Attention deficit hyperkinetic disorder.pptx

Child psychiatry

1. ADHD Dr Vivek Sharma Resident 3 RD Year Dept of Psychiatry Dr MK Shah Medical College & Research Centre, Ahmedabad

2. Introduction Attention-deficit/hyperactivity disorder (ADHD) is the most common childhood behavioral disorder diagnosed in outpatient settings. It is a chronic disorder which can cause impairment into adolescence and adulthood.

3. Nosology Evolution Historical Facts S.No . Description 1 First Described by George Still in 1902 2 In 1920 termed as “minimal brain damage syndrome,” children who survived the flu frequently developed severe behavior problems and are now thought to have suffered organic brain damage. 3 In the early 1960s , the condition was renamed “minimal brain dysfunction.” 4 The ninth revision of the International Classification of Diseases and Related Health Problems (ICD-9) and the second edition of the DSM adopted the same descriptive term for the condition— hyperkinetic syndrome of childhood In ICD 10 it is called Hyperkinetic Disorder 5 The 1980 version of the APA classificatory system, DSM-III , renamed this diagnosis attention-deficit disorder (ADD) 6 Much of the diagnostic criteria for ADHD has remained the same between DSM-IV in 1994, the text revision, DSM-IV-TR in 2000

4. Nosology Evolution Historical Facts S.No . Description 7. Criteria were revised in DSM-5 in May 2013 & kept same in DSM -5TR which was released in March 2022 . 8. DSM -4 DSM -5 Age limit was 7 years 12 years two subtypes : Inattentive and Hyperactive/Impulsive type . three specifiers , which essentially denote the same groups: (1) combined presentation , (2) predominantly inattentive presentation , and (3) predominantly hyperactive/impulsive presentation . Additional changes in DSM-5 include permitting a comorbid ADHD and autism spectrum diagnosis to be made. Finally, in DSM-5, for adolescents 17 years and older and for adults , only five symptoms, rather than six symptoms of either inattention or hyperactivity and impulsivity are required. In addition, to reflect the developmental differences in ADHD across the life span, examples of symptoms have been added to the DSM-5 criteria for ADHD. To confirm a diagnosis of ADHD, impairment from inattention and/or hyperactivity and impulsivity must be present in at least two settings and interfere with developmentally appropriate social or academic functioning

5. Epidemiology Prevalance : 7 to 8 percent in prepubertal elementary school children . 5 percent of youth including children and adolescents 2.5 percent of adults. ADHD is more prevalent in boys than in girls , with the ratio ranging from 2: 1 to as high as 9: 1

6. Etiology ADHD is a complex disorder of multifactorial etiology , thought to have multiple genetic and environmental variables of small effect acting together to produce vulnerability to ADHD. 1) Genetic Factors 2) Neuro Chemical Factors 3) Neuroanatomical Factors 4) Neuro Physiological Factors 5) Developmental Factors 6) Psychosocial Factors

7. Genetic Factors Twin, sibling, adoption, and family studies all suggest a strong genetic component in the development of hyperactivity, inattention, and impulsivity, with heritability index estimated to range from 0.6 to 0.98 . Heritability estimates include both genetic influences , as well as the effects of gene–environment interaction .

8. Genetic Factors ADHD-like behaviors have been reported in rare genetic disorders such as Fragile X syndrome Neurofibromatosis type 1, DiGeorge syndrome, tuberous sclerosis, Turner syndrome, Williams syndrome, Angelman and Prader-Willi .

9. Genetic Factors Twin Studies. 76 percent of the variance in the transmission of ADHD is attributable to genetics, making ADHD one of the most heritable psychiatric disorders. The concordance rate among monozygotic twins ranges from 59 to 92 percent, whereas the concordance rate in dizygotic twins ranges from 29 to 42 percent.

10. Genetic Factors Adoption Studies . Studies have found that the biological relatives of hyperactive children are more likely to be hyperactive themselves. This relationship is not seen in adoptive relatives of hyperactive children. Adoptive relatives of children with ADHD have risk of ADHD similar to relatives of control children the biological relatives of children with ADHD are more likely to have ADHD or associated disorders.

