA via mesolimbic pathways in the ventral tegmental area (VTA).  Specifically, stimulation of mu-opioid receptors in the VTA inhibits GABA and releases dopamine.

Moreover, the decrease in GABA and increase in dopamine is accompanied by aforestated changes in neurotransmission such as elevated norepinephrine, as well as the stimulatory hormone “cortisol.”  The entire cascade of neurochemical changes that occur within the body of a pathological gambler, as well as individuals with other forms of ICDs is complex.  That said, it is likely that for many, the opioid system is implicated.

  • Source: http://www.ncbi.nlm.nih.gov/pubmed/15288706
  • Source: http://www.ncbi.nlm.nih.gov/pubmed/10388157

Cortisol: Among individuals with impulse control disorders, there are thought to be abnormalities in circulating concentrations of cortisol.  Cortisol classified as a glucocorticoid steroid hormone and is manufactured in the adrenal cortex.  In stressful situations or upon activation of survival mechanisms (e.g. freeze-fight-flight response), cortisol levels tend to increase.

Though cortisol dysregulation may play a less significant role in ICDs compared to other neurotransmitters, evidence indicates an inverse relationship between levels of cortisol levels and impulsivity in adolescents.  Other research has suggested that cortisol reactivity has a major influence upon development of addictions, and possibly inability to resist impulsive tendencies.  Particularly, stress has been found to decrease cortisol reactivity and increase impulsive behaviors.

Further evidence from rodent studies suggests that specific cortisol receptors such as the mineralocorticoid receptor (MR) and glucocorticoid receptor (GR) modulate our ability to feel rewards from dopaminergic drugs.  We could speculate that among those with ICDs such as problem gamblers, the mineralocorticoid receptor may be overstimulated whereas the glucocorticoid receptor may be underactive.  Among pathological gamblers especially, cortisol, cortisol reactivity, and corticoid receptors affect impulses.

  • Source: http://www.ncbi.nlm.nih.gov/pubmed/20217435/
  • Source: http://www.ncbi.nlm.nih.gov/pubmed/12404678
  • Source: http://www.ncbi.nlm.nih.gov/pubmed/23085387

Genetics & Epigenetics

Scientific literature has revealed genetic correlates that increase susceptibility to develop an impulse control disorder.  Possessing certain genes and/or lacking others may increase your underlying predisposition to behave impulsively and may lead you to develop an ICD.  Furthermore, your epigenetics or how your genes are altered in expression by environmental factors also may affect inclination to develop a particular impulse control disorder.

Dopaminergic genes

DRD4: There is evidence that variations of the DRD4 gene, which influences the expression of D4 dopamine receptors, can increase likelihood of an impulse control disorder.  Children with ADHD tend to exhibit variations in DRD4, as well as the gene SLC6A3 (which alters function of the dopamine transporter).  Research suggests that certain polymorphisms, as well as epigenetic influences (e.g. parenting) affect impulsivity.

SLC6A3: This gene is responsible for encoding the dopamine transporter (DAT) and is associated with ADHD, especially when accompanied by DRD4.  When expressed along with DRD4 variations, impulsivity is a likely manifestation.  Even when expressed without DRD4 variants, SLC6A3 as a standalone can contribute to impulsive tendencies.

D2A1: Those with the A1 allele of the D2 receptor are more likely to abuse drugs, compulsively eat, and smoke.  Additionally, pathological gamblers tend to express D2A1 at nearly a 2-fold higher rate when compared to controls.  Although not all pathological gamblers may have the A1 allele of the D2 gene, it may be associated with the pathological gambling ICD subtype.

DRD1: There is evidence to suggest that expression of the DRD1 gene influences likelihood of addiction and compulsive behaviors.  Specifically, individuals who are carrying the DRD1 “11” genotype are more likely to engage in gambling, compulsive buying, and alcohol use.  The DRD1 “22” genotype also appears to increase likelihood of addictive and compulsive tendencies, but not to the same extent as DRD1 “11” genotypes.

