Can a Baby Be Affected With Add When Born
J Psychiatry Neurosci. 2005 Mar; xxx(ii): 120–126.
Linguistic communication: English |
Perinatal complications in children with attention-arrears hyperactivity disorder and their unaffected siblings
Abstract
Objectives
Genetic and nonshared environmental factors (experienced by 1 family member to the exclusion of the others) have been strongly implicated in the causes of attention-deficit hyperactivity disorder (ADHD). Pregnancy, labour/delivery and neonatal complications (PLDNC) have often been associated with ADHD; however, no investigations aimed at delineating the shared or nonshared nature of these factors have been reported. We aimed to identify those elements of the PLDNC that are more likely to be of a nonshared nature.
Methods
We used an intrafamily study pattern, comparing the history of PLDNC between children diagnosed with ADHD, according to the criteria of the Diagnostic and Statistical Transmission of Mental Disorders, fourth edition (DSM-Four), and their unaffected siblings. Children with ADHD were recruited from the outpatient, day-handling program of the Child Psychiatry Department, Douglas Hospital, Montréal. The unaffected sibling closest in age to the child with ADHD was used as a control. The history of PLDNC was assessed using the Kinney Medical and Gynecological Questionnaire and the McNeil–Sjöstrom Scale for both children with ADHD and their siblings. Seventy children with ADHD forth with 50 of their unaffected siblings agreed to participate in the study. Child Behavior Checklist (CBCL), Continuous Functioning Examination (CPT) and Restricted Academic Situation Scale (RASS) scores were also used as measures of ADHD symptoms in children with ADHD.
Results
The children with ADHD had significantly higher rates of neonatal complications compared with their unaffected siblings (F 4,196 = 3.67, p < 0.006). Furthermore, neonatal complications in the children with ADHD were associated with worse CBCL total and externalizing scores and with poorer operation on the CPT.
Conclusions
These results propose that neonatal complications are probably a nonshared environmental gamble factor that may be pathogenic in children with ADHD.
Medical subject headings: attention arrears disorder with hyperactivity, child, perinatal intendance, pregnancy complications, siblings
Abstruse
Objectifs
On a incriminé fortement des facteurs génétiques et des facteurs environnementaux non partagés (vécus par united nations membre de la famille seulement) dans les causes du trouble d'hyperactivité avec déficit de l'attention (THADA). On a souvent établi united nations lien entre la grossesse, le travail et l'accouchement et les complications néonatales (GTACN) et le THADA, mais on northward'a fait rapport d'aucune étude visant à définir la nature partagée ou non partagée de ces facteurs. Nous voulions déterminer les éléments des facteurs GTACN les plus susceptibles ne pas être partagés.
Méthodes
Nous avons procédé à une étude intrafamiliale et comparé les antécédents de GTACN entre enfants chez lesquels on a diagnostiqué un THADA, en fonction des critères de la quatrième édition du Diagnostic and Statistical Transmission of Mental Disorders (DSM-IV), et des frères et sœurs non touchés. On a recruté des enfants atteints du THADA à partir du program de traitement de jour en service externe de la Partitioning de pédopsychiatrie de l'Hôpital Douglas à Montréal. On a utilisé comme témoin le frère ou la sœur non touché qui avait l'âge le plus proche de celui de l'enfant atteint du THADA. On a évalué les antécédents des facteurs GTACN au moyen du questionnaire médical et gynécologique de Kinney et de l'échelle McNeil-Sjöstrom à la fois chez les enfants atteints du THADA et chez leur frère ou sœur. Soixante-dix enfants atteints du THADA et fifty de leurs frères ou sœurs non atteints ont consenti à participer à fifty'étude. Pour mesurer les symptômes de THADA chez les enfants atteints, on a utilisé aussi les résultats de la liste de vérification des comportements des enfants (Kid Behavior Checklist), du exam de rendement continu (Continuous Functioning Test) et de l'échelle des situations scolaires restreintes (Restricted Academic State of affairs Scale).
Résultats
Les enfants atteints du THADA avaient eu beaucoup plus de complications néonatales que leurs sœurs ou frères not atteints (F 4,196 = 3,67, p < 0,006). On a de plus établi united nations lien entre les complications néonatales chez les enfants atteints du THADA et de plus mauvais résultats totaux et externalisants à la liste de vérification ainsi que des résultats plus faibles au test de rendement.
Conclusions
Ces résultats indiquent que les complications néonatales constituent probablement un facteur de risque environnemental non partagé qui peut être pathogène chez les enfants atteints du THADA.
