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• Reports published over the past decade indicate that attention deficit hyperactivity disorder (ADHD) is a cause of significant psychological impairment in adults.
  
• The adulthood disorder occurs as a continuation of its childhood counterpart, with the full ADHD syndrome persisting into early adulthood in about a third of those with childhood ADHD.
  
• Despite advances in the understanding of the neurobiology of adult ADHD, the diagnosis is made clinically by establishing a retrospective childhood diagnosis, evaluating the current symptom profile and excluding alternative medical or psychiatric causes of symptoms.
  
• Adults with ADHD have high rates of comorbid psychiatric disorder and suffer significant relationship dysfunction, work and educational failure.
  
• There is emerging evidence for the effectiveness of specific treatments for adult ADHD, including stimulant medications and some antidepressants.
  
• Clinicians should be aware of this potentially treatable disorder in young adults presenting with psychological difficulties and a history of childhood ADHD symptoms.

Definition

The diagnosis of adult ADHD, as with most psychiatric disorders, is made on clinical grounds. Case identification is based on systematic assessment of symptom profile and exclusion of alternative psychiatric or medical causes. The Diagnostic and statistical manual of mental disorders, 4th edition¹ (DSM-IV), reflects the recent conceptual shift in ADHD diagnosis by using wording applicable to adults as well as children (Box 1). Because some ADHD symptoms (eg, inattention, forgetfulness, motor restlessness) occur commonly in the community to a varying extent, it is difficult to decide where the boundary should be drawn between normal and pathological. This dilemma is partly answered in DSM-IV by allowing only those symptoms that are persistent and maladaptive to be counted toward diagnosis. In addition, impairment in at least two settings (eg, work, university, home or social life) is required before a diagnosis of ADHD can be made. Facility exists in DSM-IV for clinicians to specify "ADHD in partial remission" for patients in whom the full diagnostic criteria, although met in childhood, are no longer fulfilled. The clinical status of this less severely affected group awaits clarification.

Relationship to childhood ADHD

ADHD symptoms must have been present in childhood (although not necessarily recognised) for an adulthood diagnosis to be sustainable. Follow-up studies of childhood ADHD cohorts show considerable discrepancy in reported rates of retention of ADHD diagnosis by early adulthood. Such discrepancies are multifactorial and relate to different diagnostic and exclusion criteria used for study entry, variation in illness severity in original cohorts and differences in age at follow-up. Although up to two-thirds of patients may continue to have symptoms of ADHD as adults,⁴ only a third will satisfy full diagnostic criteria at age 18,^2,3 with further age-dependent decline continuing into the mid 20s.^5,6

Comorbidity in adult ADHD

Rates of psychopathology among ADHD children in adulthood are high (2-2.5 times those of controls), with a particularly high risk for antisocial personality disorder (up to 10 times that of controls) and drug or alcohol misuse (4-5 times that of controls).^4,7 ADHD adults have elevated rates of mood disorder (2-6 times),^7,8 anxiety disorders (2-4 times),^7,8 relationship dysfunction (2 times),⁷ and learning disorder⁷ compared with control populations. The high rate of comorbid psychopathology seen in adult ADHD may be in part a reflection of the impact of longstanding adaptive impairments on development, as well as shared familial, environmental and possibly genetic vulnerabilities. Theoretical and practical implications of comorbidity in adult ADHD have been reviewed in detail elsewhere.⁹

Pathophysiology

Despite its proposed neurobiological basis and predominantly biological treatment, the precise pathophysiological mechanisms of adult ADHD remain obscure. A complete review of this area is beyond the scope of this article and has been provided elsewhere.^10,11 Research has focused on a hypothesised functional deficit of monoamines, especially dopamine and noradrenaline. An understanding of the functional¹² and structural^13-15 neuroanatomy of ADHD is beginning to emerge, implicating dysfunctional prefrontal-striatal circuits in the pathogenesis of ADHD.

The need for a diagnostic hierarchy

The key steps in the diagnostic assessment of adults presenting with possible ADHD are shown in the Figure. Many presenting for assessment readily identify with the symptoms of the disorder. However, up to half of those presenting to specialty clinics for assessment of possible ADHD do not have ADHD as the primary diagnosis.¹⁶ Thus, approach to this popular diagnosis demands a standardised and objective assessment.