  • Source: http://www.ncbi.nlm.nih.gov/pubmed/7550364/
  • Source: http://www.ncbi.nlm.nih.gov/pubmed/17063402/
  • Source: http://www.ncbi.nlm.nih.gov/pubmed/8807661/
  • Source: http://www.ncbi.nlm.nih.gov/pubmed/10402503/

Serotonergic genes

TPH1: Research indicates that the serotonin system generally plays a significant role in the development of impulse control disorders.  Some speculate that the TPH1 gene (tryptophan hydroxylase 1) may reduce serotonin production, thereby increasing susceptibility to impulse control disorders.  Those with ICDs tend to have lower levels of 5-HIAA metabolites in cerebrospinal fluid than those without ICDs – indicating that serotonin production is deficient.  Impulsive violent criminals are more likely to express the TPH1 variant than usual.

SLC6A4: Impulsivity and substance abuse have been associated with deficits in functionality of the serotonin transporter.  Polymorphisms in the SLC6A4 gene, particularly those that lead to production of less protein, are associated with an array of neuropsychiatric conditions such as anxiety and depression.  Researchers believe that short alleles of the SLC6A4 gene may play a role in the development of ICDs – especially in males.

MAOA: The gene MAOA encodes the enzyme MAO-A which breaks down dopamine, norepinephrine, and serotonin.  Polymorphisms and mutations of the MAOA gene may be associated with ICDs.  For example, one mutation known as “Brunner Syndrome” involves a mutation of the MAOA gene resulting in impulsive behavior (e.g. hypersexuality, pyromania, etc.) as well as a reduced IQ.

  • Source: http://www.ncbi.nlm.nih.gov/pubmed/10471073/

Opioidergic genes

OPRM1: Polymorphisms in the OPRM1 gene are known to alter binding of endorphins to the mu receptor.  As an example, the A118G variant results in 3-fold more binding and activation, leading opioid users to experience more potent rewards upon stimulation.  This increases likelihood of addiction to any behaviors (e.g. pathological gambling) that activate the mu opioid receptors with endogenous beta-endorphin.

OPRK1: Various haplotypes of the OPKR1 gene have been associated with opioid dependence.  The OPRK1 gene modulates perception, pain, motor control, and mood.  Dynorphin binds to the receptor which can alleviate pain, but also tends to induce dysphoria.  Those with ICDs are thought to encode polymorphisms of the OPKR1 gene that activate p38, resulting in kappa-opioid receptor dependent behaviors.

  • Source: http://www.ncbi.nlm.nih.gov/pubmed/9689128/
  • Source: http://www.ncbi.nlm.nih.gov/pubmed/12884968/

Brain damage

Those who’ve endured any form of brain damage may be at increased risk of an impulse control disorder.  Damage to subregions of the prefrontal cortex such as the orbitofrontal cortex are well-documented as increasing susceptibility to impulsive behaviors.  The damage inflicted upon various areas of the brain, regardless of whether stemming from drug abuse, neurodegeneration, or head trauma – can also have epigenetic implications that could increase likelihood of ICD development.

Acquired brain injury: Some individuals experience an acquired brain injury (ABI) as inflicted by tumors, hypoxia, and strokes.  While rehabilitation may prevent significant long-term damage stemming from an ABI, some of the damage may be irreversible.  This irreversible damage may lead to an impulse control disorder or excessive, bizarre forms of impulsivity.

In one clinical example, a 49-year-old man suffered a stroke that damaged regions such as the: ipsilateral striatum, dorsolateral, and orbitofrontal cortex.  Although he seemed to have recovered well without characteristics of apathy, mania, or depression – the man exhibited pathologically impulsive generosity.  Acquired brain injuries, particularly unilateral lesions, may trigger unpredictable impulsive behaviors.

  • Source: http://www.ncbi.nlm.nih.gov/pubmed/23962063

Neurodegenerative diseases: Individuals with neurodegenerative diseases tend to experience an insidious decline in brain function accompanied by structural decay and brain cell death.  Various common neurodegenerative diseases include: ALS, Alzheimer’s, Huntington’s, and Parkinson’s disease.  Currently there are no known ways to inhibit nor reverse the progression of such diseases.  Furthermore, the structural damage and death of precious neurons may increase susceptibility to ICDs during the progression of the disease.

