Attention-Deficit Hyperactivity Disorder
Research Re: Cause
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Benson DF: THE ROLE OF FRONTAL DYSFUNCTION IN ATTENTION DEFICIT HYPERACTIVITY DISORDER. [REVIEW]. Journal of Child Neurology 1991; 6 Suppl:S9-12. Summary: Among diverse populations concerning the etiology of attention deficit hyperactivity disorder (ADHD), frontal dysfunction remains strong. The influences of frontal systems on attention, particularly the elements of higher mental control postulated as prefrontal functions, are illustrated through presentation of a number of syndromes of abnormal mental awareness associated with prefrontal brain damage. Against this background, a theory explaining part (but not all) of the problem seen in ADHD children is postulated, and a firm stand for prefrontal dysfunction as one element in the disorder is presented. [References: 31]
Elia J: STIMULANTS AND ANTIDEPRESSANT PHARMACOKINETICS IN HYPERACTIVE CHILDREN. [REVIEW]. Psychopharmacology Bulletin 1991; 27(4):411-5. Summary: Psychopharmacological treatment of attention-deficit hyperactivity disorder (ADHD), is well established. The central nervous system stimulants, especially dextroamphetamine and methylphenidate, are the drugs of choice. Response is rapid, consistent and predictable. Most children respond to one or the other when a trial of both stimulants are given across wide dose ranges (Elia et al. 1991). The efficacy of pemoline is also well established, but its variable onset and duration of action in children has made it a secondary treatment. Tricyclic antidepressants also produce rapid behavioral effects in ADHD, at doses less than those used for depression. Adverse effects are a limiting factor for continued treatment as well as the fact that beneficial effects are often short-lived. [References: 28]
Gans DA: SUCROSE AND DELINQUENT BEHAVIOR: COINCIDENCE OR CONSEQUENCE? [REVIEW]. Critical Reviews in Food Science & Nutrition 1991; 30(1):23-48. Summary: Over the past decade, a number of theories have appeared that are attempts to relate consumption of simple sugars to violent or delinquent behavior. Such claims have been based mainly on anecdotal reports, misinterpretations of scientific literature, or flawed interpretation of questionable data. Thus, these claims remain unsubstantiated. There are data that suggest that a very few individual hyperactive children may respond adversely to a sucrose challenge, but most carefully designed and controlled studies with children offer no convincing evidence that sucrose ingestion exacerbates hyperkinetic behavior. While provocative evidence is beginning to emerge from studies of incarcerated juvenile delinquents, as well as from studies of adult criminals habitually violent under the influence of alcohol, that anomalies in carbohydrate metabolism may in some way be related to expression of antisocial behavior, there is no evidence to suggest that consuming sucrose causes violent behavior. On the contrary, ingestion of foods that contain simple carbohydrates may elicit beneficial responses, at least in behavioral subgroups of adolescent males. [References: 153]
Heilman KM, Voeller KK, Nadeau SE: A POSSIBLE PATHOPHYSIOLOGIC SUBSTRATE OF ATTENTION DEFICIT HYPERACTIVITY DISORDER. [REVIEW]. Journal of Child Neurology 1991; 6 Suppl:S76-81. Summary: The attention deficit hyperactivity disorder (ADHD) is associated with defective attention and response inhibition and motor restlessness. Inattention, defective response inhibition, and impersistence are more commonly seen in adults with right than with left hemisphere dysfunction. In light of this fact and because children with ADHD not only appear to demonstrate these symptoms but also neglect the left side and have decreased activation of their right neostriatum, we propose that these children have a right hemisphere dysfunction. In addition, because both inattention and defective response inhibition can be seen in children with ADHD and in patients and animals who have frontal lobe and striatal dysfunction, we propose that children with ADHD have dysfunction in a right-sided frontal-striatal system. Motor restlessness may reflect frontal lobe dysfunction due to impairment of the mesocortical dopamine system. [References: 50]
Swanson JM, Posner M, Potkin S, Bonforte S, Youpa D, Fiore C, Cantwell D, Crinella F: ACTIVATING TASKS FOR THE STUDY OF VISUAL-SPATIAL ATTENTION IN ADHD CHILDREN: A COGNITIVE ANATOMIC APPROACH. [REVIEW]. Journal of Child Neurology 1991; 6 Suppl:S119-27. Summary: The clinical label attention deficit hyperactivity disorder (ADHD) suggests that this syndrome is a disorder of attention. However, the presumed attentional deficits have not been linked either to specific cognitive operations or to specific neural systems. To provide this link, theories of the cognitive anatomy of attention were used to generate hypotheses about specific visual-spatial attentional deficits in children with ADHD. A cued reaction-time test was used to assess covert and overt shifts of attention theoretically linked to two neuroanatomically defined attentional systems in the posterior and anterior parts of the human brain. The early, posterior-based covert shift of attention was found to be normal in ADHD children, but a later, anterior-based overt shift of attention was abnormal as reflected by a significant lateral difference in reaction time. This was interpreted as a failure to sustain focused attention. [References: 30]
de Rijk-van Andel JF, Catsman-Berrevoets CE, van Hemel JO, Hamers AJ: CLINICAL AND CHROMOSOME STUDIES OF THREE PATIENTS WITH SMITH-MAGENIS SYNDROME. Developmental Medicine & Child Neurology 1991; 33(4):343-7. Summary: The authors report three patients with Smith-Magenis syndrome; only 21 patients with this syndrome have been described previously in the literature. The syndrome is related to a deletion of chromosome 17p11 x 2, and differs from Miller-Dieker syndrome on clinical criteria and in that the latter is related to a deletion of 17p13 x 3.
Biederman J, Faraone SV, Keenan K, Steingard R, Tsuang MT: FAMILIAL ASSOCIATION BETWEEN ATTENTION DEFICIT DISORDER AND ANXIETY DISORDERS. American Journal of Psychiatry 1991; 148(2):251-6. Summary: BACKGROUND AND METHOD: This study tested hypotheses about patterns of familial association between attention deficit disorder (ADD) and anxiety disorders among 356 first-degree relatives of 73 clinically referred children with ADD and 26 normal comparison children. Through structured diagnostic interviews with trained raters, relatives were assessed for adult and childhood psychopathology. After stratifying the sample of ADD probands into those with anxiety disorders and those without, the authors examined patterns of aggregation of ADD and anxiety disorders in the relatives of these probands as well as in the relatives of the normal comparison subjects. RESULTS: Familial risk analyses revealed that 1) familial risk for anxiety disorders was higher among all ADD probands than among the normal subjects; 2) familial risk for ADD was similar in the relatives of the ADD probands and of the probands with ADD and anxiety disorder; 3) the relatives of the ADD probands with and without anxiety disorders were at greater risk for ADD than the relatives of the normal subjects; 4) the risk for anxiety disorders was two times higher in the relatives of the probands who had ADD with anxiety disorder than in those of the ADD probands without anxiety disorders; and 5) there was a tendency for ADD probands' relatives who themselves had ADD to have a higher risk for anxiety disorders than ADD probands' relatives who did not have ADD (cosegregation). CONCLUSIONS: The results were most consistent with the hypotheses indicating that ADD and anxiety disorders segregate independently in families.
Faraone SV, Biederman J, Keenan K, Tsuang MT: SEPARATION OF DSM-III ATTENTION DEFICIT DISORDER AND CONDUCT DISORDER: EVIDENCE FROM A FAMILY-GENETIC STUDY OF AMERICAN CHILD PSYCHIATRIC PATIENTS. Psychological Medicine 1991; 21(1):109-21. Summary: Using family study methodology and assessments by blind raters, this study tested hypotheses about patterns of familial association between DSM-III attention deficit disorder (ADD) and antisocial disorders (childhood conduct (CD) and oppositional disorder (OPD) and adult antisocial personality disorder) among 457 first-degree relatives of clinically referred children and adolescents with ADD (73 probands, 264 relatives), psychiatric (26 probands, 101 relatives) and normal controls (26 probands, 92 relatives). Among the 73 ADD probands, 33 (45%) met criteria for OPD, 24 (33%) met criteria for CD, and 16 (22%) had no antisocial diagnosis. After stratifying the ADD sample into those with CD (ADD + CD), those with OPD (ADD + OPD) and those with neither (ADD) familial risk analysis revealed the following: (1) relatives of each ADD proband subgroup were at significantly greater risk for ADD than relatives of both psychiatric and normal controls: (2) the morbidity risk for ADD was highest among relatives of ADD + CD probands (38%), moderate among relatives of ADD + OPD (17%) and ADD probands (24%) and lowest among relatives of psychiatric and normal controls (5% for both); (3) the risk for any antisocial disorder was highest among relatives of ADD + CD (34%) and ADD + OPD (24%) which were significantly greater than the risk to relatives of ADD probands (11%), psychiatric (7%) and normal controls (4%); and (4) both ADD and antisocial disorders occurred in the same relatives more often than expected by chance alone. Although these findings suggest that ADD with and without antisocial disorders may be aetiologically distinct disorders, they are also consistent with a multifactorial hypothesis in which ADD, ADD + OPD and ADD + CD fall along a continuum of increasing levels of familial aetiological factors and, correspondingly, severity of illness.
Faraone SV, Biederman J, Keenan K, Tsuang MT: A FAMILY-GENETIC STUDY OF GIRLS WITH DSM-III ATTENTION DEFICIT DISORDER. American Journal of Psychiatry 1991; 148(1):112-7. Summary: OBJECTIVE: The authors evaluated family-genetic risk factors in girls with attention deficit disorder and compared these results to findings in the authors' previous study of boys with attention deficit disorder. METHOD: Twenty-one girls with attention deficit disorder and 20 normal comparison girls were consecutively ascertained from a pool of existing and new referrals from a pediatric psychopharmacology unit and a medical pediatric unit of the same urban hospital. First-degree relatives of the attention deficit disordered girls (N = 69) and of the normal girls (N = 71) were also assessed. Both groups of girls and their relatives were evaluated on the basis of structured diagnostic interviews conducted by raters who were blind to the clinical status of the probands. RESULTS: The relatives of the girls with attention deficit disorder had higher risks for attention deficit disorder, antisocial disorders, major depression, and anxiety disorders. The higher risk for attention deficit disorder could not be accounted for by gender or generation of relative, age of proband, social class, or family intactness. These findings are highly consistent with the findings in the authors' previous study of boys with attention deficit disorder, which was conducted with identical methods. CONCLUSIONS: This study provides further support for the validity of the diagnosis of attention deficit disorder in girls and suggests that the genders share a common biological substrate.
Baker GB, Bornstein RA, Rouget AC, Ashton SE, van Muyden JC, Coutts RT: PHENYLETHYLAMINERGIC MECHANISMS IN ATTENTION-DEFICIT DISORDER. Biological Psychiatry 1991; 29(1):15-22. Summary: Urinary excretion (24-hr) of beta-phenylethylamine (PEA), phenylacetic acid (PAA), phenylalanine (Phe), and p-tyrosine (Tyr), and plasma levels of PAA, Phe, and Tyr were examined in 18 normal children and 26 children diagnosed as having attention-deficit hyperactivity disorder (ADHD). The results indicated that urinary excretion (expressed per g of creatinine) of free and total PEA was significantly lower in the ADHD patients, and plasma levels of Phe and Tyr were also decreased in the ADHD subjects compared with the normal controls.
Cadoret RJ, Stewart MA: AN ADOPTION STUDY OF ATTENTION DEFICIT/HYPERACTIVITY/AGGRESSION AND THEIR RELATIONSHIP TO ADULT ANTISOCIAL PERSONALITY. Comprehensive Psychiatry 1991; 32(1):73-82. Summary: This study used an adoption design to investigate the relationships among genetic background, environmental factors, and clinical outcome of attention deficit/hyperactivity, aggressivity, and adult antisocial personality (ASP) in a sample of 283 male adoptees. A biologic parent adjudged to be delinquent or to have an adult criminal conviction predicted increased attention deficit/hyperactivity in the adopted away sons, as well as increased adult ASP diagnosis. Aggressivity in the adoptee was predicted by attention deficit/hyperactivity, and aggressivity in turn predicted increased adult ASP. Environmental factors of socioeconomic status (SES), and psychiatric problems in adoptive family members correlated significantly with various clinical outcomes of aggressivity, attention deficit/hyperactivity, and ASP. The results suggest that attention deficit/hyperactivity should be considered a syndrome that has a variety of correlated behaviors, such as aggressivity, and that each of these correlated behaviors is influenced by different genetic and environmental factors and their interactions. Depending on the mix of factors, adult ASP can be one of the outcomes.
