Review article

Attention Deficit and Hyperactivity Disorder in Adulthood

Dtsch Arztebl Int 2008; 105(17): 311-7; DOI: 10.3238/arztebl.2008.0311

Philipsen, A; Heßlinger, B; Elst, L T v

Introduction: Until the late nineties, attention deficit and hyperactivity disorder (ADHD) was often regarded in Germany as a disorder that fades away in late adolescence. However, it has recently become clear from numerous studies that core symptoms of ADHD persist into adulthood in a substantial subgroup of patients.
Methods: Selective review of relevant literature in Medline, up to September 2007.
Results: The prevalence of ADHD in adulthood is estimated at about 2%. Core symptoms include attention deficit in the presence of understimulation, chronic restlessness, impulsivity, disorganized behaviour, and disorders of affect regulation. The extent of psychosocial impairment depends on symptom severity, psychiatric comorbidity (such as addiction or depression), and psychosocial support.
As in childhood, ADHD in adulthood is a clinical diagnosis. Genetic factors probably play a key role in primary ADHD. Treatment should include psychotherapy and medical treatment.
Discussion: ADHD in adulthood is commoner than for example bipolar disorder or schizophrenia. It may be regarded as a risk factor for the development of other psychiatric conditions. Highly effective treatment is possible not only in childhood but also in adulthood. The problem of off-label use of psychotrophic medication in adults limits treatment in adult ADHD.
Dtsch Arztebl Int 2008; 105(17): 311–7
DOI: 10.3238/arztebl.2008.0311
Key words: ADHD, adulthood, diagnosis, treatment,
methylphenidate
Until the late 1990s, attention deficit hyperactivity disorder (ADHD) was often regarded in the German speaking countries as a disorder affecting only children and adolescents and which fades away with the onset of adulthood. Research has shown, however, that ADHD frequently persists into adulthood and is a relevant differential diagnosis for many psychiatric disorders (13). A factor of particular importance for family medicine is the high genetic penetrance of ADHD. In the majority of cases several generations of a family are affected.

Methods
An overview of the diagnosis, etiology and therapeutic options of adult ADHD is presented, based on an analysis of the results of a selective literature search in Medline up to August 2007 including review articles and monographs.

Diagnosis and classification systems
The prevalence of ADHD is estimated at 4% to 5% in childhood and about 2% in adulthood when the diagnosis is based on ICD-10 (2, 4). When applying the DSM-IV diagnostic system of the American Psychiatric Association the prevalence rates are twice as high (2).

The diagnosis of ADHD is a clinical diagnosis established on the basis of patient-reported medical history – whenever possible supported by a carer based history – and the results of a psychopathologic evaluation. As with other psychiatric disorders there are no somatic findings to demonstrate the correctness of the diagnosis.

The accepted diagnostic systems require the symptoms to have been present before the age of seven years, a fact often difficult to validate in older adults. Moreover, there is a subgroup of patients in whom the onset of this condition can only be demonstrated in early youth.

The German guidelines according to Ebert et al., which were elaborated with the support of the German Society for Psychiatry, Psychotherapy and Neurology (DGPPN) (4) do not give preference to any of the internationally established diagnostic systems, but do require physicians to state which system was used.

ICD international classification system
The "childhood hyperkinetic syndrome" (F90.0) was first introduced in 1978 within the WHO ICD-9 Classification System. In the ICD-10, the option of also diagnosing ADHD in adults was added in 1992. However, there are no specific diagnostic criteria for the diagnosis in adulthood.

DSM diagnostic system
According to the DSM-IV diagnostic system of the American Psychiatric Association, persistence of the symptoms into adulthood was already defined as "residual type" in 1980. As with the ICD-10, one problem is that the criteria are defined on a child-specific basis and have to be modified for adults (box 1 gif ppt) (5). According to DSM-IV, the inattentive, hyperactive-impulsive and combined subtype are distinguished. The combined subtype is most commonly encountered in adulthood. A further requirement is that the symptoms should cause marked impairments in at least two areas of life.