Whether an individual is likely to develop an ICD as a result of a particular neurodegenerative disease may depend on interindividual disease progression, severity, and treatment.  As was already mentioned, many treatments for Parkinson’s disease, particularly dopamine agonists, result in 10% of patients developing an impulse control disorder.  However, a decline in prefrontal function and/or centers of the brain responsible for impulse regulation may provoke an ICD in susceptible populations.

Deficits in long-term planning and impulse control have been discussed among individuals with nearly every type of neurodegenerative disease.  Loss of dopaminergic function and damage to various structures within the brain as a result of disease progression may spur an impulse control disorder among those suffering from neurodegeneration.

  • Source: http://www.ncbi.nlm.nih.gov/pubmed/25925985
  • Source: http://www.ncbi.nlm.nih.gov/pubmed/18580596
  • Source: http://www.ncbi.nlm.nih.gov/pubmed/24765067

Neurotoxicity: Many neurotoxins can inflict similar damage upon brain structures and neurotransmission as neurodegenerative diseases.  Continuous exposure to certain drugs (e.g. MTPT) and environmental pollutants (e.g. toxic mold, lead, etc.) can induce neurotoxicity, leading to apoptosis (programmed neuronal death).  Even slight damage to regions such as the prefrontal cortex could have disastrous implications for impulse control.

Furthermore, it is understood that toxins alter expression of various genes (via epigenetics) and can cause genetic mutations.  Changes to genes and epigenetic expression following toxic exposures may lead to the development of an impulse control disorder.  An individual regularly exposed to neurotoxins, either knowingly (e.g. illicit drugs) or unknowingly (e.g. pesticide inhalation) – may develop an impulse control disorder as a result of the cumulative exposure.

Traumatic brain injury: Traumatic brain injuries (TBIs) can increase impulsive behaviors, and possibly lead to development of impulse control disorders.  Examples of common TBIs include: concussions, contusions, and penetrations.  Concussions, for example, can detrimentally affect the blood-brain-barrier (BBB), allowing chemicals to enter the brain that would otherwise have been blocked.

Although the site of the specific TBI matters in regards to prediction of symptoms and functional outcomes, any TBI could lead to impulse control disorder.  It is understood that traumatic brain injuries often lead to impairments in executive functions (e.g. critical thinking, problem solving, attention, etc.) – and may increase likelihood of impulsivity.  While rehabilitation may be a viable strategy for offsetting a TBI-induced ICD, rehab may not always prove efficacious.

  • Source: http://www.ncbi.nlm.nih.gov/books/NBK185336/

Autonomic nervous system

There appear to be differences in activation of the autonomic nervous system (ANS) of those with impulse control disorders and those without.  Specifically, when presented with cues related to the uncontrollable impulse (e.g. buying), there may be increased activation of the sympathetic nervous system.  This increased activation of the sympathetic nervous system is associated with release of catecholamines (e.g. dopamine and norepinephrine) and hormones such as cortisol.

  • Overactive sympathetic nervous system
  • Underactive parasympathetic nervous system
  • Autonomic nervous system dysfunction

Among pathological gamblers, for example, research has shown differences in skin conductance and heart rate during cues related to a gambling task – indicating heightened sympathetic activity.  Since those with impulse control disorders are thought to produce less serotonin and GABA, it may be that overactivation of the sympathetic nervous system is to blame.  Those without ICDs may have greater activation of the parasympathetic branch, thereby allowing for more production of serotonin and GABA.

Chronic dysfunction of the autonomic nervous system is likely perpetuated unless deliberately corrected via pharmacology or conscious upregulation of parasympathetic pathways.  Though research is highly focused on neurotransmission in the involvement of ICDs, changes in autonomic activation not only affect neurotransmitter levels, but can induce epigenetic alterations.  An imbalanced autonomic nervous system is likely overlooked as a potential direct cause of impulse control disorders.


