Year : 2019  |  Volume : 61  |  Issue : 1  |  Page : 3--12

Situating adult attention-deficit/hyperactivity disorder in the externalizing spectrum: Etiological, diagnostic, and treatment considerations

Jayant Mahadevan1, Arun Kandasamy2, Vivek Benegal2,  
1 Department of Psychiatry, National Institute of Mental Health and Neurosciences, Bengaluru, Karnataka, India
2 Department of Psychiatry, Centre for Addiction Medicine, National Institute of Mental Health and Neurosciences, Bengaluru, Karnataka, India

Correspondence Address:
Dr. Vivek Benegal
Department of Psychiatry, Centre for Addiction Medicine, National Institute of Mental Health and Neurosciences, Bengaluru - 560 029, Karnataka


Adult attention-deficit/hyperactivity disorder (ADHD) has a population prevalence of 5%. However, its prevalence is much higher in mental health and substance use treatment settings. It is associated with significant physical and psychiatric morbidity, as well as social, occupational, and legal consequences. Adult ADHD is considered to be a part of the externalizing spectrum with which it shares both homotypic comorbidity and heterotypic continuity across the lifespan. This is attributable to a shared genetic basis, which interacts with environmental risk factors such as nutritional deficiencies and psychosocial adversity to bring about epigenetic changes. This is seen to result in a lag in brain maturation particularly in the areas of the brain related to executive functioning (top-down regulation) such as the prefrontal and cingulate cortices. This delay when coupled with impairments in reward processing, leads to a preference for immediate small rewards and is common to externalizing disorders. Adult ADHD is increasingly understood to not merely be associated with the classically described symptoms of hyperactivity, impulsivity and inattention, but also issues with motivation, emotional recognition and regulation, excessive mind wandering, and behavioral self-regulation. These symptoms are also observed in other disorders which overlap with the externalizing spectrum such as oppositional defiant disorder, conduct disorder, antisocial and borderline personality disorder. It is therefore important to develop both broad-based and specific interventions to be able to target these deficits which can reduce the burden and improve outcomes.

How to cite this article:
Mahadevan J, Kandasamy A, Benegal V. Situating adult attention-deficit/hyperactivity disorder in the externalizing spectrum: Etiological, diagnostic, and treatment considerations.Indian J Psychiatry 2019;61:3-12

How to cite this URL:
Mahadevan J, Kandasamy A, Benegal V. Situating adult attention-deficit/hyperactivity disorder in the externalizing spectrum: Etiological, diagnostic, and treatment considerations. Indian J Psychiatry [serial online] 2019 [cited 2021 Oct 21 ];61:3-12
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Externalizing disorders which refer to a set of disorders which include attention-deficit/hyperactivity disorder (ADHD), oppositional defiant disorder (ODD) and conduct disorder (CD) in childhood, and substance use disorders (SUD) and antisocial personality disorder (ASPD) in adulthood have a great impact on individuals, families, and society in terms of academic underachievement, problems related to employment, criminal behavior, and incarceration.[1]

The term externalizing disorders comes from research which evaluated higher order structure of common mental disorders and found that internalization and externalization accounted for a majority of the systematic covariance among these disorders,[2] a finding that has been replicated fairly consistently in samples taken from different parts of the world.[3],[4],[5] ADHD is considered by many to be the prototype of externalizing disorders across the lifespan and often precedes the development of other conditions in the externalizing spectrum.

This narrative review traces the origins of adult ADHD and makes a case for expanding and reinterpreting its conceptual boundaries to incorporate broad externalizing spectrum psychopathology. It then describes general and specific treatment strategies for the same.

 Nosology of Adult Attention-Deficit/hyperactivity Disorder: Old and New Concepts

Historical concepts of attention-deficit/hyperactivity disorder

ADHD was first described in the early 20th century as an “abnormal defect in moral control in children”. It subsequently came to be termed “minimal brain dysfunction” which consisted of hyperkinesis, impulsivity, short attention span and learning difficulty.[6] ADHD or “hyperkinetic reaction of childhood” as it was then termed first made its appearance in 1968 as part of the American Psychiatric Association's Diagnostic and Statistical Manual of Mental Disorders–Second Edition (DSM II). DSM-III in 1980, re-conceptualized the construct, focusing on problems of attention, impulsivity and hyperactivity, and reframed it to attention-deficit disorder (with and without hyperactivity). DSM-IV, kept the term ADHD but introduced three specific subtypes (predominantly inattentive, predominantly hyperactive-impulsive, and combined), which was defined by the predominance of symptoms of inattention and/or hyperactivity-impulsivity.

