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A patient is brought to the emergency department by her daughter for bizarre behavior and symptoms of mania after gambling  from the casino for 48 continuous hours. 

A Case of Gambling Disorder

If money is not the lure for problem gamblers, what is? 

Mini Quiz: Gambling Disorder

Impulsivity has long been thought to be an important risk factor for suicide. But recent research, 

, suggests that the reality is counterintuitive.

A) Impulsivity is higher among suicide attempters than among those who consider suicide but do not attempt

B) Impulsive people tend to make impulsive suicide attempts

C) Impulsivity is similarly elevated in suicide attempters and those who have suicidal thoughts but have never attempted

D) Impulsivity has no relationship to suicidality

Impulsivity has long been thought to be an important risk factor for depression and suicide. But recent research suggests that the reality might actually be counterintuitive. 

Mini Quiz: Impulsivity Risk Factors

It is a pleasure to introduce this Special Report on impulsivity. Impulsivity, which can be defined as an overvaluation of short-term reward over long-term goals, is linked to other constructs, such as executive control and disinhibition. A transdiagnostic trait, impulsivity is a characteristic of many disorders that can appear to be rather distinct. Indeed, ADHD, gambling disorder, substance use disorders, bipolar affective disorder, borderline personality disorder, and Internet gaming disorder all share impulse dyscontrol as a prominent feature. The recent DSM-5 reclassification, with its emphasis on dimensionality, has further highlighted impulsivity, in part through the inclusion of 2 new diagnostic groupings: “obsessive-compulsive and related diorders,” which argues for a compulsive-impulsive spectrum, and “disruptive, impulse-control and conduct disorders.”

[[{"type":"media","view_mode":"media_crop","fid":"40378","attributes":{"alt":"Â© natalia_maroz/Shutterstock.com","class":"media-image media-image-right","id":"media_crop_4998202180083","media_crop_h":"0","media_crop_image_style":"-1","media_crop_instance":"4124","media_crop_rotate":"0","media_crop_scale_h":"134","media_crop_scale_w":"150","media_crop_w":"0","media_crop_x":"0","media_crop_y":"0","style":"float: right;","title":"Â© natalia_maroz/Shutterstock.com","typeof":"foaf:Image"}}]]Several advances in our understanding of the biological basis of impulsivity informed this new nosology. Neuroimaging data suggest differential activation, gray matter density, and functional connectivity in cortical areas, such as the prefrontal cortex, the orbitofrontal cortex, the anterior cingulate cortex, and the amygdala. Motor task studies, such as stop signal reaction time, show impairment in prepotent response inhibition. And, neuropsychological tests, such as the Stroop test, show distractibility and delayed cognitive processing.

The topics selected for this special issue highlight the broad relevance of this symptom domain to clinical practice in psychiatry and beyond. Suicide and self-harm, for example, are often linked to impulsivity, but what do empirical evaluations of this link actually show? This association is discussed, and challenged, in an article by E. David Klonsky, PhD, and Alexis M. May, MA, in which a 

 for assessing suicide risk is also advanced.

Parkinson disease is associated with significant morbidity, but iatrogenic impulse control disorders that can emerge during treatment add another layer of suffering and complexity. In the article by Jacob Taylor, MD, MPH, and Gregory Pontone, MD, the 

 behaviors such as hypersexuality, gambling, and excessive buying in Parkinson disease are discussed, as are ways to address them while still managing the underlying condition.

Disorders of impulse control have also been called “behavioral addictions,” since they share features with substance use disorders. In his article, Luke Clark, MD, focuses on 

, now placed under DSM-5’s “substance-related and addictive disorders,” as the “quintessential” behavioral addiction, one with similarities to other behavioral addictions that are also discussed, such as “food addiction” and “Internet gaming disorder.”

Aggression can be a manifestation of illness that is of great concern to patients, their loved ones, and clinicians. This issue is addressed in an article by Sean Z. Kaliski, MB, BCh, PhD, that explores the potentially dangerous 

Finally, pharmacological treatments that target problematic impulses are discussed in this month’s CME activity. The message from the article by Jon E. Grant, JD, MD, MPH, and Samuel R. Chamberlain, MD, PhD, is that while impulsive behavior can be a distressing sign of pathology and while there is a clear need for more research and better treatments, some impulsive patients may benefit from available interventions.

I hope this Special Report contributes to your understanding of impulsivity and that it proves beneficial for your clinical practice.

Dr Aboujaoude is Clinical Professor and Director of the OCD Clinic at the Stanford University School of Medicine, Stanford, Calif. He is the author and editor of several books, most recently, Mental Health in the Digital Age: Grave Dangers, Great Promise. He reports no conflicts of interest concerning the subject matter of this Special Report. 

The topics selected for this special issue highlight the broad relevance of this symptom domain to clinical practice in psychiatry and beyond.

Introduction: Impulsivity-A Transdiagnostic Trait

At some point in their life, most people are likely to have acted on impulses or reacted to provocations. This is accepted normal human behavior. However, in some cases it is pathological and some individuals behave this way habitually-as part of a pattern of behaviors that may have begun sometime in their youth. Although there are protean manifestations of these behaviors, ranging from suicidal gestures, substance abuse, risk taking, and antisocial behaviors, a subset of individuals are also aggressive and violent.

[[{"type":"media","view_mode":"media_crop","fid":"40384","attributes":{"alt":"Â© Cartoonresource/shutterstock.com","class":"media-image","id":"media_crop_4776623887150","media_crop_h":"0","media_crop_image_style":"-1","media_crop_instance":"4130","media_crop_rotate":"0","media_crop_scale_h":"266","media_crop_scale_w":"260","media_crop_w":"0","media_crop_x":"0","media_crop_y":"0","title":"Â© Cartoonresource/shutterstock.com","typeof":"foaf:Image"}}]]The terms “impulsivity” and “disorders of impulse control” have customarily been used interchangeably. Yet there have been contrasting definitions in the literature. “Impulsivity” has been defined as a decreased sensitivity to negative consequences, rapid unplanned reactions to stimuli (without adequate processing of information), and lack of regard for long-term consequences. “Disorders of impulse control” have been characterized as repeated failures to resist an impulse or perform an act that is harmful, with a preceding subjective sense of increasing tension (or arousal) and an experience of pleasure or gratification, ie, catharsis, while committing the act.