Biederman J, Faraone SV, Keenan K, Tsuang MT: EVIDENCE OF FAMILIAL ASSOCIATION BETWEEN ATTENTION DEFICIT DISORDER AND MAJOR AFFECTIVE DISORDERS. Archives of General Psychiatry 1991; 48(7):633-42. Summary: With the use of family study methods and assessments by "blinded" raters, we tested hypotheses about patterns of familial association between DSM-III attention deficit disorder (ADD) and affective disorders (AFFs) among first-degree relatives of clinically referred children and adolescents with ADD (73 probands, 264 relatives) and normal controls (26 probands, 92 relatives). Among the 73 ADD probands, 24 (33%) met criteria for AFFs (major depression, n = 15 [21%]; bipolar disorder, n = 8 [11%]; and dysthymia, n = 1 [1%]). After stratification of the ADD sample into those with AFFs (ADD + AFF) and those without AFF (ADD), familial risk analyses revealed the following: (1) the relatives of each ADD proband subgroup were at significantly greater risk for ADD than were relatives of normal controls; (2) the age-corrected morbidity risk for ADD was not significantly different between relatives of ADD and ADD + AFF (27% vs 22%); however, these two risks were significantly greater than the risk to relatives of normal controls (5%); (3) the risk for any AFF (bipolar disorder, major depressive disorder, or dysthymia) was not significantly different between relatives of ADD probands and ADD + AFF probands (28% and 25%), but these two risks were significantly greater than the risk to relatives of normal controls (4%); (4) ADD and AFFs did not cosegregate within families; and (5) there was no evidence for nonrandom mating. These findings are consistent with the hypothesis that ADD and AFFs may share common familial vulnerabilities.
Gross-Tsur V, Shalev RS, Amir N: ATTENTION DEFICIT DISORDER: ASSOCIATION WITH FAMILIAL-GENETIC FACTORS. Pediatric Neurology 1991; 7(4):258-61. Summary: The etiology of attention deficit disorder and hyperactivity (ADDH) is controversial because both biologic and social factors have been postulated. To study such factors, we undertook a referral study based on an entire cohort (N = 6,950) of children born in Jerusalem in 1976. Of 479 children referred for learning disabilities, hyperactivity, and behavioral problems, 381 were available for study. Information regarding obstetric, developmental, and family histories was obtained by a detailed, structured interview. A DSM-III-based questionnaire for ADDH was completed by parents and teachers. Each child underwent neurologic examination and 133 had IQ testing. Of these children, 145 fulfilled the criteria for ADDH. Our results revealed a number of significant familial-genetic factors: boys outnumbered girls by 3:1, 30% of ADDH children had siblings with learning disabilities (P less than .001); and ADDH children clustered within families of North African descent (P less than .001). The only significant developmental factor was delayed language development. Of numerous pre- and peri-natal factors investigated, only intrauterine growth retardation was significantly associated with ADDH. No correlation was found between ADDH and IQ, parental age, years of education, profession, and language spoken at home. Our study supports the hypothesis that familial-genetic factors are contributory to ADDH.
Einfeld S, Hall W, Levy F: HYPERACTIVITY AND THE FRAGILE X SYNDROME. Journal of Abnormal Child Psychology 1991; 19(3):253-62. Summary: Workers who have claimed an association between Fragile X [fra(x)] Syndrome and Hyperactivity and aggressive behavior have done so despite the lack of controlled studies using standard diagnostic criteria. Accordingly, we provided a controlled test of the hypothesis that individuals with the fra(x) Syndrome are more hyperactive and have more symptoms of aggression than other mentally retarded individuals. The test formed part of a study to assess autistic behavior in fra(x) individuals. A sample of fra(x) individuals was obtained from the register of a clinical genetics unit and individually matched for age, sex, and IQ with mentally retarded individuals selected from assessment centres. Forty-five pairs of fra(x) cases and control individuals were compared on criteria which reflected DSM-III concepts of hyperactivity and on criteria reflecting aggressive behavior. The comparison failed to find a higher prevalence of these symptoms in the fra(x) group. An analysis of the study's statistical power suggested that it is unlikely that the investigation failed to detect a large to medium difference between fra(x) individuals and control individuals in the symptoms investigated.
Levy F: THE DOPAMINE THEORY OF ATTENTION DEFICIT HYPERACTIVITY DISORDER (ADHD). [REVIEW]. Australian & New Zealand Journal of Psychiatry 1991; 25(2):277-83. Summary: Clinical, animal and neuroanatomical studies of differential isomer and dosage effects of CNS stimulant medications on behaviour are reviewed. Wender's hypothesis that an underlying biochemical abnormality and a disorder of reinforcement was the primary deficit in "MBD" children is restated in terms of a disorder of polysynaptic dopaminergic circuits, between prefrontal and striate centres. Wender's notion of a disorder of reinforcement is broadened to include a disorder of planning and correction of behaviour, including capacity for cortical control of automatic instinctual motor programmes. The dopamine hypothesis of Attention Deficit Hyperactivity Disorder (ADHD) is examined from the point of view of differential dose effects of CNS stimulant medications, and theories of neural control. Clinical, animal and neuropharmacological studies are reviewed. Implications of the findings for understanding clinical and side effects in ADHD children of stimulants are discussed. [References: 52]
Klorman R: COGNITIVE EVENT-RELATED POTENTIALS IN ATTENTION DEFICIT DISORDER. [REVIEW]. Journal of Learning Disabilities 1991; 24(3):130-40. Summary: Cognitive event-related potentials (ERPs) have been used to aid in the interpretation of findings that children with Attention Deficit Disorder (ADD) make more errors and react more slowly than nondisabled controls in tests of sustained attention. Coincident with their abnormally poor performance, children with ADD have smaller late positive components of the ERP (especially a wave known as P3b) than their peers with psychiatric diagnoses. Notably, stimulant administration improves the performance of children with ADD and enlarges the amplitude of the late positive waves of their ERPs. These findings are interpreted as reflecting reduced capacity allocation, which, in turn, is increased by stimulant medications. Research on memory scanning suggests that children with ADD are deficient in energetic aspects of information processes and that their excessive slowness in reaction time tests involves stages following memory search and decision, that is, motor processes. The same factors seem to be involved in the amelioration of performance by stimulants, which speed up motor responses but do not affect the latency of P3b. Research on ERPs during selective attention also points to possible disturbances in this aspect of processing, but further research in this area is needed. [References: 60]
Virtanen TA, Moilanen IK, Ihalainen MM: WHAT CAUSES STRESS FOR MOTHERS OF CHILDREN WITH MBD? Scandinavian Journal of Social Medicine 1991; 19(1):47-52. Summary: Adapting the paradigm developed by Richard Lazarus, parenting stress and coping were studied among mothers of 6-9-year-old children (n = 42) with different symptoms of Minimal Brain Dysfunction (MBD) (hyperkinesis, perceptual or motor deficits, learning disabilities or speech disorders) and among mothers of non-disabled children (n = 42) matched for age, sex, social status of the family and marital status. Mothers of children with MBD were found to experience more parenting difficulties and more negative cognitive appraisals of their stakes in parenting than their matched controls. The mothers of children with hyperkinesis and perceptual or motor deficits considered their mastery lower and experienced less positive affects than their matched controls. The mothers of children with speech disorders experienced less positive affects than their matched controls. Mothers of children with both few and several symptoms experienced more parenting difficulties in the child domain than their matched controls. Mothers of children with several symptoms considered their mastery lower and experienced less positive affects; mothers of children with few symptoms appraised their stakes in parenting more negatively than their matched controls. No significant differences were found between mothers of children with MBD with few and several symptoms.
Lubar JF: DISCOURSE ON THE DEVELOPMENT OF EEG DIAGNOSTICS AND BIOFEEDBACK FOR ATTENTION-DEFICIT/HYPERACTIVITY DISORDERS. [REVIEW]. Biofeedback & Self Regulation 1991; 16(3):201-25. Summary: This article presents a review of work that my colleagues and I have been doing during the past 15 years developing a rationale for the diagnosis of attention-deficit/hyperactivity disorder (ADHD) and treatment of ADHD employing EEG biofeedback techniques. The article first briefly reviews the history of research and theory for understanding ADHD and then deals with the development of EEG and event-related potential (ERP) assessment paradigms and treatment protocols for this disorder, including our work and that of others who have replicated our results. Illustrative material from our current research and child case studies is included. Suggestions for future experimental and clinical work in this area are presented and theoretical issues involving the understanding of the neurophysiological and neurological basis of ADHD are discussed. [References: 39]
Mannuzza S, Klein RG, Addalli KA: YOUNG ADULT MENTAL STATUS OF HYPERACTIVE BOYS AND THEIR BROTHERS: A PROSPECTIVE FOLLOW-UP STUDY. Journal of the American Academy of Child & Adolescent Psychiatry 1991; 30(5):743-51. Summary: This study reports on the psychiatric outcome as young adults (ages 16-23) of 50 hyperactive boys compared with their nonhyperactive brothers and to unrelated controls. Siblings provide a built-in control for potentially important factors, such as social class and parental psychopathology. Blind assessments at follow-up showed that significantly more probands (30%) than siblings (6%) and controls (10%) had multiple DSM-III diagnoses. Moreover, probands had a more severe form of antisocial disorder than siblings. In conclusion, the increased risk for multiple and more pervasive mental disorder in the young adulthood of hyperactive boys cannot be attributed to childhood factors shared with siblings.
Marazziti D, Conti L: AGGRESSION, HYPERACTIVITY AND PLATELET IMIPRAMINE BINDING. Acta Psychiatrica Scandinavica 1991; 84(3):209-11. Summary: We measured platelet 3H-imipramine binding parameters in 16 subjects affected by different types of mental deficiency, all characterized by hyperactive and/or aggressive behaviour, and in 16 healthy controls. The patients had a lower maximum binding capacity than the controls, with no difference in Kd, irrespectively of the type of mental disorder. These findings suggest a link between 5-HT disturbances, reflected by reduced imipramine binding sites, and behavioural dyscontrol, expressed as hyperactivity and aggression.
Ryback RS, Gardner EA: LIMBIC SYSTEM DYSRHYTHMIA: A DIAGNOSTIC ELECTROENCEPHALOGRAM PROCEDURE UTILIZING PROCAINE ACTIVATION. Journal of Neuropsychiatry & Clinical Neurosciences 1991; 3(3):321-9. Summary: A diagnostic method is presented that makes it possible to distinguish patients who are most likely to show a positive response to treatment with anticonvulsant medication, thereby cutting across many DSM-III-R diagnoses. Patients are evaluated to determine whether they exhibit at least 4 of 12 groups of symptoms, and the local anesthetic procaine is used, along with an electroencephalogram (EEG) to evaluate for omega band activity (30-50 Hz) of at least 50 microvolts or approximately three times baseline values in the anterior temporal leads. This method was studied in 145 patients with varying diagnoses. Eighty-three percent of patients who were symptom- and procaine-positive responded to anticonvulsants. Specific application to patients with attention-deficit hyperactivity disorder, bipolar disorder, and panic disorder is made. This method may provide a basis for identifying subpopulations of anticonvulsant-responsive patients who often are considered treatment-resistant.
Barkley RA, Grodzinsky G, DuPaul GJ: FRONTAL LOBE FUNCTIONS IN ATTENTION DEFICIT DISORDER WITH AND WITHOUT HYPERACTIVITY: A REVIEW AND RESEARCH REPORT. [REVIEW]. Journal of Abnormal Child Psychology 1992; 20(2):163-88. Summary: We review 22 neuropsychological studies of frontal lobe functions in children with attention deficit disorder with and without hyperactivity (ADD/+H, ADD/-H). Some measures presumed to assess frontal lobe dysfunctions were not reliably sensitive to the deficits occurring in either form of ADD. Tests of response inhibition more reliably distinguished ADD/+H from normal children. Where impairments were found on other tests between ADD and normal subjects, they were highly inconsistent across studies and seemed strongly related to age of the subjects and possibly to the version of the test employed. Other methodological differences across studies further contributed to the discrepant (LD) and conduct problems, with ADD may be an additional confounding factor in some, though not all, of these studies. In a separate reports. The co-morbidity of other disorders, such as learning disabilities (LD) and conduct problems, with ADD may be an additional confounding factor in some, though not all, of these studies. In a separate study, children with ADD/+H (n = 12) were then compared on frontal lobe tests to three other groups: ADD/-H (n = 12), LD but no ADD (n = 11), and normal children (n = 12) statistically covarying for differences in conduct problems across groups. Most measures did not distinguish among these groups. Both ADD groups made more omission errors on a Continuous Performance Test (CPT) than the normal group. All three clinical groups performed more poorly on the word and interference portions of the Stroop Test. Thus, while both types of ADD share some apparent similarities in deficits on a few frontal lobe tests in this study, the totality of existing findings suggests an additional problem with perceptual-motor speed and processing in the ADD/-H group. [References: 75]
Palm L, Persson E, Bjerre I, Elmqvist D, Blennow G: SLEEP AND WAKEFULNESS IN PREADOLESCENT CHILDREN WITH DEFICITS IN ATTENTION, MOTOR CONTROL AND PERCEPTION. Acta Paediatrica 1992; 81(8):618-24. Summary: In 10 children with deficits in attention, motor control and perception (DAMP), the relation between daytime vigilance and night-time sleep quality was examined with polygraphic sleep recordings, multiple sleep latency tests and measurements of reaction times. Two girls and eight boys, 6-12 years of age were studied. Eighteen normal children served as controls. Normal sleep regulation and sleep quality was found, but the children with DAMP tolerated the recording procedure less well than the controls. Most patients did not suffer from increased daytime sleepiness, but at MSLT 3, patients had short sleep latencies as in daytime hypersomnolence. Reaction times were significantly longer among the patients than among the controls. It is proposed that the findings may be related to functional changes in the forebrain.