As evident from the above early conceptualisations, ADHD is considered to be a neuro-developmental disorder with onset in childhood and resolution during adolescence and young adulthood. It has a worldwide prevalence of about 5% in the general population[7] and is more common in males than females in child and adolescent samples. Children with pre-term birth and low birth weight in conjunction with minor neuro-developmental impairments are known to be at a higher risk for the development of ADHD.[6] The DSM classifications, till as late as the DSM-IV, have placed ADHD in the section on “Disorders first diagnosed in infancy, childhood or adolescence” and thus did not seriously investigate the manifestations of ADHD in adults.

Evolution of the concept of adult attention-deficit/hyperactivity disorder

There is now a growing body of evidence to suggest that the symptoms of ADHD can persist into adulthood, and that as many as 60% of children with ADHD may go on to have significant ADHD-related impairments in social, academic, and occupational functioning as adults.[8] Studies suggest that ADHD affects approximately 4.4%–5.2% of adults between 18 and 44 years of age[9],[10],[11],[12] and the prevalence in older adults might range between 2.8% and 3.5%. A large population-based Australian study detected ADHD (using the adult ADHD Self-Report Scale [ASRS]) in 2.2% of older adults (68–74 years) compared with 6.2% of middle-aged (48–52 years) adults.[13] However, fewer than 1 of every 5 adults with ADHD are currently diagnosed or treated.[14]

The prevalence is higher in certain populations, such as in incarcerated adults and among problematic substance users.[15] Unlike in childhood, ADHD in adulthood is equally prevalent in both men and women.[16] The factors associated with the persistence of ADHD symptoms into adulthood include severity of ADHD, whether treatment for ADHD was given, presence of co-morbid CD and major depressive disorder.[17] Generally, longitudinal studies of children with ADHD have demonstrated that symptoms of hyperactivity/impulsivity tend to show greater decreases than symptoms of inattention in adulthood.[6] Adults with ADHD have more traffic violations, poor occupational performance, frequent changes of jobs and higher rates of separation and divorce. Comorbid mental disorders such as depression, anxiety, and SUDs are frequently encountered in adults with ADHD.[16]

Impact on classificatory systems

The emerging evidence for adult ADHD has influenced the descriptions of ADHD in the classificatory systems. The DSM-5 criteria[18] have increased the minimum age for displaying symptoms to make a diagnosis of ADHD from 7 years to 12 years. The symptom-domain-threshold i.e., minimum number of symptoms per symptom domain required to diagnose adolescent/adult ADHD was lowered from 6 to only 5 out of 9 symptoms, recognizing that while appropriate for young children, the stricter threshold missed out on identifying those 17 and older who experience impairments and need intervention. The DSM-5 also recommends the use of severity of presentation (mild, moderate, and severe). In addition, the earlier criterion on pervasiveness of symptoms was changed from merely requiring “evidence of impairment” to “evidence of symptoms in two or more settings.” The criterion requiring “clinically significant” impairment now only requires that functional impairments need to “reduce the quality of social, academic or occupational functioning.” Autism Spectrum Disorders are also now no longer an exclusion for a diagnosis of ADHD. The DSM-IV ADHD “sub-types” are also now referred to as “presentations.”[19] This reflects the evidence that expression of different symptoms change in an individual across the lifespan (heterotypic continuity of symptom trajectories). For example, while inattention is relatively stable across the lifespan, hyperactivity/impulsivity most often diminishes with age, and therefore those initially diagnosed with Combined-type-ADHD, might transition to a predominantly Inattentive presentation later in life.[18]

Adult onset attention-deficit/hyperactivity disorder – A new entity ?