Nature and severity of current symptoms

The symptoms of ADHD in adults are an extension of those seen in children. Patients may experience difficulty sustaining attention in a number of settings, particularly when performing demanding cognitive tasks. Hyperactivity manifests physically, but may also have a mental component (having accelerated or multiple simultaneous thoughts); however, hyperactivity is not essential for the diagnosis. Patients may manifest impulsive symptoms verbally (by making tactless comments or interrupting others), or may engage in impulsive high risk activities. Often patients have poor organisational skills and an exaggerated response to minor frustrations. A longitudinal assessment of the impact of symptoms should be consistent with impairment secondary to ADHD symptoms. Common experiences of the ADHD sufferer may include recurrent educational or occupational failure, relationship instability and poor ability to organise personal affairs.

Establishing a retrospective childhood diagnosis of ADHD

A sound retrospective diagnosis of probable ADHD in childhood should be considered as a central precursor to a diagnosis of ADHD in adulthood. A retrospective assessment of childhood symptoms should be made regardless of whether a past childhood diagnosis of ADHD has been made. A retrospective diagnosis is supported by consistent parental reports of symptoms of ADHD in one or more settings, as well as objective accounts of aberrant behaviour recorded in past school reports.

Assessing other psychological and medical problems

All patients should be asked about the presence of symptoms of common psychiatric and medical disorders (past and present) that can mimic ADHD (Box 2). This is particularly important when patients present for the first time at a relatively late age (eg, over 35 years). In some cases, diagnostic difficulty arises where superimposed symptoms of a second psychiatric disorder coexist with longstanding symptoms of ADHD.

Chronic use of many illicit drugs (eg, cannabis, cocaine, amphetamines) and alcohol should be considered as a possible cause of the presenting cognitive and behavioural symptoms. Adult ADHD patients are at high risk of comorbid drug misuse and are more likely to report failed attempts to curtail their drug use.^17,18 In patients in whom possible ADHD symptoms and drug misuse occur together, it is usually prudent to reassess for ADHD symptoms after treatment of the drug misuse. Recent (eg, within the past two or three months) or ongoing misuse of illicit substances is a relative contraindication to prescription of stimulant medication. A non-stimulant treatment may be offered to patients with significant ADHD symptoms who are unable to curtail illicit drug use.

Adjunctive diagnostic tests

Routine investigations: Routine blood tests (urea, electrolyte, creatinine levels, a full blood count, liver and thyroid function tests) are of use only when the presentation suggests an underlying medical disorder. Random urinary drug screening may be performed to monitor illicit drug use in selected patients. An electrocardiogram (EEG) is performed in older adults or those with a history or signs of cardiac disease, particularly when treatment with tricyclic antidepressants is being considered.

Rating scales: Rating scales are a useful adjunct to clinical assessment, but do not provide a diagnostic test for adult ADHD. Scales have been developed for retrospective self-report of childhood symptoms (eg, Wender-Utah Rating Scale¹⁹) and retrospective parent report of childhood symptoms (eg, Conners Abbreviated Symptom Questionnaire²⁰). Rating scales can also be used to evaluate the severity of current symptoms and to monitor treatment (eg, Patient's Behavior Checklist for ADHD Adults²¹).

Neuropsychological testing: A range of neuropsychological deficits have been reported in children and adolescents with ADHD. Preliminary neuropsychological studies of adults^22-27 have produced some conflicting findings, but, on the whole, are consistent with those in childhood, and provide some support for the validity of adult ADHD. The most commonly administered test in adults is a computerised test of sustained attention (Continuous Performance Task). At present, there is insufficient evidence to recommend detailed neuropsychological evaluation for ADHD adults on a routine basis. However, neuropsychological testing may be useful in patients in whom diagnosis is difficult, or when cognitive impairment secondary to another disorder is suspected (eg, those with previous head injury, alcohol-related cognitive deficits, or early dementias).

Neurophysiological testing: Quantitative electroencephalograph (EEG) abnormalities, including decreased power of alpha and beta bandwidths in posterior leads and increased frontal theta, have been demonstrated in ADHD children and adolescents.^28-30 Quantitative EEG findings have not yet been systematically studied in adults with ADHD and, at present, cannot be advocated for routine assessment. Studies of event-related potentials (ERPs) in children and adolescents with ADHD have found a number of abnormalities in the late positive potential (P3b) amplitude and latency,^30-32 as well as abnormalities of the early negative potentials (N1 and N2).^31,33,34 However, these findings are seen in a variety of other disorders (eg, autism, learning disability) and hence lack diagnostic specificity. There are few published studies of ERP findings in adults with ADHD, and thus at present their use is for research rather than diagnostic assessment.