11. Genetic Factors Family Studies . Family studies have shown that first-degree relatives of children with ADHD are two to eight times more likely to have the disorder.

12. Genetic Factors Molecular Genetic Studies . ( GWAS) to identify the specific “risk” genes concentrated on dopamine-related genes given the implication of dopamine dysfunction in ADHD . Candidate genes discovered so far are: . The dopamine transporter gene (DAT1) Dopamine type D2 receptor gene (DRD2). Dopamine 4 receptor seven-repeat allele gene (DRD4) . The Synaptosomal -associated protein 25 gene (SNAP25) . Genes that code for dopamine β-hydroxylase (DBH), catechol-O- methyltransferase (COMT), dopamine 5 receptor gene, norepinephrine transporter gene (SLC6A2), serotonin transporter gene (SLC6A4), α-2A adrenergic receptor (ADRA2A), thyroid receptor B gene, androgen receptors and factors in immune function and regulation have also been reported to correlate with ADHD symptoms. Subsequent studies and meta-analysis have not sufficiently supported the association between ADHD and these genes.

13. NeuroChemical Factors The nonspecific catecholamine hypothesis of ADHD posits that the psychophysiology of ADHD symptomatology emerges from an imbalance among various neurotransmitters, including norepinephrine, epinephrine, and dopamine. Dysfunction in brain norepinephrine systems, particularly a lack of inhibition of locus coeruleus neurons , could explain the inattention, cognitive deficits, and higher levels of gross motor activity seen in children with ADHD. Randomized clinical trials (RCTs) have suggested that the norepinephrine reuptake inhibitors (NRIs), tricyclic antidepressants (TCAs) and atomoxetine , are effective in reducing ADHD symptoms by restoring a more normal ratio of epinephrine and norepinephrine. Molecular genetic studies have targeted genes that code for dopamine receptors and PET scans in adults with ADHD have provided imaging data that correlate stimulant-driven increases in dopamine concentration. There is weak evidence for serotonin’s role in ADHD. Medications that exclusively affect serotonin function, such as the selective serotonin reuptake inhibitors (SSRIs), have no efficacy in the treatment of children with ADHD. For that reason, serotonin is thought to play a secondary role in the pathology of ADHD .

14. NeuroAnatomical Factors Researchers have hypothesized networks within the brain for promoting components of attention including focusing, sustaining attention, and shifting attention. They describe neuroanatomical correlations for the superior and temporal cortices with focusing attention; external parietal and corpus striatal regions with motor executive functions ; the hippocampus with encoding of memory traces ; the prefrontal cortex with shifting from one stimulus to another . the brainstem, which contains the reticular thalamic nuclei function , is involved in sustained attention.

15. NeuroAnatomical Factors magnetic resonance imaging (MRI), positron emission tomography (PET), and single photon emission computerized tomography (SPECT) show evidence of both decreased volume and decreased activity in prefrontal regions, anterior cingulated, globus pallidus , caudate, thalamus, and cerebellum with slightly larger gray matter volumes in the left posterior cingulate cortex PET scans have also shown that female adolescents with ADHD have globally lower glucose metabolism Diffusion tensor imaging (DTI) studies show white matter tract abnormalities and dysfunctional connectivity in ADHD during rest and while engaging in cognitive tasks. fMRI studies using cognitive tasks to target the neural circuits show significantly reduced frontal lobe activity

16. Neurophysiological Factors. S.No . Age Group EEG Finding 1 Children & Adoloscent Increased Theta 2 Youth Increased Beta 3 Children with Combined Presentation Increased Beta 4 Current investigation of EEG in youth with ADHD have identified behavioral symptom clusters among children with similar EEG profiles

17. Developmental Factors Higher rates of ADHD are present in children who were born prematurely and whose mothers were observed to have maternal infection during pregnancy . Perinatal insult to the brain during early infancy caused by infection, inflammation, and trauma be contributing factors in the emergence of ADHD symptoms. Children with ADHD have been observed to exhibit nonfocal (soft) neurological signs at higher rates than those in the general population. September is a peak month for births of children with ADHD with and without comorbid learning disorders.