Wender Utah criteria
In contrast, the Utah criteria for ADHD were specially developed for adulthood (modified from [4]):

1. Attention disorder in the absence of stimulation
2. Hyperactivity (for example "feeling of inner restlessness"/"nervousness")
3. Emotional lability
4. Disorganized behavior
5. Impaired affect control
6. Impulsivity
7. Emotional hyperreactivity

The diagnosis is made according to the Utah criteria when: 1. and 2. plus two criteria from 3. to 7. are fulfilled. The Utah criteria take into account the pronounced mood fluctuations commonly present in ADHD to a much greater extent than ICD-10 or DSM-IV.

Course
ADHD usually has its onset in early childhood, more rarely in adolescence. No cases with adult onset have been described. The course is chronic (3), and a phasic course should suggest the differential diagnosis of an affective disorder. When ADHD persists into adulthood, the disorder may be of mild intensity and may appear as merely a variant of "normal" personality traits ("erratic, temperamental"), but may also retain the severity of a disease associated with considerable lifestyle impairment. ADHD is associated with significantly increased rates of early unplanned pregnancies, venereal diseases, traffic accidents, divorces, lower educational achievement, frequent job changes, and unemployment (6).

Supplementary and exclusion diagnosis
Questionnaires
Questionnaires can be quite helpful to assess the extent and course of clinical symptoms and they ensure a structured assessment of symptoms as an additional expedient (7). As with other psychiatric disorders, however, they are of only indicative value and confirm neither the diagnosis nor its exclusion (8).

Neuropsychological tests
According to the guidelines (4), an examination based on psychological tests, for example of attention performance, working memory and impulse control, may contribute to confirming the diagnosis. An individual diagnosis, however, cannot be made on the basis of a test value. When interpreting the results it should be remembered that adults with ADHD can even achieve very good results if interested and stimulated, although they may be suffering from relevant restrictions in daily life.

Somatic exclusion diagnosis
A medical and neurological examination must be performed and a medicine and illicit drug abuse history should be taken for exclusion and differential diagnostic purposes. The guidelines applied in the German speaking countries recommend thyroid function tests and electroencephalography (EEG) (4).

Comorbidities
The high rate of comorbid disorders (80%) and psychosocial consequences is particularly significant in adult psychiatry and psychotherapy (1). Depression (40% to 60%), anxiety disorders (20% to 60%) and addictive diseases (50% to 60%) are among the commonest comorbidities (8). The prevalence rates of ADHD among drug dependent persons and the prison population are significantly higher compared to the general population and run at about 25%. ADHD is thus a considerable risk factor for further psychiatric morbidities (box 2 gif ppt).

At the same time, some comorbidities are also differential diagnoses, such as depressive disorder with its impairments of concentration. However, it can be distinguished from ADHD based on its usually phasic course.

Differential diagnosis from borderline personality disorder (BPD) can be particularly difficult due to the high overlap of clinical symptoms – such as impulsivity and emotional lability – and comorbidity. BPD is frequently dominated clinically by states of tension followed by self harm, chronic suicidal ideation and possible symptoms of posttraumatic stress disorder.

The results of the Nordbaden childhood study (9) and our own clinical observations in adults have shown that somatic diseases such as allergies and arterial hypertension are frequent comorbidities.

Neurobiology and differential diagnosis
The exact cause of ADHD remains unknown. Most experts agree, however, that ADHD is not a single clinical disorder but rather represents a group of etiologically heterogeneous entities which share a group of core symptoms.

Numerous genetic studies have shown that children of parents with ADHD also suffer more frequently from ADHD themselves. Parents and siblings of affected patients have a two to eight-fold risk of developing ADHD symptoms (10). A metaanalysis of six twin studies revealed that 80% of the variance of the clinical symptoms can be explained in terms of genetic factors. Adopted siblings of ADHD children have a lower risk than biological siblings, and biological siblings perform more poorly than adopted siblings in neuropsychological tests of sustained attention (10). All these findings point to an important role of genetic factors in the etiology of ADHD symptoms.