Functional neuroimaging: Positron emission tomography (PET) findings, including abnormality of glucose uptake in the premotor and frontal cortices¹² and reduced [fluorine-18] fluorodopa ratios in the prefrontal cortex,³⁵ support the hypothesis of prefrontal and dopaminergic deficits as central to the pathophysiology of adult ADHD, but do not have clinical application. Structural and functional neuroimaging studies may be appropriate in selected cases when another cause of cognitive and behavioural symptoms is suspected.

Education

Response to initial diagnosis is highly variable, with reactions ranging from relief at an explanation for the symptoms to grief over the "lost years" of the untreated disorder. Education regarding ADHD and its treatment is essential. Further information can be obtained by patients from popular books, ADHD support groups, and the Internet <http://www.nimh.nih.gov/publicat/adhdmenu.cfm>

Pharmacotherapy

There are only a few published reports examining the efficacy of pharmacotherapy for adult ADHD.³⁶ Drug treatment is generally reserved for those with moderate or severe symptoms, or when more conservative measures have failed. Current evidence supports stimulant responsiveness across age groups,³⁷ but there have only been six published double-blind placebo-controlled trials of psychostimulant use in adults. A review of these³⁶ noted considerable variability in response rates to stimulants (range, 25%-78%; mean, 52%) and attributed this to multiple factors, including diagnostic and dose variation between studies. No convincing evidence has emerged that long term supervised prescription of stimulants leads to drug tolerance or misuse. Commonly used dose ranges for the two stimulants available in Australia are the same as those for ADHD children (0.3-1.0 mg/kg per day for methylphenidate, and 0.2-0.5 mg/kg per day for dextroamphetamine). The mechanisms of action of stimulant medication have been reviewed.³⁸ Stimulants should not be taken together with other psychotropic drugs, unless recommended by an experienced clinician.

Tricyclic antidepressants

(TCAs) have been assessed as effective treatments for childhood and adolescent ADHD. Two studies of ADHD in adults^39-40 support a role for desipramine, nortriptyline and imipramine at typical antidepressant dosages as second-line treatment for adult ADHD. However, initial treatment with TCAs should be considered in selected patients (those at risk of misuse of prescribed stimulants, and those with comorbid depression and anxiety). The newer antidepressants venlafaxine^41-43 and bupropion⁴⁴ have shown promise in open studies, but further evaluation is required. Serotonin reuptake inhibitors may be appropriate for those with comorbid anxiety, depression, obsessive-compulsive symptoms and severe impulsivity, but as yet there is no evidence of their value for the treatment of ADHD symptoms alone. The monoamine oxidase-B inhibitor L-deprenyl has been shown to reduce ADHD symptoms in a single trial in adults.⁴⁵

Cognitive behavioural therapy

Cognitive and behavioural strategies have yet to be systematically evaluated as independent treatments for adult ADHD. However, to overcome skill deficits commonly seen in ADHD, patients can be taught basic skills such as time management, organisational strategies, problem solving and anger management.

Controversial treatments

A number of controversial treatments are available for adult ADHD. Dietary supplementation, exclusion diets and herbal supplements have not been shown to be of benefit in adults. EEG biofeedback is an expensive treatment of growing popularity, but has yet to be properly evaluated.

A case history of adult ADHD in a 22-year-old man is given in Box 3.

For patients commencing stimulant medication for the first time as adults, there should be clear evidence of functional improvement over the first 3-6 months of treatment. Clear short-term functional improvement justifies continuing stimulant prescription over the next 12 months. Thereafter, a patient's progress should be reviewed as above. Those with persistence of the full adult ADHD profile may require medication until educational goals have been met, or until stable employment is obtained. This allows the patient to further develop the skills needed to compensate for persisting symptoms. A small group of patients with severe symptoms may require stimulant medication indefinitely.