There is also growing awareness of the existence of a different conception of adult ADHD where ADHD symptoms may not necessarily be present in childhood but may emerge in young adulthood. The evidence of the same comes from three independent longitudinal studies following prospectively community samples. The Pelotas Birth cohort study from Brazil found that only 17% with childhood ADHD continued to have ADHD as young adults and only 13% with young adult onset ADHD had disorder in childhood.[20] There are similar findings that emerge from a four decade longitudinal cohort study from New Zealand where 90% of those with Adult ADHD lacked a history of Childhood ADHD and 85% of those with childhood ADHD did not have persistence of the disorder in adulthood suggesting that these groups were largely nonoverlapping.[21] The environmental risk (E-Risk) Longitudinal twin study which studied a birth cohort of 2322 twins from England and Wales and evaluated for ADHD at ages of 5, 7, 10, and 12 years found that more than 2/3rd of individuals diagnosed to have ADHD at the age of 18 years did not have the diagnosis in childhood.[22] These studies re-iterate that with regards to gender, while childhood ADHD is more prevalent in males, adult onset ADHD has a female preponderance. They also demonstrate that childhood ADHD may have neuro-cognitive impairments (such as slightly lower IQ), while adult onset ADHD have a more intact neuro-cognitive profile.[23] However, they showed that individuals with adult onset ADHD had impairments in adulthood related to traffic incidents, criminal behavior, incarceration, suicide attempts, and comorbidities, similar to those with residual childhood ADHD.[23] This raises the question as to whether childhood ADHD and adult onset ADHD actually represent two separate syndromes with distinct neurobiological substrates.

 Adult Attention-Deficit/hyperactivity Disorder and Co-Morbidity: The Externalizing Spectrum and Beyond

Attention-deficit/hyperactivity disorder and comorbid disorders

A-ADHD more often than not is co-morbid with a large number of other conditions, both psychiatric and metabolic. Over 80% of adults with ADHD have at least one coexisting psychiatric disorder including SUDs, personality disorders, and mood and anxiety disorders.[24] A large population-based investigation of common psychiatric and metabolic comorbidity of adult ADHD documented that both psychiatric disorders: SUD (35.12%), depression (42.28%), bipolar disorder (14.29%), and anxiety (44.65%) as well as metabolic diseases: type-2 diabetics mellitus (T2DM) (6.1%), and hypertension (16.65%) were significantly more prevalent in adults with clinically diagnosed ADHD than in those without. Among adults with ADHD, the prevalence estimates of depression, bipolar disorder, and anxiety were higher in females than in males, whereas the prevalence estimates of SUD, T2DM, and hypertension were higher in males than in females.[25] The data from the US National Comorbidity Survey Replication, documented significantly increased risk to develop co-morbid mood disorders (odds ratio [OR] = 5.0), anxiety disorders (OR = 3.7), and SUDs (OR = 3.0) in patients with adult ADHD. The degree of co-morbidity increases further while considering individual disorders such as bipolar disorder (OR = 7.4), dysthymia (OR = 7.5), and drug dependence (not including alcohol) (OR = 7.9).[26]

Substance use disorders

Alcohol, tobacco, and other substance-use disorders (SUDs) are the most problematic co-occurring disorders with A-ADHD. ADHD in childhood or adolescence is strongly associated with an increased risk for substance use or dependence later in adolescence or in early adulthood, as is CD.[27] Both ADHD and CD and their joint occurrence increase vulnerability to future alcoholism and substance abuse.[28],[29] It has been proposed that the same cognitive and affective mechanisms underlie all of the “dysregulatory” psychopathologies of hyperactivity, anti-sociality, substance abuse/dependence, impulsive aggression, and mania. A meta-analysis of the prevalence of adult ADHD in patients with SUDs places it at 23.1% (CI: 19.4%–27.2%).[30] Similar findings were seen among Indian outpatients seeking treatment for SUDs at our centre where 21.7% were found to have “highly likely ADHD” based on ASRS screening.[31] Adults with ADHD and comorbid SUD have a greater likelihood of having continuous problems, a reduced likelihood of going into remission, and take longer to reach remission. They also respond less well to SUD treatment and are less likely to remain in treatment, despite having more treatment exposure.[32] Moreover, adults with ADHD and comorbid SUD also have increased rates of criminal behavior, imprisonment, and delinquency. Co-occurring conduct or bipolar disorders (with ADHD) confer the highest risk for SUD.[33] It is a matter of concern that ADHD and its other comorbidities, remain underidentified and undertreated in addiction treatment centres, leading to greater recidivism. For example, a study from a residential drug treatment documented that although 3% of patients were noted in the records as having ADHD, systematic assessment using a standardized screener identified a rate of ADHD of 44%.[34]

