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Chapter: Essentials of Psychiatry: Impulse Control Disorders

Intermittent Explosive Disorder

Patients with intermittent explosive disorder have a problem with their temper (see DSMIV-TR criteria).

Intermittent Explosive Disorder




Patients with intermittent explosive disorder have a problem with their temper (see DSMIV-TR criteria). This definition highlights the centrality of impulsive aggression in intermittent explo-sive disorder. Impulsive aggression, however, is not specific to intermittent explosive disorder. It is a key feature of several psy-chiatric disorders and nonpsychiatric conditions and may emerge during the course of yet other psychiatric disorders. Therefore, the definition of intermittent explosive disorder as formulated in the DSM-IV-TR is essentially a diagnosis of exclusion. As described in criterion C, a diagnosis of intermittent explosive disorder is made only after other mental disorders that might ac-count for episodes of aggressive behavior have been ruled out. The individual may describe the aggressive episodes as “spells” or “attacks”. The symptoms appear within minutes to hours and, regardless of the duration of the episode, may remit almost as quickly. As in other impulse control disorders, the explosive be-havior may be preceded by a sense of tension or arousal and is followed immediately by a sense of relief or release of tension Although not explicitly stated in the DSM-IV-TR definition of intermittent explosive disorder, impulsive aggressive behavior may have many motivations that are not meant to be includedwithin this diagnosis. Intermittent explosive disorder should not be diagnosed when the purpose of the aggression is monetary gain, vengeance, self-defense, social dominance, or expressing a political statement or when it occurs as a part of gang behavior. Typically, the aggressive behavior is egodystonic to individuals with intermittent explosive disorder, who feel genuinely upset, remorseful, regretful, bewildered, or embarrassed about their impulsive aggressive acts.


Etiology and Pathophysiology


Since the second half of the 19th century, two main lines of explanation, which are to a large extent complementary, have been developed to account for the existence of individuals with episodic impulsive aggression. One line of explanation viewed the etiology of impulsive aggression as stemming from the effects of early childhood experiences and possibly childhood trauma on the development of self-control, frustration tolerance, planning ability and gratification delay, which are all important for self-prevention of impulsive aggressive outbursts. Early experiences with “good-enough” mothering that fosters phase-appropriate delay of gratification and the development of the potential for im-itation and identification with the mother are considered impor-tant for normal development. Too much or too little frustration, as well as overgratification or undergratification, may impair the normal development of the ability to anticipate frustration and delay gratification.


A second line of explanation, which has yielded numer-ous positive findings during the past 15 years, views impulsive aggression as the result of variations in brain mechanisms that mediate behavioral arousal and behavioral inhibition. A rapidly growing body of evidence has shown that impulsive aggression may be related to defects in the brain serotonergic system, which acts as an inhibitor of motor activity. Although the majority of studies involved patients who suffered from impulsive aggression in the context of disorders other than intermittent explosive dis-order, their findings may be relevant to the behavioral dimension of impulsive aggression, of which intermittent explosive disorder is a “pure” form. A number of researchers have confirmed a rela-tionship between levels of 5-hydroxyindoleacetic acid (5-HIAA) in the CSF and impulsive or aggressive behaviors. Others have divided aggressive behaviors into impulsive and nonimpulsive forms, and found that reduced CSF 5-HIAA levels were corre-lated with impulsive aggression only. Pharmacological challenge studies of the serotonergic system have also demonstrated that low serotonergic responsiveness (as measured by the neuroen-docrine response to serotonergic agonists) correlates with scores of impulsive aggression. Studies of impulsive aggression among alcoholics have further defined a probable relationship between such behaviors and diminished serotonergic function.