Many cerebral imaging studies have demonstrated both structural as well as neurochemical and functional abnormalities in ADHD patients. For example, reductions in total brain volume, prefrontal brain (especially right-sided), basal ganglia (especially the caudate nucleus) and the cerebellum (especially the vermix) have been reported (1013). Neurochemical abnormalities in various areas of the brain have also been reported (14). The good efficacy of adrenergic and dopaminergic substances point to an important role of these systems in the pathogenesis of ADHD. Abnormalities have also been demonstrated for the cerebral dopamine transporter and pre-synaptic dopamine decarboxylase activity in PET and SPECT studies (15). However, these findings have not so far been robustly replicated, and the individual measured values do not reliably differentiate between healthy and sick persons but only become significant in the group mean.

A further risk factor is chronic intrauterine nicotine exposure (10), which is associated with a 2 to 2.7-fold elevated risk for the later development of ADHD (e1). Other factors such as certain diets, lead exposure, sugar and food additives or metabolic diseases such as cryptopyrroluria are also contentiously debated as possible causes of ADHD (10). A recently published study provided support for the hypothesis that certain food additives are associated with the development of hyperactive symptoms later in life (e2). The authors are however unaware of any data that could conclusively resolve these controversies as regards the other factors mentioned.

Chronic familial conflicts, reduced familial cohesion and confrontation with parental (especially maternal) psychopathology are more often observed in families with ADHD sufferers compared to control families (13). For example, depending on the extent of the psychosocial handicap (Rutter's indicator [RI] 1–4), the odds ratio for children from psychosocially handicapped families for developing an attention deficit hyperactivity disorder increases to values of 7.4 (for RI 1) to 41.7 (for RI 4) (e3). Odds ratios > 1 indicate an increased risk.

When thinking about the causes of ADHD it is important to distinguish the elements causality (etiology), mechanisms of action (pathogenesis) and clinical picture (syndrome) from each other. The capacity of attention control, impulse control and affect regulationare pathogenically closely associated with the fronto-striato-thalamo-frontal feedback loop systems. However, these are distributed cerebral neuronal networks. Their function may be disturbed at various sites for various reasons, for example due to lesions of greatly varying origin such as perinatal asphyxia, encephalitis, metabolic disorder, intoxication and febrile seizure.

Lesions at various sites in the brain can thereby lead to a similar clinical deficit if an identical feedback loop system is affected somewhere along its course. This means that it is no longer possible to reliably deduce the site of a functional lesion and even less the cause of a disorder, on the basis of the clinical presentation. The function of these feedback loops, however, may also be systematically compromised, i.e. independently of individual lesions, due to functional disorders of the adrenergic or dopaminergic system. Because of the genetic component and the good efficacy of dopaminergic and adrenergic substances on the core symptom of attention control, it may readily be assumed that the adrenergic and dopamine systems play a central pathogenic role at least in a large subgroup of ADHD patients.

Against this background, there is much that argues in favor of distinguishing between a primary and a secondary attention deficit hyperactivity disorder from the etiologic perspective. A positive familial history and lacking evidence of mild cerebral dysfunctions then point to primary ADHD. Birth complications, inflammatory brain diseases, intoxications, head traumas or possibly a familial history of convulsive disorder would rather suggest secondary ADHD (table 1 gif ppt).

Treatment
The guidelines (4) recommend treatment if, in the presence of a definite clinical diagnosis of ADHD, at least one area of life is severely impaired or two areas of life are slightly impaired (box 3 gif ppt).

Treatment should – as in childhood and adolescence – consist of a combination of pharmacotherapy and psychotherapy. A rationale should be provided for monotherapy. If comorbid disorders such as depression or addiction dominate the clinical picture, they should be treated first, for instance with antidepressant medication, detoxification and withdrawal treatment. After treating the comorbid disorder, the extent of ADHD related impairment should be reassessed.

