Chapter 34 Attention deficit and hyperactivity disorder (ADHD)
EPIDEMIOLOGY, AETIOLOGY AND CLASSIFICATION
The worldwide prevalence rate of attention deficit and hyperactivity disorder (ADHD) has been estimated at between 2 and 29%.1 The rate at which ADHD is diagnosed and treated in both children and adults has dramatically increased since the syndrome was first recognised as a specific disorder in the Diagnostic and Statistical Manual of Mental Disorders (DSM) in the 1970s. In the United States of America as many as 10% of males and 4% of females have been diagnosed with ADHD.2 An objective epidemiological or scientific basis for the rapidly increasing prevalence of ADHD in general and the higher incidence of the syndrome in boys compared to girls is highly controversial and may reflect social issues and changes in diagnostic criteria more than actual changes in prevalence rates.3
The causes of ADHD are multifactorial. Data from twin studies show that ADHD is a highly heritable disorder4 and the risk of developing this disorder is probably influenced by genes that affect CNS transport of dopamine and serotonin.5 Other causes of ADHD include problems associated with premature birth, birth trauma, childhood illness and environmental toxins.6 Increased risk of ADHD is associated with in-utero exposure to alcohol, tobacco smoke and lead. Up to 20% of ADHD cases are probably caused by brain injury around the time of birth. Certain food preservatives exacerbate the symptoms of ADHD, but probably do not actually cause the disorder.7 Some cases of ADHD may be associated with delayed development of certain areas of the frontal and temporal lobes and relatively rapid maturation of motor areas of the brain.8 Children diagnosed with ADHD frequently experience disturbed sleep including restlessness, sleep walking, night terrors and restless leg syndrome; however, a causal relationship between sleep disorders and ADHD has not been clearly established.9 Early childhood neglect or abuse probably also increase the risk of developing ADHD. Most cases of ADHD probably result from multiple genetic, developmental, physiological, environmental and psychosocial factors.10
Three subtypes of ADHD are recognised in the DSM, depending on the type and severity of symptoms:
Symptoms of inattention, impulsivity or hyperactivity must cause clinically significant impairment in at least two spheres including social, academic or occupational functioning. Neuropsychological testing is frequently employed to assess inattention, processing speed and neurocognitive deficits. A diagnosis of ADHD should be made in childhood only after other childhood disorders, including pervasive developmental disorders, learning disorders and anxiety disorders, have been ruled out.11 Many children diagnosed with ADHD also meet criteria for conduct disorder. When evaluating adults a thorough medical history is important to rule out medical or psychiatric disorders that mimic symptoms or functional impairments that resemble ADHD. These include, for example, bipolar disorder, absence seizures, hypothyroidism, obsessive-compulsive disorder and chronic sleep deprivation.12
RISK FACTORS
The hyperactivity of ADHD often resolves by late adolescence or adulthood; however, symptoms of distractibility may not lessen with age. It has been estimated that fewer than one-fifth of adults with ADHD have been correctly diagnosed and appropriately treated, resulting in significant social and occupational risk. ADHD is highly comorbid with oppositional-defiant disorder and learning disorders in children, and with major depressive disorder, anxiety disorders and substance abuse in adults.13 It has been estimated that almost half of individuals diagnosed with ADHD never graduate from high school and fewer than 5% complete a 4-year university degree program.14 The high prevalence rate of ADHD significantly affects employment statistics. A large population survey of US adults found that a diagnosis of ADHD was associated with 35 days of lost work on average. Extrapolating these findings to the population suggests that US$19 billion in lost productivity and 120 million lost work days annually are attributable to ADHD.15
CONVENTIONAL TREATMENT
Stimulant medications are the standard Western treatment of ADHD; however, SSRIs and other antidepressants are also used with varying degrees of success. Extended-release forms of stimulants are better tolerated and less often lead to abuse. Approximately one-third of children and adolescents who take stimulants experience significant adverse effects, including abdominal pain, decreased appetite and insomnia, and 10% experience serious adverse effects.16 Because stimulants are classified as scheduled or restricted medications (depending on the country), prescriptions are usually limited to a short supply; this can result in treatment interruptions and transient symptomatic worsening when refills are not obtained on time. One-third of all individuals who take stimulants for ADHD report significant adverse effects, including insomnia, decreased appetite and abdominal pain.16 Sporadic cases of stimulant-induced psychosis have been reported.17 Neurotoxic effects associated with long-term stimulant use have not been fully elucidated; however, chronic amphetamine use in childhood is associated with slowing in growth. Stimulants and other conventional treatments of adulthood ADHD may be only half as effective as they are in children.13
Short-acting stimulants are the most prescribed conventional treatments of adult ADHD. Controlled-release stimulants, buproprion and the SSRI antidepressants are being increasingly used in the adult ADHD population; however, research findings suggest these medications may not be as efficacious as fast-released stimulants.18 The non-stimulant medication atomoxetine has less potential for abuse, but may not be as efficacious as stimulants.19 Although atomoxetine is the only non-amphetamine medication approved by the US Food and Drug Administration for the treatment of childhood ADHD, there are growing concerns about its adverse effects, including hypertension, tachycardia, nausea and vomiting, liver toxicity and possibly increased suicide risk.20,21 In Australia atomoxetine is registered for use by the Therapeutic Goods Administration.
Growing concerns about inappropriate or over-prescribing by physicians of stimulant medications and incomplete understanding of risks associated with their long-term use have led to increasing acceptance of emerging non-conventional therapies.22,23 In addition to conventional prescription medications, behavioural modification is a widely used conventional treatment of ADHD in children. Psychotherapy and psychosocial support help reduce the anxiety and feelings of loss of control that frequently accompany ADHD.