The literature on serotonin and suicide, which may be viewed as an extreme form of self-directed aggression, suggests another link between serotonin and aggression. Postmortem studies found that brain stem levels of serotonin were decreased in suicide victims, and reduced imipramine binding, which is thought to be associated with reduced presynaptic serotonergic binding sites, was found in the brains of suicide completers. Furthermore, an increase in postsynaptic 5-hydroxytryptamine (5-HT2) receptors was found in the brains of suicide completers, and this finding was confirmed in subsequent studies. An increase in 5-HT2 receptors, which are thought to be mostly postsynaptic, may reflect the brain’s reaction to a decrease in functional sero-tonergic neurons, with consequent upregulation of postsynaptic serotonin binding sites


Another line of neurobiological evidence links impulsive aggression with dysfunction of the prefrontal cortex. Studies of neuropsychiatric patients with localized structural brain lesions have demonstrated that some bilateral lesions in the prefrontal cortex may be specifically associated with a chronic pattern of impulsive aggressive behaviors. Neurological studies suggest that the prefrontal cortical regions associated with impulsive aggression syndromes are involved in the processing of affec-tive information and the inhibition of motor responsiveness, both of which are impaired in patients with impulsive aggres-sion. Interictal episodes of aggression may occur among some individuals with epilepsy. In a quantitative MRI study of such episodes among individuals with temporal lobe epilepsy (TLE) (Woermann et al., 2000) three groups (24 TLE patients with ag-gressive behavior, 24 TLE patients without such behavior and 35 nonpatient controls) were compared. The researchers concluded that the aggressive behavior was associated with a reduction of frontal neocortical gray matter.


Biological studies implicate the serotonergic system and the prefrontal cortex in the pathogenesis of impulsive aggression. The diagnosis of intermittent explosive disorder is sometimes considered in forensic settings; the biological correlates of im-pulsive aggression focus attention on, but do not solve, the com-plicated problem of personal responsibility for impulsive violent acts that are correlated with objective biological findings. Data from a study of visual-evoked potentials and EEGs in a large group of children and adolescents who demonstrated aggressive behavior also suggest that such behavior may be associated with altered innate characteristics of central nervous system function (Bars et al., 2001).


Assessment and Differential Diagnosis


Phenomenology and Variations in Presentation


Episodes of violent behavior appear in several common psychi-atric disorders such as antisocial personality disorder, borderline personality disorder and substance use disorders and need to be distinguished from the violent episodes of patients with intermit-tent explosive disorder, which are apparently rare. The study of Felthous and coworkers (1991), in which 15 men with rigorously diagnosed DSM-III-R intermittent explosive disorder were iden-tified from among a group of 443 men who complained of vio-lence, permitted some systematic observations about the “typical violent episode” as reported by patients with intermittent explo-sive disorder.


In the vast majority of instances, the subjects with inter-mittent explosive disorder identified their spouse, lover, or girl-friend or boyfriend as a provocateur of their violent episodes. Only one was provoked by a stranger. For most, the reactions occurred immediately and without a noticeable prodromal pe-riod. Only one subject stated that the outburst occurred between 1 and 24 hours after the perceived provocation. All subjects with intermittent explosive disorder denied that they intended the outburst to occur in advance. Most subjects remained well oriented during the outbursts, although two claimed to lose track of where they were. None lost control of urine or bowel function during the episode. Subjects reported various degrees of subjective feelings of behavioral dyscontrol. Only four felt that they completely lost control. Six had good recollection of the event afterward, eight had partial recollection and one lost memory of the event afterward. Most subjects with intermit-tent explosive disorder attempted to help or comfort the victim afterwards.




Special Issues in the Psychiatric Examination and History


The DSM-IV-TR diagnosis of intermittent explosive disorder is essentially a diagnosis of exclusion, and the psychiatrist should evaluate and carefully rule out more common diagnoses that are associated with impulsive violence. The lifelong nonremitting history of impulsive aggression associated with antisocial person-ality disorder and borderline personality disorder, together with other features of antisocial behavior (in antisocial personality disorder) or impulsive behaviors in other spheres (in borderline personality disorder), may distinguish them from intermittent explosive disorder, in which baseline behavior and functioning are in marked contrast to the violent outbursts. Other features of borderline personality disorder such as unstable and intense interpersonal relationships, frantic efforts to avoid abandonment and identity disturbance may also be elicited by a careful history. More than in most psychiatric diagnoses, collateral information from an independent historian may be extremely helpful. This is especially true in forensic settings. Of note, patients with in-termittent explosive disorder are usually genuinely distressed by their impulsive aggressive outbursts and may voluntarily seek psychiatric help to control them. In contrast, patients with an-tisocial personality disorder do not feel true remorse for their actions and view them as a problem only insofar as they suffer their consequences, such as incarceration and fines. Although patients with borderline personality disorder, like patients with intermittent explosive disorder, are often distressed by their im-pulsive actions, the rapid development of intense and unstable transference toward the psychiatrist during the evaluation period of patients with borderline personality disorder may be helpful in distinguishing it from intermittent explosive disorder.