 In both cases, the consequences of the acting out are usually deleterious, with subsequent feelings of regret or guilt.

No studies have directly compared individuals whose impulsivity only takes the form of acting precipitously to stimuli with those who act solely because of impelling urges. In practice, there are many who possess an admixture of both aspects, such as those with borderline personality disorder who repeatedly act out their urges and can also respond explosively to stimuli. In DSM-5, an important criterion for borderline personality disorder is impulsivity, which also encompasses risk-taking activities that are exemplars of poor impulse control, such as excessive spending, promiscuity, and reckless driving. Individuals with intermittent explosive disorder, a “pure” impulse control disorder, exhibit “impulsive (or anger-based) aggressive outbursts” in response to minor provocations or stressors. Whatever the distinctions, individuals with these disorders all have in common a deficit in inhibiting damaging behavior.

In clinical practice, it may actually be difficult to differentiate between compulsions, addictions, and irresistible impulses. Almost all self-damaging behaviors, especially if they occur in the context of a psychiatric disorder, can be reframed as impulse disorders, such is the looseness of the definitions. Commonly, individuals who habitually cannot control their aggressive impulses also have other impulse control disorders, such as gambling and alcohol and substance abuse.

Forensic psychiatrists and the courts have long grappled with the difficult distinction between “impulses that cannot be resisted” and “impulses that are not resisted”-namely the “irresistible impulse” defense. In the former, there is the possibility that the person has an inherent biological propensity to act violently and therefore ought to be excused; the latter implies that the loss of control was voluntary and consequently not excusable. This applies mostly when someone responds violently following provocation. But impulses can also build up over an extended period until they demand urgent expression. Even serial killers who plan their homicides, sometimes meticulously, often report that they had to surrender to overwhelming urges.

Over 30 years ago, Linnoila and colleagues

 found that impulsive violent offenders had significantly lower cerebrospinal fluid (CSF) concentrations of the major metabolite of serotonin, 5-hydroxyindoleacetic acid (5-HIAA). Their findings have been convincingly validated.

Serotonin is an important inhibitory neurotransmitter, especially in the amygdala, anterior cingulated cortex, and dorsal-lateral prefrontal and orbitofrontal cortices. Reduced or dysregulated serotonin activity is associated with impulsivity and aggression. The possible mechanism may be the disruption of circuits between the amygdala and the medial prefrontal cortex, which results in amygdala hyperactivity and reduced prefrontal inhibition.

 Impulsive aggression presumably occurs consequent to ongoing arousal (from the amygdala) that primes negative urgency-the tendency to respond impulsively and aggressively to provocations or perceptions of threat.

Individuals who have the X-linked allele that codes for low-functioning monoamine oxidase A (MAOA-L), the most important enzyme for the metabolism of central serotonin, tend to display enhanced activation in subcortical limbic areas (especially the amygdala) and reduced prefrontal inhibition. This allele has now acquired the moniker “warrior gene” because of its consistent association with impulsive aggressive behavior.

Individuals who have the s/s allele for the serotonin transporter promoter gene also tend to exhibit patterns of impulsive violence, probably because of the reduced presynaptic re-uptake of serotonin. It may seem paradoxical that low-functioning versions of 

 and serotonin promoter genes are associated with impulsive aggression because these genes lead to increased levels of serotonin. The most likely mechanism is that increased levels of serotonin occupy serotonin 1A and serotonin 1B autoreceptors that “switch” the presynaptic neuron off and functionally cause a serotonin deficiency.

Men who have high CSF levels of free testosterone (which possibly mediates dominance-seeking) and low CSF levels of 5-HIAA are even more likely to be aggressive. Genes that determine the activities of the dopamine transporter protein and low levels of D2/D3 receptors in the nucleus accumbens have also been associated with impulsivity traits, possibly by interfering with the neural reward system.

Why don’t all individuals with the above genotypic profiles act impulsively and aggressively? Epigenetic factors that modulate gene expression may either potentiate or ameliorate these traits. This was investigated as part of the seminal longitudinal Dunedin Multidisciplinary Health and Development Study that followed up 1037 people born around 1973. The findings strongly suggest that boys with low MAOA activity but who had been severely maltreated before age 12 had, by their third decade, markedly the highest rates of convictions for violent offenses and dispositions toward violence.

 There were, nevertheless, some individuals who had not been maltreated and had high MAOA activity that ultimately also had violent convictions and dispositions. In other words, there are obviously a host of other factors that predispose persons to violent behavior (including the subset of impulsive aggressors).

These data have been confirmed by other studies, although generally, none of the studies seem to have differentiated between impulsive and non-impulsive violence.

 A notable exception was the large National Longitudinal Study of Adolescent to Adult Health (Add Health study) in which severe maltreatment was the sole factor that seemed to determine adult violence and the 

 genotype only seemed to contribute to a disposition toward violence.

 This suggests that the actual mechanisms by which environmental (and situational) factors interact with genotypes to produce habitually impulsively aggressive individuals are not yet fully understood.

Alcohol and substance abuse are probably the most powerful facilitators for impulsive aggression, increasing the risk almost exponentially. Alcohol abuse reduces serotonin neurotransmission, and intoxication may particularly provoke intemperate violent outbursts in individuals who have inherited dysregulated serotonergic neurotransmission.

 Findings suggest that intoxication with stimulant drugs, such as methamphetamine, promotes disinhibition via the enhancement of dopamine and epinephrine pathways, but not consistently.

There are many experiential and situational factors that are important, but it is difficult to prove their effects empirically. Apart from maltreatment, exposure to violence in the community also increases the risk for poor impulse control.