The role of neuroplasticity in development of ICDs may be more significant than is discussed in literature.  For example, someone who engages in addictive behaviors from a young age (e.g. pathological gambling, compulsive buying, etc.) may be shaping his/her brain via neuroplastic reinforcement to engage in more similar behaviors in the future.  The influence of neuroplasticity in the onset of ICDs may be particularly significant among adolescents and young adults who lack a fully formed prefrontal cortex.

Prior to full development of the prefrontal cortex, neuroplastic changes to support an impulse control disorder may serve to impair prefrontal development while simultaneously increasing rewarding sensations associated with a particular impulse.  This may generate a particular addiction or the inability to resist ongoing temptations.  Research has suggested that the mesolimbic reward pathways of the brain may be heavily influenced by neuroplastic changes and contribute to ICDs.

Among those with Parkinson’s disease subject to treatment with dopamine agonists, onset of ICDs is facilitated by dysfunction in the mesocorticolimbic network.  Engagement in any particular ICD (e.g. compulsive buying) shapes the brain activation to support that activity with greater frequency in the future.  Ongoing pathological gambling reduces activation in regions such as the thalamus, basal ganglia, and cortical areas of the brain.

In other words, the more you use or don’t use a particular region and/or neural network in the brain (as a result of an ICD), the tougher it will be to treat an ICD in the future.  Fortunately, cessation and/or proper management of an impulse for an extended period of time may correct dysfunctional neural activation as was induced by neuroplastic changes stemming from the ICD.

Psychological aspects

Though many factors such as genetics and/or neuroactivation can increase susceptibility to impulse control disorders – or perhaps directly cause them – psychological factors should be discussed as potential influential causes.  Certain individuals may have a tendency to seek out impulsive behaviors and repeat them uncontrollably based on a combination of cognitive-behavioral learning and to cope with emotional voids and/or unpleasant emotion.

  • Cognitive: A person may learn a particular behavior via observation of a friend or family member. He/she may engage in the same behavior to mimic the observations of others in his/her environment and/or to “fit in.” Upon doing so, the individual may cognitively “learn” that the particular behavior gives rise to rewarding feelings of pleasure.  This strengthens circuitry in the brain to promote thoughts that increase likelihood of that behavior in the future.
  • Emotional: In addition to the emotional response elicited by the particular behavior, some individuals may engage in impulsive behaviors as a means of filling an emotional void. For example, it is well-understood that those with covert schizoid personality disorder frequently pursue anonymous sexual encounters to cope with the emotional void (e.g. flat affect) induced by the disorder.  Certain individuals may end up engaging in these impulsive behaviors to fill the void only to have them spiral out of control; consuming their existence.  In other cases, the impulsive behaviors may be engaged in as a means of coping with unpleasant emotions (e.g. anxiety) rather than a particular emotional void.

Impulse Control Disorder (ICD) Treatment

There is no universally established treatment for individuals with impulse control disorders, particularly if they are drug-induced.  Therefore, treatment for impulse control disorders should be determined based on the specific ICD subtype, as well as hypothesized causative underpinnings (e.g. serotonergic deficits, reduced activity in the prefrontal cortex, overactive reward centers, etc.).  Due to the inexact science of psychiatry and significant potential for causative interindividual variation, it may take some trial and error to optimize interventions.

Antidepressants: Antidepressants are considered common first-line treatments for ICDs, but their clinical efficacy is regarded as questionable.  Efficacy of antidepressants, particularly serotonergic agents may be subject to interindividual variation based on the specific neurochemical abnormalities associated with the ICD.  If serotonin deficits contributed heavily to a person’s ICD, then utilization of an SSRI may provide significant benefit.