Introduction
Attention-arrears hyperactivity disorder (ADHD) assembly inattention, hyperactivity and impulsivity and has a prevalence of 5%–10%.1 Although the cause of ADHD is not known, it has been well established that ADHD has a large genetic component equally shown by family,ii , 3 , 4 twin5 , 6 and adoptionseven studies. In particular, twin studies take shown that ADHD heritability is high, ranging from 75% to 90%. In add-on, these studies indicate that the rest of the variance in the ADHD phenotype (10%–25%) is accounted for generally by nonshared environmental factors (experienced by i member of the family to the exclusion of his or her siblings). In contrast, the interest of shared ecology factors (shared by all the individuals in the aforementioned family) in increasing the risk for ADHD is estimated to exist minimal.8
Instance–command epidemiologic studies indicate that pregnancy, labour/commitment and neonatal complications (PLDNC) are more frequent environmental factors in children diagnosed with ADHD compared with healthy controls.9 , 10 , eleven , 12 It is believed that such early on trauma on the brain during crucial periods of development may take long-lasting effects on knowledge and behaviour,13 although the relevant mechanisms mediating the furnishings of these events remain undetermined. To our knowledge, all studies of PLDNC in ADHD have used case–control designs, comparison children with ADHD with healthy, unrelated controls regarding their history of PLDNC. In addition to the archetype limitations of case–control take chances studies,14 such experimental designs cannot address the between-relatives differences in exposure to environmental factors. Furthermore, the causal nature of the clan betwixt these putative ecology factors and ADHD needs to be clarified, considering the same heritable characteristics may increment the take chances for these factors (such as smoking and alcohol consumption past mothers) and for ADHD.15 , 16
Smoking during pregnancy is i of the near studied and consistently identified perinatal factors in ADHD.17 Milberger et al18 compared boys with ADHD with unrelated controls regarding maternal history of smoking during pregnancy. They plant that children with ADHD were more than likely to take a maternal history of smoking during pregnancy than controls. In a later report, Milberger et al19 reported, in a sample of siblings of children with ADHD and siblings of healthy controls, that the unaffected siblings of children with ADHD had a statistically significantly more than frequent history of maternal smoking during pregnancy compared with the siblings of healthy controls. The fact that unaffected siblings of probands also have a statistically significantly more frequent history of maternal smoking compared with siblings of healthy controls suggests that the association between smoking during pregnancy and ADHD is not limited to children afflicted with ADHD only extends to their unaffected siblings. This may be at least partially compatible with the hypothesis that mothers of children with ADHD are more prone to smoke during all their pregnancies. This maternal lifestyle may exist the result of a mutual familial predisposition to smoking and to ADHD. Consistent with this shared intrafamilial risk hypothesis, children with ADHD and their unaffected siblings were establish to be at higher risk for early onset of smoking.20 , 21
Maternal alcohol consumption has been proposed equally a hazard factor in ADHD.xi Indeed, ADHD is often diagnosed in children with fetal alcohol syndrome and in the children of alcoholics. Chocolate-brown et al22 and Aronson et al23 reported that children born to mothers who had abused alcohol throughout pregnancy had more behavioural and attention problems than children built-in to mothers with no alcohol consumption during pregnancy. There was a correlation between the occurrence and the severity of psychiatric disorders, including attending deficit, and the degree of booze exposure of the children in utero.24 Notwithstanding, these dose-dependent furnishings on neurobehavioural part were not limited to attention but also extended to other disorders such as learning problems. In add-on, Hill et al25 found that family history of alcoholism, only non alcohol consumption during pregnancy, is associated with ADHD, suggesting that alcoholism and ADHD may share some of their genetic determinants.
In decision, the relation between environmental factors (i.eastward., maternal smoking and alcohol consumption) and ADHD is complex and points to the difficulty of determining the nature of the environmental risk factors in ADHD and their relation with genetic factors. In the two examples cited, the correlation betwixt these risk factors and ADHD may be secondary, at least in function, to a common underlying gene, such as shared genes that increase the take chances for these behaviours and ADHD. A study with an intrafamilial design, comparing children with ADHD with their unaffected siblings, would have the advantage of controlling for 50% of the genetic variability. In addition, this design will control for many confounding factors, because all siblings share their socioeconomic status, family surroundings and history. The within-family design tin as well help differentiate the critical shared and nonshared nature of these ecology factors.
