Assessment
Medical, laboratory and other special investigations Psychometric evaluation Comorbidity Medical, laboratory and other special investigations A thorough medical history and physical examination should be completed to exclude any causative or comorbid medical disorders confounding the diagnosis. It is also important to document baseline blood pressure, pulse rate, height and weight, which should b
Medical, laboratory and other special investigations
Medical, laboratory and other special investigations
A thorough medical history and physical examination should be completed to exclude any causative or comorbid medical disorders confounding the diagnosis. It is also important to document baseline blood pressure, pulse rate, height and weight, which should be monitored at follow-up consultations.24
Most patients with ADHD do not require laboratory investigations, which should be reserved to eliminate suspected pathology (e.g. iron deficiency) or for safety monitoring with the use of certain medications (e.g. liver function tests with the use of atomoxetine [ATX]).
An electrocardiogram (ECG) may be required if there is a history or family history of significant cardiac pathology, particularly congenital cardiac defects or cardiac surgery. Visual and auditory screening should be done with a referral to optometrists or audiologists for further investigation when indicated. Neurological symptoms may require referral to a neurologist. Routine electroencephalogram (EEG) is not recommended as part of the diagnostic workup for ADHD.
If epilepsy is suspected, an EEG should be performed. Although extended-length EEGs have a higher likelihood of detecting interictal phenomena, cost and convenience factors should be considered.26 Despite the United States Food and Drug Administration’s approval of the NEBA (Neuropsychiatric EEG-based Assessment Aid) system to evaluate theta and beta wave ratios, studies have not found this to be a reliable method to diagnose ADHD and the use of EEG biomarkers for diagnostic purposes is not supported as yet.27,28
Although neuroimaging, brain mapping and event-related potentials have detected structural and functional differences in ADHD research studies, there are currently no indications for these costly and inaccessible investigations in clinical practice.11,25
Psychometric evaluation
There are currently no neuropsychological tests for ADHD with sufficient sensitivity and specificity to serve as an individual diagnostic test.11 Neuropsychological and psychoeducational evaluations should be interpreted within the broader clinical evaluation and are not in themselves diagnostic. These tests can be useful where comorbidity and diagnostic uncertainty exist and to individualise interventions. Computerised assessments such as the Test of Variable Attention (TOVA),29 MOXO d-CPT 8,30 and QbTest 31 have not yet been established as useful in children and adolescents.
Comorbidity
Comorbid conditions are very common with ADHD and often complicate the clinical presentation. Fifty to ninety per cent of children have at least one comorbid condition, while 50% have two or more comorbid conditions.25,32 Follow-up studies of children with ADHD and comorbidity show poorer outcomes and greater social, emotional and psychological difficulties.
Comorbid conditions are either current, episodic conditions – the most frequent in childhood being disruptive behavioural disorders (e.g. oppositional defiant disorder, conduct disorder), anxiety disorders (e.g. generalised anxiety disorder, social anxiety and obsessive-compulsive disorder) and mood disorders (e.g. depression and bipolar disorder). Others represent lifespan disorders, such as specific developmental disorders of language, learning and motor development, ASD and intellectual disability.25,32
Attention-deficit/hyperactivity disorder does not have any one symptom that is pathognomonic for the condition and overlap with other disorders can be significant. Comorbid conditions differ according to developmental stage and change over time. In early childhood, the most common comorbid disorders are oppositional defiant disorder, language disorders and anxiety disorders. In middle school children, anxiety and tic disorders become more common. In adolescence, mood disorders and substance use disorders become more prevalent.25
Oppositional defiant disorder and conduct disorder are common comorbidities with ADHD in childhood and adolescence, with 30%–50% fulfilling the criteria for one of these two conditions. Other externalising disorders such as disruptive mood dysregulation disorder and intermittent explosive disorder also occur relatively commonly.
These comorbidities are associated with greater functional impairment, higher rates of learning disabilities and academic problems, behavioural problems, aggression and later, substance use and delinquent behaviour.33 Treatment should be multimodal, including medication, parent management training, cognitive behavioural therapy and family interventions.
Anxiety disorders and mood disorders also commonly co-occur with ADHD. Anxiety disorders are seen in 15%–35% of children with ADHD and depressive disorders in 20%–50%. 34 For bipolar disorder, the rates vary widely across studies.35 The most impairing condition should be treated first, though both conditions usually require treatment. The comorbid condition may be aggravated by the others’ treatment, thus slow titrations and careful monitoring are necessary.