18. Dietary Influences Dietary factors as a cause and possible treatment of ADHD are controversial. There have been reports of a connection between ADHD and nutritional deficiencies of iron, zinc, and essential fatty acids (omega-3 and omega-6), but the beneficial effects of supplementation are inconclusive. Some studies have indicated that a small subset of children may have sensitivity to certain foods, additives, excess sugar or nutritional deficiencies , causing behavioral effects. There has been some support for elimination diets to treat ADHD, such as the Feingold (additive and salicylate-free) diet, oligoantigenic (hypoallergenic) diet, and ketogenic diet

19. Psychosocial Factors. Severe chronic abuse, maltreatment, and neglect are associated with certain behavioral symptoms that overlap with ADHD including poor attention and poor impulse control. Predisposing factors may include the child's temperament and genetic-familial factors.

20. Diagnosis The diagnosis of ADHD requires the integration of data from multiple sources, Detailed History School history and teachers' reports MSE Physical Examination to rule out associated Genetic & Developmental Abnormalities Investigations as and when Necessary Applying Diagnostic Criteria to confirm Diagnosis Behavior Assessment Scales

21. Detailed History The medical history should cover the prenatal, perinatal, toddler, and preschool phases of development. Inquiries should be made about pregnancy complications, such as maternal illness ( eclampsia , diabetes), maternal smoking, alcohol, or illicit drug use. The perinatal period should identify the presence of labor problems, delivery complications, prematurity, jaundice, and low birth weight. Feeding and sleeping routines during the perinatal and postnatal periods need to be described. Developmental milestones, illnesses, injuries, and symptomatology need to be reviewed. A detailed family, medical, and psychiatric history should be completed

22. School History & Teacher’s Report School history and teachers' reports are critical in evaluating whether a child's difficulties in learning and school behavior are caused primarily by inattention or compromised understanding of the academic material . In addition to intellectual limitations, poor performance in school may result from maturational problems, social rejection, mood disorders, anxiety, or poor self-esteem due to learning disorders. Assessment of social relationships with siblings, peers, and adults, and engagement in free and structured activities may yield valuable diagnostic clues to the presence of ADHD.

23. MSE , Physical & Neurological Examination The mental status examination in a given child with ADHD who is aware of his or her impairment may reflect a demoralized or depressed mood ; however, thought disorder or impaired reality testing is not expected. A child with ADHD may exhibit distractibility and perseveration and signs of visual-perceptual, auditory-perceptual, or language-based learning disorders . Height and weight at baseline to be recorded A neurological examination may reveal visual, motor, perceptual, or auditory discriminatory immaturity or impairments without overt signs of visual or auditory disorders. Children with ADHD often have problems with motor coordination and difficulty copying age-appropriate figures, rapid alternating movements, right-left discrimination, ambidexterity, reflex asymmetries, and a variety of subtle non focal neurological signs (soft signs)

24. Investigations There are no blood, genetic, or neuroimaging tests available to diagnose ADHD. Medical problems that might aid in the differential diagnosis, such as petit mal epilepsy, hearing and vision difficulty, thyroid dysfunction, and hypoglycemia , all need to be ruled out. ECG to rule out (Arrhythmia, tachycardia, or hypertension) that can increase the risk of serious adverse events should a stimulant medication treatment be initiated.

25. Investigations A continuous performance task, a computerized task in which a child is asked to press a button each time a particular sequence of letters or numbers is flashed on a screen, is not specifically a useful diagnostic tool for ADHD; however, it may be useful in comparing a child's performance before and after medication treatment, particularly at different doses. Children with Poor Attention tend to make errors of omission that is, they fail to press the button when the sequence has flashed. Impulsivity is often manifested by errors of commission , in which an impulsive child cannot resist pushing the button, even when the desired sequence has not yet appeared on the screen.

26. SCALES Commonly used rating scales for ADHD include Conners Rating Scales for parents (CPRS-R) and teachers (CTRSR), Conners Wells Adolescent Self-Report Scale, Vanderbilt ADHD Diagnostic Parent and Teacher Scales, Swanson, Nolan and Pelham (SNAP IV), Brown ADD Rating Scales for Children, Adolescents, and Adults. Only the Conners Comprehensive Behavior Rating Scales and the ADHD Rating Scale IV have been validated in preschool-aged children .