It is rare for violent individuals to seek help voluntarily. Treatment may be a consequence of an involuntary admission, ie, court mandated. In such cases, the individual may be unwilling or embarrassed to provide information; he or she will likely be angry and not very treatment-adherent-a good clinician-patient relationship will need to be established quickly. Collateral information will be useful for the initial assessment.

Impulsive aggression can occur as an isolated singular event, but usually is expressed as part of a defined disorder (

). When no other disorder accounts for the behavior, intermittent explosive disorder (IED) is diagnosed. This disorder is characterized (in DSM-5) by verbal aggression that occurs twice a week for 3 months and 3 behavioral outbursts over a 12-month period that resulted in damage or destruction of property or physical assault that resulted in injury. These phenomena need to occur independent of other mental disorders, comorbid medical conditions, or the effects of any psycho- tropic substances. To make this diagnosis confidently, the clinician has to have detailed and reliable information about the patient. The true prevalence of this disorder in the community is not known, although estimates indicate a life-time prevalence of 1% to 11%.

 An exact diagnosis of IED on the basis of aggressive outbursts is complicated, especially when there is a comorbid disorder-just over a fifth of patients may have another impulse control disorder, such as obsessive-compulsive disorder.

In most cases, treatment of the presenting psychiatric disorder should reduce the violent behavior. Alternatively, treatment of the aggressive or violent behavior should also address the problem of impulsivity. Most treatment strategies are guided by a structured assessment that identifies important dynamic risk factors and helps treatment decision making for each patient.

There is evidence that mood stabilizers, SSRIs, atypical antipsychotics, Î²-blockers (eg, propranolol), and Î±2-agonists have some efficacy in treating impulsive aggression.

 A recent meta-analysis of randomized controlled trials suggests that mood stabilizers are effective, especially carbamazepine, phenytoin, and lithium.

 Dialectical behavioral therapy–corrections modified, cognitive-behavioral therapy, group therapy, family therapy, and social skill training are also considered to be valid interventions.

 Despite the current dearth of good evidence for treatment strategies, it is probably prudent to use multimodal treatments-namely, a combination of drugs and psychotherapeutic approaches. When or if one should ever withdraw treatment remains a moot issue.

Dr Kaliski is Associate Professor/Senior Specialist for the Forensic Mental Health Service, Western Cape, department of psychiatry, University of Cape Town, South Africa. He reports no conflicts of interest concerning the subject matter of this article.

 Moeller FG, Barratt ES, Dougherty DM, et al. Psychiatric aspects of impulsivity. 

 Dell’Osso B, Altamura AC, Allen A, et al. Epidemiologic and clinical updates on impulse control disorders: a critical review.

 Linnoila M, Virkkunen M, Scheinin M, et al. Low cerebrospinal fluid 5-hydroxyindoleacetic acid concentration differentiates impulsive from nonimpulsive violent behaviour. 

 Mehlman PT, Higley JD, Faucher I, et al. Low CSF 5-HIAA concentrations and severe aggression and impaired impulse control in nonhuman primates. 

 Pavlov KA, Chistiakov DA, Chekhonin VP. Genetic determinants of aggression and impulsivity in humans. 

 Dorfman HM, Meyer-Lindenberg A, Buckholtz JW. Neurobiological mechanisms for impulsive-aggression: the role of MAOA. 

 Caspi A, McClay J, Moffitt TE, et al. Role of genotype in the cycle of violence in maltreated children. 

 Krakowski M. Violence and serotonin: influence of impulse control, affect regulation, and social functioning. 

 Haberstick BC, Lessem JM, Hewitt JK, et al. MAOA genotype, childhood maltreatment, and their interaction in the etiology of adult antisocial behaviors. 

 Virkkunen M, Eggert M, Rawlings R, Linnoila M. A prospective follow-up study of alcoholic violent offenders and fire setters. 

 Tyner EA, Fremouw WJ. The relation of methamphetamine use and violence: a critical review. 

 Sharkey PT, Tirado-Strayer N, Papachristos AV, Raver CC. The effect of local violence on children’s attention and impulse control. 

 McElroy SL, Soutullo CA, Beckman DA, et al. DSM-IV intermittent explosive disorder: a report of 27 cases. 

 Jones RM, Arlidge J, Gillham R, et al. Efficacy of mood stabilisers in the treatment of impulsive or repetitive aggression: systematic review and meta-analysis. 

 Shelton D, Sampl S, Kesten KL, et al. Treatment of impulsive aggression in correctional settings. 

The authors explore ways to address aggression in clinical practice and examine the potentially dangerous impulsivity-violence link across a broad range of conditions. 

Impulse Control, Impulsivity, and Violence: Clinical Implications

Impulsivity, a frequently misunderstood aspect of suicide risk, has long been considered important to the etiology and prediction of suicide. In particular, impulsivity is highlighted for its role in facilitating suicidal actions among those with suicidal ideation. Mann and colleagues

 developed a clinical model of suicidal behavior which suggests that impulsivity makes individuals “more likely to act on suicidal feelings.” Similarly, Bryan and Rudd

 state that impulsivity “may actually be a more significant indicator of suicide attempt than the presence of a specific suicide plan.”

Impulsivity has been adopted as a risk factor or warning sign for suicide. 

 includes impulsivity as both a chronic and an 

. Impulsivity is also highlighted by the American Foundation for Suicide Prevention and the Substance Abuse and Mental Health Services Administration.

 However, as discussed below, these widely held perceptions about impulsivity do not appear to be supported by research.

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The claim that impulsivity facilitates transition from suicidal thoughts to suicide attempts suggests a clear and testable prediction: trait impulsivity should be higher among those who attempt suicide than among those who only consider suicide. However, to the surprise of many, research on the role of impulsivity has routinely failed to support this claim. For example, a 2007 study of young adults by 

 found that attempters scored no higher on the Barratt Impulsiveness Scale than patients with suicidal ideation who had never attempted suicide.