Silverman IW, Ragusa DM: A SHORT-TERM LONGITUDINAL STUDY OF THE EARLY DEVELOPMENT OF SELF-REGULATION [PUBLISHED ERRATUM APPEARS IN J ABNORM CHILD PSYCHOL 1993 APR;21(2):231]. Journal of Abnormal Child Psychology 1992; 20(4):415-35. Summary: A short-term longitudinal study was conducted to determine whether self-regulation at 4 years could be predicted from child and maternal measures obtained when the children were age 24 months. The subjects were 69 children and their mothers drawn from the general community. Criterion behaviors assessed at 4 years were those suggestive of attention-deficit hyperactivity disorder. Of the 24-month child measures, maternal ratings of the child's impulsivity and attention span, plus an objective measure of delay ability, were the most effective predictors. Maternal negativity, as assessed in mother-child interaction, predicted the criterion behaviors, even after the child's behavior as an elicitor of maternal behavior was controlled. Maternal child-rearing attitudes on the dimensions of warmth and aggravation were also effective predictors, even after controlling for the child's emotionality as a possible determinant of maternal attitudes. It is argued that the results with the maternal attitude measures provide support for the hypothesis that maternal behavior is a contributor to the development of self-regulation.
Koziol LF, Stout CE: USE OF A VERBAL FLUENCY MEASURE IN UNDERSTANDING AND EVALUATING ADHD AS AN EXECUTIVE FUNCTION DISORDER. Perceptual & Motor Skills 1992; 75(3 Pt 2):1187-92. Summary: A primary characteristic of Attention Deficit Hyperactivity Disorder (ADHD) is an inability to establish and maintain sustained attention, which is speculated to reflect frontal lobe involvement. The Knight Verbal Fluency measure was administered to 19 ADHD inpatient boys and to a cohort group of 7 children who were matched for mean age, psychiatric diagnosis (depression), treatment facility, and examiner but were without the diagnosis of ADHD. Analysis indicated that ADHD children performed significantly lower than expected and lower than the similar non-ADHD children. These findings lend support to the hypothesis that frontal lobe dysfunction is involved in attentional process disorders and suggests the potential clinical usefulness in the diagnostic screening of ADHD children of a simply administered measure amenable to interpretation of frontal lobe function.
Mann CA, Lubar JF, Zimmerman AW, Miller CA, Muenchen RA: QUANTITATIVE ANALYSIS OF EEG IN BOYS WITH ATTENTION-DEFICIT-HYPERACTIVITY DISORDER: CONTROLLED STUDY WITH CLINICAL IMPLICATIONS. Pediatric Neurology 1992; 8(1):30-6. Summary: Sixteen-channel topographic brain mapping of electroencephalograms of 25 right-handed males, 9-12 years of age, with attention-deficit-hyperactivity disorder revealed increased theta (4-7.75 Hz) and decreased beta 1 (12.75-21 Hz) when compared with 27 controls matched for age and grade level. The differences were greater when patients were tested for reading and drawing skills, but were decreased when they were at rest during visual fixation. Although the differences in patients with attention-deficit-hyperactivity disorder were generalized, increased theta was more prominent in frontal regions, while beta 1 was significantly decreased in temporal regions. Principal component analysis was used to combine the variables into 2 components which accounted for 82% of the total variance. A discriminant function analysis using these components was able to predict group membership for attention-deficit-hyperactivity disorder patients 80% of the time and 74% for controls. These findings support the use of topographic electroencephalography for further elucidation of the neurophysiology of attention-deficit-hyperactivity disorder.
Ornitz EM, Hanna GL, de Traversay J: PRESTIMULATION-INDUCED STARTLE MODULATION IN ATTENTION-DEFICIT HYPERACTIVITY DISORDER AND NOCTURNAL ENURESIS. Psychophysiology 1992; 29(4):437-51. Summary: Startle modulation was induced by prestimulation in 43, 6-11 year old boys with attention-deficit hyperactivity disorder (ADHD), 13 of whom were or had been enuretic, 17 age-matched enuretic boys, and 42 age-matched normal boys, using 60-ms and 120-ms prestimulation intervals and a 4000-ms continuous tone. There was a significant multivariate effect of enuresis on startle amplitude modulation. This effect was attributed primarily to the reduction of amplitude inhibition following the 120-ms prestimulation interval regardless of whether or not enuresis was associated with ADHD. There was no effect of ADHD on startle modulation by prestimulation. The inhibition following the 120-ms prestimulation interval in the enuretic boys was reduced to the level of 5-year-old normal children, suggesting a maturational component of the deficient startle inhibition. The neurophysiologic dysfunction underlying the deficient startle inhibition in enuresis, but not ADHD, is discussed in terms of a possible dysfunction of mesopontine reticular mechanisms mediating preattentive processing of signals associated with spinal reflexes involved in urinary bladder control.
Dykman RA, Ackerman PT, Oglesby DM: HEART RATE REACTIVITY IN ATTENTION DEFICIT DISORDER SUBGROUPS. Integrative Physiological & Behavioral Science 1992; 27(3):228-45. Summary: Beat-to-beat heart rate (HR) was analyzed for 9 contiguous seconds in a warned reaction time (RT) paradigm. Imperative stimuli were tones of three intensity levels (55, 78, and 100 db); a visual warning signal occurred 5 sec before tone onset. Baseline and reward conditions were run. Normal controls were contrasted with three Attention Deficit Disorder (ADD) subgroups: ADD-only, ADD with hyperactivity (ADDH), ADD with hyperactivity and aggression (ADDHA). The ADD subgroups were predicted to show less deceleration in HR because of their problem sustaining readiness to respond. Significant sex x group differences in HR levels and change scores were found. Overall, girls had higher HR levels than boys and the ADD-only group (boys and girls) had lower HRs than the other ADD groups. But, the ADD-only boys had more marked deceleration to the warning signal and acceleration to the tones than the other ADD boys, whereas the ADD-only girls were no more reactive than the ADDH and ADDHA girls. Control girls had the highest HR levels and were the most reactive to stimuli. Control boys and ADD-only boys had similar HR levels and reaction patterns. ADD-only girls appear to be underaroused, whereas ADD-only boys do not. Results suggest that cardiac measures can provide external validation of disruptive and nondisruptive ADD subtypes.
Gillis JJ, Gilger JW, Pennington BF, DeFries JC: ATTENTION DEFICIT DISORDER IN READING-DISABLED TWINS: EVIDENCE FOR A GENETIC ETIOLOGY. Journal of Abnormal Child Psychology 1992; 20(3):303-15. Summary: In order to assess the genetic etiology of attention deficit hyperactivity disorder (ADHD), the basic regression model for the analysis of selected twin data (DeFries & Fulker, 1985, 1988) was fitted to questionnaire data (DICA: Diagnostic Interview for Children and Adolescents; Herjanic, Campbell, & Reich, 1982) for 37 identical and 37 fraternal twin pairs tested in the Colorado Reading Project. Results of this analysis suggest that ADHD is highly heritable. Moreover, adjusting DICA scores for either IQ or reading performance differences did not substantially change parameter estimates. In future analyses of larger data sets, distinguishing between possible subtypes of attentional problems (e.g., ADD with or without hyperactivity) may facilitate tests of more searching etiological questions.
Gilger JW, Pennington BF, DeFries JC: A TWIN STUDY OF THE ETIOLOGY OF COMORBIDITY: ATTENTION-DEFICIT HYPERACTIVITY DISORDER AND DYSLEXIA. Journal of the American Academy of Child & Adolescent Psychiatry 1992; 31(2):343-8. Summary: Monozygotic and dizygotic twin pairs, in which at least one member of each pair is reading disabled (RD), were assessed for attention-deficit hyperactivity disorder (ADHD). Within pair cross-concordances of the RD and ADHD qualitative diagnoses for monozygotic twins were larger than for dizygotic twins, although not significantly so (p less than 0.10). Thus, the data suggest that RD and ADHD may be primarily genetically independent. However, trends in the data and subtype analyses suggest that in some cases RD and ADHD may occur together because of a shared genetic etiology and that a genetically mediated comorbid subtype may exist.
Stevenson J: EVIDENCE FOR A GENETIC ETIOLOGY IN HYPERACTIVITY IN CHILDREN. Behavior Genetics 1992; 22(3):337-44. Summary: There has been considerable controversy over the nosology of hyperactivity and attention deficit hyperactivity disorder (ADHD). There have been suggestions that genetic influences may play a role in the origins of individual differences on this dimension or dimensions of behavior and that an understanding of the significance of genetic factors might help to clarify the classification of these disorders. Multiple regression is used to analyze data from a sample of 91 pairs of identical twins and 105 pairs of same sex fraternal twins. The heritability of extreme group membership (h2g = 0.75) was significant for activity rated by the mother. The heritability for one of the measures of attention deficit was also significant (h2g = 0.76). The results are consistent with a significant genetic contribution to individual differences in activity levels and attention abilities.
Egger J, Stolla A, McEwen LM: CONTROLLED TRIAL OF HYPOSENSITISATION IN CHILDREN WITH FOOD-INDUCED HYPERKINETIC SYNDROME. Lancet 1992; 339(8802):1150-3. Summary: Food intolerance seems to be an important cause of the hyperkinetic syndrome, but restricted diets are expensive, socially disruptive, and often nutritionally inadequate. Enzyme-potentiated desensitisation (EPD) may overcome some of these difficulties. EPD was tested in a double-blind placebo-controlled trial among 40 children with food-induced hyperkinetic behaviour disorder. A total of 185 children with established hyperkinetic syndrome underwent oligoantigenic dietary treatment for four weeks. 116 whose behaviour responded had provoking foods identified by sequential reintroduction. Foods that reproducibly provoked overactivity were avoided. 40 patients who were then invited to take part in the hyposensitisation trial were randomly assigned to treated and control groups. Treated patients received three doses of EPD (beta-glucuronidase and small quantities of food antigens) intradermally at two-monthly intervals. Controls received buffer only. Thereafter, patients were allowed to eat known provoking foods. Of 20 patients who received active treatment, 16 became tolerant towards provoking foods compared with 4 of 20 who received placebo (p less than 0.001). Our results show that EPD permits children with food-induced hyperkinetic syndrome to eat foods that had previously been identified as responsible for their symptoms. These results also support the notion that food allergy is a possible mechanism of the hyperkinetic syndrome.
Biederman J, Faraone SV, Keenan K, Benjamin J, Krifcher B, Moore C, Sprich-Buckminster S, Ugaglia K, Jellinek MS, Steingard R, et al: FURTHER EVIDENCE FOR FAMILY-GENETIC RISK FACTORS IN ATTENTION DEFICIT HYPERACTIVITY DISORDER. PATTERNS OF COMORBIDITY IN PROBANDS AND RELATIVES PSYCHIATRICALLY AND PEDIATRICALLY REFERRED SAMPLES. Archives of General Psychiatry 1992; 49(9):728-38. Summary: We examined 140 probands with attention deficit hyperactivity disorder, 120 normal controls, and their 822 first-degree relatives using "blind" raters and structured diagnostic interviews. Compared with controls, probands with attention deficit hyperactivity disorder were more likely to have conduct, mood, and anxiety disorders. Compared with relatives of controls, relatives of probands with attention deficit hyperactivity disorder had a higher risk for attention deficit hyperactivity disorder, antisocial disorders, major depressive disorder, substance dependence, and anxiety disorders. Patterns of comorbidity indicate that attention deficit hyperactivity disorder and major depressive disorders may share common familial vulnerabilities, that attention deficit hyperactivity disorder plus conduct disorder may be a distinct subtype, and that attention deficit hyperactivity disorder and anxiety disorders are transmitted independently in families. These results extend previous findings indicating family-genetic influences in attention deficit hyperactivity disorder by using both pediatrically and psychiatrically referred proband samples. The distributions of comorbid illnesses in families provide further validation for subgrouping probands with attention deficit hyperactivity disorder by comorbidity.