27. Clinical Features Hyperactivity. Hyperactivity describes the inappropriate excessive motor activity observed in ADHD, including restlessness, fidgeting, and appearing to be “driven by a motor.” These behaviors are often first noticed when the child is a toddler, but can be normative before age 4.

28. Clinical Features Impulsivity. . Impulsiveness and an inability to delay gratification are character. Impulsive actions occur without forethought about consequences and may be associated with desire for immediate rewards or to avoid delay. Impulsivity might be seen when the child engages in dangerous activities, yells out in class, or interrupts or intrudes on others during games or conversations.

29. Clinical Features Attentional Difficulties . Inattention includes difficulty sustaining focus, trouble maintaining organization, and being easily distracted by extraneous stimuli. Sluggish Cognitive Tempo (SCT) is a type of attentional difficulty that has been closely associated with the inattentive subtype of ADHD. SCT describes a constellation of symptoms such as daydreaming, staring, tendency toward confusion, mental fogginess, sleepiness, apathy, and physical hypoactivity . There is growing evidence suggesting that SCT is a condition distinct from ADHD, however, SCT is currently not considered a separate disorder or diagnostic subtype. .

30. Clinical Features Associated features includes memory and thinking deficits, specific learning disabilities, and speech and hearing deficits. often include perceptual motor impairment, emotional lability, and developmental coordination disorder. A significant percent of children with ADHD show behavioral symptoms of aggression and defiance. School difficulties, both learning and behavioral , commonly exist with ADHD. Comorbid communication disorders or learning disorders that hamper the acquisition, retention, and display of knowledge complicate the course of ADHD.

31. Differential Diagnosis Oppositional defiant disorder. Individuals with oppositional defiant disorder may resist work or school tasks that require self-application because they resist conforming to others' demands. Their behavior is characterized by negativity, hostility, and defiance.

32. Differential Diagnosis Autism spectrum disorder . Individuals with ADHD and those with autism spectrum disorder exhibit inattention, social dysfunction, and difficult-to-manage behavior . The social dysfunction and peer rejection seen in individuals with ADHD must be distinguished from the social disengagement, isolation, and indifference to facial and tonal communication cues seen in individuals with autism spectrum disorder. Children with autism spectrum disorder may display tantrums because of an inability to tolerate a change from their expected course of events. In contrast, children with ADHD may misbehave or have a tantrum during a major transition because of impulsivity or poor self-control.

33. Differential Diagnosis Specific learning disorder. Children with specific learning disorder alone may appear inattentive because of frustration, lack of interest, or limited ability in neurocognitive . Intellectual developmental disorder (intellectual disability). A diagnosis of ADHD in intellectual developmental disorder requires that inattention or hyperactivity be excessive for mental age. The symptoms in ID are evident ONLY during Academic tasks as compare to ADHD in academic as well as Non Academic task

34. Differential Diagnosis Anxiety disorders. Restlessness might be seen in anxiety disorders. However, in ADHD, the symptom is not associated with worry and rumination. Depressive disorders. Individuals with depressive disorders may present with inability to concentrate. However, poor concentration in mood disorders becomes prominent only during a depressive episode.

35. Differential Diagnosis Bipolar disorder. Individuals with bipolar disorder may have increased activity, poor concentration, and increased impulsivity, but these features are episodic, unlike ADHD, in which the symptoms are persistent.

36. Course & Prognosis the school-aged child often experiences academic failure and peer rejection. In childhood 65 to 75 percent of children with ADHD have one or more comorbid conditions, which in addition to ODD, can include conduct disorder (CD), anxiety and mood disorders, tics or Tourette syndrome, learning disorders, and autistic spectrum disorders. Many of these comorbidities continue into adolescence. The adolescent with ADHD continues to have academic and social problems, which erode his/her self-esteem and at times promote the gravitation to a negative peer group have a threefold increase in substance use and abuse, more frequent delinquent acts and trouble with the law, and increased rates of car accidents when they begin to drive. . Gambling and other addictions are also frequently seen.