  • SSRIs: Selective serotonin reuptake inhibitors function by inhibiting the reuptake of 5-HT (serotonin), allowing for increased signaling in the neuronal cleft (synapse). Several randomized controlled trials (RCTs) have investigated the efficacy of SSRIs for the treatment of ICDs, but results are mixed.  Some trials have demonstrated significant benefit over a placebo, while others document no improvement compared to a placebo.  Drugs like Celexa, Lexapro, Luvox, and Prozac were no more effective than placebos for trichotillomania, hypersexuality, and compulsive buying.  While they may reduce symptoms related to ICDs (e.g. anxiety, depression, sex drive) – they may not fully alleviate ICDs as standalone interventions.
  • Tricyclics: Some TCA (tricyclic antidepressants) have been tested in randomized controlled trials (RCTs) for the treatment of trichotillomania. In a head-to-head comparison trial between clomipramine and desipramine, it was discovered that clomipramine significantly reduced trichotillomania symptoms whereas desipramine provided no benefit.  Perhaps some patients may respond better to tricyclic antidepressants than serotonergic antidepressants (SSRIs) for certain ICDs.

Mood stabilizers: Some believe that mood stabilizers may improve outcomes among individuals with impulse control disorders.  Mood stabilizers appear to provide significant benefit in reducing comorbid ICDs among those diagnosed with bipolar disorder.  Like antidepressants, the efficacy of mood stabilizers for the treatment of impulse control disorders (among those without bipolar disorder) isn’t fully elucidated.  Most research suggests that they may provide limited, patient-specific benefit.

  • Lithium: Evidence indicates that treatment with lithium carbonate (~0.87 mEq/L) is superior to a placebo in decreasing symptoms of pathological gambling over the course of 10 weeks. Lithium appears to decrease gambling urges and thoughts, however, it may not affect number of gambling episodes per week nor money lost from such behaviors.  Although it decreases urges, it may not be entirely effective for the treatment of ICDs.
  • Depakote: In a randomized, double-blind study over the course of 12-weeks, divalproex sodium appeared to provide no benefit for those with intermittent explosive disorder, a subtype of ICD. The treatment failed to reduce aggression and outbursts among those with a primary IED (intermittent explosive disorder) diagnosis.
  • Valproate: There is evidence to suggest that valproate may be effective for those with pathological gambling subtypes of impulse control disorders. It appears to modulate both GABA and serotonin systems to decrease inclination to engage in pathological gambling.

Opioid antagonists: As was discussed, opioidergic systems may contribute to the maintenance of an impulse control disorder.  Targeting opioid systems with pharmacology may prove efficacious for reducing likelihood of an ICD.  Particularly, treatment with opioid receptor antagonists appears to offer some benefit.

  • Naltrexone: Administration of naltrexone has shown efficacy for the treatment of pathological gambling, compulsive buying, and hypersexuality. Perhaps of all agents utilized to treat ICDs, naltrexone has the best track-record.
  • Nalmefene: At a dose of 40 mg/day, this long-acting opioid receptor antagonist has proven efficacious in the management of pathological gambling among individuals with Parkinson’s disease. Due to the fact that it functions similar to naltrexone (as an opioid receptor antagonist), it may also be a viable intervention for compulsive buying and hypersexuality.

Glutamatergics: The rewarding behaviors associated with ICDs (e.g. gambling) appear to affect neuroplasticity of extracellular glutamate in the nucleus accumbens.  Emerging evidence indicates that administration of glutamatergic agents (as to bolster glutamatergic activity in the nucleus accumbens) may decrease reward-seeking tendencies among those with addictions and ICDs.  In particular, they appear effective in treating pathological gambling and trichotillomania.

  • N-acetylcysteine (NAC): Administration of the amino acid known as N-acetylcysteine (a cysteine prodrug) increases concentrations of extracellular glutamate while concurrently activating inhibitory metabotropic glutamate receptors. This decreases the release of glutamate from synapses and replenishes extracellular glutamate in the nucleus accumbens.  Trials indicate that NAC can decrease cravings and compulsions related to pathological gambling ICDs.

Source: http://www.ncbi.nlm.nih.gov/pubmed/24219002

Psychostimulants: Many people find that psychostimulants such as Adderall, Vyvanse, and methylphenidate (Ritalin) decrease impulsivity.  It is unclear as to whether these agents would simultaneously improve symptoms of ICDs.  There is evidence to suggest that they may improve self-control in many users.  They may provide most benefit to those with prominent dopaminergic underpinnings associated with their ICDs.