Pharmacotherapy
In contrast to child and adolescent psychiatry, no medication has yet (as at October 2007) been approved in Germany for the management of adult ADHD (off-label use) (box 4 gif ppt).

Stimulant therapy
According to the German guidelines, the first-line medication is methylphenidate. Its prescription is subject to the provisions of the German Narcotics Prescription Act. The available meta-analyses rate the efficacy of methylphenidate as very good (16). The dosage and choice of product – for example as a sustained release formulation – depend on the patient's needs and therapeutic response (17). The Federal Institute for Drugs and Medical Devices recommends a dose range similar to that for pediatric use of 0.5 to 1.0 mg/kg body weight (BW) daily, although in some studies better efficacy was achieved with higher dosages up to 1.4 mg/kg BW daily. In daily clinical practice, however, it has been found that lower dosages are often sufficient for long-term therapy, especially since many adults aspire to achieve a reduction but not complete suppression of the symptoms.

Medical contraindications (box 5 gif ppt) for methylphenidate include untreated arterial hypertension and cardiac arrhythmias. Before starting medication, electrocardiography (ECG) and measurement of blood pressure and pulse are recommended. These parameters should be monitored in all patients receiving methylphenidate treatment since patients without arterial hypertension may also experience a mild increase in blood pressure and pulse rate. Monitoring of body weight is also recommended because loss of appetite is a common undesirable effect. Methylphenidate should not be prescribed during pregnancy and lactation.

Abuse potential of methylphenidate
Oral use as directed in the therapeutic dose range is not generally associated with an increased dependence potential (18), although some cases of abuse involving intranasal or intravenous use have been documented. The sustained release formulations have an even lower abuse potential because of the slower rate of drug influx.

Comorbid addictions are usually treated initially with alternative therapy options such as noradrenergic substances like atomoxetine.

However, patients with dependence diseases can also be treated with stimulants under controlled conditions, i.e. with regular negative substance abuse screening.

Atomoxetine and other substances
If methylphenidate is ineffective or if the patient has contraindications or comorbities such as depression or anxiety disorders, frequently used alternative medications include atomoxetine or antidepressants such as venlafaxine, reboxetine and desipramine. As regards significant efficacy in adult ADHD, however, so far only the selective noradrenaline reuptake inhibitor atomoxetine has been evaluated – also in larger studies – in comparison to placebo (19, 20). Atomoxetine is approved for the treatment of adult ADHD if it was already prescribed before the patient was 18 years old. Atomoxetine is also associated with mild increases in blood pressure and resting pulse as well as palpitations. The target dose is 1.2 mg/kg BW. Treatment should be in progress for 3 to 4 weeks before performing a maximal efficacy assessment. Comparative studies on the efficacy of methylphenidate and atomoxetine are still lacking. Other active agents such as modafinil, bupropion and nicotine patch are under investigation but usually in small case numbers and over only a few weeks.

Duration of treatment
Adult ADHD usually exhibits a chronic course and therefore requires long-term medication. In most cases, symptoms reappear after terminating medication.

Psychotherapy
Since the psychosocial consequences such as job loss and/or interrupted relationships are frequently predominant features in adult ADHD and these aspects cannot be influenced directly by medicinal therapy, psychotherapeutic interventions are also recommended. The group and individual psychotherapy concepts evaluated so far are based on cognitive-behavioral and/or dialectic-behavioral therapy and show positive results (2124). Both patients without medication and patients who still have residual symptoms after ADHD specific medication derive benefits. Psychotherapy can reduce the severity of ADHD and provide an improvement in commonly associated symptoms such as depression and anxiety and in self esteem. Initial evidence suggests that combination therapy comprising pharmacologic and psychotherapeutic components may be superior to medication alone (25). However, no study has yet evaluated the efficacy of psychotherapy compared to ADHD specific medication on a randomized, blind basis. The Federal Ministry for Education and Research is therefore sponsoring a large, randomized, multicenter study to further evaluate structured psychotherapy compared to one-to-one psychiatric interview (clinical management) in combination with methylphenidate or placebo.

