Attention Deficit Hyperactivity Disorder in Adults
Attention Deficit Hyperactivity Disorder (ADHD) is the most frequently diagnosed and widely studied mental disorder of childhood and adolescence, yet is attended by increasing controversy about its diagnosis and treatment (Connor, 2011). Among the chief areas of controversy are its occurrence and symptomatology in adults, and the appropriateness of pharmacologic treatment in adults generally and particularly the long-term use of stimulant medications (Hodgkins, Arnold, Shaw, Caci, Kahle, Woods & Young, 2011). There is now general consensus that ADHD persists into adulthood more often than had once been thought, and has a distinct clinical profile and often significant adverse consequences for patients (Gentile, Atiq & Gillig, 2006). Controversy has lately been reactivated, however, by evidence that there has been a marked increase in the prevalence of attention disorders requiring pharmacological treatment in the past 5 years, particularly among adults (Muzina, 2014).
The first medical description of ADHD is thought to have been by Weikard in 1775, who described shallow and inattentive people who embarked imprudently on many projects that they completed recklessly or incompletely, and advocated confinement in darkness and solitude along with cold baths, exercise and quinine treatment to focus attention (Barkley & Peters, 2012). Molière may have depicted an étourdi ( “scatterbrain” or “bungler”) with ADHD in his 1653 comedy, L’ètourdi ou le contretemps, however (Bange & Mouren, 2009). A more detailed clinical description of “incapacity of attending with a necessary degree of constancy to any one object” was published in 1798 by Sir Alexander Crichton, and the association of motor restlessness with inattention was described in the 1840s by Heinrich Hoffmann, who was both a clinician and one of the founders of German psychiatry and a noted author of children’s stories, among them Fidgety Phillip and Johnny Look-in-the-Air (Lange, Klaus, Reichl, S., Lange, Katharina, Tucha, Lara & Tucha, Oliver, 2010).
In 1902, British pediatrician Sir George Still described children with a “defect of moral control”, meaning difficulty in controlling behavior and maintaining concentration and obedience, without impairment of intelligence or physical symptoms. Still noted a marked preponderance of boys and associated characteristics of impulsivity and low threshold for frustration. Many of his patients had more severe disobedience and delinquency, and some had suffered previous neurological insults, so in addition to ADHD this patient population had what was later to be called minimal brain damage or dysfunction (Conners, 2000). Many cases of behavioral disturbance were reported after the epidemic of encephalitis lethargia (von Economo’s disease) that followed the influenza pandemic of 1917-18; inattention, hyperactivity and often unruly and antisocial behavior were noted in children but also described in adults (Rafalovich, 2001).
The treatment of inattentive and hyperactive patients, mainly children, began at Bradley Hospital in Rhode Island in 1937, when patients with headache after then-standard diagnostic pneumoencephalograms were given Dexedrine in order to stimulate the choroid plexus to produce more cerebrospinal fluid to alleviate the headache. The stimulant had little effect on the headaches, but the school performance of treated children markedly improved, and subsequent systematic studies showed subdued behavior, decreased motor activity and increased attentiveness. Stimulant therapy was found to work best in children with “short attention span, dyscalculia, hyperactivity, impulsiveness and poor memory”, and was postulated to work by enhancing inhibition by higher brain centers (Gross, 1995). Methylphenidate, a phenylethylamine derivative which augments dopamine as well as catecholamines, was synthesized in 1944 and came to replace dextroamphetamine; it was also useful for a variety of other psychiatric disorders and was marketed as Ritalin in 1954, named for Margherita Pannizon, the wife of its discoverer (Lange et al., 2010).
ADHD was not included in the first edition of the Diagnostic and Statistical Manual of Mental Disorders (American Psychiatric Association, 1952), and at that time hyperkinetic and inattentive behavior was largely ascribed to minimal brain damage or treated with psychoanalysis (Conners, 2000). In the second edition of the DSM, it was classified as Hyperkinetic Reaction of Childhood (American Psychiatric Association, 1968). The distinction between Attention Deficit Disorder with and without Hyperactivity was introduced in DSM-3(American Psychiatric Association, 1980), and the two symptoms were combined as ADHD when the manual was revised in 1987. Subtypes of ADHD were created and the occurrence of symptoms in adolescents recognized in the fourth edition and its subsequent revisions (American Psychiatric Association, 2000), but the applicability of these criteria to attentional problems in adults was increasingly questioned (Fischer & Barkley, 2007).