Personality disorders

Prospective studies have shown a significant association of ADHD diagnoses in childhood and the later development of personality disorders in adulthood. Prevalence of personality disorder diagnoses in adult ADHD patients range from 10% to 75%. Personality disorders from cluster B and to a lesser extent cluster C have been prominently found in ADHD populations.[35] There is a significant co-morbidity of adult ADHD with borderline, histrionic, narcissistic, and antisocial personality disorders.[36] The co-occurrence of ADHD and borderline personality disorder is one of the most common overlaps, with 40% of those diagnosed with borderline personality disorder likely to have a diagnosis of ADHD.[37]

Bipolar disorder

Lifetime ADHD is frequently co-morbid in adults with bipolar disorder (BD). Systematic studies of children and adolescents with BD show rates of ADHD ranging from 60% to 90%.[38] Comorbid ADHD and BD is associated with earlier age of BD onset, a more severe disease course, more severe mood disorder symptoms, lower functional scores and greater burden of other psychiatric comorbid conditions.[38] A recent study detected co-morbid ADHD in 48% of bipolar patients and 25% of patients with unipolar depression, compared to 12% in healthy controls. ADHD and comorbid BD had higher frequency of suicide attempts and significant association with depressive, cyclothymic, irritable, and anxious temperament.[39] The co-segregation of these two conditions makes ADHD diagnosis challenging because its symptoms are often mistakenly assumed to be part of BD. So, patients with comorbid ADHD/BD are underdiagnosed and under-treated. There is even some evidence that the presence of ADHD symptoms may be indicative of pre-morbid schizophrenia or even be linked with a “distinct neurodevelopmental progression of schizophrenia.”[40]

Autism spectrum disorders

ADHD and autism spectrum disorder (ASD) are neurodevelopmental conditions that frequently co-occur, with ADHD presenting in 30%–80% of individuals with ASD,[41] and ASD presenting in 20–50% of individuals with ADHD.[42] Below-threshold cross-disorder symptoms are also common.[43] Adults having concurrent symptoms of ASD and ADHD are at higher risk of poorer cognitive, emotional and functional outcomes including mood disorders, sleep problems and unfavorable psychosocial outcomes, such as poorer academic performance and lower employment levels.[44] Since dual-diagnosis of ADHD and ASD was not permitted till recently (DSM-IV TR had specified that ASD was an exclusion criterion for ADHD), this link has been under-diagnosed, thereby limiting research of this common clinical co-occurrence.[11] Though substance use-related problems have traditionally been considered rare in ASD, a recent large population register Swedish study observed that ASD was associated with increased risk for a range of substance use-related problems and that the risk was the highest among individuals with ASD and co-occurring ADHD.[45] Those with ASD and ADHD may represent a group which is at high risk for problems such as excessive and problematic gaming.[46]

Anxiety disorders

Anxiety disorders have been reported in around 50% of individuals with ADHD[10] and has been reportedly commoner with social phobia than panic disorder.[47] Obsessive compulsive disorder is highly comorbid with ADHD particularly in males in whom the rate of comorbidity is about 50%.[48] Individuals with anxiety disorders and ADHD have more severe anxiety symptoms, earlier age of onset of anxiety, and more frequent additional comorbid psychiatric diagnoses and substance. ADHD is under-diagnosed and diagnosed later in individuals with comorbid anxiety.[49]

The externalizing spectrum of adult attention-deficit/hyperactivity disorder and other psychopathologies