More recently, my colleagues and I examined a military population and found that while both suicide attempters and patients with suicidal ideation scored higher on a measure of impulsivity than those who had never been suicidal, impulsivity scores were equivalent between attempters and patients with suicidal ideation who had never attempted suicide.

 In other words, impulsivity was moderately elevated in anyone with a history of suicidality (thoughts or behavior), but the study failed to show any further elevation among those who acted on their ideation and progressed to suicide attempts.

On the basis of these surprising findings, we conducted a subsequent analysis using the UPPS Impulsive Behavior Scale. The UPPS developers, Whiteside and Lynam,

 suggest that impulsivity is a heterogeneous construct. They used a series of factor and psychometric analyses to identify 4 distinct impulsivity-related traits: Urgency (responding rashly to negative emotions), poor Premeditation (difficulties in foreseeing consequences of actions), poor Perseverance (tendency to give up easily), and Sensation seeking (preference for excitement and stimulation).

Using a brief version of the UPPS in a large sample of adolescents and young adults, we found that attempters and individuals with suicidal ideation exhibited equivalent scores on 3 of the dimensions (Urgency, Perseverance, and Sensation seeking) and that attempters scored only very slightly higher on the fourth (Premeditation). Taken together, the findings suggest that suicide attempters and individuals with suicidal ideation exhibit similar levels of trait impulsivity, a pattern that is contrary to clinical beliefs and guidelines.

The studies described above examined impulsivity as a personality trait that could occur at higher or lower levels within an individual. However, there is a second body of research that is also relevant to the role of impulsivity in suicide.

This research examines the impulsive nature of the suicide attempt itself. Many different definitions of attempt impulsivity have been used, including degree of forethought, amount of time between the decision to choose suicide and the actual suicide attempt, time spent contemplating the attempt before making the attempt, presence of a suicide plan, and amount of time spent making a plan, among many others. Given the many ways to define or identify an impulsive attempt, it is not surprising that studies on attempt impulsivity produce widely divergent results. For example, the percentage of suicide attempts estimated to be impulsive has ranged from a low of 20% to a high of 85%.

Perhaps one of the most surprising findings is that trait impulsivity and attempt impulsivity appear to be unrelated. In other words, among individuals who have made suicide attempts, those who score higher on personality measures of impulsivity are not the ones making the more impulsive suicide attempts. This pattern has been found and reported by 2 separate research teams and thus appears to be true despite its counterintuitive nature.

Taken together, studies indicate 2 critical limitations of current knowledge. First, when it comes to characterizing impulsivity in suicide, there is a disconnect between clinical guidelines and research. The way impulsivity is described in lists of suicide risk factors and warning signs is not supported-and is in some cases disputed-by empirical research. Second, the field continues to struggle to understand the role impulsivity plays in influencing the likelihood and nature of suicide attempts, as well as how to best understand suicide and suicide risk.

 examined the association between measures of impulsivity and measures of suicidal behavior (eg, non-lethal attempts, death by suicide). Across all studies, the relationship between impulsivity and suicidal behavior was modest (Hedges’ g = 0.37). However, most of these studies were cross-sectional; current impulsivity was used to predict a history of suicidal behavior. In the studies that explored impulsivity as a predictor of future suicidal behavior, the association was even smaller, barely above 0 (Hedges’ g = 0.09). The researchers conclude that the role of impulsivity in suicide is likely to be small and indirect rather than central or causal.

Anestis and colleagues next proposed a model specifying the role of impulsivity in suicide. In particular, the authors noted work by Joiner

 that suggested that to make a potentially lethal suicide attempt, one must have the capability to make an attempt. Pain and fear of death serve as barriers to making a suicide attempt, and certain kinds of experiences can allow people to habituate to pain and fear of death and overcome these barriers. These experiences are referred to by Joiner as painful and provocative events and can include a variety of experiences and events, such as exposure to violence, nonsuicidal self-injury, and substance use.

 theorized that rather than a direct relationship, impulsivity has a distal relationship to suicidal behavior by virtue of increasing one’s exposure to painful and provocative events. Indeed, they noted that initial studies have found that painful and provocative events mediate the relationship between impulsivity and suicidal behavior. In short, it appears that impulsivity exhibits its small relationship to suicidal behavior because it facilitates a lifestyle in which painful and provocative events are more likely to be experienced.

If, contrary to commonly held clinical beliefs, impulsivity is not a strong or central predictor of suicide or suicide risk, what may be a more accurate, more useful alternative model?

The often cited risk factors for suicide, such as impulsivity as well as depression, hopelessness, and most mental disorders, are indeed greater among suicidal populations, but they distinguish poorly between those who attempt suicide and those who consider but never attempt suicide.

 In other words, once an individual is known to have suicidal ideation, assessing his or her depression, hopelessness, psychiatric diagnosis, and impulsivity offers little to no information about the risk of acting on that ideation and making a suicide attempt. This distinction is critical because most individuals with suicidal ideation do not go on to attempt suicide.

This pattern of findings, replicated in numerous studies by numerous investigators, led to the ideation-to-action framework. From this perspective, predictors and explanations for suicide should be classified as to how they address (a) the risk of suicide ideation, (b) the risk of suicide attempts among those with suicidal ideation, or (c) both. For example, depression, hopelessness, impulsivity, and most psychiatric disorders appear to be best characterized as predictors of suicidal ideation.

In contrast, fearlessness and reduced pain sensitivity appear to specifically characterize suicide attempters, but not patients with suicidal ideation.

 Other risk factors, such as nonsuicidal self-injury, appear to confer risk of both suicidal ideation and attempts.

 Thus, conceptual and clinical models guided by an ideation-to-action framework can greatly improve models of suicide risk as well as efforts to understand and prevent suicide.

A new theory of suicide positioned within the ideation-to-action framework is the 3-step theory (3ST). The 3ST makes 3 central claims, all of which are consistent with existing evidence that is supported by recent findings.