Chandola CA, Robling MR, Peters TJ, Melville-Thomas G, McGuffin P: PRE- AND PERINATAL FACTORS AND THE RISK OF SUBSEQUENT REFERRAL FOR HYPERACTIVITY. Journal of Child Psychology & Psychiatry & Allied Disciplines 1992; 33(6):1077-90. Summary: Possible pre- and perinatal risk factors for subsequent referral for hyperactivity were assessed by comparing birth records of 129 referrals with the remaining 24,656 members of a geographically defined birth cohort. Relationships between the risk factors were accounted for using logistic regression methods. The significant factors were: social class, maternal age, antepartum haemorrhage, length of labour (second stage), 1-min Apgar and sex. Associations between referral for hyperactivity and the pregnancy, labour and birth outcome factors were not explained by the socio-demographic variables. The results suggest that such factors have a statistically significant association with referral for hyperactivity and may be of modest aetiological importance. However, the predictive power of the final set of factors remained low even on the original data set.
Shue KL, Douglas VI: ATTENTION DEFICIT HYPERACTIVITY DISORDER AND THE FRONTAL LOBE SYNDROME. Brain & Cognition 1992; 20(1):104-24. Summary: The usefulness of frontal lobe (FL) dysfunction as a conceptual model for Attention Deficit Hyperactivity Disorder (ADHD) was investigated. Twenty-four ADHD and 24 normal control (NC) children were tested using two batteries of tasks. The first was sensitive to FL deficits in motor control and problem solving skills. The second consisted of memory tasks sensitive to temporal lobe dysfunction. ADHD children differed significantly from NCs on measures of FL function, but not on tests of temporal lobe functions. Where norms were available for normal children on the same FL tests, ADHDs performed like 6- to 7-year-olds, despite their mean age of 10 years and minimum age of 8 years. The differential performance of ADHDs on tasks sensitive to FL and temporal lobe dysfunction supports the hypothesis that ADHD deficits are analogous to FL dysfunction and demonstrates that the children's deficits do not reflect generalized cognitive impairment.
Hoegerman GS, Resnick RJ, Schnoll SH: ATTENTION DEFICITS IN NEWLY ABSTINENT SUBSTANCE ABUSERS: CHILDHOOD RECOLLECTIONS AND ATTENTION PERFORMANCE IN THIRTY-NINE SUBJECTS. Journal of Addictive Diseases 1993; 12(1):37-53. Summary: Attention deficits were studied among 67 consecutive admissions to an adult tertiary care in-patient substance abuse unit. Fifty-four patients completed the testing; of these 15 were excluded due to confounding variables. The majority of the remaining 39 subjects had evidence of current and/or childhood attention dysfunction. There was no correlation with current performance and childhood recollection of dysfunction even when the effect of gender, race and alcohol abuse were taken into account. There are intriguing educational and therapeutic implications of the similarities between cognitive impairments of newly sober substance abusers and adults with persistence of attention deficit-hyperactivity disorder (ADHD).
Winsberg BG, Javitt DC, Silipo GS, Doneshka P: MISMATCH NEGATIVITY IN HYPERACTIVE CHILDREN: EFFECTS OF METHYLPHENIDATE. Psychopharmacology Bulletin 1993; 29(2):229-33. Summary: This pilot study investigates electrophysiological correlates of methylphenidate (MP) treatment among hyperkinetic children who are clinical responders to therapy. Event-related potentials were obtained from a small sample (6 hyperactive and 5 controls) during an auditory "oddball" task. In the ignore condition, oddball tones elicited a frontocentral "mismatch" negativity (MMN) during the 100- to 200-msec latency range following stimulus presentation. In the attend condition, oddball target tones elicited a centroparietal P3 as well. MP significantly decreased hyperkinetic behaviors. Preliminary analyses of the electrophysiological data indicated a decreased amplitude of the P3 waveform among hyperkinetic children and a trend toward normalization on MP. Waveform abnormalities in the latency range of control MMN suggested either a decrease in MMN amplitude or an increase in MMN latency in hyperactive subjects along with a trend toward normalization by MP. The preliminary data are suggestive of information-processing abnormalities among hyperactive children that may be sensitive to MP therapy.
Pontius AA: NEUROETHICS VS NEUROPHYSIOLOGICALLY AND NEUROPSYCHOLOGICALLY UNINFORMED INFLUENCES IN CHILD-REARING, EDUCATION, EMERGING HUNTER-GATHERERS, AND ARTIFICIAL INTELLIGENCE MODELS OF THE BRAIN. Psychological Reports 1993; 72(2):451-8. Summary: Potentially negative long-term consequences in four areas are emphasized, if specific neuromaturational, neurophysiological, and neuropsychological facts within a neurodevelopmental and ecological context are neglected in normal functional levels of child development and maturational lag of the frontal lobe system in "Attention Deficit Disorder," in education (reading/writing and arithmetic), in assessment of cognitive functioning in hunter-gatherer populations, specifically modified in the service of their survival, and in constructing computer models of the brain, neglecting consciousness and intentionality as criticized recently by Searle.
Soorani-Lunsing RJ, Hadders-Algra M, Huisjes HJ, Touwen BC: MINOR NEUROLOGICAL DYSFUNCTION AFTER THE ONSET OF PUBERTY: ASSOCIATION WITH PERINATAL EVENTS. Early Human Development 1993; 33(1):71-80. Summary: In order to study the hypotheses that puberty is related to a decrease of minor neurological dysfunction (MND) and that persisting MND is associated with perinatal factors, two groups (174 normal, 172 MND) of the Groningen Perinatal Project were followed from 12 to 14 years. At 14 years almost all the children had entered puberty (n = 329) defined as the presence of three or more puberty signs. In the MND group 55% of the children were normal at 14 years and in 45% MND signs were still present, though in a less extensive form. The latter phenomenon was most clear in children who had just begun puberty. The effect of puberty was similar in both sexes. MND which persisted into puberty was related to neonatal neurological deviancy, lower social class, lower obstetrical optimality score and male sex. After differentiation with specific MND clusters, it appeared that fine manipulative disability was associated with neonatal neurological deviancy, with minor physical anomalies and with lower social class; choreiform dyskinesia with asphyxia; hypotonia with constitutionally related factors; and coordination problems with pre-maturity (< 32 weeks).
Valdizan JR, Andreu AC: TEST OF REPEATED OPERATIONS AND LOGISTIC REGRESSION AS TO THE EFFICACY OF BRAIN MAPPING. Clinical Electroencephalography 1993; 24(2):89-92. Summary: The object of this paper is to apply two new methods, those of repeated observations and logistic regression in order to verify the validity of qEEG. These methods are applied using children with hyperactivity and attentional disorders, according to DSM III-R. The results of sensitivity and specificity were similar.
Pliszka SR, Hatch JP, Borcherding SH, Rogeness GA: CLASSICAL CONDITIONING IN CHILDREN WITH ATTENTION DEFICIT HYPERACTIVITY DISORDER (ADHD) AND ANXIETY DISORDERS: A TEST OF QUAY'S MODEL. Journal of Abnormal Child Psychology 1993; 21(4):411-23. Summary: Quay (1988) put forward a model of childhood mental disorders based on Gray's (1982) theory that there exists within the brain a behavioral inhibition system (BIS), which processes signals related to aversive or punishing stimuli. According to this model, children with attention deficit hyperactivity disorder (ADHD) show lower than optimal levels of activity in this system, which leads to less responsiveness at a physiological level to signals related to punishment. Children with ADHD and controls were compared on a classical conditioning paradigm. Skin conductance and cardiac responses were measured in response to a conditioned stimulus that had been paired with an aversive unconditioned stimulus. There were no differences between the groups, suggesting that, in terms of classical conditioning, ADHD children are equally responsive to signals related to punishment as controls.
DiBattista D, Shepherd ML: PRIMARY SCHOOL TEACHERS' BELIEFS AND ADVICE TO PARENTS CONCERNING SUGAR CONSUMPTION AND ACTIVITY IN CHILDREN. Psychological Reports 1993; 72(1):47-55. Summary: The available body of scientific evidence does not support the notion that sugar consumption has significant adverse effects on children's behaviours; however, responses to a mailed questionnaire indicated that more than 80% of 389 Canadian primary school teachers believed that sugar consumption contributes to increasing activity of normal children and to the behavioural problems of hyperactive children. Moreover, in the previous three years, 55% of all respondents had counselled the parents of children whom they believed to be hyperactive to consider reducing their child's sugar consumption to control the child's activity, and parents frequently did so. These results indicate that teachers need to be provided with accurate and up-to-date information about the effects of sugar on children's behaviour and about effective treatments for hyperactivity. Possible origins of beliefs about the reputed adverse behavioural effects of sugar and about factors that may serve to perpetuate these beliefs are discussed.
McGee R, Stanton WR, Sears MR: ALLERGIC DISORDERS AND ATTENTION DEFICIT DISORDER IN CHILDREN. Journal of Abnormal Child Psychology 1993; 21(1):79-88. Summary: It has been suggested that children with attention deficit disorder-hyperactivity (ADDH) are likely to show allergic disorders, and that both ADDH and allergic disorders may share a common biological background. In a large sample of children from the general population we found no association between parent, teacher, and self-reports of ADDH behaviors and a history of allergic disorders (asthma, eczema, rhinitis, and urticaria) at ages 9 or 13 years. Similarly, reports of ADDH behaviors at age 13 years were not related to level of atopic responsiveness by skin test or serum IgE levels. Our findings call into question the hypothesis that there is a relationship between ADDH and allergic disorder.
Phillips BB, Drake ME Jr, Hietter SA, Andrews JE, Bogner JE: ELECTROENCEPHALOGRAPHY IN CHILDHOOD CONDUCT AND BEHAVIOR DISORDERS. Clinical Electroencephalography 1993; 24(1):25-30. Summary: The pathophysiology of behavior disorders in children is controversial. In particular, the relationship of episodic behavior disturbance to epilepsy and chronic behavior problems to subclinical neurologic disorder has been debated. It has been suggested that EEG may assist in this sometimes difficult determination. We report on routine screening EEGs in children hospitalized over an 18-month period for behavior problems. Eighty-six children were admitted for conduct disorder, attention deficit hyperactivity disorder, or both. Seventy-eight tracings (91%) were normal or showed normal variant patterns. Eight records (9%) were abnormal, showing background slowing or paroxysmal discharges not associated with behavioral manifestations. None of these neurologically normal, nonretarded patients had epilepsy or other known cerebral disorder. This suggests that routine EEG screening may be of limited value in childhood behavior problems without clinical evidence of neurologic disorder.
Baker GB, Bornstein RA, Douglass AB, Van Muyden JC, Ashton S, Bazylewich TL: URINARY EXCRETION OF MHPG AND NORMETANEPHRINE IN ATTENTION DEFICIT HYPERACTIVITY DISORDER. Molecular & Chemical Neuropathology 1993; 18(1-2):173-8. Summary: Twenty-four-hour excretion (expressed per gram of creatinine) of the norepinephrine metabolites 3-methoxy-4-hydroxyphenylethylene glycol (MHPG) and normetanephrine (NME) was measured in children with attention deficit hyperactivity disorder (ADHD) and in normal subjects matched for age and education. In contrast to findings with Tourette syndrome patients, in the ADHD patients there was no significant difference in excretion of MHPG and NME from control values.
Kelly DP, Kelly BJ, Jones ML, Moulton NJ, Verhulst SJ, Bell SA: ATTENTION DEFICITS IN CHILDREN AND ADOLESCENTS WITH HEARING LOSS. A SURVEY. American Journal of Diseases of Children 1993; 147(7):737-41. Summary: OBJECTIVES--To determine the prevalence of reported attention deficits in a sample of children who are deaf or hard of hearing and to examine associated variables. DESIGN--Cross-sectional survey. SETTING--Residential school for the deaf. PARTICIPANTS--All students attending the school (n = 238; median age, 16.0 years; range, 4 to 21 years). Subjects were subgrouped by cause of deafness for further analyses. INTERVENTION--None. MEASUREMENTS/MAIN RESULTS--School personnel completed questionnaires that are commonly used in the assessment of attention problems. Teachers completed the Attention Deficit Disorder With Hyperactivity (ADD-H) Comprehensive Teacher Rating Scale (ACTeRS) and an abbreviated version of the Attention-Activity section of the ANSER (Aggregate Neurobehavioral Student Health and Education Review) System Questionnaires. Dormitory supervisors rated students on the Conners' Parent Rating Scale and the ANSER System Questionnaires. The mean factor scores for the total sample of deaf and hard-of-hearing students on the Attention and Hyperactivity scales of the ACTeRS and Conners' questionnaires did not differ from the normative data. The 64 students with hereditary deafness received significantly better ratings than the 75 with an acquired cause of deafness such as bacterial meningitis or congenital rubella. Raw scores on the ACTeRS were converted to percentile equivalents based on the normative sample. On the Attention Scale, 38.7% of those with acquired deafness were rated below the 20th percentile (indicative of problems); only 14.1% of the students with hereditary deafness were in this range (P = .002). CONCLUSIONS--Ratings of attention for students with hearing loss, attending a residential school, did not differ from the normative data. However, the subgroup of children with acquired sensorineural deafness appear to be at increased risk for attention problems.