It will be evident, that although conceptualised as a single disorder, ADHD is a much more heterogeneous disorder, with great variability between individuals, not only in children but to an even greater extent, in adults. The symptoms associated with ADHD can be viewed as dimensional markers of a spectrum of related disorders that have as part of their characteristics impairments of attention and impulsivity. The spectrum also accommodates the wide array of comorbid psychiatric disorders associated with ADHD. This comorbidity is bidirectional. Those diagnosed with ADHD have one or more psychiatric disorders, while patients with a primary diagnosis of one of several psychiatric disorders also meet criteria for ADHD at rates higher than the general population. Grouping disorders according to their patterns of covariation (i.e., comorbidity), it has been argued, can reveal the natural classification of mental illness, since conditions that tend to co-occur more frequently, possibly belong to the same underlying class and share etiologies. Research on disorder dimensionality and comorbidity suggests that many mental disorders are manifestations of relatively few core underlying dimensions. Factor analytic studies of symptoms of psychiatric disorders have found support for two factors, internalizing and externalizing, underlying common psychopathology in adults. Internalization is the propensity to express distress inwards, while Externalization describes the propensity to express distress outwards. The internalizing dimension appears to represent the higher-order factor which accounts for much of the covariation among first-order factors accounting for comorbidity among major depression, generalized anxiety disorder, dysthymia, panic disorder, social and specific phobias, obsessive-compulsive disorder, posttraumatic stress disorder, separation anxiety disorder, and so on. Whereas the externalizing dimension is the latent factor underlying ADHD, ODD, CD, ASPD, and SUDs. There is also ample evidence of co-occurrence between internalizing and externalizing disorders.

The externalizing spectrum per se is seen to be related to an “externalizing liability” which is a common vulnerability factor that underlies all externalizing spectrum disorders from childhood to young adulthood. This liability corresponds to the neuropsychological and behavioral constructs of trait impulsivity and executive functioning deficits which in turn are thought to be related to common, heterogeneous neural substrates, which can account for a range of neurological, cognitive, and psychiatric disorders.[1] This liability is highly heritable (h2 = 0.84) and twin studies have supported evidence for common genetic influences hypothesized to be what contributes to high heritability noted amongst externalizing spectrum disorders. However, this genetic risk ultimately has to interact with environmental risk to culminate in symptomatology.[50]

 Attention-Deficit/hyperactivity Disorder Etiological Evidence

Construct of attention-deficit/hyperactivity disorder

ADHD is currently considered to be a disorder of deficient self-regulation in the areas of attention, motivation, arousal as well as affect.[51]

The ability to self-regulate is in turn dependent on its component abilities, including self-awareness, response inhibition, executive attention or attentional management, verbal self-instruction or working memory, nonverbal working memory or visual imagery, problem-solving, self-motivation, and emotional self-regulation.[51] These deficits are present in varying degrees across the externalizing spectrum disorders and contribute to the difficulties encountered by individuals afflicted with them.

Neurobiological substrates and mechanisms of attention-deficit/hyperactivity disorder and externalizing spectrum disorders

Multiple neurobiological models have been proposed for the symptoms of ADHD. There is growing interest in exploring the trans-diagnostic neural deficits that underlie ADHD, and the spectrum of externalizing disorders, including subjects at high risk for alcohol and SUDs. Delayed development within the later maturing areas of the brain has been suggested as a causal mechanism. Several studies, including some longitudinal cohorts of children with externalizing disorders, have observed that various brain measures differed widely from that in normal controls, in early childhood but tended to converge with age.[52] In fact some cross-sectional studies found no difference between adults with ADHD and age-matched controls, supporting this hypothesis of normalization with age. Also the externalizing disorder group had very similar growth trajectories (developmental curves) to the control groups, suggesting a maturational lag. The brain measures implicated include, brain volume,[53] cortical thickness,[54],[55] electrophysiological measures like the P300 component of the evoked response potential.[56] In summary, neuropsychological studies in adults with ADHD have shown impairments in the domains of attention, memory, and behavioral inhibition. Structural MRI studies in adults with ADHD are more inconsistent wherein one meta-analysis showed differences in anterior cingulate cortex volumes[57] while another showed no differences.[58] Resting state functional MRI studies, which assess connectivity in and between brain networks, show reduced connectivity within the default mode network (DMN) and between the DMN and the fronto-parietal (executive control) and ventral attention (salience) networks in patients with ADHD.[59] It has also been hypothesized that individuals with ADHD have lapses of attention related to failure of suppression of the DMN.[59] Recent neurobiological theories of ADHD have revolved around two common, but not mutually exclusive models. One emphasizes top-down, self-regulation processes, associated with cognitive control or executive functioning.[60] Another emphasizes bottom-up, motivational, and incentive or reward response.[61] There is evidence to support the involvement of both these psychobiological systems.