First, the combination of pain and hopelessness is what brings about suicidal ideation. The nature of pain is intentionally not specified. Any type of pain that makes daily life aversive, regardless of its source, can be implicated in suicidal ideation. When efforts to engage with life are paired with emotional, psychological, or physical pain, the individual is behaviorally conditioned to want to avoid engaging with life, which, in turn, decreases the desire to live. Furthermore, if the experience of pain is accompanied by hopelessness (over the idea that the pain will never improve), suicidal thinking begins. However, if there is hope that one’s situation can improve, then one will continue to engage with life. It is the confluence of pain and hopelessness that leads to suicidal thoughts.

Indeed, pain and hopelessness are the two primary motivations for suicide.

 More to the point, recent research suggests that it is the 

 of pain and hopelessness that matters. Specifically, suicidal ideation was negligible in those low on both pain and hopelessness and was negligible in those either high on pain or high on hopelessness; in contrast, suicidal ideation was elevated only in the subgroup high on both pain and hopelessness.

Second, the 3ST suggests that connectedness prevents suicidal ideation from escalating in those at risk (ie, those experiencing both pain and hopelessness). In other words, if connectedness to life-to loved ones, to a valued role, or to any sense of meaning or purpose-exceeds the pain, suicidal ideation will remain at modest levels. However, if pain exceeds the connectedness to or investment in life, suicidal ideation becomes strong and active. Recent findings support this notion: connectedness was found to be a significant buffer against suicidal ideation only in those with pain and hopelessness; in everyone else, connectedness is negligibly related to suicidal ideation.

Finally, the 3ST states that strong suicidal ideation leads to a suicide attempt if, and only if, one has the capacity to make an attempt. Three specific categories of variables contribute to suicide capacity: dispositional, acquired, and practical. Recent research has found that each of these 3 variables predicts suicide attempt history, even when controlling for past and current suicidal ideation.

Dispositional variables are driven largely by genetics, such as pain sensitivity. For example, someone born with low pain sensitivity will have a higher capacity to carry out a suicide attempt. Indeed, more recent work from Smith and colleagues

 indicates that capability for suicide may be largely genetic. Acquired variables are experiences associated with pain, injury, fear, and death, and they can lead over time to a higher capacity for a suicide attempt.

 Practical variables are concrete factors that make a suicide attempt easier. These factors include access to, knowledge of, comfort with, and practice with lethal means. There are countless ways for someone to increase practical capacity. Each of these 3 factors-dispositional, acquired, practical-contribute to the capacity for attempted suicide, and an individ- ual with strong suicidal ideation will only make a suicide attempt if and when he has the capacity to do so.

One reason the 3ST is useful is that it suggests clear clinical implications. To reduce suicide risk, clinicians can reduce pain, increase hope, foster connection, and/or decrease capacity. Although these domains require more study and validation, they may be a useful way to conceptualize how a specific set of interventions with a particular patient can target and impact suicide risk.

Contrary to commonly held beliefs, a large body of research suggests that impulsivity is not a strong predictor or cause of suicidal behavior. Instead, trait impulsivity appears to be a modest and distal predictor of suicide; however, large, prospective studies that could best address this issue are still needed.

Future studies guided by the ideation-to-action framework may be able to specifically test the degree to which the impulsivity-suicidality relationship is explained by impulsivity’s impact on the pain and hopelessness that cause ideation and/or on suicide capacity. Instead of focusing on impulsivity, it may be fruit- ful to focus on domains that have been consistently shown to predict and motivate suicidal ideation and suicide attempts, including pain and hopelessness (especially in combination), connectedness, and suicide capacity. Interventions for suicide risk may be most effective when one or more of these domains is improved.

Dr Klonsky is Associate Professor and Ms May is a Doctoral Candidate in the department of psychology at the University of British Columbia in Vancouver. The authors report no conflicts of interest concerning the subject matter of this article.

 Mann JJ, Waternaux C, Haas GL, Malone KM. Toward a clinical model of suicidal behavior in psychiatric patients. 

 Bryan CJ, Rudd MD. Advances in the assessment of suicide risk. 

 American Association of Suicidology. Risk factors for suicide and suicidal behaviors I. 2013. 

http://suicidology.org/Portals/14/docs/Resources/FactSheets/Risk-Factors_2013.pdf

 American Foundation for Suicide Prevention. What is the most frequent cause of suicide? 2015.

 www.afsp.org/understanding-suicide/frequently-asked-questions%20February%201,%202015

 Substance Abuse and Mental Health Services Administration. Shared risk and contributing factors (slide 12). 2014. 

http://www.samhsa.gov/sites/ default/files/suicide-prevention-samhsa.pptx

 Brezo JB, Paris J, Tremblay R, et al. Identifying correlates of suicide attempts in suicidal ideators: a population-based study. 

 Klonsky ED, May A. Rethinking impulsivity in suicide. 

 Whiteside SP, Lynam DR. The Five Factor Model and impulsivity: using a structural model of personality to understand impulsivity. 

 Bagge CL, Littlefield AK, Lee HJ. Correlates of proximal premeditation among recently hospitalized suicide attempters. 

 Witte TK, Merrill KA, Stellrecht NE, et al. “Impulsive” youth suicide attempters are not necessarily all that impulsive. 

 Wyder M, De Leo D. Behind impulsive suicide attempts: indications from a community study. 

 Anestis MD, Soberay KA, Gutierrez PM, et al. Reconsidering the link between impulsivity and suicidal behavior. 

. Cambridge, MA: Harvard University Press; 2005.

 Klonsky ED, May AM. Differentiating suicide attempters from suicide ideators: a critical frontier for suicidology research. 

 Kessler RC, Borges G, Walters EE. Prevalence of and risk factors for lifetime suicide attempts in the National Comorbidity Survey. 

 Apter A, Horesh N, Gothelf D, et al. Relationship between self-disclosure and serious suicidal behavior. 