Daugherty TK, Quay HC, Ramos L: RESPONSE PERSEVERATION, INHIBITORY CONTROL, AND CENTRAL DOPAMINERGIC ACTIVITY IN CHILDHOOD BEHAVIOR DISORDERS. Journal of Genetic Psychology 1993; 154(2):177-88. Summary: We screened students (N = 710) in grades four through six at two public elementary schools for behavior problems, using the Revised Behavior Problem Checklist. Five groups of children were identified: conduct disorder (n = 8), attention deficit disorder (n = 9), conduct disorder plus attention deficit disorder with hyperactivity (n = 11), anxiety-withdrawal (n = 12), and normal control (n = 15). A response perseveration task, inhibitory control task, and a noninvasive measure of dopaminergic activity were administered to selected students, and group differences were predicted based on Quay's hypotheses as derived from Gray's theory of brain function. Hypothesized group differences were not found, although analyses revealed dimensional relationships that were consistent with the hypotheses. Results are discussed in terms of Quay's hypotheses and potential modifications to tasks for future research.
Faraone SV, Biederman J, Lehman BK, Keenan K, Norman D, Seidman LJ, Kolodny R, Kraus I, Perrin J, Chen WJ: EVIDENCE FOR THE INDEPENDENT FAMILIAL TRANSMISSION OF ATTENTION DEFICIT HYPERACTIVITY DISORDER AND LEARNING DISABILITIES: RESULTS FROM A FAMILY GENETIC STUDY. American Journal of Psychiatry 1993; 150(6):891-5. Summary: OBJECTIVE: The purpose of the study was to clarify the relationship between attention deficit hyperactivity disorder and learning disabilities. METHOD: The authors assessed learning disabilities in a sample of 140 children with attention deficit hyperactivity disorder and in 120 normal comparison children. They also assessed a sample of the probands' 822 first-degree relatives. RESULTS: The risk for learning disabilities was highest among relatives of probands with both attention deficit hyperactivity disorder and learning disabilities. The two disorders did not cosegregate in families. There was nonrandom mating between spouses with attention deficit hyperactivity disorder and learning disabilities. CONCLUSIONS: The two disorders are transmitted independently in families, and their co-occurrence may be due to nonrandom mating. Attention deficit hyperactivity disorder is likely to be etiologically independent from learning disabilities.
Matochik JA, Nordahl TE, Gross M, Semple WE, King AC, Cohen RM, Zametkin AJ: EFFECTS OF ACUTE STIMULANT MEDICATION ON CEREBRAL METABOLISM IN ADULTS WITH HYPERACTIVITY. Neuropsychopharmacology 1993; 8(4):377-86. Summary: Recent work in our laboratory has demonstrated both global and regional reductions in cerebral glucose metabolism in adult subjects with attention-deficit hyperactivity disorder (ADHD). The purpose of the present study was to examine the effects of an acute dose of stimulant medication on cerebral metabolism in adults with ADHD using positron emission tomography with fluorodeoxyglucose-18 as the tracer. Each subject underwent scanning twice, once off-drug and again after receiving a single oral dose of either dextroamphetamine (0.25 mg/kg) or methylphenidate (0.35 mg/kg). Subjects completed behavioral self-report measures before and after the scan and performed an auditory continuous performance task during the tracer uptake period. Neither drug changed global metabolism. Both drugs increased systolic blood pressure, and dextroamphetamine improved performance on the auditory attention task. Each stimulant produced a differential pattern of increases and decreases in regional metabolism throughout the regions of interest that were sampled. Rather than increasing glucose utilization in specific brain regions with lowered metabolic rates in adults with ADHD, stimulants may act by altering glucose use throughout the brain.
Kaneko M, Hoshino Y, Hashimoto S, Okano T, Kumashiro H: HYPOTHALAMIC-PITUITARY-ADRENAL AXIS FUNCTION IN CHILDREN WITH ATTENTION-DEFICIT HYPERACTIVITY DISORDER. Journal of Autism & Developmental Disorders 1993; 23(1):59-65. Summary: Examined hypothalamic-pituitary-adrenal axis (HPA axis) function in 30 children with attention-deficit hyperactivity disorder (ADHD) by measuring the diurnal variation and response to the dexamethasone suppression test (DST) of saliva cortisol. Normal diurnal saliva cortisol rhythm was found in only 43.3% of the ADHD children. DST showed suppression in 46.7% of the ADHD children. An abnormal diurnal rhythm and nonsuppression to the DST were more frequent in the severely hyperactive group than in the mildly were more frequent in the severely hyperactive group than in the mildly hyperactive group of children with ADHD. These results suggest abnormalities in HPA axis function in some children with ADHD, especially those exhibiting severe hyperactivity.
Singer HS, Reiss AL, Brown JE, Aylward EH, Shih B, Chee E, Harris EL, Reader MJ, Chase GA, Bryan RN, et al: VOLUMETRIC MRI CHANGES IN BASAL GANGLIA OF CHILDREN WITH TOURETTE'S SYNDROME. Neurology 1993; 43(5):950-6. Summary: To define the site of pathology in Tourette's syndrome (TS), we performed a volumetric MRI study of basal ganglia structures and lateral ventricles on 37 children with this disorder and 18 controls. There were no statistically significant differences in the size of the right or left caudate, putamen, globus pallidus, or ventricles in these populations. In contrast, there were significant differences for measures of symmetry in the putamen and the lenticular region. Virtually all controls (17 right- and one left-handed) had a left-sided predominance of the putamen, whereas in 13 of 37 TS subjects, a right predominance exceeded that of any control. Statistical comparisons among TS patients, with (n = 18) or without (n = 19) attention-deficit hyperactivity disorder (ADHD), and controls showed significant differences for the volume of the left globus pallidus and for lenticular asymmetry. Post hoc evaluations showed that in the TS + ADHD group, the volume of the left globus pallidus was significantly smaller than the volume of the right and that lenticular asymmetry was due to a greater right-sided predominance in the TS+ADHD group. This study lends further support to proposals that claim the basal ganglia is involved in the pathogenesis of TS and also suggests that the comorbid problem of ADHD is related to regional changes that differ from those primarily associated with tics.
Faraone SV, Biederman J, Lehman BK, Spencer T, Norman D, Seidman LJ, Kraus I, Perrin J, Chen WJ, Tsuang MT: INTELLECTUAL PERFORMANCE AND SCHOOL FAILURE IN CHILDREN WITH ATTENTION DEFICIT HYPERACTIVITY DISORDER AND IN THEIR SIBLINGS. Journal of Abnormal Psychology 1993; 102(4):616-23. Summary: We made psychiatric and intellectual assessments of 140 children with attention deficit hyperactivity disorder (ADHD), 120 normal controls, and their 303 siblings. The index children were white, non-Hispanic boys. ADHD children were more likely to have had learning disabilities, repeated grades, been placed in special classes, and received academic tutoring. They also did worse on the Wechsler Intelligence Scale for Children--Revised (WISC-R). Among ADHD probands, comorbid conduct, major depressive, and anxiety disorders predicted school placement more than school failure or WISC-R scores. However, the neuropsychological disability of all ADHD children could not be attributed to comorbid disorders because those without comorbidity had more school failure and lower WISC-R scores than normal controls. Intellectual impairment was also increased among siblings of ADHD children. This provides converging evidence that the ADHD syndrome is familial.
Hynd GW, Hern KL, Novey ES, Eliopulos D, Marshall R, Gonzalez JJ, Voeller KK: ATTENTION DEFICIT-HYPERACTIVITY DISORDER AND ASYMMETRY OF THE CAUDATE NUCLEUS. Journal of Child Neurology 1993; 8(4):339-47. Summary: The neurologic basis of attention deficit-hyperactivity disorder (ADHD) is poorly understood. Based on previous studies that have implicated metabolic deficiencies in the caudate-striatal region in ADHD, we employed magnetic resonance imaging to investigate patterns of morphology of the head of the caudate nucleus in normal and ADHD children. In normal children, 72.7% evidenced a left-larger-than-right (L > R) pattern of asymmetry, whereas 63.6% of the ADHD children had the reverse (L < R) pattern of asymmetry of the head of the caudate nucleus. This reversal of normal asymmetry in ADHD children was due to a significantly smaller left caudate nucleus. The reversal in asymmetry of the head of the caudate was most notable in ADHD males. These results suggest that normal (L > R) morphologic asymmetry in the region of the caudate nucleus may be related to asymmetries observed in neurotransmitter systems implicated in ADHD. The behavioral symptoms of ADHD may reflect disinhibition from normal levels of dominant hemispheric control, possibly correlated with deviations in asymmetric caudate-striatal morphology and deficiencies in associated neurotransmitter systems.
Stevenson J, Pennington BF, Gilger JW, DeFries JC, Gillis JJ: HYPERACTIVITY AND SPELLING DISABILITY: TESTING FOR SHARED GENETIC AETIOLOGY. Journal of Child Psychology & Psychiatry & Allied Disciplines 1993; 34(7):1137-52. Summary: The influence of genetic factors in the comorbidity of spelling disability and hyperactivity was investigated in two samples of 190 and 260 same sex twin pairs. The method of bivariate group heritability was used to estimate the genetic correlation for spelling disability and hyperactivity. A similar though not statistically significant value for the genetic correlation was obtained for the two samples (0.29 and 0.42). It was estimated that approximately 75% of the co-occurrence of these two conditions was due to shared genetic influences.
Knell ER, Comings DE: TOURETTE'S SYNDROME AND ATTENTION-DEFICIT HYPERACTIVITY DISORDER: EVIDENCE FOR A GENETIC RELATIONSHIP. Journal of Clinical Psychiatry 1993; 54(9):331-7. Summary: BACKGROUND: Attention deficit disorder with or without hyperactivity (ADD) is present in 49% to 83% of patients with Tourette's syndrome (TS), and up to 50% of children with attention-deficit hyperactivity disorder (ADHD) have chronic tics or a family history of chronic tics. Two explanations have been offered for this association: (1) ADHD is part of the pleiotropic expression of the Gilles de la Tourette (Gts) gene(s), or (2) the presence of ADHD in TS is due to ascertainment bias. METHOD: To avoid ascertainment bias, we examined 338 first-degree relatives of 131 TS probands utilizing a structured questionnaire and the DSM-III criteria for ADD and DSM-III-R criteria for ADHD. All probands and many relatives were personally interviewed. RESULTS: Of the relatives with TS, 61% had ADD and 36% had ADHD. Of the relatives with chronic tics, 41% had ADD and 26% had ADHD. Log-linear analysis showed a major, significant association between tics and ADHD. CONCLUSION: These results indicate that ADHD is part of the pleiotropic expression of the Gts gene(s).
Pauls DL, Leckman JF, Cohen DJ: FAMILIAL RELATIONSHIP BETWEEN GILLES DE LA TOURETTE'S SYNDROME, ATTENTION DEFICIT DISORDER, LEARNING DISABILITIES, SPEECH DISORDERS, AND STUTTERING. Journal of the American Academy of Child & Adolescent Psychiatry 1993; 32(5):1044-50. Summary: OBJECTIVE: This study examined the familial relationship between Gilles de la Tourette's syndrome (GTS) and attention deficit disorder (ADD), learning problems, speech disorders, and stuttering. METHOD: This family study consisted of 338 first degree relatives of 85 GTS probands and 113 controls. All available relatives were personally assessed using structured interviews, and family history information was collected from all family members. Best-estimate diagnoses were assigned for GTS, ADD, learning problems, speech disorders, and stuttering. Analyses examined whether ADD, learning problems, speech disorders, and stuttering by themselves represent genetically variant expressions of GTS. RESULTS: There was no evidence that ADD, learning problems, speech disorders, or stuttering represent variant expressions of GTS. However, relatives with GTS were at increased risk for ADD regardless of the ADD diagnosis of the GTS proband. CONCLUSIONS: ADD, learning problems, stuttering, and speech problems by themselves are not variant forms of GTS. However, GTS and ADD may be etiologically related in some persons. There may be two types of individuals with GTS and ADD: ones in whom ADD is independent of GTS, and others in whom ADD is secondary to occurrence of GTS.