It was long believed that the symptoms of ADHD resolved with maturation (Faraone, Biederman & Mick, 2006). Still, Kraepelin and other clinicians in the early 20th century noticed the occurrence of ADHD symptoms in adults, and it was gradually recognized that the parents of ADHD children often had similar symptoms (Arnold, Strobl & Weisenberg, 1972). Clinical trials in adults began soon thereafter and established that the symptoms also responded to stimulants (Wood, Reimherr, Wender & Johnson, 1976). Multiple subsequent studies have indicated that ADHD symptoms persist across the lifespan, although with different manifestations and consequences at different ages (Young & Amerasinghe, 2010), and ADHD has been demonstrated in aged individuals (Brod, Schmidt, Goodwin, Hodgkins & Niebler, 2012).
ADHD affects between 4 and 12 per cent of school age children, and persists into adulthood in 10 to 60 per cent of patients, with an estimated 4.5 per cent of adults manifesting the disorder (Gillig, Gentile & Atiq, 2005). As many of 15 per cent of adults with ADHD do not know that they have the condition (Adler, 2008). Adult ADHD presupposes the presence of the disorder in childhood, but it is not necessary to meet all the childhood diagnostic criteria if inattention or hyperkinesis cause impairment in multiple domains in adulthood, such as relationships, occupational performance and academic achievement. The symptoms decrease in intensity with age, particularly those of hyperactivity, and the incidence of comorbid psychiatric diagnoses increase, which suggests that, rather than remitting as had previously been supposed, individuals with childhood ADHD compensate for their symptoms and develop coping mechanisms both appropriate and inappropriate (Silver, 2000).
The chief manifestations of adult ADHD are procrastination and difficulty initiating tasks, variable and often insufficient attention to detail, disorganization and inefficient setting of priorities, task impersistence and disorganization. Hyperactivity, low frustration tolerance and impulsivity are less frequent, but chaotic lifestyles, substance abuse and other psychiatric disorders are more often noted. The socioeconomic consequences of adult ADHD are substantial: a 2004 study estimated that high school graduates with ADHD earned about $11,000 less per year than their non-ADHD counterparts, while the discrepancy for college graduates was approximately $4,500; lost productivity on account of ADHD was estimated at $77 billion annually, which was more than the effects of depression, alcoholism and drug addiction (Biederman & Faraone, 2006). Adults with ADHD have greater rates of job change, separation and divorce and legal difficulties, and as many as 80 per cent may have comorbid psychiatric diagnoses (Kattragada & Schubiner, 2007).
The National Comorbidity Survey Replication study (Kessler, Adler, Barkley, Biederman, Conners, Demler, Faraone, Greenhill, Howes, Secnik, Spencer, Usten, Walters & Zaslavsky, 2006) found that individuals with ADHD were significantly more likely to have mood disorder, anxiety disorder or substance use disorder. ADHD is also strongly associated with learning disability, particularly developmental dyslexia (Eden & Vaidya, 2008).
Recently-revised DSM-5 criteria (American Psychiatric Association, 2013) provide for the first time for a specific ADHD diagnosis in adults. Children up to age 16 must have 6 or more symptoms of inattention, present for at least 6 months and inappropriate for developmental level. Adolescents and adults need to have 5 or more inattentive symptoms. These include: failing to give close attention to details or making careless mistakes; difficulty holding attention on tasks and activitie; seeming not to listen when spoken to directly; frequent inability to complete schoolwork, chores or workplace duties; difficulty organizing tasks and activities; avoidance or dislike of activities that require prolonged mental effort; frequent loss of necessary objects; or forgetfulness.
There must similarly be at least 6 symptoms of hyperactivity and impulsivity in children and at least 5 in adolescents and adults, present for at least 6 months, inappropriate for developmental leval and disruptive in effect. These are: frequent fidgeting or squirming; leaving one’s seat when it is customary to remain seated; inappropriate running or climbing in children and restlessness in adolescents and adults; inability to play or recreate quietly; frequent hyperactivity; excessive talking; blurting out answers; difficulty waiting one’s turn; and frequent interrupting.
These symptoms must have been present before age 12 and must manifest themselves in 2 or more different settings. They must interfere with schoolwork, occupational performance or social function. They must also not be due to a psychotic disorder, or be better explained by another mental disorder. Three distinct presentations of ADHD are now recognized: predominantly inattentive/impulsive, predominantly hyperactive and combined, based on the admixture of symptoms over the previous 6 months.