In this study, nosotros aimed to place those elements amongst PLDNC that are potentially nonshared ecology factors by using an intrafamilial case–command design. More specifically, we hypothesized that some of the PLDNC, which are often reported to be associated with ADHD, may correspond shared environmental factors, whereas some other PLDNC may stand for nonshared (specific to the afflicted child) ecology factors with dissimilar potential roles in increasing the risk for ADHD within families. To distinguish betwixt shared and nonshared PLDNC factors, nosotros first compared children with ADHD with their unaffected siblings with regard to PLDNC. Second, PLDNC that are significantly more than mutual in children with ADHD than in siblings were studied with regard to the severity of ADHD symptoms, on the basis of the assumption that these factors may be correlated with the expression of ADHD.
Methods
This study was part of a larger placebo-controlled clinical trial of methylphenidate in children with ADHD. Clinical data from baseline assessments (before administration of placebo or methylphenidate) were used in this study. Among the 70 children with ADHD, aged 6–12 years, recruited in this study from the Douglas Hospital Child Psychiatry Division, Montréal, 50 had unaffected siblings and 20 children had no unaffected siblings or no siblings at all. 5 children agreed to participate in the PLDNC study but not in the methylphenidate clinical trial. The Douglas Hospital Ethics Commission approved the enquiry protocol, and parents gave written informed consent later an caption of the study purposes and procedures was given. The nature of the study was also explained to the children, who gave their assent to their participation.
2 experienced child psychiatrists made a best-estimate diagnosis of ADHD based on a clinical evaluation according to the criteria of the Diagnostic and Statistical Manual of Mental Disorders, quaternary edition (DSM-Iv),26 and on reports from teachers and parents. Parents also completed a structured interview, the Diagnostic Interview Schedule for Children Version IV (DISC-IV).27 Children with an IQ lower than 70 (Wechsler Intelligence Scale for Children III [WISC-3])28 or psychosis were excluded.
Mothers were interviewed, using DISC-IV, with respect to the history of ADHD in all their children. Siblings who did non come across ADHD criteria were identified, and the child closest in age to and of the same sexual activity as the affected child was included in the study. In addition to the structured interviews, all children were assessed with the Child Beliefs Checklist (CBCL).29
The Kinney Medical and Gynecological Questionnaire was used in interviews with the mothers with regard to prenatal, perinatal or postnatal complications that had occurred during all their pregnancies, labours and deliveries and during the neonatal history of all their children.30 This questionnaire was complemented with data from infirmary files in 60% of cases. The McNeil–Sjöstrom calibration for obstetric complications was used for scoring. The scoring takes into business relationship the severity of complications during the offset, second and 3rd trimesters of pregnancy, labour, delivery and the neonatal period (start eight weeks). It includes vi severity levels, reflecting the ordinal degree of potential harm to the cardinal nervous system.31 For all the children, scoring was done by the same clinician who was blinded to the subjects' status (ADHD or unaffected sibling). A enquiry banana blinded to the interview and scoring data selected the siblings to be included as controls.
As part of the clinical trial, performance on the Continuous Operation Exam Overall Index (CPT-OI)32 and the Restricted Bookish Situation Calibration (RASS)33 was assessed. The CPT is a 15-minute computerized examination that measures sustained attention ability, and the RASS is a 15-minute test that provides information about motor activity during academic piece of work.
Statistical analysis
For demographic and clinical characteristics, the 2 groups were compared using a t test. Considering of the tight matching betwixt cases (children with ADHD) and controls (unaffected siblings), we used a repeated-measures analysis of variance (ANOVA) with a inside-subject repeated measure out (scores of the field of study and of his or her sibling) and a repeat over time for the developmental periods (3 trimesters of pregnancy, labour/delivery and neonatal period). Fisher exact tests were performed to compare the frequency of PLDNC in children with ADHD and their siblings. The effects of PLDNC that differed significantly betwixt subjects and siblings were assessed within the group of children with ADHD. Among the affected children, nosotros compared the ADHD characteristics for those with and those without PLDNC. Statistical significance was ready at p < 0.05.
Results
Children with ADHD who had unaffected siblings (n = 50 pairs) were significantly younger than their unaffected siblings (mean age viii.viii [standard deviation {SD} one.vii] yr v. 10.1 [SD three.7] yr, respectively, p = 0.031) (Table 1). Birth rank was higher in the ADHD group compared with the sibling group (median 2 v. 1 respectively, p = 0.001). As expected, boys were overrepresented in our study group. For children with ADHD and siblings, mean DISC-Four total scores were respectively 13.8 [SD 3.iii] and ii.6 [SD iii.0] (the normal score beingness < half-dozen). Mean CBCL full scores were respectively 72.5 [SD 8.5] and 55.7 [SD 16.ii] (the normal score being < 65).