Other causes of episodic impulsive aggression are sub-stance use disorders, in particular alcohol abuse and intoxication. When the episodic impulsive aggression is associated only with intoxication, intermittent explosive disorder is ruled out. How-ever, as discussed earlier, intermittent explosive disorder and al-cohol abuse may be related, and the diagnosis of one should lead the psychiatrist to search for the other.


Neurological conditions, such as dementias, focal frontal lesions, partial complex seizures and postconcussion syndrome after recent head trauma, may all present as episodic impulsive aggression and need to be differentiated from intermittent explo-sive disorder. Other neurological causes of impulsive aggression include encephalitis, brain abscess, normal-pressure hydrocepha-lus, subarachnoid hemorrhage and stroke. In these instances, the diagnosis would be personality change due to a general medical condition, aggressive type, and it may be made with a careful his-tory and the characteristic physical and laboratory findings.



Individuals with intermittent explosive disorder may have comorbid mood disorders. Although the diagnosis of a manic epi-sode excludes intermittent explosive disorder, the evidence for serotonergic abnormalities in both major depressive disorder and impulse control disorders supports the clinical observation that impulsive aggression may be increased in depressed patients, leading ultimately to completed suicide.


Physical Examination and Laboratory Findings


The physical and laboratory findings relevant to the diagnosis of intermittent explosive disorder and the differential diagnosis of impulsive aggression may be divided into two main groups: those associated with episodic impulsive aggression but not diagnostic of a particular disorder and those that suggest the diagnosis of a psychiatric or medical disorder other than intermittent explosive disorder. No laboratory or physical findings are specific for inter-mittent explosive disorder.


The first group of findings that are associated with impul-sive aggression across a spectrum of disorders includes soft neuro-logical signs such as subtle impairments in hand–eye coordination and minor reflex asymmetries. These signs may be elicited by a comprehensive neurological examination and simple pencil-and-paper tests such as parts A and B of the Trail Making Test. Mea-sures of central serotonergic function such as CSF 5-HIAA lev-els, the fenfluramine neuroendocrine challenge test, and positron emission tomography of prefrontal metabolism also belong to this group. Although these measures advanced our neurobiological understanding of impulsive aggression, their utility in the diagno-sis of individual cases of intermittent explosive disorder and other disorders with impulsive aggression is yet to be demonstrated.


The second group of physical and laboratory findings is useful in the diagnosis of causes of impulsive aggression other than intermittent explosive disorder. The smell of alcohol on a patient’s breath or a positive alcohol reading with a Breathalyzer may help reveal alcohol intoxication. Blood and urine toxicology screens may reveal the use of other substances, and track marks on the forearms may suggest intravenous drug use. Partial com-plex seizures and focal brain lesions may be evaluated by use of the EEG and brain imaging. In cases without a grossly abnormal neurological examination, magnetic resonance imaging may be more useful than computed tomography of the head. Magnetic resonance imaging can reveal mesiotemporal scarring, which may be the only evidence for a latent seizure disorder, sometimes in the presence of a normal or inconclusive EEG. Diffuse slowing on the EEG is a nonspecific finding that is probably more com-mon in, but not diagnostic of, patients with impulsive aggression. Hypoglycemia, a rare cause of impulsive aggression, may be de-tected by blood chemistry screens.


Differential Diagnosis


As discussed earlier, the differential diagnosis of intermittent ex-plosive disorder covers the differential diagnosis of impulsivity and aggressive behavior in general. Aggression and impulsivity are defined as follows:


Aggression is defined as forceful physical or verbal action, which may be appropriate and self-protective or inappropriate as in hostile or destructive behavior. It may be directed against another person, against the environment, or toward the self. The psychiatric nosology of aggression is still preliminary. Impul-sivity is defined as the tendency to act in a sudden, unpremedi-tated, and excessively spontaneous fashion.


