ADHD Diagnostic Criteria and Management Guidelines PDF

Attention Deficit Hyperactivity Disorders, (ADHD) Intended Learning Objectives 1. Define ADHD as a neurodevelopmental disorder affecting a great proportion of children. 2. Identify the different diagnostic criteria of ADHD and its developmental course. 3. Know the etiology and...

Attention Deficit Hyperactivity Disorders, (ADHD) Intended Learning Objectives 1. Define ADHD as a neurodevelopmental disorder affecting a great proportion of children. 2. Identify the different diagnostic criteria of ADHD and its developmental course. 3. Know the etiology and comorbidities of ADHD. 4. Describe the different therapeutic regimens of ADHD. Attention deficit hyperactivity disorders (ADHD) is a persistent pattern of inattention and/or hyperactivity-impulsivity that interfere with functioning and development (DSM- 5). ADHD is serious as it is likely to impair academic and social functioning during a period of mental and behavioral maturation. Diagnostic and Statistical Manual of mental disorders (DSM-5) states that patients must have experienced a minimum of six symptoms of inattention (e.g. failing to sustain attention in tasks or play activities, not listening when being spoken to directly), or six symptoms of hyperactivity/impulsivity (e.g. talking excessively, fidgeting with hands or feet). The manual distinguishes between three subtypes of the disorder: 1. Predominantly hyperactive/impulsive type, 2. Predominantly inattentive type 3. Combined type (Inattentive & hyperactive/impulsive) In order to reach diagnosis according to the latest version of the DSM, symptoms must have: 1. Onset before the age of 12 (rather than an age 7 cut-offs for symptom-related impairment in DSM-IV). 2. Be pervasive across different settings (e.g. home and school). 3. Associated with substantial impairment in psychosocial functioning. Diagnostic criteria for ADHD 2. Six (or more) of the following symptoms of hyperactivity/impulsivity A. Either 1 or 2: have persisted for at least 6 months to 1. Six (or more) of the following a degree that is maladaptive and symptoms of inattention have persisted inconsistent with developmental level: for at least 6 months to a degree that is Hyperactivity maladaptive and inconsistent with developmental level: (a) Often fidgets with hands or feet or squirms in seat. Inattention (b) Often leaves seat in classroom or in (a) Often fails to give close attention to other situations in which remaining details or makes careless mistakes in seated is expected. schoolwork, work, or other activities. (c) Often runs about or climbs (b) Often has difficulty sustaining excessively in situations in which it is attention in tasks or play activities. inappropriate (in adolescents or adults, (c) Often does not seem to listen when may be limited to subjective feelings of spoken to directly. restlessness). (d) Often does not follow through on (d) Often has difficulty playing or instructions and fails to finish engaging in leisure activities quietly. schoolwork, chores, or duties in the (e) Is often “on the go” or often acts as if workplace (not due to oppositional “driven by a motor”. behavior or failure to understand instructions). (f) Often talks excessively. (e) Often has difficulty organizing tasks Impulsivity and activities. (g) Often blurts out answers before (f) Often avoids, dislikes, or is reluctant questions have been completed. to engage in tasks that require sustained (h) Often has difficulty awaiting turn. mental effort (such as schoolwork or homework). (i) Often interrupts or intrudes on others (e.g., butts into conversations or games). (g) Often loses things necessary for tasks or activities (e.g., toys, school B. Some hyperactive/impulsive or assignments, pencils, books, or tools). inattentive symptoms that caused impairment were present before age 12. (h) Is often easily distracted by extraneous stimuli. C. Some impairment from the symptoms is present in two or more settings (e.g., at (i) Is often forgetful in daily activities. school [or work] and at home) D. There must be clear evidence of schizophrenia, or other psychotic clinically significant impairment in disorder and are not better accounted for social, academic, or occupational by another mental disorder (e.g., mood functioning disorder, anxiety disorder, dissociative disorder, or a personality disorder) E. The symptoms do not occur exclusively during a pervasive disorder, Clinicians, parents and/or teachers must report the presence of at least six of nine behaviors from either list to warrant consideration of an ADHD diagnosis of predominantly inattentive type or hyperactive/ impulsive type. For a diagnosis of ADHD combined type, more than six symptoms must be present from both lists. Such behaviors have an onset prior to 12 years of age (DSM-5), duration of at least 6 months They must be evident in two or more settings (home & school at least), have a clear impact on psychosocial functioning. Prevalence  ADHD is common, with worldwide prevalence estimated at approximately 5%.  