Table 1
Repeated-measures ANOVA revealed that the inside-pair difference in the full score for PLDNC tended to be statistically pregnant (F one,49 = 3.56, p = 0.06). Patients with ADHD showed a tendency to accept higher scores for PLDNC than their unaffected siblings. A pregnant result of the flow of development (starting time, 2nd and third trimesters of pregnancy, labour/delivery and neonatal period) was too observed (F iv,196 = 3.67, p < 0.006). The main finding of this study is that the 2 profiles of PLDNC over the developmental periods in children with ADHD and their unaffected siblings were not parallel, as indicated by a significant interaction between grouping and periods of development (F four,196 = 3.89, p < 0.004). Post hoc comparisons using Tukey's Honestly Significant Difference (HSD) showed that this deviation stemmed from a significantly greater number of neonatal complications in the children with ADHD compared with the unaffected siblings (p < 0.006) (Table 2).
Tabular array 2
Fisher exact tests were performed to compare the frequency of PLDNC in children with ADHD and their siblings. Children with ADHD had significantly more neonatal admissions to hospital and/or therapeutic interventions (36% v. 16%, p = 0.02). During gestation, children with ADHD had more of a history of early contractions that required medication (14% 5. 2%, p = 0.05).
It is noteworthy that the factors often reported to be associated with ADHD in case–control (unrelated) studies, such every bit maternal smoking and alcoholism, did non evidence significant differences betwixt patients and their unaffected siblings (58% v. 58%, and iv% v. 8%, respectively, for smoking and alcoholism). Unaffected siblings had a more frequent history of forceps delivery (4% v. 18%, p = 0.05).
Among the initial group of 70 patients, 65 subjects completed the clinical trial in which behavioural and therapeutic responses to methylphenidate were assessed using a ii-calendar week double-bullheaded crossover design (0.five mg/kg per d). Afflicted children with neonatal complications (n = 45) and those without neonatal complications (n = 20) did not differ with regard to age, sex ratio and family income. Within the group of children with ADHD, the subgroup of children with a history of neonatal complications showed significantly higher mean scores on the full CBCL (72.0 [SD 6.7] 5. 66.3 [SD 14.1], p = 0.031) and tended to have significantly college mean CBCL externalizing subscores, such as attention and impulsivity (72.7 [SD 7.5] v. 67.4 [SD 14.3], p = 0.05), but non on the CBCL internalizing subscore, such equally feet (64.7 [SD ten.0] 5. 62.2 [SD 14.0], p = 0.twoscore), compared with those without neonatal complications (normal scores < 65). In that location was no difference between children with and without PLDNC with regard to IQ (95.1 v. 97.one, p = 0.67) (Tabular array 3).
Table 3
We besides compared the average measurements on the CPT-OI and RASS (before medication) in patients with and without neonatal complications. Patients with neonatal complications showed a poorer performance on the CPT-OI (F ane,threescore = 10.59, p = 0.001), and no differences on motor activity were observed (F 1,62 = two.59, p = 0.12) (Tabular array 3).
Discussion
PLDNC have been the nigh studied of the environmental factors implicated in the pathogenesis of ADHD and have received some validity from animal studies.34 The literature indicates that many confounding factors (socioeconomic status, maternal IQ, family history) tin can limit the interpretation of case–command studies. An intrafamilial report comparing children with ADHD with their unaffected siblings may provide first-class-to-good matching between cases and controls for several ecology factors and, to a sure extent, for the genetic background. Genetic epidemiologic studies identify mainly nonshared environmental factors, whereas case–command studies identify factors that are more than likely to be common to all children in the same family, such as maternal smoking and alcohol consumption, both of which may share genetic determinants with ADHD. Thus, using intrafamilial case–command studies may assistance to analyze the complexity of the interaction betwixt genetic and environmental factors that may be implicated in this disorder.
The first main finding of this study is that the profile of PLDNC during developmental periods in children with ADHD and their unaffected siblings was not parallel. This is mainly because of an increased level of neonatal complications in the children with ADHD.