INTEGRATIVE MEDICAL DIAGNOSIS AND TREATMENT OPTIONS
Many individuals diagnosed with ADHD use alternative therapies alone or adjunctively with conventional pharmacological treatments.24 Over half of parents of children diagnosed with ADHD treat their children’s symptoms using one or more CAM therapies, including vitamins, dietary changes and expressive therapies, but few disclose this to their child’s paediatrician.25 Most CAM therapies for ADHD are supported by limited evidence; however, when any herbal or other naturopathic therapy is used to treat ADHD it is regarded as the primary treatment over 80% of the time.25 Appropriate CAM and integrative treatment strategies for ADHD will depend on the subtype of ADHD that is being addressed, symptom severity, previous treatment outcomes using conventional or CAM modalities, adverse effect issues, psychiatric or medical comorbidities, patient preferences, the availability of qualified CAM practitioners and access to reputable brands of specific supplements. Dietary modifications, including reduced sugar and caffeine intake and specialised restrictive diets, are reasonable first-line strategies in ADHD-diagnosed children who are predominantly hyperactive. There are no contraindications to taking stimulant medications while following a restrictive diet; however, parents of ADHD children should first consult their child’s paediatrician before initiating a strict dietary regimen, and ideally with a nutritionist who can provide them with expert guidance. Preliminary findings suggest that omega-3 essential fatty acids in doses up to 16 g/day are effective adjuvants when combined with stimulants for both hyperactivity and inattention; however, more studies are needed to confirm this. Preliminary findings suggest that a standardised extract of the bark of the French maritime pine tree may be beneficial in some cases of ADHD; however, it is not clear whether this product has adjunctive benefits when combined with stimulants. Zinc supplementation may enhance the efficacy of prescription stimulants permitting reductions in stimulant doses in some cases, and preliminary findings suggest that acetyl-L-carnitine at doses up to 1500 mg/day may significantly ameliorate symptoms of inattention, but not hyperactivity. Other reasonable integrative treatment strategies for ADHD combine specific EEG biofeedback protocols with restrictive diets, the above supplements and stimulants. When EEG biofeedback training is pursued on a regular basis, effective doses of conventional stimulants can sometimes be reduced, resulting in fewer adverse effects, improved treatment adherence and better outcomes.
INTEGRATIVE MEDICAL TREATMENT AIMS
Dietary modification
Early studies on a restrictive diet that eliminates all processed foods reported promising findings in children with ADHD;26 however, a review of controlled studies failed to support these findings.27 The oligoantigenic diet (OAD) is a highly restrictive multiple elimination diet that excludes food colourings and additives, in addition to dairy products, sugar, wheat, corn, citrus, eggs, soy, yeast, nuts and chocolate. Most OAD research protocols consist of two lean meats, two fruits, two sources of complex carbohydrates, some vegetables, water and salt. Studies involve several phases requiring many weeks to complete. During phase I, which typically lasts 4 weeks, specific food items are withheld from the diet and the patient is monitored using standardised symptom rating scales. In cases where symptoms improve during the initial treatment phase, specific foods are gradually re-introduced in phase II. A third phase follows a placebo-controlled crossover design in which the patient is randomised to a food item that initially caused symptoms or an acceptable placebo for 1 week, followed by a washout period, and subsequently exposed to either placebo or a specific food item or additive for an additional week.
THE PUTATIVE ROLE OF SUGAR IN ADHD
Several studies on the OAD regimen reported significant reductions in hyperactivity in children diagnosed with ADHD when specific food items were eliminated from the diet using the above protocol.28,29,30 In all of these studies behavioural symptoms improved during the elimination and placebo phases and recurred when children were subsequently challenged with the eliminated food item following a blinded protocol. Although these results are promising they cannot be used to develop general ADHD treatment protocols because of study design flaws, including heterogeneity of patient populations, absence of standardised outcome measures, high drop-out rates and, in some studies, non-blinded researchers.31
EEG biofeedback
Many individuals diagnosed with ADHD have abnormal patterns of brain electrical activity, including ‘under-arousal’ in frontal and midline cortical regions and frontal ‘hyper-arousal’ that is more frequent in stimulant non-responders.36 Electroencephalographic (EEG) biofeedback is aimed at normalising EEG activity in order to correct the brain’s state of relative under-arousal and improve cognitive and behavioural functioning.37 Two EEG biofeedback protocols have been extensively evaluated as treatments of ADHD. Sensorimotor rhythm (SMR) training reinforces EEG activity in the faster ‘beta’ frequency range (16–20 Hz) in the midline cortical regions with the goal of reducing symptoms of impulsivity and hyperactivity. ‘Theta suppression’ reduces EEG activity in the slower ‘theta’ frequency range (4–8 Hz) and is primarily used to treat symptoms of inattention. Controlled studies comparing EEG biofeedback to a stimulant medication versus a waitlist report positive clinical effects and EEG normalisation with select protocols have been conducted; however, it has not yet been established whether improved alertness is associated with increased or decreased alpha activity (12–18 Hz).38,39 The significance of research findings is limited by small study sizes, heterogeneous populations, absence of a control group, inconsistent outcome measures and limited or absent follow-up. Large studies in which patients are randomly allocated to true versus sham biofeedback are needed to rule out positive group expectation effects. The use of sophisticated QEEG analysis with reference to a normative database may help future clinicians select the most efficacious treatment protocols for a particular ADHD symptom pattern.
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