Conclusions
Adult ADHD is a disorder that can be validly diagnosed and which, as in pediatric and adolescent psychiatry, can be treated medicinally and with psychotherapy with positive results. Further scientific research into the long-term course of this condition and the efficacy and tolerability of different therapeutic strategies is necessary. The treatment of adult patients in clinical practice is impeded at present by the lack of an approved medication.

Conflict of Interest Statement
Dr. Philipsen has received fees for lectures and advisory activities and travel expense reimbursements from the companies Medice, Janssen-Cilag, Novartis, and Lilly. She has also received research sponsorship from Medice and Janssen-Cilag.
PD Dr. Heßlinger has received lecture fees from the companies Boehringer, AstraZeneca, Lilly, Pfizer, and Medice.
Prof. Dr. Tebartz van Elst has received lecture fees and travel expense reimbursements from the companies Janssen-Cilag, Lilly, Wyeth, AstraZeneca, and Otsuka.

Manuscript received on 24 October 2007, revised version accepted on 21 January 2008.

Translated from the original German by mt-g.


Corresponding author
Dr. med. Alexandra Philipsen
Abteilung für Psychiatrie und Psychotherapie
Universitätsklinikum Freiburg
Hauptstr. 5
79104 Freiburg, Germany
alexandra.philipsen@uniklinik-freiburg.de
1.
Krause J: Die Aufmerksamkeitsdefizit-/Hyperaktivitätsstörung bei Erwachsenen. Fortschr Neurol Psychiat 2007; 75: 293–305.
2.
Sobanski E, Alm B: Aufmerksamkeitsdefizit-/Hyperaktivitätsstörung (ADHS) bei Erwachsenen. Nervenarzt 2004; 75: 697–716. MEDLINE
3.
Wilens TE, Biederman J, Spencer, TJ: Attention deficit/hyperactivity disorder across the lifespan. Annu Rev Med 2002; 53: 113–31. MEDLINE
4.
Ebert D, Krause J, Roth-Sackenheim C et al.: ADHS im Erwachsenenalter – Leitlinien auf der Basis eines Expertenkonsensus mit Unterstützung der DGPPN. Nervenarzt 2003; 939 –45. Weitere Details: http://www.dgppn.de/stellungnahmen/adhs MEDLINE
5.
Aufmerksamkeitsdefizit-/Hyperaktivitätsstörung (ADHS). Stellungnahme herausgegeben vom Vorstand der Bundes­ärzte­kammer auf Empfehlung des Wissenschaftlichen Beirats. Köln: Deutscher Ärzte-Verlag, 2007.
6.
Rösler M, Retz W: Sozialmedizinische Aspekte der ADHS – über die Ursachen und Folgen komorbider Störungen. PychoNeuro 2007, 33: 390–394.
7.
Rösler M, Retz-Junginger P, Retz W, Stieglitz RD: Homburger ADHS-Skalen für Erwachsene. Untersuchungsverfahren zur syndromalen und kategorialen Diagnostik der Aufmerksamkeitsdefizit-/Hyperaktivitätsstörung (ADHS) im Erwachsenenalter (HASE). Göttingen: Hogrefe Verlag für Psychologie 2007.
8.
Rösler M, Heßlinger B, Philipsen A: ADHS im Erwachsenenalter. In: Voderholzer U, Hohagen F (Hrsg.): Therapie psychischer Erkrankungen – State of the Art. 2. Auflage. München: Urban & Fischer 2007.
9.
Schlander M, Schwarz O, Trott GE, Viapiano M, Bonauer N: Who cares for patients with attention-deficit/hyperactivity disorder (ADHD)? Insights from Nordbaden (Germany) on administrative prevalence and physician involvement in health care provision. Eur Child Adolesc Psychiatry 2007; 16: 430–38. MEDLINE
10.
Biederman JF, Faraone SV: Current concepts on the neurobiology of attention-deficit/hyperactivity disorder. J Atten Disord 2002; 6 Suppl 1: 7–16. MEDLINE