Unfortunately, psychostimulants are associated with rapid onset tolerance and if abused, can decrease control of impulses.  Therefore, it is unlikely that most individuals pursuing psychopharmacological treatment for ICDs will receive a psychostimulant intervention unless comorbid ADHD is apparent.

Eugeroics: Eugeroics such as modafinil appear to decrease risky decision making, desire to gamble, and disinhibited behaviors among those with high baseline impulsivity.  Since most individuals with ICDs are thought to have high baseline impulsivity, perhaps treatment with modafinil or similar substances (e.g. armodafinil) would effectively treat ICD symptoms.  Among those with low baseline impulsivity (e.g. those without ICDs), eugeroics have propensity to increase impulsive behaviors.  Among populations with ICDs, and especially in cases of comorbid narcolepsy, modafinil may be an optimal intervention.

  • Source: http://www.ncbi.nlm.nih.gov/pubmed/19300566

Cognitive Behavioral Therapy (CBT): All individuals with an impulse control disorder should pursue cognitive behavioral therapy.  While pharmacological treatments may help adjust neurophysiological activity to increase self-control and/or decrease temptation to engage in an impulsive behavior, the simultaneous potential benefit to be attained from CBT may be equally as significant.  CBT helps patients learn strategies to successfully manage impulsive tendencies without pharmacology, although when employed simultaneously (with pharmacology), benefits may be synergistic.

Furthermore, modification of cognition and behavior with CBT will facilitate rewiring of the brain through neuroplasticity.  Although activity in the centers of the brain associated with reward-seeking is likely high and activity in regions associated with self-control is likely reduced among those with ICDs, implementation of regular CBT can help a patient correct these abnormalities in activation.  The speed by which activation is normalized may depend on the severity of the underlying impulse control disorder and duration over which a person has engaged in the impulsive behaviors.

Additionally, the specific CBT techniques employed may differ based on the particular patient and subtype of impulse control disorder.  As an example, for the treatment of pathological gambling, a cognitive behavioral therapist may employ techniques such as: systematic desensitization, aversion therapy, relaxation training, covert sensitization, or imaginal desensitization.  In addition to the aforestated techniques, psychoeducation, cognitive-restructuring, and relapse prevention exercises may be conducted.

  • Source: http://www.ncbi.nlm.nih.gov/pubmed/17713695

Self-Directed Neuroplasticity: Someone may also want to implement changes in their own thinking and behavior via self-directed neuroplasticity as a complement to psychotherapy and/or psychopharmacology.  This can be accomplished by consciously overriding impulsive urges with pre-planned, non-addictive behaviors (e.g. gardening).  As an example, consider the hypersexual individual who is constantly thinking about sex and cannot control such impulses.

If you have the awareness that you suffer from hypersexuality, you can take steps to intervene and ultimately rewire your brain.  This would involve disposing of all “triggers” and/or cues that may lead to engagement in unwanted behavior.  Next, you’d want a list of numerous alternative activities to engage in each time you have the urge to seek out sex, masturbation, porn, etc.

The goal is to consciously shift your focus away from the problematic, overactive network that’s facilitating the ICD.  This can be accomplished by carrying a notepad full of alternative activities to do each time hypersexual thoughts or urges arise (e.g. going for a walk, exercising, reading a book, gardening, etc.).  Over time, your brain will naturally rewire itself to engage in more of the newly introduced activity (e.g. gardening) and be less prone to future hypersexuality.

Self-directed neuroplasticity may not work for everyone due to the fact that many don’t understand how to properly use it.  Those interested in learning how to overcome any addiction and/or ICD – should understand how to use neuroplasticity to their advantage.

What if the ICD was drug-induced? (Treatments)

If your impulse control disorder was induced by a drug, the most logical solution is to discontinue the particular drug in favor of another.  If you’re unable to discontinue the drug (for some reason), a dosing adjustment (e.g. reduction) would be your best bet.  If the adjustment in your dosing fails to provide benefit, your doctor may prescribe an adjunctive drug to combat the impulsivity.