The demoralisation and low mood resulting from living with ADHD are differentiated from depressive disorders that have an independent and distinct course from ADHD. In bipolar disorder, one should stabilise the mood first and then treat the ADHD.36 When these two disorders co-occur, patients have poorer global functioning and greater symptom severity than for either alone.37
Tic disorders including Tourette syndrome are highly comorbid with ADHD, with prevalence rates of 55%–90%. The presence of tics is not a contraindication to using stimulants for ADHD, but careful monitoring is required. If stimulants do increase tics in a particular individual, then ATX should be considered, as it has a lower potential to aggravate tics.38 The co-occurrence of obsessive-compulsive disorder and ADHD further increases the risk for tic disorders and Tourette syndrome.39
In previous editions of the DSM, the diagnosis of ADHD and ASD was mutually exclusive. However, since the publication of DSM-5, there has been a substantial increase in the prevalence of these two disorders, which can now be diagnosed in combination. Thirty to seventy per cent of patients with ASD meet the criteria for ADHD, while many individuals with ADHD display social deficits and ASD-like symptoms.40,41,42
Children with combined ADHD and ASD have more severe symptoms across most domains including sleep disturbances.43 Trials have shown that treating ADHD with comorbid ASD is effective, but side effects may be more prevalent, and medication should be started at lower doses and titrated carefully.44
Attention-deficit/hyperactivity disorder is two to three times more common in children with developmental disabilities, borderline IQ and intellectual disabilities. Around 45% of children with ADHD have a specific learning disorder, including disorders of reading, written expression, auditory processing, visual processing and processing speed. Children with either ADHD or a learning difficulty should be screened for the other condition, – as outcomes are significantly improved if both conditions are receiving necessary intervention.45
Sleep disturbance occurs in around 50% of individuals with ADHD, most commonly initial insomnia. There is growing evidence that individuals with ADHD may be more susceptible to circadian rhythm disruptions.46 Sleep problems may also aggravate ADHD symptoms, and pharmacological interventions for ADHD may impact sleep. Although methylphenidate does not alter sleep architecture, it may delay sleep onset, reduce sleep efficiency and shorten total sleep duration.47 Behavioural sleep interventions and melatonin are considered effective interventions for sleep disturbances in the child and adolescent populations.48,49
Developmental and acquired brain injuries are also associated with ADHD-like symptoms. The association between foetal alcohol syndrome and ADHD is strong and can be particularly difficult to manage.50 Children with moderate to severe brain injury have up to a 48% chance of secondary ADHD and should receive treatment with close monitoring for side effects.51
Comorbidity between epilepsy and ADHD is common. Identification of ADHD in patients with epilepsy is difficult because the symptoms and management related to epilepsy can directly contribute to attention deficits.52 Twenty to forty per cent of children with epilepsy have ADHD, with significant ADHD symptoms present in up to 82% of children before the onset of the first seizure. Children with ADHD have a two to fourfold higher risk for epilepsy when compared to controls (1.2%–14% of children).53
Vigilance is important, especially in female patients and those with the predominantly inattentive subtype. Both conditions require rigorous management to improve clinical outcomes and quality of life. Anticonvulsants should be chosen with a view to minimising behavioural and cognitive side effects. There is no strong evidence to suggest that psychostimulants increase the severity or frequency of seizures in patients with stable epilepsy.54,55
The prevalence of ADHD in eating disorders (such as anorexia nervosa and bulimia nervosa) is around 11%, while roughly 20% of children with ADHD also develop eating disorders.56 Screening for ADHD should be part of an eating disorder history and vice versa.57 There is also a bidirectional relationship between ADHD and obesity.58 Attention-deficit/ hyperactivity disorder and ASD are more prevalent in children and adolescents with obesity than in those without obesity.59 Suggested mechanisms include impulsive eating, common genetic underpinnings involving the dopaminergic system and obesity-related risk factors such as sleep-disordered breathing.60
Attention-deficit/hyperactivity disorder increases the risk for an elimination disorder (enuresis and encopresis) two to three times. Elimination disorders should be investigated and managed, but recent studies have found that treatment of ADHD with both psychostimulants and ATX can result in an improvement in enuresis and encopresis.61
Time spent using digital media for leisure purposes has increased exponentially in the last decade among children and adolescents, and social media use has been found to be just as addictive as gaming. Longitudinal studies have looked at the direction of association between digital media use and ADHD and have revealed that excessive digital media use (EDMU) is a risk factor for the onset of ADHD symptoms, while ADHD predisposes to EDMU. Furthermore, ADHD and EDMU mutually aggravate each other over time.62
A recent study showed that 44% of children and adolescents with ADHD met the criteria for internet gaming disorder (IGD), compared to 9.5% of controls. Attention-deficit/hyperactivity disorder patients with IGD presented with greater severity and impairment, more severe ADHD symptomatology, more internalising symptoms (particularly withdrawal/depression and socialisation problems), and a greater likelihood of other addictive behaviours.63
Therefore, from a clinical perspective, it is important for practitioners to educate parents and children about how EDMU may aggravate ADHD symptoms. Various bodies, such as the American Academy of Pediatrics have published guidelines for recreational screen time in children (www. healthychildren.org).
Belsham B, Kelly L, Schoeman R_The SASOP/PsychMg child and adolescent attention-deficit/hyperactivity disorder guidelines_South African Journal of Psychiatry; 25 February 2025