A more detailed account of the neurobiological substrates of ADHD and other externalizing disorders using a variety of measures of CNS structure and functioning is beyond the purview of this review and have been excellently reviewed in recent publications.[62],[63]

Genetics of adult attention-deficit/hyperactivity disorder

There is consistent evidence to suggest that ADHD risk is genetically mediated with heritability estimates of approximately 80%.[16] This has been noted in adult ADHD as well suggesting that the heritability is stable from childhood to adulthood.[64] Candidate gene studies have implicated six genes linked to catecholaminergic neuro-transmission.[65] The dopamine transporter gene (SLC6A3) 40 base pair variable number of tandem repeats regulatory polymorphism produces two alleles with 9 and 10 repeats (9R and 10R).[66] The 9R variant is associated with adult ADHD and is related to increased dopamine transporter activity, which may result in a baseline “hypo-dopaminergia” and reward deficit.[67] Meta-analysis of genome wide association studies in ADHD, found that 12 loci reached genome wide significance and that the genes involved were biologically relevant. However, they were not the ones expected based on candidate gene approaches.[68] One of these, FOXP2 has been related to adult ADHD and speech and language disorders. It is also associated with dopamine regulation in certain parts of the brain.[64]

The common genetic variants account for only about one third of the total heritability of ADHD predicted from familial studies. The remaining heritability is therefore most likely linked to gene–gene and gene–environment interactions.[64] Externalizing disorders such as CD, anti-social personality disorder, alcohol and drug dependence are also highly heritable, where a general vulnerability factor accounts for familial resemblance in these disorders.[69] There is also evidence to suggest that in ADHD and other externalizing disorders, environmental exposure may play a key role to shape temperament and psychopathology and that the same is mediated through epigenetic changes leading to variations in brain development.[70]

The role of the environment and epigenetics in attention-deficit/hyperactivity disorder and the externalizing spectrum

As mentioned in the previous section, there is a significant component of the heritability in ADHD that is explained by gene-environment interactions. In other words, it is only when the genetic risks for ADHD and the externalizing spectrum interact with varied environmental exposures, such as nutritional deficiencies, toxin exposures and psychosocial adversity through epigenetic mechanisms, do they result in the different symptoms of externalizing spectrum disorders.[50] This has led to the emergence of the “exposome” concept which is composed of every exposure to which an individual is subjected from conception to death being an integral component of etiological studies.[71] There are several environmental risk factors which have been seen to be related to the development of ADHD. These include low maternal folate levels, exposure to tobacco smoke, alcohol, and polychlorinated biphenyls during the gestational period.[50] The presence of family dysfunction, lack of social support for mothers, adverse life events, disagreements in the course of pregnancy and exposure to violence in intrauterine life and childhood, including domestic violence are also associated with an increased risk of ADHD.[72] Epigenetic studies have pointed to lower DNA methylation levels in DRD4 and 5-HTT genes which were associated with higher ADHD scores. However, systematic analysis of environmental exposures were not conducted for correlations to be made as to what factors influenced the methylation profile.[73]

 Assessment of Adult Attention-Deficit/hyperactivity Disorder

Most often, patients with Adult ADHD have already seen other doctors and sought treatment for other co-occurring conditions like SUDs, behavioral addictions such as internet use and gaming disorder, mood disorders, or anxiety. Both patients and their spouses or parents often complain about occupational difficulties (educational dropout, repeated disciplinary incidents, irregular job records), problems with organization (time and money management problems, personal and administrative difficulties) and tendency to procrastination. Often intelligent patients develop complicated strategies to counteract their lack of attention and poor concentration to cope with the difficulties in school and college or at work, which often put a strain on their cognitive resources. Many will have faced repeated difficulties in personal relationships and have been frustrated by their repeated lack of success despite relatively higher intelligence and creativity, accompanied by demoralization and depression. Clinicians need to be aware that the common clinical presentations of adult ADHD may be different from the standard representation of the hyperactive child [Box 1].[63],[74][INLINE:1]