  • Reduce dosage: Sometimes a simple reduction in dosing can mitigate drug-induced impulse control disorders. The only problem with reductions is that they may compromise the efficacy of the drug to treat a particular medical condition.
  • Discontinuation: A subset of users may need to discontinue a drug if it is causing an impulse control disorder. For example, many people taking dopamine agonists such as Mirapex experience gambling-related ICDs and are recommended to discontinue by medical professionals (in favor of another option).
  • Adjunctive agents: Preliminary research indicates that antidepressants, mood stabilizers, glutamatergics, and opioid receptor antagonists – may benefit those with impulse control disorders. Your doctor may be able to come up with a safe adjunct prescription that attenuates impulse control issues induced by another drug.

How does an impulse control disorder differ from similar psychiatric disorders?

Many individuals diagnosed with ADHD (attentional deficit/hyperactivity disorder), a well-documented psychiatric disorder, exhibit symptoms of impulsivity.  However, among those diagnosed with ADHD, impulsivity is generally neither the predominant nor standalone symptom.  Those with ADHD tend to experience a cornucopia of other symptoms such as inability to maintain attention, disorganized thoughts, fidgetiness, and hyperactivity.

Another common psychiatric diagnosis is bipolar mania which is often associated with heightened impulsivity acted out in the form of sexual encounters, shopping sprees, etc.  In this case, the impulsivity does not occur as a standalone symptom, it is one of many symptoms including: euphoria, rapid speech, excessive energy, insomnia, irritability, etc.  Upon treatment of bipolar mania, the impulsivity abates.

To fit the diagnostic criteria for an impulse control disorder, the chief symptom should be an inability to resist urges, temptations, or impulses.  The predominant, all-encompassing feature of ICDs is impulsivity yielding deleterious consequences.  Moreover, in legitimate diagnoses of ICD, the impulsivity is often isolated to just one (possibly two) niches such as: gambling, sex, shopping, etc.

Could someone get diagnosed with ICD and another psychiatric disorder?

Yes.  Impulse control disorder may be diagnosed concurrently along with various psychiatric conditions such as: ADHD, anxiety disorders, depression, PTSD, substance abuse, etc.  For example, a patient may appear to struggle with an inability to resist the urge to gamble while simultaneously suffering from major depression.  In this case, the individual may be diagnosed with major depression and ICD.

For a valid diagnosis, a skilled psychiatrist will need to distinguish the ICD from impulsivity as a symptom of another condition such as ADHD or bipolar disorder.  If symptoms of the initially diagnosed condition are successfully managed with pharmacology, yet the inability to resist impulsive urges remain, an ICD comorbidity may be apparent.  This may require treatment with a cocktail of medications – some of which target one condition and the others of which target the impulse control disorder.

Impulse Control Disorder (Risk Factors)

Evidence suggests that some individuals may be more likely to develop impulse control disorders than others.  Keep in mind that just because you may exhibit many risk factors for an impulse control disorder, it does not mean that you’re automatically guaranteed to develop one.  However, if these risk factors are presented in a family member or friend – you may want to monitor his/her behavior to ensure that they aren’t struggling with an ICD.