It is one of the more common childhood disorders, representing one third to one half of referrals to child mental health services.  ADHD also occurs more often in boys than in girls. Developmental course  Although originally seen as a disorder of childhood, evident in preschool children and although symptoms may decline with age in some cases, about 40% of children cases continue to meet full criteria of ADHD in the adult years.  Predominantly hyperactive/impulsive and combined subtypes are more common than the inattentive subtypes among younger children.  Progression of the disorder from predominantly hyperactive/impulsive or combined to predominantly inattentive as children got older (adolescents and adults).  First display of clear signs as developmentally inappropriate inattentive and overactive behavior suggestive of ADHD peaks between 3 and 4 years of age. For a smaller number of children, ADHD symptoms may not be evident until 5 or 6 years of age, corresponding with school entry.  Psychosocial impairment in relationships and functioning across multiple settings becomes more apparent in middle childhood (home and school).   At home, parents must contend with ongoing behavior problems around chores, self-help activities (e.g., dressing, bathing, etc.), and interactions with siblings.  At school, academic performance and classroom behavior are often erratic over time, contributing to under-achievement relative to ability and impaired relationships with teachers and peers.  Poor social skills eventually create a pattern of social rejection.  By late childhood and preadolescence, these patterns of academic, familial, and social impairment have become well established, and secondary comorbid problems have emerged. Comorbidity ADHD is often comorbid with a number of other psychiatric conditions, developmental and health risks, in addition to functional impairments. Comorbid disease states: 44%–87% of children with ADHD have at least one other disorder 1. Psychiatric disorders: Disruptive behavioral disorders (DBDs):  Oppositional defiant disorders (ODD) and conduct disorders (CD) are the most common comorbid disorders with ADHD.  About 50-60% of children with ADHD meet criteria for ODD. Most common comorbid disorder in adolescents. ODD is characterized by a negativistic, hostile and defiant behavior, often directed towards authority figures. Presence of ADHD increases the odds of oppositional defiant disorder almost 11-fold.  About 25% of children meet CD criteria, that describe a pattern of behavior in which age-appropriate social norms and the rights of others are violated. This behavior includes aggressiveness to people and animals, destruction of property, deceitfulness and serious violation of rules. Mood and anxiety disorders:  Mood disorders (depression and bipolar disorder) and anxiety disorders are also commonly observed in children with ADHD.  Anxiety disorder: May exist in about 25% of children with ADHD Tics:  21%–90% of children with Tourette syndrome may also have ADHD.  May not be exacerbated by stimulant agents, as once thought 2. Functional impairment: Neuropsychological functioning:  These include deficits in executive functions (EF), delay aversion and temporal processing.  EF is used to describe high-order cognitive functions including working memory cognitive flexibility and inhibitory control. EF deficits may manifest as forgetfulness and difficulty in planning and coordinating everyday tasks as getting ready for schools.  Delay aversion is evidenced by the fact that children with ADHD display preference for smaller immediate rewards rather than larger later ones.  Temporal processing deficits is defined as slower rate at which the brain process auditory information. A person must be able to process auditory information at a rapid pace to develop appropriate listening and language skills. Studies reported that there are “Structural brain differences in areas involved in the rapid processing of hearing, vision and touch in affected people, and that people with these speech and learning disorders require 300 milliseconds to process basic speech sounds, where normal processing takes about 25 milliseconds. Social/peer functioning:  Children with ADHD often display impaired social performance and are more likely to be nominated by their peer as someone they would least like be friends with.  For example, children with ADHD combined type are more aggressive and intrusive during social interactions, whereas primarily inattentive children may appear withdrawn and display poorer memory of interactions. Academic functioning:  Academic under-achievement is a common feature of children with ADHD and is evident from pre-school through to adolescence.  