Several screening tools are available for ADHD in adults. It may be prudent to utilise these tools in addiction treatment settings and psychiatric treatment facilities in patients with bipolar disorder or anxiety, where the prevalence of adult ADHD is quite high. Two tools which are free to access and commonly used are:

The ASRS is a validated tool which is recognized by the World Health Organization and has recently been updated to reflect changes in DSM 5 criteria. The ASRS has been translated into many languages, including Indian languages. The ASRS has been extensively studied in many general population clinical settings, and has good sensitivity (91.4%) and specificity (96.0%)[75]The Wender Utah Rating Scale assesses ADHD but also a broader spectrum of associated and comorbid symptoms. Its aims to assess an adults' retrospective account of their own childhood symptoms of ADHD. It is widely used but has been criticized for using outdated criteria and lacking proper validation.[76]

Other screening tools such as Conners Adult ADHD Rating Scale and the Adult ADHD Investigator Rating Scale require author permissions for use.

While the gold standard for diagnosis is a clinical interview, several free to use interviews are available for diagnostic assessment of ADHD in adulthood. These include:

Diagnostic Interview for Adult ADHD (DIVA 2.0) is based on the criteria for ADHD in DSM-IV. DIVA 2.0 asks about the presence of ADHD symptoms in adulthood as well as childhood, chronicity of these symptoms, and significant clinical or psychosocial impairments due to these symptoms.[77] It is available in English but not in any Indian languagesADHD Child Evaluation + (ACE+) is a semi-structured interview which is built upon ADHD Child Evaluation (ACE) and is free to use, but is not available in Indian languages.[78]

Other interviews such as the Conners Adult ADHD Diagnostic Interview (CAADID), Adult ADHD Clinical Diagnostic Scale (ACDS) require author permissions.

 Treatment of Adult Attention-Deficit/hyperactivity Disorder and Externalizing Spectrum Conditions

Given the wide overlap between ADHD and other disorders, consideration of treatment is often dictated by the presence of co-occuring disorders. As a thumb rule, comorbidities require to be diagnosed at the outset, so that the best order of treatment can be decided in discussion with the patient. In general, disorders such as psychosis, bipolar disorder, severe depression and severe anxiety are usually treated first.[63] Drug and alcohol abuse should usually be stabilized but may also treated concurrently with ADHD. Milder mood or anxiety disorders, and emotional instability, may actually respond to treatment of ADHD and should be treated at the same time.

Based on our understanding of the underpinnings of ADHD and externalizing disorders described previously, there are different strategies that can be adopted for treatment. These can be understood as trans-diagnostic or disorder-specific interventions.

Trans-diagnostic interventions include nutritional supplementation, cognitive retraining and brain gyms, brain stimulation interventions, psychotherapy, yoga and meditation. Disorder-specific interventions for adult ADHD are pharmacotherapy.

Transdiagnostic interventions

Nutritional interventions

A systematic review has found that supplementation of n-3 polyunsaturated fatty acids in children and adolescents with ADHD improve clinical scores and cognition.[79] These findings are not however replicated in adult ADHD. There is also some evidence for the use of micronutrient supplementation such as iron, zinc and selenium in individuals with ADHD for improvements in attention, however only if there is evidence of deficiency.[80]

Cognitive retraining

These include cognitive training such as working memory training which can be delivered by trained professionals or through commercially available mobile and computer applications. These may lead to improvements in neuropsychological test outcomes, however do not translate into improvements of symptoms of ADHD measured objectively.[81] A meta-analysis of neuro-feedback studies in individuals with ADHD showed large effect sizes for inattention and impulsivity and medium effect sizes for hyperactivity.[82]

Brain stimulation interventions

A meta-analysis of transcranial magnetic stimulation and direct current stimulation studies has shown preliminary evidence that there are improvements in symptoms of ADHD. These are interventions that hold promise for the future.[83]