11.
Spencer TJ, Biederman J, Biederman JF, Mick E: Attention-deficit/hyperactivity disorder: diagnosis, lifespan, comorbidities, and neurobiology. J Pediatr Psychol 2007; 32: 631–42. MEDLINE
12.
Bush GF, Valera EM, Seidman L, Seidman LJ: Functional neuroimaging of attention-deficit/hyperactivity disorder: a review and suggested future directions. Biol Psychiatry 2005; 1: 1273–84. MEDLINE
13.
Biederman J: Attention-deficit/hyperactivity disorder: a selective overview. Biol Psychiatry 2005; 1: 1215–20. MEDLINE
14.
Perlov E, Philipsen A, Hesslinger B et al.: Reduced cingulate glutamate/glutamine-to-creatine ratios in adult patients with attention deficit/hyperactivity disorder – A magnet resonance spectroscopy study. J Psychiatr Res 2007; 41: 934–41. MEDLINE
15.
Huber MF, Kirchler E, Niederhofer HF, Gruber L: Neuropsychiatrie des Methylphenidat bei der Aufmerksamkeits-Defizit/Hyperaktivitäts-Störung (ADHS). Fortschr Neurol Psychiatr 2007; 75: 275–84. MEDLINE
16.
Faraone SV, Spencer T, Aleardi M, Pagano C, Biederman J: Meta-analysis of the efficacy of methylphenidate for treating adult attention-deficit/hyperactivity disorder. J Clin Psychopharmacol 2004; 24: 24 –9. MEDLINE
17.
Biederman J, Mick EO, Surman C et al.: Comparative acute efficacy and tolerability of OROS and immediate release formulations of methylphenidate in the treatment of adults with attention-deficit/hyperactivity disorder. BMC Psychiatry 2007; 7: 49ff. MEDLINE
18.
Katusic SK, Barbaresi WJ, Colligan RC, Weaver AL, Leibson CL, Jacobsen SJ: Psychostimulant treatment and risk for substance abuse among young adults with a history of attention-deficit/hyperactivity disorder: a population-based, birth cohort study. J Child Adolesc Psychopharmacol 2005; 15: 764–76. MEDLINE
19.
Adler LA, Sutton VK, Moore RJ: Quality of life assessment in adult patients with attention-deficit/hyperactivity disorder treated with atomoxetine. J Clin Psycho-pharmacol 2006; 26: 648–52. MEDLINE
20.
Sevecke K, Battel S, Dittmann R, Lehmkuhl G, Döpfner M: Wirksamkeit von Atomoxetin bei Kindern, Jugendlichen und Erwachsenen mit ADHS – Eine systematische Übersicht. Nervenarzt 2005; 77: 294 – 308. MEDLINE
21.
Hesslinger B, Tebartz van Elst L, Nyberg E et al.: Psychotherapy of attention deficit hyperactivity disorder in adults – a pilot study using a structured skills training program. Eur Arch Psychiatry Clin Neurosci 2002; 252: 177–84. MEDLINE
22.
Stevenson CS, Whitmont S, Bornholt L et al.: A cognitive remediation programme for adults with attention deficit hyperactivity disorder. Aust N Z J Psychiatry 2002; 36: 610–6. MEDLINE
23.
Rostain AL, Ramsay JR: A combined treatment approach for adults with ADHD – results of an open study of 43 patients. J Atten Disord 2006; 10: 150–9. MEDLINE
24.
Philipsen A, Richter H, Peters J: Structured group psychotherapy in adults with attention deficit hyperactivity disorder: results of an open multicentre study. J Nerv Ment Dis 2007; 195: 1013–9. MEDLINE
25.
Safren SA, Otto MW, Sprich S et al.: Cognitive-behavioral therapy for ADHD in medication-treated adults with continued symptoms. Behav Res Ther 2005; 43: 831–42. MEDLINE
e1.