ADHD children are more likely to require specialist academic support, repeat a school year. 3. Developmental risks Motor coordination:  About 30-50% of children with ADHD often demonstrate poor motor coordination or motor performance and balance.  Difficulties in motor coordination can result in clumsiness, perhaps explaining the high rates of injuries in children with ADHD. 4. Health risks Sleep disturbances:  Studies reported that sleep problems occurred twice as often in ADHD as in control children.  The problems are mainly more behavioral and include settling difficulties, a longer time to fall asleep, instability of sleep duration, tiredness at awakening or frequent night waking. Etiology  Underlying etiological explanation of ADHD can be simply divided into biological and environmental.  Biological explanations include genetics and brain structure and their influence on neuropsychology.  Environmental explanations include parenting, diet, problem during and after birth and exposure to environmental toxins. 1. Genetics  ADHD is considered one of the most heritable psychiatric conditions by being clustered significantly among the biological relatives of children with the disorder.  Genetic factors are accounted for 80% of the etiology of ADHD.  Among the genes involved in such disorders include those regulating dopaminergic transmission such as DAT1 gene (dopamine transporter 1), overexpression of DRD4/7R gene (dopamine receptor subtype D/7-repeat variant).  Several reasons exist for the particular focus on dopaminergic transmission, since dopaminergic drugs as methylphenidate are clinically efficacious in addressing the core symptoms of ADHD.  Moreover, neuroimaging of ADHD children’s brain has implicated the fronto- striatal circuitry, an area rich in dopaminergic acivity.  Norepinephrine and serotonin transporter have been also implicated in the pathophysiology of ADHD. 2. Brain structure  Using brain scan technology such as MRI, these studies suggest that the brain circuit linking the pre-frontal cortex, striatum and cerebellum are not functioning normally in children with ADHD.  Studies proved that compromised brain morphology of these selected regions is related to behavioral measures of inhibition and attention. 3. Parenting:  ADHD is best viewed as a “gene x environment interaction”.  Children who have a genetic predisposition will express the disorder when put in the correct environment, typically one characterized by chaotic parenting.  The best evidence for environmental influences on ADHD come from intervention studies which have demonstrated improvements in ADHD symptoms, when parents have been taught alternative parenting skills.  The relationship between ADHD and parenting may result from both negative aspects of the child influencing the parents’ behavior, and negative aspects of the parents influencing the child’s behavior (bi-directional). 4. Diet:  Data driven from a large randomized control trial demonstrated a general adverse effect of food coloring agents and benzoate preservatives on hyperactive behavior based on parental reports.  Despite the lack of scientific evidences and explanations of this observation, parents report particular diet as a factor that exacerbates their child’s ADHD symptoms. Management of ADHD  The Multi-modal Treatment study of ADHD (MTA) results along with those of many other studies suggest that a combination of pharmacological and psychosocial treatment provide better long term outcome. Pharmacological treatment: 1. Stimulants as methylphenidate & lisdexamphetamine dimesylate (LDX). 2. Non-stimulant as atomoxetine (ATX). 3. For comorbid conditions as CD or ODD or affection disorder: anticonvulsant (divalproex), atypical antipsychotic (risperidone) or lithium may be added. Dosage and regimen: 1. Methylphenidate  Methylphenidate is a CNS stimulant (Schedule 2 controlled drug) prescribed under specialist supervision.  Methylphenidate is thought to block the reuptake of norepinephrine and dopamine into the presynaptic neuron and increase the release of these monoamines into the extra-neuronal space.  It is available in modified-release formulations that enable once-daily dosing (Concerta XL®), also available as transdermal delivery patch.   The recent availability of extended release forms of stimulants provides continuous coverage for controlling ADHD symptoms throughout the school day and has eliminated the need for in-school dosing in most cases.  Furthermore, the recently FDA-approved transdermal system minimizes the potential for diversion because once the patch is applied, it cannot be reapplied to another individual.  Treatment with modified-release formulation (Concerta XL®) is used to replace the immediate-release formulation (liability of addiction) and is used where treatment effects are required to persist into the evening.  