Sprich-Buckminster S, Biederman J, Milberger S, Faraone SV, Lehman BK: ARE PERINATAL COMPLICATIONS RELEVANT TO THE MANIFESTATION OF ADD? ISSUES OF COMORBIDITY AND FAMILIALITY. Journal of the American Academy of Child & Adolescent Psychiatry 1993; 32(5):1032-7. Summary: OBJECTIVE: We evaluated the role of pregnancy, delivery, and infancy complications (PDICs) in the etiology of attention deficit disorder (ADD) addressing issues of comorbidity and familiarity by formulating and testing multiple hypotheses. METHOD: Subjects were six to 17-year-old boys with DSM-III attention deficit disorder (ADD, N = 73), psychiatric (N = 26), and normal (N = 26) controls and their relatives. Information on PDICs was obtained from the mothers in a standardized manner blind to the proband's clinical status. RESULTS: Using odds ratio analyses, an association was found between ADD and PDICs that was strongest for the comorbid and nonfamilial subtypes. In contrast, noncomorbid and familial ADD subgroups differed less from normal controls in the risk for PDICs. CONCLUSIONS: The increased risk for PDICs in nonfamilial ADD children and the lack of evidence for increased risk among familial ADD patients suggests that PDICs may be part of nongenetic etiologic mechanisms in this disorder, especially for children who have comorbid disorders.
Ernst M, Zametkin AJ, Matochik JA, Liebenauer L, Fitzgerald GA, Cohen RM: EFFECTS OF INTRAVENOUS DEXTROAMPHETAMINE ON BRAIN METABOLISM IN ADULTS WITH ATTENTION-DEFICIT HYPERACTIVITY DISORDER (ADHD). PRELIMINARY FINDINGS. Psychopharmacology Bulletin 1994; 30(2):219-25. Summary: The effects on brain metabolism of the intravenous (i.v.) administration of dextroamphetamine was assessed by positron emission tomography (PET) with [18F]-fluorodeoxyglucose (18-FDG) in 8 adults with attention-deficit hyperactivity disorder (ADHD). During the 3-hour 18-FDG PET session, each adult underwent the initial scan following i.v. infusion of placebo and a second scan following i.v. infusion of 0.15 mg/kg dextroamphetamine in a single-blind design. All subjects showed increased systolic/diastolic blood pressure and improved continuous performance task scores after dextroamphetamine. Global and regional metabolic rates were not significantly altered by the stimulant. When regional and global rates were normalized, the metabolic rates of only three cortical regions differed significantly between conditions. Individually, global metabolism increased in 4 subjects, was unchanged in 2, and decreased in 2 after stimulant infusion. No clinical characteristics differentiated these patients. I.V. infusion of dextroamphetamine did not significantly alter brain metabolism in ADHD adults in this preliminary study.
Gerra G, Caccavari R, Fontanesi B, Delsignore R, Fertonani-Affini G, Marcato A, Maestri D, Avanzini P, Perna G, Brambilla F: ALPHA-2-ADRENOCEPTOR SENSITIVITY IN HEROIN ADDICTS WITH AND WITHOUT PREVIOUS ATTENTION DEFICIT DISORDER/HYPERACTIVITY AND CONDUCT DISORDER. Neuropsychobiology 1994; 30(1):15-9. Summary: Growth hormone (GH) and beta-endorphin (beta-EP) responses to clonidine stimulation were examined in 18 male heroin addicts, 9 with and 9 without previous histories of attention deficit disorder with hyperactivity (ADD-H) and conduct disorder (CD). Ten psychophysically healthy volunteers were used as controls. ADD-H/CD addicts had blunted GH and beta-EP responses as compared to controls while those of non-ADD-H/CD addicts were normal. This suggests that postsynaptic adrenoceptor sensitivity is decreased and, possibly, that presynaptic noradrenaline secretion is increased in ADD-H/CD patients with heroin addiction.
Ackerman PT, Dykman RA, Oglesby DM, Newton JE: EEG POWER SPECTRA OF CHILDREN WITH DYSLEXIA, SLOW LEARNERS, AND NORMALLY READING CHILDREN WITH ADD DURING VERBAL PROCESSING. Journal of Learning Disabilities 1994; 27(10):619-30. Summary: EEG power spectra were studied in two poor reader groups (with dyslexia and slow learning) and a normally reading clinic control group (with attention deficit disorder) as the children viewed strings of words and letters (seven categories). The children ranged in age from 7.5 to 12 years; 33 were girls, 86 were boys. Bilateral temporal and parietal sites and four midline sites were used. The major difference between groups was in the low beta band, where the ADD group had greater power at the parietal and midline sites. Also, the slow learner group had marginally greater low beta at the left than right temporal site, with the opposite trend found for the dyslexic and ADD groups. Across groups, power was greater at the right than at the left parietal site in the delta and alpha bands and at the right than at the left temporal site in the low beta band. Stimulus category effects were modest, with some alpha suppression to word strings, relative to letter strings, found in the poor readers. In correlational analyses, the combination of greater low beta and less theta power significantly predicted better reading and spelling. Results indicate that the adequate readers more actively processed the stimuli than did the poor readers.
Halperin JM, Sharma V, Siever LJ, Schwartz ST, Matier K, Wornell G, Newcorn JH: SEROTONERGIC FUNCTION IN AGGRESSIVE AND NONAGGRESSIVE BOYS WITH ATTENTION DEFICIT HYPERACTIVITY DISORDER. American Journal of Psychiatry 1994; 151(2):243-8. Summary: OBJECTIVE: This study was designed to assess central serotonergic (5-HT) function in aggressive and nonaggressive boys with attention deficit hyperactivity disorder. METHOD: Prolactin response to a challenge dose of the 5-HT agonist d,l-fenfluramine was assessed in 25 7-11-year-old boys with attention deficit hyperactivity disorder who were divided into aggressive and nonaggressive subgroups. In addition, the subgroups were compared on plasma catecholamine metabolites and platelet 5-HT. RESULTS: The aggressive group had a significantly greater prolactin response to the fenfluramine challenge than the nonaggressive subgroup. The groups did not differ on peripheral measures of neurotransmitter function. CONCLUSIONS: These data suggest that aggressive and nonaggressive children with attention deficit hyperactivity disorder differ in central 5-HT functioning.
Tzourio N, Heim A, Zilbovicius M, Gerard C, Mazoyer BM: ABNORMAL REGIONAL CBF RESPONSE IN LEFT HEMISPHERE OF DYSPHASIC CHILDREN DURING A LANGUAGE TASK. Pediatric Neurology 1994; 10(1):20-6. Summary: This study used xenon 133 inhalation and single-photon computed tomography to measure regional cerebral blood flow during a quiet resting condition, a simple auditory task, and an auditory phonemic discrimination task in 3 age-matched groups of children suffering from developmental language disabilities: expressive dysphasia, expressive-receptive dysphasia, and attention-deficit hyperactivity disorder. An absence of left hemisphere activation was observed in the expressive-receptive group during the phonemic discrimination task as compared to both expressive and attention-deficit hyperactivity disorder children, together with an absence of left inferior parietal region activation in dysphasics as compared to hyperactive children. These results favor the hypothesis of an abnormal lateralization for language in dysphasic children and point toward possible different pathologic localizations in the different clinical subtypes of dysphasia.
Gillberg IC, Gillberg C, Ahlsen G: AUTISTIC BEHAVIOUR AND ATTENTION DEFICITS IN TUBEROUS SCLEROSIS: A POPULATION-BASED STUDY. Developmental Medicine & Child Neurology 1994; 36(1):50-6. Summary: In a population-based sample of 28 individuals under the age of 20 years, autistic symptoms were present in 24 and DSM-III-R autistic disorder in 17. Many of the children and adolescents diagnosed as autistic also showed attention deficit/hyperactivity. There was no specific association between autistic behaviour and the presence of infantile spasms. Some of the children with tuberous sclerosis and autism were of near-normal intelligence. Indirectly, the results suggest that as many as 9 per cent of all children with autism may have tuberous sclerosis.
Newton JE, Oglesby DM, Ackerman PT, Dykman RA: VISUAL SLOW BRAIN POTENTIALS IN CHILDREN WITH ATTENTION DEFICIT DISORDER. Integrative Physiological & Behavioral Science 1994; 29(1):39-54. Summary: Using a two-stimulus reaction time paradigm, with two separate reward conditions (contingent and noncontingent), we compared slow wave brain potentials (ERPs) in 144 children with attention deficit disorder (ADD) and 30 normal control children. This article reviews the findings during the 900 msec visual warning stimulus. As we had expected, based on ERP work of Forth and Hare (1989) and Raine, Venables and Williams (1990), and on previous work from our own laboratory, the group differences were found in the negative slow wave portions of the ERP complex during the contingent reward condition but not during the noncontingent condition. Aggressive hyperactive subjects with attention deficit disorder (ADDHA) were discriminated from nonaggressive subjects (including control subjects) during the contingent reward condition in the following ways: (1) greater fronto-central negativity (640-900 msec slow wave) and (2) greater right parietal than left parietal negativity (430-750 msec slow wave). All ADD subgroups, when compared to control (CONTR) subjects, showed greater slow wave negativity (700-900 msec) at the midline occipital electrode site during the contingent reward condition. This could be explained in part as an IQ effect on ERPs reflecting the IQ difference between the ADD subgroups and the controls. These slow wave findings seem to relate to attentional problems of these children. They are discussed in terms of a psychobiological model of inhibition/disinhibition and appetitive activation.
Arcia E, Gualtieri CT: NEUROBEHAVIOURAL PERFORMANCE OF ADULTS WITH CLOSED-HEAD INJURY, ADULTS WITH ATTENTION DEFICIT, AND CONTROLS. Brain Injury 1994; 8(5):395-404. Summary: The symptoms experienced by people with mild closed-head injury (mCHI) and by people with attention deficit disorder (ADD) are similar in many aspects. We examined the performance of 26 adults with mCHI, 23 adults with ADD, and 25 matched controls on four functional areas: (1) simple motor response, (2) response speed and attention, (3) complex perceptual-motor performance, and (4) memory and learning. Analyses of variance and multivariate analyses of variance were used to compare the performance of the three groups. Test results were also plotted to examine patterns of performance and similarities between the groups. Both groups with mCHI and ADD had significantly more difficulty than controls with sustained attention. However, whereas the group with mCHI was characterized by generalized slowness in their response times, the group with ADD was characterized by impulsivity or an inability to regulate their attention and responses.
Steyaert J, Borghgraef M, Fryns JP: APPARENTLY ENHANCED VISUAL INFORMATION PROCESSING IN FEMALE FRAGILE X CARRIERS: PRELIMINARY FINDINGS. American Journal of Medical Genetics 1994; 51(4):374-7. Summary: Eighteen normally intelligent adult female fragile X carriers were tested with the "de Sonneville Visual Attention Tasks," a computer-based set of reaction-time experiments, in order to assess different aspects of their attention capacity. The subject group was compared with a group of 48 adults, who were not known to be fragile X carriers. We publish preliminary results of this study. These show that the fragile X carriers have significantly faster reaction times at a substantial number of the tests. This suggests that normally intelligent female fragile X carriers might process simple visual information, such as the targets offered in these reaction time experiments, at a faster rate than control women.
Biederman J, Milberger S, Faraone SV, Guite J, Warburton R: ASSOCIATIONS BETWEEN CHILDHOOD ASTHMA AND ADHD: ISSUES OF PSYCHIATRIC COMORBIDITY AND FAMILIALITY. Journal of the American Academy of Child & Adolescent Psychiatry 1994; 33(6):842-8. Summary: OBJECTIVE: In this paper we evaluate the association between asthma and attention-deficit hyperactivity disorder (ADHD), addressing issues of comorbidity and familiality by formulating and testing competing hypotheses. METHOD: Subjects were 6- to 17-year-old boys with DSM-III-R ADHD (N = 140) and normal controls (N = 120) and their first-degree relatives. Information on asthma was obtained from the mothers in a standardized manner blind to the proband's clinical status. RESULTS: The risk for asthma did not meaningfully differ between ADHD and control children. Relatives of ADHD probands with and without asthma were at significantly greater risk for ADHD than relatives of normal controls. In contrast, the risk for asthma was significantly elevated only among relatives of children with ADHD plus asthma. CONCLUSIONS: These findings argue against a substantial etiological or pathophysiological relationship between the two conditions but suggest that ADHD and asthma are independently transmitted in families. Thus, the observation of ADHD symptoms in an asthmatic child should not be dismissed out of hand as being a consequence of asthma since many asthmatic ADHD children may actually have ADHD.