1. American Psychiatric Association. Diagnostic and statistical manual of mental disorders, 4th edition. Washington, DC: American Psychiatric Association, 1994: 83-85.
2. Gittleman R, Mannuzza S, Shenker R, Bonagura N. Hyperactive boys almost grown up: I. Psychiatric status. Arch Gen Psychiatry 1985; 42: 937-947.
3. Mannuzza S, Klein RG, Bonagura N, et al. Hyperactive boys almost grown up: V. Replication of psychiatric status. Arch Gen Psychiatry 1991; 48: 77-83.
4. Weiss G, Hechtman L, Milroy T, Perlman T. Psychiatric status of hyperactives as adults: a controlled prospective 15-year follow-up of 63 hyperactive children. J Am Acad Child Psychiatry 1985; 24: 211-220.
5. Mannuzza S, Klein RG, Bessler A, et al. Adult outcome of hyperactive boys: educational achievement, occupational rank and psychiatric status. Arch Gen Psychiatry 1993; 50: 565-576.
6. Mannuzza S, Klein RG, Bessler A, et al. Adult psychiatric status of hyperactive boys grown up. Am J Psychiatry 1998; 155: 493-498.
7. Biederman J, Faraone SV, Spencer T, et al. Patterns of psychiatric comorbidity, cognition, and psychosocial functioning in adults with attention deficit hyperactivity disorder. Am J Psychiatry 1993; 150: 1792-1798.
8. Biederman J, Newcorn J, Sprich S. Comorbidity of attention deficit hyperactivity disorder with conduct, depressive, anxiety and other disorders. Am J Psychiatry 1991; 148: 564-577.
9. Horning M. Addressing comorbidity in adults with Attention Deficit Hyperactivity Disorder. J Clin Psychiatry 1998; 59 [Suppl 7]: 69-75.
10. Castellanos FX. Toward a pathophysiology of attention deficit hyperactivity disorder. Clin Paediatr 1997; 36: 381-393.
11. Faraone SV, Biederman J. Neurobiology of Attention-Deficit Hyperactivity Disorder. Biol Psychiatry 1998; 44: 951-958.
12. Zametkin AJ, Nordahl TE, Gross M, et al. Cerebral glucose metabolism in adults with hyperactivity of childhood onset. N Engl J Med 1990; 323: 1361-1366.
13. Castellanos FX, Giedd JN, Eckburg P, et al. Quantitative morphology of the caudate nucleus in attention deficit hyperactivity disorder. Am J Psychiatry 1994; 151: 1791-1796.
14. Semrud-Clikeman M, Filipek PA, Biederman J, et al. Attention-deficit hyperactivity disorder: magnetic resonance imaging morphometric analysis of the corpus callosum. J Am Acad Child Adolesc Psychiatry 1994; 33: 875-881.
15. Castellanos FX, Giedd JN, Marsh WL, et al. Quantitative brain magnetic resonance imaging in attention deficit hyperactivity disorder. Arch Gen Psychiatry 1996; 53: 607-616.
16. Roy-Byrne P, Scheele L, Brinkley J, et al. Adult attention deficit hyperactivity disorder: assessment guidelines based on clinical presentation to a specialty clinic. Compr Psychiatry 1997; 38: 133-140.
17. Goodwin DW, Schulsinger F, Hermansen L, et al. Alcoholism and the hyperactive child syndrome. J Nerv Ment Dis 1975; 160: 349-353.
18. Carroll KM, Rounsaville BJ. History and significance of childhood attention deficit hyperactivity disorder in treatment-seeking cocaine abusers. Compr Psychiatry 1993; 34: 75-82.
19. Ward MF, Wender PH, Reimherr FW. The Wender Utah Rating Scale: an aid in the retrospective diagnosis of childhood attention deficit hyperactivity disorder. Am J Psychiatry 1993; 150: 885-890.
20. Goyette CH, Conners CK, Ulrich RF. Normative data on Revised Conners Parent and Teacher Rating Scales. J Abnorm Child Psychol 1978; 6: 221-236.
21. Patient's Behaviour Checklist for ADHD Adults. In: Barkley RA, ed. Attention deficit hyperactivity disorder: a clinical workbook. New York: The Guilford Press, 1991: 43.
22. Seidman LJ, Biederman J, Weber W, et al. Neuropsychological function in adults with attention deficit hyperactivity disorder. Biol Psychiatry 1998; 44: 260-268.
23. Matochik JA, Rumsey JM, Zametkin AJ, et al. Neuropsychological correlates of familial attention deficit hyperactivity disorder in adults. Neuropsychiatry, Neuropsychol Behav Neurol 1996; 9: 186-191.
24. Downey KK, Stelson FW, Pomerleau OF, Giordani B. Adult attention deficit hyperactivity disorder: psychological test profiles in a clinical population. J Nerv Ment Dis 1997; 185: 32-38.