Treatment should be initiated at a dose of 18 mg once daily (in the morning), and increased if necessary up to a maximum of 54 mg once daily.  Common adverse effects of treatment include: o insomnia, nervousness, headache, decreased appetite, o abdominal pain and cardiovascular effects such as tachycardia, palpitations and minor increases in blood pressure. 2. Atomoxetine (ATX)  In 2002, Strattera® (atomoxetine) was the first non-stimulant medication approved for use in the treatment of ADHD.  Although the effect size of ATX is generally lower than that of stimulants, updated guidelines recommend ATX as a first line treatment option.  Although some improvement may be seen in a patient as early as one week after the initiation of treatment, ATX generally take longer to have a full effect.  ATX is dispensed in capsules of 10, 18, 25, 40, 60, 80, and 100 mg. The mechanism of action of ATX is thought to be related to inhibition of the presynaptic norepinephrine transporter.  The maximum daily dose approved by the US FDA for children and adolescents who weight ≤ 70 Kg is 1.4 mg/kg/day; for children and adolescents who weight ≥ 70 kg and adults, it is 100 mg/day.  When discontinuing ATX, tapering is not necessary as stopping the medication is not associated with acute discontinuation symptoms.  Common adverse effects of treatment include: o Abdominal pain, decreased appetite, nausea and vomiting, o Early morning awakening, irritability and mood swings. o Increased heart rate and small increases in blood pressure have been reported. Available pharmacologic agents I. Stimulant medications: Some children with ADHD respond better to one stimulant type than another; therefore, both methylphenidate- and amphetamine-containing products should be tried before stimulant treatment is deemed a failure. 1. Methylphenidate-containing products  Ramp effect: Behavioral effects are proportional to the rate of methylphenidate absorption into the central nervous system.  Adverse effects and precautions: o Headache, stomachache, loss of appetite, and insomnia o Use with caution in patients with glaucoma, tics, psychosis, and concomitant monoamine oxidase inhibitor use. o Insomnia, anorexia, and tics occur more often with transdermal patch, also mild skin reactions. 2. Amphetamine-containing products  Adverse effects and precautions: o Loss of appetite, insomnia, abdominal pain, and nervousness o May exacerbate preexisting hypertension and tic disorders o Labeling change warns of potential association with sudden cardiac death (SCD); therefore, not recommended for patients with known structural heart defects. Potential association of stimulants with SCD  No established evidence of causative relationship between stimulants and SCD  The frequency of SCD is no higher in children taking stimulants than in the general pediatric population.  The AAP recommends targeted cardiac history and careful physical examination before initiating stimulant therapy. o Routine electrocardiography is not recommended unless history and physical examination suggest cardiac disease. o For otherwise healthy children, stimulant therapy should not be withheld because of the inability to obtain an electrocardiogram or assessment by a pediatric cardiologist. II. Non-stimulant medications 1. Norepinephrine reuptake inhibitors  Adverse effects: Dyspepsia, decreased appetite, weight loss, and fatigue  Labeling change warns of potential for severe liver injury, although routine monitoring of hepatic function is not necessary.  Black box warning about increased risk of suicidal ideation in children and adolescents  Does not exacerbate tics 2. α-Adrenergic receptor agonists: 3. Antidepressants: Non-FDA label approved for the treatment of ADHD  Noradrenergic antidepressant (e.g., bupropion [Wellbutrin]) o May use immediate- or extended-release product given in two or three doses o Contraindicated for children with active seizure disorder  Tricyclic antidepressants (e.g., imipramine, nortriptyline) o Baseline electrocardiogram is recommended before therapy initiation and after each dose increase. o Desipramine should be used with extreme caution because of reports of sudden death. Non-pharmacological treatment:  Parenting interventions o Parent training typically involves 8 to 12 weekly sessions with a trained therapist with the aim of improving parents' or caregivers' understanding of the child's behavior and teaching them skills to deal with behavioral difficulties related to ADHD.  Classroom interventions o Classroom-based interventions usually include behavioral strategies for the teacher to improve problematic classroom behavior and academic performance.  Child psychosocial therapy o Include sessions covering social skills training, anger management and problem solving.