Ernst M, Liebenauer LL, King AC, Fitzgerald GA, Cohen RM, Zametkin AJ: REDUCED BRAIN METABOLISM IN HYPERACTIVE GIRLS. Journal of the American Academy of Child & Adolescent Psychiatry 1994; 33(6):858-68. Summary: OBJECTIVE: This study assesses the effect of attention-deficit hyperactivity disorder (ADHD) and gender on cerebral glucose metabolism (CMRglu), using positron emission tomography and 18F-fluorodeoxyglucose. METHOD: Nineteen normal (6 females; 14.3 +/- 1.3 years old) and 20 ADHD adolescents (5 females; 14.7 +/- 1.6 years old) participated in the study. An auditory continuous performance task was used during the 30-minute uptake of 18F-fluorodeoxyglucose. RESULTS: There were no statistically significant differences in global or regional CMRglu between ADHD (N = 20) and normal (N = 19) adolescents. However, the global CMRglu in ADHD girls (N = 5) was 15.0% lower than in normal girls (N = 6) (p = .04), while global CMRglu in ADHD boys was not different than in normal boys. Furthermore, global CMRglu in ADHD girls was 19.6% lower than in ADHD boys (p = .02) and was not different between normal girls and normal boys. Clinical rating scales did not differentiate ADHD girls from ADHD boys, nor normal girls from normal boys. CONCLUSIONS: The greater brain metabolism abnormalities in females than males strongly stress that more attention be given to the study of girls with ADHD.
Ross RG, Hommer D, Breiger D, Varley C, Radant A: EYE MOVEMENT TASK RELATED TO FRONTAL LOBE FUNCTIONING IN CHILDREN WITH ATTENTION DEFICIT DISORDER. Journal of the American Academy of Child & Adolescent Psychiatry 1994; 33(6):869-74. Summary: OBJECTIVE: Attention-deficit hyperactivity disorder (ADHD) has been postulated to be related to dysfunction of the prefrontal cortex. In the oculomotor delayed response task, a subject is cued as to where he or she should look (shift visual gaze to) but must delay a short period and then shift gaze to the location where the cue previously existed but no longer exists (a memory-guided saccade). Dependent measures from this task provide information on three functions tentatively tied to prefrontal cortex functioning: the ability to inhibit response (during the delay period), preparation of motor response (inversely tied to the latency of shifting visual gaze), and accuracy of working visuospatial memory (accuracy of the memory-guided saccade). METHOD: Thirteen children with ADHD and 10 normal controls, aged 9 to 12 years, were tested using an 800-msec delay period. RESULTS: Children with ADHD showed, relative to normal controls, deficits on inhibiting response during the delay period but no differences in latency (preparation of motor response) or accuracy of visuospatial memory. CONCLUSIONS: These results support the hypothesis that the primary deficit in ADHD is difficulty in inhibition of response. This deficit may be associated with pathology located outside the dorsolateral prefrontal cortex.
Semrud-Clikeman M, Filipek PA, Biederman J, Steingard R, Kennedy D, Renshaw P, Bekken K: ATTENTION-DEFICIT HYPERACTIVITY DISORDER: MAGNETIC RESONANCE IMAGING MORPHOMETRIC ANALYSIS OF THE CORPUS CALLOSUM. Journal of the American Academy of Child & Adolescent Psychiatry 1994; 33(6):875-81. Summary: OBJECTIVE: The following study seeks to document possible differences in corpus callosal area and shape between children with attention-deficit hyperactivity disorder (ADHD) and controls. METHODS: Fifteen carefully diagnosed right-handed male subjects with ADHD with overactivity symptomatology were compared to 15 right-handed male control subjects. The corpus callosum was divided into seven areas on the midsagittal slice of a magnetic resonance image with shape analysis also conducted. RESULTS: An exploratory shape analysis showed no significant differences in shape between the groups. No group differences were found in the area, length, or anterior regions of the corpus callosum. The ADHD subjects were found to have significantly smaller posterior corpus callosum regions than the control group, with the splenium accounting for most of the variance between the groups. CONCLUSIONS: The splenial area of the corpus callosum is smaller in children with ADHD than in a sample of normally developing children. These smaller areas may relate to commonly seen sustained attention deficits which in turn negatively impact on the development of more advanced levels of attention such as self-regulation. Further study of the regions surrounding the splenial area is suggested to determine whether they are correlated in size to the smaller corpus callosum.
Crawford SG, Kaplan BJ, Kinsbourne M: ARE FAMILIES OF CHILDREN WITH READING DIFFICULTIES AT RISK FOR IMMUNE DISORDERS AND NONRIGHTHANDEDNESS? Cortex 1994; 30(2):281-92. Summary: This study used questionnaire data to examine immune disorders and nonrighthandedness in the families of children enrolled in a learning disabilities school and children attending regular classrooms in public schools. Groups were organized according to their performance on a standardized test of reading comprehension to avoid overlap. In total, 468 questionnaires were returned, from which we were able to derive a final sample of carefully matched subjects: 55 subjects undergoing remediation for reading problems and 55 age- and sex-matched control subjects. The results indicated that children with reading problems and their families more frequently suffered from some immune and autoimmune disorders, particularly those involving the gastrointestinal tract and the thyroid gland. In addition, symptoms of attention deficit hyperactivity disorder were associated with Crohn's disease and migraine headache in the families. There was no evidence of an elevated prevalence of nonrighthandedness in the children with reading problems and their families.
Weiss RE, Stein MA, Duck SC, Chyna B, Phillips W, O'Brien T, Gutermuth L, Refetoff S: LOW INTELLIGENCE BUT NOT ATTENTION DEFICIT HYPERACTIVITY DISORDER IS ASSOCIATED WITH RESISTANCE TO THYROID HORMONE CAUSED BY MUTATION R316H IN THE THYROID HORMONE RECEPTOR BETA GENE. Journal of Clinical Endocrinology & Metabolism 1994; 78(6):1525-8. Summary: Resistance to thyroid hormone (RTH) is a syndrome of reduced responsiveness of tissues to thyroid hormone. The clinical manifestations are variable and 46-50% of children with RTH have attention deficit hyperactivity disorder (ADD). We present a new family with RTH (F120) found to have a mutation R316H in the thyroid hormone receptor beta (TR beta) gene identical for that reported in an unrelated family. Assignment of the mutant allele and haplotyping based on CA repeat polymorphism were done on 16 family members. Semistructured diagnostic interviews and psychometric testing were used to determine the psychiatric diagnosis of 12 family members by examiners blinded to the genotype. Three subjects were identified to have the R316H allele as well as mildly elevated free T4 index (168 +/- 12; normal range 77-135) and nonsuppressed TSH (4.1 +/- 1.7 mU/L). Only 2 of the subjects with RTH were found to have ADD, while one family member homozygous for the wild type TR beta and normal thyroid function tests also had ADD. Unaffected family members had higher full scale intelligence quotients (IQ) (93 +/- 7) than any of the 3 family members with RTH (77 +/- 5, p = 0.006). These data do not support the genetic linkage of ADD and RTH, but do suggest that RTH is associated with lower IQ scores that may confer a high likelihood of exhibiting ADD symptoms.
Comings DE: GENETIC FACTORS IN SUBSTANCE ABUSE BASED ON STUDIES OF TOURETTE SYNDROME AND ADHD PROBANDS AND RELATIVES. I. DRUG ABUSE. Drug & Alcohol Dependence 1994; 35(1):1-16. Summary: There have been relatively few studies of genetic factors in drug abuse. Childhood Attention Deficit Hyperactivity Disorder (ADHD) has been implicated as a risk factor, and pedigree studies of Tourette Syndrome (TS), a hereditary impulse disorder closely related to ADHD, show an increased prevalence of substance abuse in relatives. These observations suggest the genes for TS and ADHD may play an important role in the development of drug abuse. To examine this hypothesis 217 TS probands and 328 of their relatives, 58 ADHD probands and 35 of their relatives, and 50 controls were prospectively studied using a structured questionnaire based on the Diagnostic Interview Schedule. All subjects were Caucasians 16 to 49 years of age. The responses concerning the use of 8 different drugs and 8 different symptoms of drug abuse were compared. The results showed a highly significant increase in positive responses with increased loading for the TS and ADHD genes for 6 of the 8 drugs and all of the drug abuse symptoms. The percentage of positive responses in TS probands was markedly influenced by the presence of comorbid ADHD, as well as discipline, obsessive-compulsive, or alcohol problems. These results suggest that the genes responsible for TS and ADHD play an important role in drug abuse/dependence. The dopamine D2 receptor gene (DRD2) appears to be one of these genes since variants at this locus are significantly increased in frequency in TS, ADHD, conduct disorder and drug abuse.
Comings DE: GENETIC FACTORS IN SUBSTANCE ABUSE BASED ON STUDIES OF TOURETTE SYNDROME AND ADHD PROBANDS AND RELATIVES. II. ALCOHOL ABUSE. Drug & Alcohol Dependence 1994; 35(1):17-24. Summary: Prior studies have suggested childhood attention deficit hyperactivity disorder (ADHD) as a risk factor for alcohol abuse in adults. Gilles de la Tourette Syndrome, a hereditary tic and impulse disorder, is clinically and genetically similar to ADHD. To examine the hypothesis that individuals carrying the Gts gene are at increased risk to develop alcohol use problems, the same TS (Tourette Syndrome) and ADHD probands, relatives and controls used in the prior study of drug abuse were also studied using a structured questionnaire based on the Diagnostic Interview Schedule and the MAST test. The frequency of a positive response to any of 16 different questions concerning alcohol abuse showed a highly significant increase with increased genetic loading for Gts and ADHD genes. The percentage of more than one positive response in TS probands was markedly influenced by the presence of comorbid ADHD, discipline, obsessive-compulsive or drug abuse problems. Comorbid drug abuse problems were the best predictor of alcohol abuse problems. These results suggest that the genes responsible for TS and ADHD play an important role in alcohol abuse/dependence as well as drug abuse/dependence. One of the elements common to all of these disorders may be mutant genes affecting serotonin metabolism.
Faraone SV, Biederman J, Milberger S: AN EXPLORATORY STUDY OF ADHD AMONG SECOND-DEGREE RELATIVES OF ADHD CHILDREN. Biological Psychiatry 1994; 35(6):398-402. Summary: Family-genetic studies consistently show that attention deficit hyperactivity disorder (ADHD) aggregates in nuclear families. Little is known about the aggregation of ADHD in second-degree relatives. We examined the prevalence of ADHD in second-degree relatives of 140 ADHD probands and 120 normal controls. Information pertinent to the diagnosis of ADHD in second-degree relatives was collected from the probands' parents. The second-degree relatives of ADHD probands were at increased risk for ADHD compared with the second-degree relatives of normal control probands. These risks were greatest when the second-degree relative was biologically related to an ADHD parent of an ADHD proband. Consistent with the greater prevalence of ADHD among boys compared with girls, grandfathers were at greater risk than grandmothers and uncles were at greater risk than aunts. Our results support the usefulness of ascertaining information from second-degree relatives in studies evaluating the genetic epidemiology of ADHD. If confirmed, such studies may help clarify the mechanism of familial transmission of ADHD.
Biederman J, Lapey KA, Milberger S, Faraone SV, Reed ED, Seidman LJ: MOTOR PREFERENCE, MAJOR DEPRESSION AND PSYCHOSOCIAL DYSFUNCTION AMONG CHILDREN WITH ATTENTION DEFICIT HYPERACTIVITY DISORDER. Journal of Psychiatric Research 1994; 28(2):171-84. Summary: Since left motor preference has been hypothesized to lead to increased risk for psychopathology and cognitive deficits, it is possible that it may confer greater vulnerability for these problems to attention deficit hyperactivity disorder (ADHD) children. Subjects were 6-17 year-old boys with DSM-III-R ADHD (N = 140) and normal controls (N = 120) and their first-degree relatives. Information on motor preference was obtained in a standardized manner blind to the proband's clinical status. Although no excess of non-right motor preference was identified in ADHD probands compared with normal controls, the non-right motor preference observed in ADHD probands was partly familial and was associated with significantly increased risk for major depressive disorder and impaired psychosocial functioning. Non-right motor preference in ADHD probands significantly increases the risk for major depression and impaired psychosocial functioning. These findings raise the possibility of alterations in cerebral dominance which may be implicated in the expression of specific problems in some patients with ADHD. Further research is needed to replicate these findings and to directly assess cerebral functioning in ADHD.