  • Bipolar diagnosis: If you have a family member that has been diagnosed with bipolar disorder, you may be more likely to develop an ICD. This is due to the fact that a symptom of the manic state of bipolar disorder is impulsivity.  Those with family members that’ve been diagnosed with bipolar disorder may share similar neural features and/or genetics to bolster propensity of ICD development.
  • Cigarette smoking: Those who smoke cigarettes are at higher risk than average to experience an impulse control disorder. Smoking cigarettes is a sign that individual have difficulty resisting temptation (e.g. the nicotine buzz).  Additionally, smoking may reinforce other addictive behaviors via association and/or by increasing activation within reward centers of the brain.  Some individuals may smoke for modulation of neurotransmitters and/or to reverse deficiencies in arousal – possibly reasons to explain desire to engage in impulsive behaviors.
  • Familial gambling problems: If you have a problem gambler in your family, you have a greater risk of developing an ICD. Although you may be most likely to develop the similar ICD subtype of pathological gambling, you could also develop a distinctively different ICD such as: hypersexuality or compulsive buying.
  • Family members with ICD: If you have a family member with an impulse control disorder (ICD), you are at greater risk of developing the condition. There may be certain social, genetic and/or environmental links to ICD via families that increase your susceptibility.  For example, if your dad or brother is a pathological gambler – it may increase likelihood that you’ll follow in his footsteps.
  • Impulsive personality: Those with a personality style characterized by impulsiveness are thought to be at greater risk for development of an ICD. This impulsive personality style may have been influenced by genetic, epigenetic, neurotransmitters, and neuroplasticity.  Should a person with an impulsive personality continue to engage excessively in impulsive behaviors, he/she may develop a full-blown ICD.
  • Living in the United States: Individuals living in the United States have been documented as being at highest risk of developing an ICD. This may be due to the abundant opportunities to act upon impulses such as in betting online, shopping online, or finding sexual partners online.  It could also be due to social differences such as greater independence and less collective monitoring and/or intervention of behaviors among those afflicted.
  • Male sex: Research indicates that men tend to experience impulse control disorders to a greater extent than females. This may be due to the fact that males are inherently more likely to engage in risky behaviors than females.  If you are male, understand that you are at greater risk of developing an ICD by comparison to female counterparts.
  • Parkinson’s disease: Those with Parkinson’s disease exhibit dopaminergic dysfunction in the striatum and basal ganglia regions of the brain. In addition, neurodegeneration in a multitude of areas can lead to manifestation of unpredictable symptoms.  The pathology of Parkinson’s itself may cause impulse control disorders in some users.  However, most commonly is that the treatments used for Parkinson’s disease (e.g. dopamine agonists) tend to provoke drug-induced ICDs.
  • Substance abuse history: Individuals that personally have a history of substance abuse are more likely to experience an impulse control disorder. This may be due to the fact that substance abuse can inflict dysfunction within neurotransmitter systems, decrease prefrontal activation, and enhance connectivity in regions associated with addiction.  It should be noted that familial substance abuse is also a risk factor; if your family members struggled with substance abuse – you’re at greater risk for an ICD.
  • Unmarried: Exactly how or why an unmarried individual is more likely to develop an impulse control disorder is unclear. Perhaps married individuals are monitored more carefully by spouses and therefore, when any excessive shopping, gambling, etc. occurs – the spouse intervenes.  Single individuals have nobody to monitor their behavior, and impulse control disorders may go undetected for a longer duration.  Furthermore, there may be some links between the autonomy, choices, and personality styles of unmarried persons that increase odds of an ICD.
  • Younger age: Younger individuals more frequently develop impulse control disorders than older or elderly adults. This is especially noticeable among those diagnosed with Parkinson’s disease.  Younger onset of Parkinson’s disease is associated with increased likelihood of developing an ICD.  It could also be that ICDs are more likely in younger individuals due to the fact that they do not have a fully developed brain (e.g. prefrontal cortex isn’t fully formed).
  • Source: http://www.ncbi.nlm.nih.gov/pubmed/25370355
  • Source: http://www.ncbi.nlm.nih.gov/pubmed/20457959

Do you have an impulse control disorder?

If you have an impulse control disorder (ICD), share a comment below describing your condition.  Mention the specific subtype of ICD that you struggle with (e.g. kleptomania) and the age at which it first became a problem.  Do you believe anything (or things) in particular influenced your development or susceptibility to developing an impulse control disorder?

Upon self-realization that you struggle with an inability to control impulses, did you seek psychological or psychiatric help?  If you sought help, be sure to mention the efficacy of the specific interventions (e.g. CBT, SSRIs, etc.).  If you never sought help for your condition, do you have any particular reason for avoiding professional guidance and treatment?

For the subset of individuals that are experiencing drug-induced impulse control disorder, what medication were you taking and what was the dosage?  Discuss how the impulse control disorder has detrimentally affected your life and/or the lives of others (e.g. family, friends, etc.).  Understand that if you (or someone you know) is struggling with an impulse control disorder, it’s never too late to seek treatment.

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