Banerjee TD, Middleton F, Faraone SV: Environmental risk factors for attention-deficit hyperactivity disorder. Acta Pædiatrica 2007; 96, 1269–74. MEDLINE
e2.
McCann D, Barrett A, Cooper A et al.: Food additives and hyperactive behaviour in 3-year-old and 8/9-year-old children in the community: a randomised, double-blinded, placebo-controlled trial. Lancet 2007;370:1560–7. Erratum in: Lancet 2007; 370: 1542. MEDLINE
e3.
Biederman J, Milberger S, Faraone SV et al.: Family-environment risk factors for attention deficit hyperactivity disorder: a test of Rutter's indicators of adversity. Arch Gen Psychiatry 1995; 52: 464–70. MEDLINE
Universitätsklinikum Freiburg, Abteilung für Psychiatrie und Psychotherapie: Dr. med. Philipsen, PD Dr. med. Heßlinger, Prof. Dr. med. Tebartz van Elst
1. Krause J: Die Aufmerksamkeitsdefizit-/Hyperaktivitätsstörung bei Erwachsenen. Fortschr Neurol Psychiat 2007; 75: 293–305.
2. Sobanski E, Alm B: Aufmerksamkeitsdefizit-/Hyperaktivitätsstörung (ADHS) bei Erwachsenen. Nervenarzt 2004; 75: 697–716. MEDLINE
3. Wilens TE, Biederman J, Spencer, TJ: Attention deficit/hyperactivity disorder across the lifespan. Annu Rev Med 2002; 53: 113–31. MEDLINE
4. Ebert D, Krause J, Roth-Sackenheim C et al.: ADHS im Erwachsenenalter – Leitlinien auf der Basis eines Expertenkonsensus mit Unterstützung der DGPPN. Nervenarzt 2003; 939 –45. Weitere Details: http://www.dgppn.de/stellungnahmen/adhs MEDLINE
5. Aufmerksamkeitsdefizit-/Hyperaktivitätsstörung (ADHS). Stellungnahme herausgegeben vom Vorstand der Bundes­ärzte­kammer auf Empfehlung des Wissenschaftlichen Beirats. Köln: Deutscher Ärzte-Verlag, 2007.
6. Rösler M, Retz W: Sozialmedizinische Aspekte der ADHS – über die Ursachen und Folgen komorbider Störungen. PychoNeuro 2007, 33: 390–394.
7. Rösler M, Retz-Junginger P, Retz W, Stieglitz RD: Homburger ADHS-Skalen für Erwachsene. Untersuchungsverfahren zur syndromalen und kategorialen Diagnostik der Aufmerksamkeitsdefizit-/Hyperaktivitätsstörung (ADHS) im Erwachsenenalter (HASE). Göttingen: Hogrefe Verlag für Psychologie 2007.
8. Rösler M, Heßlinger B, Philipsen A: ADHS im Erwachsenenalter. In: Voderholzer U, Hohagen F (Hrsg.): Therapie psychischer Erkrankungen – State of the Art. 2. Auflage. München: Urban & Fischer 2007.
9. Schlander M, Schwarz O, Trott GE, Viapiano M, Bonauer N: Who cares for patients with attention-deficit/hyperactivity disorder (ADHD)? Insights from Nordbaden (Germany) on administrative prevalence and physician involvement in health care provision. Eur Child Adolesc Psychiatry 2007; 16: 430–38. MEDLINE
10. Biederman JF, Faraone SV: Current concepts on the neurobiology of attention-deficit/hyperactivity disorder. J Atten Disord 2002; 6 Suppl 1: 7–16. MEDLINE
11. Spencer TJ, Biederman J, Biederman JF, Mick E: Attention-deficit/hyperactivity disorder: diagnosis, lifespan, comorbidities, and neurobiology. J Pediatr Psychol 2007; 32: 631–42. MEDLINE
12. Bush GF, Valera EM, Seidman L, Seidman LJ: Functional neuroimaging of attention-deficit/hyperactivity disorder: a review and suggested future directions. Biol Psychiatry 2005; 1: 1273–84. MEDLINE
13. Biederman J: Attention-deficit/hyperactivity disorder: a selective overview. Biol Psychiatry 2005; 1: 1215–20. MEDLINE