Boris M, Mandel FS: FOODS AND ADDITIVES ARE COMMON CAUSES OF THE ATTENTION DEFICIT HYPERACTIVE DISORDER IN CHILDREN. [REVIEW]. Annals of Allergy 1994; 72(5):462-8. Summary: The attention deficit hyperactive disorder (ADHD) is a neurophysiologic problem that is detrimental to children and their parents. Despite previous studies on the role of foods, preservatives and artificial colorings in ADHD this issue remains controversial. This investigation evaluated 26 children who meet the criteria for ADHD. Treatment with a multiple item elimination diet showed 19 children (73%) responded favorably, P < .001. On open challenge, all 19 children reacted to many foods, dyes, and/or preservatives. A double-blind placebo controlled food challenge (DBPCFC) was completed in 16 children. There was a significant improvement on placebo days compared with challenge days (P = .003). Atopic children with ADHD had a significantly higher response rate than the nonatopic group. This study demonstrates a beneficial effect of eliminating reactive foods and artificial colors in children with ADHD. Dietary factors may play a significant role in the etiology of the majority of children with ADHD. [References: 33]
Diaz-Granados JL, Greene PL, Amsel A: SELECTIVE ACTIVITY ENHANCEMENT AND PERSISTENCE IN WEANLING RATS AFTER HIPPOCAMPAL X-IRRADIATION IN INFANCY: POSSIBLE RELEVANCE FOR ADHD. Behavioral & Neural Biology 1994; 61(3):251-9. Summary: We examined the effects of focal X-irradiation of the hippocampus in infancy on the partial reinforcement extinction effect (PREE) in weanling rats in a runway and on running wheel activity at 40 days of age. Our results show a dose-dependent X-irradiation-related reduction in granule cell neurogenesis. Weanling rats showed a corresponding increase in running speed in both acquisition and extinction and a dose-dependent reduction in the PREE--an increase in persistence after CRF and a decrease in persistence after PRF training. The same degree of hippocampal granule cell agenesis had no effect on running wheel activity. These results suggest that the enhanced speeds in the runway are incentive-related and do not reflect simple hyperactivity but rather hyperreactivity. The discussion of these results is in part a speculation regarding their possible relation to some explanations of attention deficit-hyperactivity disorder in children.
Hechtman L: GENETIC AND NEUROBIOLOGICAL ASPECTS OF ATTENTION DEFICIT HYPERACTIVE DISORDER: A REVIEW. [REVIEW]. Journal of Psychiatry & Neuroscience 1994; 19(3):193-201. Summary: This paper reviews key studies that have addressed genetic and neurobiological aspects in attention deficit hyperactive disorder. Genetic studies can be divided into three distinct types: twin, adoption, and family studies. Evidence for a particular mode of inheritance and the possible specific genetic abnormalities are also explored. There is strong evidence of genetic involvement in this condition, although a clear-cut mode of inheritance and specific genetic abnormalities are yet to be determined. Neurobiological aspects such as the neuroanatomical and neurochemical evidence of various neurotransmitter system involvement is explored. Frontal lobe and dopamine and norepinephrine neurotransmitter systems appear to be involved in attention deficit hyperactive disorder. [References: 65]
Kanarek RB: DOES SUCROSE OR ASPARTAME CAUSE HYPERACTIVITY IN CHILDREN? [REVIEW]. Nutrition Reviews 1994; 52(5):173-5. Summary: Anecdotal evidence has led to the hypothesis that there is a relationship between sugar intake and hyperactive behavior. To assess this hypothesis, a recent study using a range of behavioral and cognitive measures evaluated the effects of diets high in sucrose, aspartame, and saccharin on the performance of school-aged children believed to be sensitive to sugar, and preschool children. Although intakes exceeded average dietary levels, neither sucrose nor aspartame negatively affected behavior. Taken together with previous work, these results indicate that sugar is not a major cause of hyperactivity. [References: 19]
Aust PH: WHEN THE PROBLEM IS NOT THE PROBLEM: UNDERSTANDING ATTENTION DEFICIT DISORDER WITH AND WITHOUT HYPERACTIVITY. Child Welfare 1994; 73(3):215-27. Summary: Attention Deficit Disorder with, and Attention Deficit Disorder without, Hyperactivity, are common neurobiological conditions that cause or exacerbate many learning, social, and emotional problems. Understanding the significant interactions of biological, cognitive, and psychological factors in AD(H)D and informing clients of all treatment options, including pharmacological intervention, are essential to treatment. Counseling alone, without providing multimodal treatments that acknowledge the core medical problem, has limited positive effect.
Frank Y, Seiden JA, Napolitano B: EVENT-RELATED POTENTIALS TO AN "ODDBALL" AUDITORY PARADIGM IN CHILDREN WITH LEARNING DISABILITIES WITH OR WITHOUT ATTENTION DEFICIT HYPERACTIVITY DISORDER. Clinical Electroencephalography 1994; 25(4):136-41. Summary: Event Related Potentials (ERP) were recorded during a two-tone discrimination task in 18 children with Learning Disabilities (LD) and 36 children with Learning Disabilities and Attention Deficit Hyperactivity Disorder (LD-ADHD). Twenty-seven normal children served as a control group. P3 wave amplitude was significantly smaller in the LD and LD-ADHD groups compared with normal children. There was no difference between the LD and LD-ADHD groups. It is suggested that the smaller P3 amplitude in children with LD-ADHD syndromes reflects cognitive and processing difficulties, which frequently coexist with ADHD in these children and is not specifically related to an attention deficit.
Grizenko N, Pawliuk N: RISK AND PROTECTIVE FACTORS FOR DISRUPTIVE BEHAVIOR DISORDERS IN CHILDREN. American Journal of Orthopsychiatry 1994; 64(4):534-44. Summary: Biological, psychological, and social risk and protective factors in the development of disruptive behavior disorders were assessed in 50 disordered and 50 control preadolescents. Significant risk factors included learning difficulties, hyperactivity, perinatal complications, and violence in the home. Significant protective factors included ability to express feelings and a good relationship with grandparents.
Scerbo AS, Kolko DJ: SALIVARY TESTOSTERONE AND CORTISOL IN DISRUPTIVE CHILDREN: RELATIONSHIP TO AGGRESSIVE, HYPERACTIVE, AND INTERNALIZING BEHAVIORS. Journal of the American Academy of Child & Adolescent Psychiatry 1994; 33(8):1174-84. Summary: OBJECTIVE: To test predictions that basal salivary testosterone and cortisol are related to antisocial and internalizing behaviors, respectively, and that cortisol moderates the testosterone-aggression relationship. METHOD: Saliva samples were assayed to determine testosterone and cortisol levels in 40 clinic-referred disruptive children (aged 7 through 14 years) who were rated on aggression, inattention/overactivity, and internalizing behavior by parents, teachers, and clinic staff members. RESULTS: Results indicated significant positive relationships between testosterone and staff-rated aggression and between cortisol and parent-rated internalizing behavior. A significant negative relationship was found between cortisol and staff-rated inattention/overactivity. No interactions between testosterone and cortisol were found. These results were maintained regardless of age, racial background, height, weight, diagnosis, or medication status. CONCLUSIONS: Results suggest moderate relationships between testosterone and observed aggression, and between cortisol and emotional behaviors, in a group of disruptive children. Cortisol did not moderate the testosterone-aggression relationship in this population.
Lombroso PJ, Pauls DL, Leckman JF: GENETIC MECHANISMS IN CHILDHOOD PSYCHIATRIC DISORDERS. [REVIEW]. Journal of the American Academy of Child & Adolescent Psychiatry 1994; 33(7):921-38. Summary: OBJECTIVE: This review summarizes research findings on the genetics of several childhood psychiatric disorders. METHOD: One hundred fifty papers were reviewed from the past several decades and were selected because they have suggested that genetic factors may play a role in the etiology of certain childhood disorders. This review is not meant to be exhaustive but rather has emphasized those disorders for which a genetic etiology has been proposed by different research groups. RESULTS: The more classical approaches to genetic research are reviewed and critiqued. The status of research for a number of childhood disorders is summarized. The molecular basis for several developmental disorders is presented and the prospects for arriving at a similar molecular understanding for other childhood psychiatric illnesses are discussed. CONCLUSIONS: Genetic factors play a determining role for certain developmental disorders. However, the molecular basis for other psychiatric disorders has yet to be elucidated and there are complicating factors that bear on genetic research of complex behavioral disorders. [References: 119]
Comings DE: ROLE OF GENETIC FACTORS IN HUMAN SEXUAL BEHAVIOR BASED ON STUDIES OF TOURETTE SYNDROME AND ADHD PROBANDS AND THEIR RELATIVES. American Journal of Medical Genetics 1994; 54(3):227-41. Summary: Most significant variations in the expression of human sexuality are considered to be the result of learned behavior or psychological problems. Tourette syndrome (TS) is a common, hereditary tic and disinhibition disorder sometimes associated with compulsive use of obscene words (coprolalia) and previously reported to be occasionally associated with exhibitionism. To further explore the relationship between the Gts genes and sexual behavior, questions concerning a wide range of such behaviors were administered to 1,040 subjects, 14 years of age or older, consisting of 358 TS probands, 101 non-proband relatives with TS, 359 non-TS first degree relatives, 79 attention deficit hyperactivity disorder (ADHD) probands, 70 unaffected relatives of the ADHD probands, and 73 controls. The behaviors included magnitude of sex drive, sex orientation, exhibitionism, transvestitism, transsexualism, sadism, masochism, pedophilia, fetishism, aversion to being touched, and aversion to sex. While most of these behaviors occurred in a distinct minority of TS subjects, there was a significant positive correlation between each behavior examined and the degree of genetic loading for the Gts gene(s). The nature of these behaviors and their association with TS suggests many are variants of obsessive-compulsive disorder. Studies in animals indicate that changes in serotonin and dopamine play a significant role in the sexual behavior and many lines of evidence are consistent with the hypothesis that TS is due to genetic changes in serotonin and dopamine metabolism. These studies suggest that genetic factors play a much greater role in a wide range of forms of sexual expression than previously thought.
Robaey P, Cansino S, Dugas M, Renault B: A COMPARATIVE STUDY OF ERP CORRELATES OF PSYCHOMETRIC AND PIAGETIAN INTELLIGENCE MEASURES IN NORMAL AND HYPERACTIVE CHILDREN. Electroencephalography & Clinical Neurophysiology 1995; 96(1):56-75. Summary: Verbal and performance scores of the Wechsler Intelligence Scale for Children-Revised (WISC-R 1981) and of a Piagetian battery, the Cognitive Development Scale for Children (EDC 1984), were obtained on 30 normal control and 19 hyperactive 6-8-year-old children. Amplitudes and latencies of a fronto-central P250 and of the parieto-occipital N250, P350 and P500 were measured concurrently in 4 categorization tasks derived from tests of the WISC-R and EDC batteries. Spearman correlations were computed between the intelligence and the ERP factor scores. Results showed that age-related and age-corrected Wechsler's scores were correlated with similar ERP changes (reduced amplitude, decreased latency). With regard to the amplitude changes, each type of intelligence was associated with a specific ERP pattern. The verbal scores were correlated with the P350 and the P500 amplitudes, and the performance scores with the frontal P250 and occipital N250 amplitudes. By contrast, Piagetian development and intelligence scores yielded ERP correlates in the opposite direction: P500 amplitude was negatively correlated with raw EDC scores, but positively with scaled EDC scores. In addition, Piagetian intelligence was not related to the general peak latency decrease with age. In hyperactive children, additional negative correlations were found between P250 amplitude and the subjects' verbal test scores. Correlations with some performance tests that were negative in normal controls, were positive in hyperactive children. In addition, latency-based correlations found in normal controls were lacking in hyperactive children. These findings provide strong evidence that intelligence comprises different components related to different subsets of cognitive processes, as indexed by different ERP waves. They also suggest that the development and intelligence do not always rely on the same changes, and that intelligence forms may not be referred to the same use of the same processes in hyperactive and normal children.
Biederman J, Faraone SV, Mick E, Spencer T, Wilens T, Kiely K, Guite J, Ablon JS, Reed E, Warburton R: HIGH RISK FOR ATTENTION DEFICIT HYPERACTIVITY DISORDER AMONG CHILDREN OF PARENTS WITH CHILDHOOD ONSET OF THE DISORDER: A PILOT STUDY. American Journal of Psychiatry 1995; 152(3):431-5. Summary: OBJECTIVE: Although well-documented in clinical and epidemiological studies of attention deficit hyperactivity disorder (ADHD) in children, the familial nature of the adult syndrome has not been well investigated. One approach to evaluate the familial nature of adult ADHD is through a high-risk design aimed at estimating the risk for the disorder in children of parents with child-hood-onset ADHD. METHOD: Children at risk for ADHD were ascertained from the study group of 84 referred adults with clinical diagnoses of childhood onset of the disorder, confirmed by structured interviews. Diagnostic information on the disorder was derived from the ADHD module of the Schedule for Affective Disorders and Schizophrenia for School Age Children--Epidemiologic Version, supplemented with information regarding treatment for ADHD for the affected child and school history including repeated grades, placement in special classes, and tutoring. RESULTS: Of the 84 children at risk, 48 (57%) met criteria for ADHD. The rate of the disorder in children of adults with the disorder was significantly higher than the previously reported rate of ADHD among siblings of children with the disorder. Of the 48 ADHD children of parents with the disorder, 36 (75%) were treated for it. The rates of school failure were almost identical to those previously reported in a group of referred children and adolescents with ADHD. CONCLUSIONS: These results support the validity of the adult diagnosis of ADHD and suggest that the adult form of this disorder may have stronger familial etiological risk factors than its pediatric form. If these results are confirmed, families selected through adult probands with ADHD might be especially useful for testing genetic hypotheses about the disorder.
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