The goals of ADHD treatment in adults are enhanced attention, improved working memory, better occupational and educational performance and decreased aggression, hyperactivity and inappropriate behavior if present. As in childhood ADHD, treatment options involve pharmacologic management with stimulants or other psychotropic drugs, cognitive and behavioral therapy or supportive psychotherapy. There has been much controversy about possible predisposition to substance abuse by prolonged treatment with stimulant medications (Humphreys, Eng & Lee, 2013): the current consensus is that childhood stimulant treatment does not increase the later likelihood of substance use disorders, but caution is still appropriate because of the substantial comorbidity of the latter and adult ADHD. Another concern in adults is the greater likelihood of cardiovascular disease in adults, to which adrenergic stimulants and also antidepressants might contribute; although most investigations of the cardiovascular effects of stimulants have not shown an increased risk, 2 of 3 adult studies have suggested an association between stimulant use and adverse cardiovascular outcomes (Westover & Halm, 2012).
Methylphenidate and amphetamine compounds block norepinephrine and dopamine reuptake and therefore increase extraneuronal catecholamines. Synaptic dopamine is also increased by inhibiting the dopamine transporter protein, and amphetamine increases presynaptic dopamine release while methylphenidate enhances hippocampal norepinephrine release. The effect of these is to enhance noradrenergic neurotransmission, particularly in frontal and prefrontal cortex responsible in part for attention direction and redirection, and for behavioral self-regulation. The stimulants have wide-ranging beneficial effects on ADHD symptoms in about 70 per cent of patients. Insomnia, anorexia, nausea, weight loss, headache, irritability and abdominal pain are the principal non-cardiovascular adverse effects and diminish with time, and the pediatric concerns about stimulant effects on growth are less do not apply. Long-acting preparations are preferred because of lesser abuse risk. Mania, psychosis, aggravation of tics, aggression and suicidality rarely occur, and active psychosis, bipolar 1 disorder, Tourette’s syndrome and cardiovascular disease are felt to be contraindications (Kolar, Keller, Golfinopoulos, Cumyn, Syer & Hechtman, 2008).
Non-stimulant pharmacotherapy may be needed in those prone to stimulant abuse and the 10 to 30 per cent of patients who are unresponsive or intolerant. Atomoxetine, which inhibits presynaptic norepinephrine transport, has a more gradual onset of action and can cause anorexia, nausea and insomnia, but is mildly anxiolytic and has no apparent potential for abuse or cardiovascular effects. It is metabolized by the cytochrome P450 D26 system, so interaction with SSRI antidepressants may occur. Buproprion inhibits dopamine and norepinephrine reuptake, and is also effective for anxiety and does not precipitate mania in bipolar disorder; it too is slower in onset of action than stimulants, and can have interactions with SSRIs, especially fluoxetine, as it is also metabolized by CYP (in this case, the 2B6 isoenzyme). Headache, dry mouth, sweating, nausea, constipation and insomnia occasionally occur and sexual dysfunction is much less than with SSRIs, but it can precipitate seizures. Tricyclic antidepressants, especially despiramine and sometimes imipramine, inhibit presynaptic norepinephrine reuptake and improve mood and decrease hyperactivity, although concentration and cognitive performance are not helped. Lower efficacy than stimulants, anticholinergic side effects and QT interval prolongation on ECG are limiting factors in their use. The alpha2-adrenergic receptor agonist clonidine is effective against hyperactivity and impulsivity but not against inattention; it is most useful with comorbid Tourette syndrome or other tic disorders. Guanfacine acts on alpha2-adrenergic receptors in the locus ceruleus and prefrontal cortex and is therefore effective against inattention, with less sedation and longer duration of action than clonidine. Modafinil is approved for narcolepsy and sleep apnea, and activates adrenergic and histamine-containing centers involved in wakefulness, as well as augmenting glutamate release in thalamus and hippocampus that promotes vigilance and promoting arousal by increasing production of hypocretin in the lateral hypothalamus, which in turn increases histamine release. It can be taken once daily, and has a low incidence of headache, anorexia and insomnia as adverse effects (Biederman, 2006).
Cognitive-behavioral Therapy promotes self-control of behavior, and is thought to affect the psychological symptoms of adult ADHD while stimulants and other drugs ameliorate the neurobiological symptoms and supportive psychotherapy may help with peripheral features of the disorder, such as relational , social and occupational impairment (Rapport, Chung, Shore & Isaacs, 2001). It has also been suggested that cognitive therapy works primarily on the various psychiatric symptoms comorbid with ADHD (Rostain & Ramsey, 2006). Several protocols for cognitive-behavioral treatment have been published (Safren, 2006), and randomized controlled trials have recently demonstrated its efficacy (Weiss, Murray, Wasdell, Greenfield, Giles & Hechtman, 2012; Mongia & Hechtman, 2012).
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