14. Perlov E, Philipsen A, Hesslinger B et al.: Reduced cingulate glutamate/glutamine-to-creatine ratios in adult patients with attention deficit/hyperactivity disorder – A magnet resonance spectroscopy study. J Psychiatr Res 2007; 41: 934–41. MEDLINE
15. Huber MF, Kirchler E, Niederhofer HF, Gruber L: Neuropsychiatrie des Methylphenidat bei der Aufmerksamkeits-Defizit/Hyperaktivitäts-Störung (ADHS). Fortschr Neurol Psychiatr 2007; 75: 275–84. MEDLINE
16. Faraone SV, Spencer T, Aleardi M, Pagano C, Biederman J: Meta-analysis of the efficacy of methylphenidate for treating adult attention-deficit/hyperactivity disorder. J Clin Psychopharmacol 2004; 24: 24 –9. MEDLINE
17. Biederman J, Mick EO, Surman C et al.: Comparative acute efficacy and tolerability of OROS and immediate release formulations of methylphenidate in the treatment of adults with attention-deficit/hyperactivity disorder. BMC Psychiatry 2007; 7: 49ff. MEDLINE
18. Katusic SK, Barbaresi WJ, Colligan RC, Weaver AL, Leibson CL, Jacobsen SJ: Psychostimulant treatment and risk for substance abuse among young adults with a history of attention-deficit/hyperactivity disorder: a population-based, birth cohort study. J Child Adolesc Psychopharmacol 2005; 15: 764–76. MEDLINE
19. Adler LA, Sutton VK, Moore RJ: Quality of life assessment in adult patients with attention-deficit/hyperactivity disorder treated with atomoxetine. J Clin Psycho-pharmacol 2006; 26: 648–52. MEDLINE
20. Sevecke K, Battel S, Dittmann R, Lehmkuhl G, Döpfner M: Wirksamkeit von Atomoxetin bei Kindern, Jugendlichen und Erwachsenen mit ADHS – Eine systematische Übersicht. Nervenarzt 2005; 77: 294 – 308. MEDLINE
21. Hesslinger B, Tebartz van Elst L, Nyberg E et al.: Psychotherapy of attention deficit hyperactivity disorder in adults – a pilot study using a structured skills training program. Eur Arch Psychiatry Clin Neurosci 2002; 252: 177–84. MEDLINE
22. Stevenson CS, Whitmont S, Bornholt L et al.: A cognitive remediation programme for adults with attention deficit hyperactivity disorder. Aust N Z J Psychiatry 2002; 36: 610–6. MEDLINE
23. Rostain AL, Ramsay JR: A combined treatment approach for adults with ADHD – results of an open study of 43 patients. J Atten Disord 2006; 10: 150–9. MEDLINE
24. Philipsen A, Richter H, Peters J: Structured group psychotherapy in adults with attention deficit hyperactivity disorder: results of an open multicentre study. J Nerv Ment Dis 2007; 195: 1013–9. MEDLINE
25. Safren SA, Otto MW, Sprich S et al.: Cognitive-behavioral therapy for ADHD in medication-treated adults with continued symptoms. Behav Res Ther 2005; 43: 831–42. MEDLINE
e1. Banerjee TD, Middleton F, Faraone SV: Environmental risk factors for attention-deficit hyperactivity disorder. Acta Pædiatrica 2007; 96, 1269–74. MEDLINE
e2. McCann D, Barrett A, Cooper A et al.: Food additives and hyperactive behaviour in 3-year-old and 8/9-year-old children in the community: a randomised, double-blinded, placebo-controlled trial. Lancet 2007;370:1560–7. Erratum in: Lancet 2007; 370: 1542. MEDLINE
e3. Biederman J, Milberger S, Faraone SV et al.: Family-environment risk factors for attention deficit hyperactivity disorder: a test of Rutter's indicators of adversity. Arch Gen Psychiatry 1995; 52: 464–70. MEDLINE

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