25. Lovejoy DW, Ball JD, Keats M, et al. Neuropsychological performance of adults with attention deficit hyperactivity disorder (ADHD): diagnostic classification estimates for measures of frontal lobe/executive functioning. J Int Neuropsychol Soc 1999; 5: 222-233.
26. Corbett B, Stanczak DE. Neuropsychological performance of adults evidencing attention-deficit hyperactivity disorder. Arch Clin Neuropsychol 1999; 14: 373-387.
27. Jenkins M, Cohen R, Malloy P, et al. Neuropsychological measures which discriminate among adults with residual symptoms of attention deficit disorder and other attentional complaints. Clin Neuropsychol 1998; 12: 74-83.
28. Mann CA, Lubar JF, Zimmerman AW, et al. Quantitative analysis of EEG in boys with attention deficit hyperactivity disorder: a controlled study with clinical implications. Paediatr Neurol 1992; 8: 30-36.
29. Chabot RJ, Merkin H, Wood LM. Sensitivity and specificity of QEEG in children with attentional deficits or specific developmental learning disorders. Clin Electroencephalogr 1996; 27: 26-34.
30. Kuperman S, Johnson B, Arndt S, et al. Quantitative EEG differences in a nonclinical sample of children with ADHD and undifferentiated ADD. J Am Acad Child Adolesc Psychiatry 1996; 35: 1009-1017.
31. Loiselle DL, Stamm JS, Maitinsky S, Whipple SC. Evoked potential and behavioral signs of attentive dysfunctions in hyperactive boys. Psychophysiology 1980; 17: 193-201.
32. Holcomb PH, Ackerman PT, Dykman RA. Cognitive event-related potentials in children with attentional and reading deficits. Psychophysiology 1985; 22: 656-667.
33. Satterfield JH, Schell AM, Nicholas T, Backs RW. Topographic study of auditory event-related potentials in normal boys and boys with attention deficit disorder with hyperactivity. Psychophysiology 1988; 25: 591-606.
34. Klorman R, Brumaghim JT, Salzman LF, et al. Effects of methylphenidate on processing negativities in patients with attention-deficit hyperactivity disorder. Psychophysiology 1990; 27: 328-337.
35. Ernst M, Zametkin AJ, Matochik JA, Cohen RM. Dopa decarboxylase activity in attention deficit hyperactivity disorder adults -- a [fluorine-18] fluorodopa positron emission tomographic study. J Neurosci 1998; 18: 5901-5907.
36. Wilens TE, Biederman J, Spencer TJ, Prince J. Pharmacotherapy of adult attention deficit hyperactivity disorder: a review. J Clin Psychopharmacol 1995; 15: 270-279.
37. Spencer T, Biederman J, Wilens T, et al. Pharmacotherapy of attention-deficit hyperactivity disorder across the life cycle. J Am Acad Child Adolesc Psychiatry 1996; 35: 409-432.
38. Solanto M. Neuropsychopharmacological mechanisms of stimulant drug action in attention-deficit hyperactivity disorder: a review and integration. Behav Brain Res 1998; 94: 127-152.
39. Wilens TE, Biederman J, Mick E, Spencer TJ. A systematic assessment of tricyclic antidepressants in the treatment of adult attention-deficit hyperactivity disorder. J Nerv Ment Dis 1995; 183: 48-50.
40. Wilens TE, Biederman J, Prince J, et al. Six-week, double-blind, placebo-controlled study of desipramine for adult attention deficit hyperactivity disorder. Am J Psychiatry 1996; 153: 1147-1153.
41. Adler LA, Resnick S, Kunz M, Devinsky O. Open-label trial of venlafaxine in adults with attention deficit disorder. Psychopharmacol Bull 1995; 31: 785-788.
42. Hedges D, Reimherr FW, Rodgers A, et al. An open trial of venlafaxine in adult patients with attention deficit hyperactivity disorder. Psychopharmacol Bull 1995; 31: 779-783.
43. Findling RL, Schwartz MA, Flannery DL, Manos MJ. Venlafaxine in adults with attention-deficit hyperactivity disorder: an open clinical trial. J Clin Psychiatry 1996; 57: 184-189.
44. Wender PH, Reimherr FW. Buproprion treatment of attention deficit hyperactivity disorder in adults. Am J Psychiatry 1990; 147: 1018-1020.
45. Wood DR, Reimherr FW, Wender PH. The use of l-deprenyl in the treatment of attention deficit disorder, residual type (ADD, RT). Psychopharmacol Bull 1983; 19: 627-629.

Reprints will not be available from the author.
Correspondence: Dr J N Trollor, Neuropsychiatric Institute, McNevin Dickson Building, Prince of Wales Hospital, Randwick, NSW 2031.
J.TrollorATunsw.edu.au

©MJA 1999
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