Psychotherapeutic interventions

This includes psycho-education and cognitive behavioral therapy. A meta-analysis of cognitive behavioral therapy trials for Adult ADHD showed that it was superior to waitlist and active comparison groups.[84] Components of CBT for Adult ADHD include training in time management, prioritization, organization, problem solving, motivation, and emotional regulation. This can be considered as an adjunct to pharmacological therapy.[16]

Yoga, mindfulness, and meditation-based interventions

Yoga, mindfulness-based interventions, and/or meditation had a statistically significant effect on the outcomes of ADHD symptoms such as hyperactivity, and inattention as well as executive functioning and on-task behavior with effect sizes ranging from small to large across outcomes. However due to the considerable risk for bias inherent to these studies, further extensive research is required to validate the efficacy of these interventions.[85]

Disease-specific interventions

Pharmacological interventions are the first line of management of Adult ADHD and have definite benefits in the short term which include reduction of symptoms and improvement of functioning. There is less that is known about the long-term benefits or risks of these medications. This is important to know since most often sustained treatment is needed.[16] The approved medications used for the treatment of adult ADHD are stimulants (methylphenidate and amphetamine) and nonstimulants (atomoxetine). There are also some off label non stimulant medications (modafinil, guanfacine, venlafaxine, bupropion, and desipramine) which may also be used.


Stimulants include amphetamines (amphetamine, dextroamphetamine and lisdexamphetaminedimesylate) and methylphenidate (methylphenidate and dexmethylphenidate). Stimulant medications through various mechanisms increase dopaminergic and noradrenergic transmission. Amphetamines have an elimination half-life of 4–6 h while for methylphenidate it is 2–3 h.[16] They are available as immediate release preparations requiring dosing up to 4 times per day and sustained release preparations, for once or twice daily administration. Methylphenidate is also available in an OROS preparation for once daily administration. It is also the only stimulant medication available in India. Amphetamines and methylphenidate are equally efficacious and nearly 70% report an almost immediate improvement in attentiveness and distractibility, with moderate-to-large effect sizes.[16] The common adverse effects of stimulants are insomnia, dry mouth, decreased appetite, weight loss, headaches, and in some case a worsening of anxiety. It is also associated with an increase in resting heart rate and blood pressure and needs to be used with caution in people with hypertension and heart disease. It is also contraindicated in psychosis and tics which can be exacerbated by stimulants.[16] Stimulants also have abuse potential particularly in individuals with co-morbid SUDs and should be prescribed with caution. However, the risks of misuse are often overstated in this population and it should be considered if medically indicated. This is also because in terms of short-term outcomes, the effect sizes for stimulants are larger than those for nonstimulants.[86]


Atomoxetine is the only non-stimulant medication approved for the treatment of adult ADHD. It is a norepinephrine reuptake inhibitor and is supposed to increase noradrenergic and dopaminergic transmission in frontal brain regions.[16] A meta-analysis found that atomoxetine was more efficacious than placebo in the treatment of adult ADHD. It was found to be more efficacious in treating inattention domain than hyperactivity/impulsivity domain.[87] However, unlike stimulants it takes 1-2 weeks for beneficial effects to emerge. It may be an attractive option in patients with co-morbid SUDs because of its low abuse potential compared to stimulants. It can also be used in patients with psychosis and tic disorders.[16] A retrospective review of atomoxetine treatment of patients with co-morbid SUDs and externalizing symptoms (ES) found that it led to significant treatment benefits such as reduction of ES scores, shorter turnaround time, longer periods of abstinence, and better quality of life.


Adult ADHD is a commonly encountered disorder with significant impact on physical and psychological health and is associated with social, occupational, and legal consequences. It is a disorder which frequently co-occurs with other disorders of the externalizing spectrum to which it appears to be biologically linked. It is most often characterised not just by the classical symptoms of hyperactivity, impulsivity, and inattention, but with prominent issues with motivation and emotional regulation, which are linked to delays and deviations in brain development in terms of structure and function. This seems to be mediated by an interaction of genetic and environmental risk. It is thus important to develop both broad-based and specific interventions to be able to target these deficits which can reduce the burden and improve outcomes.

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