 Rudd MD, Joiner T, Rajab MH. Relationships among suicide ideators, attempters, and multiple attempters in a young-adult sample. 

 Smith PN, Cukrowicz KC, Poindexter EK, et al. The acquired capability for suicide: a comparison of suicide attempters, suicide ideators, and non-suicidal controls. 

 Klonsky ED, May AM, Glenn CR. The relationship between nonsuicidal self-injury and attempted suicide: converging evidence from four samples. J

 Klonsky ED, May AM. The three-step theory (3ST): a new theory of suicide rooted in the “ideation-to-action” framework. 

 May AM, Klonsky ED. Assessing motivations for suicide attempts: development and psychometric properties of the Inventory of Motivations for Suicide Attempts. 

 Smith AR, Ribeiro JD, Mikolajewski A, et al. An examination of environmental and genetic contributions to the determinants of suicidal behavior among male twins. 

Suicide and self-harm are often linked to impulsivity, but what do empirical evaluations of this link actually show? This association is discussed and challenged in this article.

Impulsivity and Suicide Risk:  Review and Clinical Implications

Parkinson disease (PD) is a progressive neurodegenerative illness that is recognized clinically by its cardinal motor features: tremor, rigidity, and bradykinesia. However, it is increasingly clear that much of the suffering and disability associated with PD is caused by psychiatric disorders. Some of these seem to be intrinsic to PD and likely emerge from the same pathogenic process that gives rise to the motor symptoms. For example, depression, anxiety disorders, and dementia are all common in PD and likely occur because the same process that damages motor circuits can also affect brain regions that subserve mood and cognition. Other psychiatric problems are associated with PD because they are caused-at least in part-by the dopaminergic medications prescribed for motor symptoms. These include delirium, psychosis, and impulse control disorders.

[[{"type":"media","view_mode":"media_crop","fid":"40379","attributes":{"alt":"Â© Lightspring/shutterstock.com","class":"media-image media-image-right","id":"media_crop_1597874128056","media_crop_h":"0","media_crop_image_style":"-1","media_crop_instance":"4126","media_crop_rotate":"0","media_crop_scale_h":"150","media_crop_scale_w":"124","media_crop_w":"0","media_crop_x":"0","media_crop_y":"0","style":"float: right;","title":"Â© Lightspring/shutterstock.com","typeof":"foaf:Image"}}]]Impulse control disorders, also described as “behavioral addictions,” include phenomena such as pathological gambling, compulsive shopping, hypersexuality (including paraphilic behavior), and binge eating. The failure to resist engaging in these behaviors rises to the level of a disorder when it causes distress or impaired occupational or social functioning. Such disorders often go un- recognized, only becoming obvious once they have wreaked havoc on the lives of patients and their families.

There may be a “Parkinson personality” characterized by cautious temperament and a decreased tendency to indulge in hedonic pleasures.

 Yet when treated with dopaminergic medication, a substantial portion of such patients have problems with an overzealous pursuit of pleasurable experiences. A better understanding of how this happens and why it happens in some but not others, might shed light on the underlying mechanisms of impulsivity and related behavioral disturbances in both persons with PD and the general population.

The association between impulse control disorders and PD seems to be driven by the dopamine replacement medications used to treat the motor symptoms of PD. A recent case-control study that compared 168 patients with newly diagnosed PD who had never received treatment with 143 healthy controls found no evidence for an increased prevalence of impulse control disorders.

 However, most studies that compare PD patients who are receiving treatment for their motor symptoms with healthy controls do find an increased prevalence of impulse control disorders in the PD patients. One cross-sectional study by Weintraub and colleagues

 of more than 3000 patients being treated for PD found a point prevalence of at least one impulse control disorder of 13.6%. The study looked specifically for pathological gambling (5.0%), sexual impulsivity (3.5%), impulse buying (5.7%), and binge eating disorder (4.3%) and found that 3.9% of patients engaged in more than one of these behaviors.

Impulse control disorders are much more common in patients who are receiving treatment with a dopamine agonist (such as pramipexole or ropinirole) than in patients treated only with the dopamine precursor levodopa. In the study by Weintraub and colleagues,

 17.1% of patients who were taking a dopamine agonist had an impulse control disorder compared with 6.9% of patients who were treated with levodopa.

The increased risk of an impulse control disorder developing during treatment with a dopamine agonist does not seem to be dose-dependent. Indeed, there have been reports of impulse control disorders in patients treated with dopamine agonists for conditions such as restless legs syndrome, for which these drugs are prescribed in substantially lower doses than in PD. By contrast, treatment with very high doses of levodopa seems to confer higher risk than treatment with low or moderate doses. Patients receiving treatment with both dopamine agonists and levodopa seem to be at the highest risk.

Other risk factors for impulse control disorders in patients being treated for PD include having a personal or family history of impulse control disorders or addictions and having premorbid novelty-seeking or impulsive traits.

 There are sex differences in risk for particular impulse control disorders, with men more likely to engage in hypersexual behavior and women more likely to engage in impulse buying or binge eating.

 Other clinical factors that appear to be associated with impulse control disorders include depressive symptoms, irritability, and appetite changes.

The motor symptoms in PD are caused by the destruction of dopaminergic neurons in the ventral portion of the substantia nigra pars compacta within the midbrain. These neurons project to the caudate and putamen and are involved in regulating motor function. This is the same system implicated in the extrapyramidal adverse effects of neuroleptics that block dopamine receptors. Medications for the motor symptoms of PD work by increasing dopaminergic neurotransmission within this circuit. Levodopa is a precursor to dopamine, while dopamine agonists act directly on dopamine receptors.

While dopaminergic neurons in the ventral part of the substantia nigra modulate motor circuits, other dopamine-producing neurons located in the dorsal part of the substantia nigra project to forebrain and limbic regions. These mesocortical and mesolimbic circuits are involved in voluntary driven behaviors through the assessment of and response to rewards and risks. While the ventral neurons are primarily destroyed in PD, the treatments for PD increase dopaminergic transmission in both sets of circuits. It is likely that excessive stimulation of dopamine receptors in limbic and forebrain regions contributes to the pathophysiology of impulse control disorders.