The diagnosis of intermittent explosive disorder should be con-sidered only after all other disorders that are associated with impulsivity and aggression have been ruled out. Chronic impul-sivity and aggression may occur as part of a cluster B person-ality disorder (antisocial and borderline); during the course of substance use disorders and substance intoxication; in the setting of a general medical (usually neurological) condition; and as part of disorders first diagnosed during childhood and adolescence such as conduct disorder, oppositional defiant disorder, attention-deficit/hyperactivity disorder and mental retardation. In addition, impulsive aggression may appear during the course of a mood disorder, especially during a manic episode, which precludes the diagnosis of intermittent explosive disorder, and during the course of an agitated depressive episode. Impulsive aggression may also be an associated feature of schizophrenia, in which it may occur in response to hallucinations or delusions. Impulsive aggression may also appear in variants of OCD, which may pres-ent with concurrent impulsive and compulsive symptoms.


A special problem in the differential diagnosis of impulsive aggression, which may arise in forensic settings, is that it may rep-resent purposeful behavior. Purposeful behavior is distinguished from intermittent explosive disorder by the presence of motivation and gain in the aggressive act, such as monetary gain, vengeance, or social dominance. Another diagnostic problem in forensic settings is malingering, in which individuals may claim to have intermittent explosive disorder to avoid legal responsibility for their acts.

Figure 60.2 presents the differential diagnosis of aggression





Prevalence and Incidence


Intermittent explosive disorder has been subjected to little systematic study. The exclusionary criterion in the DSM-IV-TR definition (criterion C) reflects an ongoing debate over the boundaries of this disorder. In an early study of the prevalence of DSM-III-R intermittent explosive disorder among violent men, Felthous and colleagues (1991) found that of 443 sub-jects who complained of violence, only 15 (3.4%) met crite-ria for intermittent explosive disorder. However, the recently completed National Comorbidity Survey Replication (NCS-R) (Kessler et al., 2005) found that intermittent explosive disorder (12 month prevalence 2.6%) was as nearly common as panic disorder (12 month prevalence 2.7%).




The DSM-IV-TR definition of intermittent explosive disorder allows signs of generalized impulsivity or aggressiveness to be present between episodes. It also allows the psychiatrist to give an additional diagnosis of intermittent explosive disorder in the presence of another disorder if the episodes are not better ac-counted for by the other disorder. The clinical reality is that most individuals who have intermittent episodes of aggressive behavior also have some impulsivity between episodes and often present with other past or current psychiatric disorders. There is minimal research-based data available regarding comorbidity. But the lit-erature on the comorbidity of impulsive aggressive episodes sug-gests that it often occurs with three classes of disorders:


·   Personality disorders, especially antisocial personality disor-der and borderline personality disorder. By definition, antiso-cial personality disorder and borderline personality disorder are chronic and include impulsive aggression as an essential feature. Therefore, their diagnosis effectively excludes the di-agnosis of intermittent explosive disorder (Figure 60.2).


·    A history of substance use disorders, especially alcohol abuse. A concurrent diagnosis of substance intoxication excludes the diagnosis of intermittent explosive disorder. However, many patients with intermittent explosive disorder report past or family histories of substance abuse, and in particular alcohol abuse. In light of evidence linking personal and family history of alcohol abuse with impulsive aggression and the evidence (reviewed later) linking both with low central serotonergic function, this connection may be clinically relevant. There-fore, when there is evidence suggesting that alcohol abuse may be present, a systematic evaluation of intermittent explo-sive disorder is warranted, and vice versa.


·   Neurological disorders, especially severe head trauma, partial complex seizures, dementias and inborn errors of metabolism. Intermittent explosive disorder is not diagnosed if the aggres-sive episodes are a direct physiological consequence of a gen-eral medical condition. Such cases would be diagnosed as per sonality change due to a general medical condition, delirium, or dementia. However, individuals with intermittent explo-sive disorder often have nonspecific findings on neurologi-cal examination, such as reflex asymmetries, mild hand–eye coordination deficits, and childhood histories of head trauma with or without loss of consciousness. Their EEGs may show nonspecific changes. Such isolated findings are com-patible with the diagnosis of intermittent explosive disorder and preempt the diagnosis only when they are indicative of a definitely diagnosable general medical or neurological condi-tion. Such “soft” neurological signs may be diagnosed by a full neurological examination and neuropsychological testing


McElroy and coworkers (McElroy et al., 1998; McElroy, 1999) studied 27 individuals who had symptoms that met criteria for intermittent explosive disorder (IED) and reported: “Twenty-five (93%) subjects had lifetime DSM-IV-TR diagnoses of mood disorders; 13 (48%), substance use disorders; 13 (48%), anxiety disorders; 6 (22%), eating disorders; and 12 (44%), an impulse control disorder other than intermittent explosive disorder. Sub-jects also displayed high rates of comorbid migraine headaches. First-degree relatives displayed high rates of mood, substance use, and impulse control disorders”.


Some children with Tourette’s disorder may be prone to rage attacks. The clinical manifestation of these rage attacks are similar to IED and may be more common among children with To-urette’s who have comorbid mood disorders. On the basis of these observations, the rage attacks of these children may flow from an underlying dysregulation of brain function (Budman et al., 2000).


Course, Natural History and Prognosis


Little systematic study has been done on the course of inter-mittent explosive disorder. The onset of the disorder appears to be from late adolescence to the third decade of life, and it may be abrupt and without a prodromal period. Intermittent explosive disorder is apparently chronic and may persist well into middle life unless treated successfully. In some cases, it may decrease in severity or remit completely with old age.




Given the rarity of pure intermittent explosive disorder, it is not surprising that few systematic data are available on its response to treatment and that some of the recommended treatment ap-proaches to intermittent explosive disorder are based on treat-ment studies of impulsivity and aggression in the setting of other mental disorders and general medical conditions. Thus, no stan-dard regimen for the treatment of intermittent explosive disorder can be recommended at this time.


Psychological Treatment


Lion (1992) has described the major psychotherapeutic task of teaching individuals with intermittent explosive disorder how to recognize their own feeling states and especially the affective state of rage. Lack of awareness of their own mounting anger is presumed to lead to the build-up of intolerable rage that is then discharged suddenly and inappropriately in a temper outburst. Patients with intermittent explosive disorder are therefore taught how to first recognize and then verbalize their anger appropri-ately. In addition, during the course of insight-oriented psycho-therapy, they are encouraged to identify and express the fantasies surrounding their rage. Group psychotherapy for temper-prone patients has also been described. The cognitive–behavioral model of psychological treatment may be usefully applied to problems with anger and rage management.


Somatic Treatments


Several classes of medications have been used to treat inter-mittent explosive disorder. The same medications have also been used to treat impulsive aggression in the context of other disorders. These included beta-blockers (propranolol and meto-prolol), anticonvulsants (carbamazepine and valproic acid), lithium, antidepressants (tricyclic antidepressants and serotonin reuptake inhibitors) and antianxiety agents (lorazepam, alpra-zolam and buspirone). Mattes (1990) compared the effectiveness of two commonly used agents, carbamazepine and propranolol, for the treatment of rage outbursts in a heterogeneous group of patients. He found that although carbamazepine and propranolol were overall equally effective, carbamazepine was more effective in patients with intermittent explosive disorder and propranolol was more effective in patients with attention-deficit/hyperactiv-ity disorder. A substantial body of evidence supports the use of propranolol – often in high doses – for impulsive aggression in patients with chronic psychotic disorders and mental retardation. Lithium has been shown to have antiaggressive properties and may be used to control temper outbursts. In patients with comor-bid major depressive disorder, OCD, or cluster B and C personal-ity disorders, SSRIs may be useful. Overall, in the absence of more controlled clinical trials, the best approach may be to tailor the psychopharmacological agent to coexisting psychiatric co-morbidity. In the absence of comorbid disorders, carbamazepine, titrated to antiepileptic blood levels, may be used empirically.


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