How does this explanation account for the fact that dopamine agonists seem to pose a higher risk than levodopa for the development of impulse control disorders? This is likely due to the localization of different receptor subtypes within these circuits. While D1 and D2 receptors are primarily located within motor circuits, D3 receptors are distributed within both motor and limbic circuits. In some individuals, increased agonism of D3 receptors seems to weaken mechanisms that would normally keep risky, pleasure-seeking behaviors in check.

Compared with the dopamine that is synthesized from levodopa, dopamine receptor agonists in use today have increased affinity for D3 receptors relative to D1 and D2 receptors. Higher affinity for D3 receptors might explain not only the elevated risk for impulse control disorders with dopamine agonists, but also their increased association with hallucinations and delusions. Similarly, dopamine metabolized from levodopa has relatively greater affinity for D1 and D2 receptors, which may be why levodopa is more effective than dopamine agonists as a first-line treatment for motor symptoms.

Unlike other, more conspicuous psychiatric adverse effects, such as hallucinations and delusions, impulsivity is often missed. Patients often lack insight that the impulse control disorder represents a problem because the impulsivity may be within the normal range of human behaviors except for the unusual extent or frequency. One of our patients, a married man in his 60s, took a several hundred–mile road trip during which he visited strip clubs and erotic massage parlors, shortly after he had started taking the dopamine agonist pramipexole. However, it was not until much later, after experiencing negative consequences from this behavior, that he recognized that he had a problem.

Another reason why impulse control disorders can be difficult to identify is that patients may not be forthcoming because they are ashamed or embarrassed. Thus, many patients are reluctant to discuss impulse control disorders with their clinicians unless asked directly. Even then, patients may minimize the extent of these behaviors. Thus, when performing psychiatric evaluations, especially in patients being treated with dopamine agonists, it is important to ask directly about gambling and other financial indiscretions as well as about changes in sexual and eating behaviors. It is also important, when possible, to ask collateral informants about such behavior. A final challenge in diagnosing dopamine agonist–induced impulse control disorders is that they often emerge insidiously, sometimes years after the offending medication is first prescribed. Thus, patients and their clinicians must remain vigilant.

Impulse control disorders in patients with PD should be distinguished from other pathological behavioral phenomena that arise from treatment with dopaminergic medications. Impulsive behaviors are distinct from compulsive behaviors in that the former are motivated by a potential hedonic reward with inadequate consideration of risk, where-as the latter are attempts to relieve anxiety or avoid harm. Compulsive behaviors seen in PD include punding (repetitive, purposeless behaviors, such as arranging or taking apart objects), hobbyism (eg, compulsive exercise, Internet use, work on projects), walkabouts (aimless wandering), and hoarding.

Another important phenomenon seen in patients treated for PD is the dopamine dysregulation syndrome. This describes the pathological overuse of dopaminergic medications. Like other chemical addictions, this behavior can be motivated by both a desire for an intrinsic reward associated with these drugs and a desire to avoid anxiety and other dysphoric emotions associated with withdrawal. Unsurprisingly, the overuse of dopaminergic medications commonly co-occurs with, and likely worsens, other impulsive behaviors as well as other psychiatric syndromes, including mania and psychosis.

The key to managing impulse control disorders in patients with PD is close coordination between the patient’s psychiatrist and neurologist. If a dopamine agonist has been prescribed, the first step is usually to discontinue this medication. However, abrupt discontinuation can theoretically precipitate a neuroleptic malignant-like syndrome. Therefore, it must be tapered carefully. Even when a patient requires higher doses of levodopa to control his or her motor symptoms, impulsive behavior may improve once the dopamine agonist is stopped.

Although case studies describe the use of neuroleptics and other psychotropic medications in the management of impulse control disorders in PD, benefits have generally been seen while concomitantly reducing dopamine agonist medications. There has been some excitement around using naltrexone. However, a 2014 randomized control trial that included 50 patients with PD and various impulse control disorders, including gambling, impulse buying, sexual impulsivity, and binge eating disorder, did not show any benefit.

 In our experience, there is no clear role for psychotropic medications in isolated impulse control disorders attributable to dopamine agonist therapy. That said, impulse control disorders are often comorbid with other psychiatric syndromes, such as mood and anxiety disorders. It is important that any comorbid disorders be identified and managed appropriately.

Of course, some patients do not tolerate completely eliminating dopamine agonist therapy and others have residual impulse control disorder symptoms even when treated with levodopa monotherapy. In many cases, the management of impulse control disorders in patients with PD represents a balancing act. We work closely with our patients, their families, and our neurology colleagues to find the lowest amount of dopaminergic medication necessary and to manage impulsivity through behavioral interventions. In fact, for many patients, once a dysfunctional pattern of behavior has been established, it takes more than pharmacological optimization to break this pattern. Thus, it is common for us to refer patients for behavioral therapy and 12-step groups aimed at interrupting these behaviors once their dopaminergic medications have been reduced as much as possible.

Impulse control disorders are common in patients with PD. They result from treatment with dopaminergic medications targeting parkinsonian motor symptoms. Their pathophysiology is likely related to increased dopaminergic transmission in mesolimbic and mesocortical circuits that play a role in assessing and acting on information about potential rewards and risks of volitional behaviors. These disorders can have devastating effects on the lives of patients and their families. Yet they are often insidious and difficult to recognize clinically, only coming to attention as the result of major consequences.

More judicious prescribing of dopamine agonists for PD and greater efforts to educate patients and their families about the risks of impulse control disorders would likely reduce the frequency of these disorders. When these disorders are discovered, their management requires close coordination between psychiatry and neurology. Reducing offending medications as much as possi-ble, treating comorbid psychiatric illness, and using interventions aimed at interrupting dysfunctional reward-seeking behavior are keys to optimal management.

Dr Taylor is a Psychiatry Resident at the Johns Hopkins Hospital in Baltimore. Dr Pontone is Assistant Professor of Psychiatry and Behavioral Sciences at Johns Hopkins University School of Medicine in Baltimore. Dr Taylor reports no conflicts of interest concerning the subject matter of this article. Dr Pontone reports that he has received research support from the National Institutes of Health (NIH), the National Institute on Aging, the Michael J. Fox Foundation, and UCB (supplier of drugs and placebo for NIH-funded clinical trials); he has also provided expert testimony for Allergan.

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 Weintraub D, Koester J, Potenza MN, et al. Impulse control disorders in Parkinson disease: a cross-sectional study of 3090 patients. 

 Weintraub D, David AS, Evans AH, et al. Clinical spectrum of impulse control disorders in Parkinson’s disease [published correction appears in Mov Disord. 2015;30:1010]. 

 Pontone G, Williams JR, Bassett SS, Marsh L. Clinical features associated with impulse control disorders in Parkinson disease. 

 Holden C. “Behavioral” addictions: do they exist? 

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The challenges of recognizing behaviors such as hypersexuality, gambling, and excessive buying in Parkinson disease are discussed, as are ways to address them while still managing the underlying condition. 

Implications of Impulse Control Disorder in Parkinson Disease

One of the many interesting shifts in DSM-5 was the reclassification of pathological gambling from the impulse control disorders category to substance addictions (“substance-related and addictive disorders”). The shift effectively recognized (the now re-labeled) “gambling disorder” as the first behavioral addiction. This is a fascinating construct in psychiatry. The other diagnoses in this category involve the compulsive administration of exogenous drugs. Much of our knowledge of addiction comes from studying the pharmacology of these drugs and their ability to “hijack” reward-oriented behavior in animal models.

[[{"type":"media","view_mode":"media_crop","fid":"40387","attributes":{"alt":"Â© katalinks/shutterstock.com, gambling","class":"media-image media-image-right","id":"media_crop_4132918533744","media_crop_h":"0","media_crop_image_style":"-1","media_crop_instance":"4131","media_crop_rotate":"0","media_crop_scale_h":"200","media_crop_scale_w":"130","media_crop_w":"0","media_crop_x":"0","media_crop_y":"0","style":"float: right;","title":"Â© katalinks/shutterstock.com","typeof":"foaf:Image"}}]]In the case of gambling disorder, there is no exogenous substance; rather, there is excessive engagement in a behavior in which money is wagered on the uncertain prospect of a larger monetary prize. Even the role of money is unclear in this equation. While money is self-evidently a potent incentive, at a psychological level, it is a complex, learned reinforcer (as distinct from a natural reward, such as food or sex). For at least some gamblers, winning money appears to play a negligible role in maintaining their behavior.

So what is it about this behavior that enables gambling to yield a power that is comparable to drugs such as cocaine, heroin, and alcohol? And might other behaviors, such as video gaming, food addictions, shopping, and sex, be conceptualized as addictive behaviors in the future?

The DSM-5 diagnosis of gambling disorder uses a threshold of 4 of 9 symptoms. These symptoms have changed little from the original list in DSM-III, which was based on the diagnostic criteria for substance dependence. The symptoms include classic hallmarks of an addiction syndrome: preoccupation with gambling, gambling with larger amounts over time (akin to tolerance), and agitation when stopping gambling (akin to withdrawal).

The criteria also emphasize the negative consequences of gambling, such as occupational or interpersonal difficulties, borrowing money, and lying about gambling. Certainly, financial debt is ubiquitous in individuals with gambling disorder, and in the rare cases that do not involve significant debts, there is usually either some form of bailout from others or bankruptcy.

Gambling disorder is linked to high rates of criminal acts to support gambling, although clinicians should note that criminality was dropped as a specific criterion in DSM-5. Homelessness, physical health burden, and suicidal behavior are further corollaries that highlight the ultimately catastrophic downward spiral of gambling disorder.

Another feature that does not have an obvious counterpart in drug addiction is loss-chasing: continuing to play or returning to the venue at a later date in an effort to claw back recent debts. Loss-chasing is often regarded as a tipping point at which recreational gambling becomes problematic. In epidemiological datasets, loss-chasing is generally the most endorsed feature.

 These population studies also illustrate how the harms of gambling are continuously distributed: individuals who do not meet diagnostic criteria can nonetheless experience clear harm from gambling. The prevalence estimates for “at risk” gambling are in the range of 2% to 7%, with full DSM diagnosis in 0.5% to 1%.

One of the pivotal lines of evidence that shaped the DSM-5 reclassification was the neurobiological overlap between gambling disorder and the substance use disorders. From a neurocognitive perspective, elevated impulsivity is a reliable feature in patients with gambling disorder.

 This personality trait refers to the tendency for rapid responses and unplanned decisions. It can be measured with either questionnaires or behavioral tasks, and is conceptualized as arising from an imbalance between overactive subcortical reward systems and underactive prefrontal cortical control mechanisms.

Now placed “substance-related and addictive disorders” in DSM-5, gambling disorder has similiarities to other behavioral addictions, such as “food addiction” and “Internet gaming disorder.” 

Impulse Control Disorder

A Case of Gambling Disorder

Mini Quiz: Gambling Disorder

Mini Quiz: Impulsivity Risk Factors

Introduction: Impulsivity-A Transdiagnostic Trait

Impulse Control, Impulsivity, and Violence: Clinical Implications

Impulsivity and Suicide Risk: Review and Clinical Implications

Implications of Impulse Control Disorder in Parkinson Disease

From Impulsivity to Addiction: Gambling Disorder and Beyond

Impulse Control Disorders: Clinical Characteristics and Pharmacological Management

Temper Tantrums, Mental Disorder, and DSM-5: The Case for Caution