In contrast to pregnancy, labour and delivery, events experienced in the neonatal menstruation, when the kid is more contained of the mother, are conceivably more than likely to be specific to each individual, that is, a nonshared gene. This consequence may propose that neonatal complications may exist a risk gene with a putative causal link to the development of ADHD. This result is also consistent with the fact that genetic epidemiologic studies have identified mainly nonshared environmental factors in ADHD. Surprisingly, in the literature, low birth weight (LBW) (≤ 2500 1000) as a neonatal hazard cistron was nigh exclusively associated with ADHD.35 , 36 , 37 , 38 In these studies, ADHD was a frequent outcome for LBW children; however, LBW children also experienced greater developmental filibuster. This association may be the upshot of the effects of general developmental problems. Moreover, other studies12 , 39 , 40 have reported that LBW was associated but with lower IQ scores merely non with ADHD. The consequence of LBW on attention and motor behaviour remains controversial.13 Apart from LBW, no other aberrant neonatal conditions have been reported to exist associated with ADHD.
In the study group, medical conditions that were more frequent in ADHD included several events occurring during the first ii months of life: neonatal access to hospital, having been in an incubator, oxygen therapy, general anesthesia and surgery being the virtually frequent. Although these findings do not bespeak to a single event that may atomic number 82 to behavioural or cognitive problems, they practice support past research indicating that children with ADHD take a college prevalence of stressful events in early life.12 Moreover, these factors, consequent with previous enquiry, suggest that prolonged chronic rather than astute stresses are more likely to be associated with ADHD. It is interesting that some of these factors are clearly associated with hypoxia (e.g., oxygen therapy). This is consistent with findings from animal models indicating that neonatal hypoxia tin outcome in increased locomotor activity later in life.41 , 42 , 43 The relation of these neonatal events to pregnancy and labour/delivery needs to be analyzed in order to assess their specific part in increasing the adventure for ADHD.
Surprisingly, smoking and booze consumption during pregnancy, which are frequently reported as ecology run a risk factors for ADHD, did not differ between patients and their unaffected relatives. Smoking was equally common (58%) in pregnancies leading to affected and unaffected children. Remarkably, this rate is higher than the rate observed in the general population of Quebec (40%).44 This may indicate that smoking in our population is a trait associated non with ADHD but with an intrafamilial nature shared by all the family members. A recent review of the literature17 constitute that smoking during pregnancy is one of the almost ofttimes reported risk factors but with a small outcome. More recently, a big twin study found that maternal smoking during pregnancy explains a small but significant proportion (2%) of the variance in the ADHD phenotype.45 It is, therefore, possible that our written report has missed this effect because of the small sample or the fact that intrafamilial studies (including twin studies) tend to obscure the relationship for shared chance factors considering of the lack of variability in exposure to some risk factors. A much larger sample with more variability in maternal smoking from i pregnancy to the other is needed to investigate adequately the relationship betwixt genetic factors, smoking and ADHD.
The second master finding of this written report is that among the children diagnosed with ADHD, neonatal complication was associated with worse full and externalizing CBCL scores, including hyperactivity and inattention. Neonatal complications were as well associated with higher scores on the CPT just not with RASS scores. This interesting result suggests that neonatal complications may take a greater touch on attention deficit but non on motor hyperactivity.
The presence of an association between neonatal complications and the severity of the ADHD (with a worse CBCL score and lower CPT performance), combined with the putative nonshared nature of these complications, suggests that indeed these events may play a role in the pathogenesis of ADHD. Although the mechanism for a positive association betwixt neonatal complications and ADHD has non been established, this finding can exist interpreted as consistent with the early dopaminergic disruption hypothesis for this disorder.46 In fact, several studies have linked postnatal insults with amending in dopaminergic circuits such equally the prefrontal cortex and basal ganglia structures that are involved in the development of ADHD. In detail, neuroimaging studies take shown that, in children with ADHD, growth curves of brain structures are parallel to normal growth curves, which suggests that brain abnormalities in ADHD are more than probable to be fixed during early development rather than an ongoing process.47
Interestingly, the fact that neonatal complications were associated with worse CBCL scores and poorer CPT performance, but not RASS scores, may suggest that this constellation of personal history events and behavioural characteristics may delineate a specific subgroup within the ADHD syndrome. Kotimaa et al,10 in a recent prospective report, found that maternal smoking during pregnancy is associated merely with hyperactivity. This may suggest that other risk factors may be more closely associated with different behavioural dimensions of ADHD. Further investigation of the human relationship between neonatal complications and other relevant factors (due east.g., genetic and biologic indicators, therapeutic response) is needed to further this hypothesis.48
Several limitations should be kept in mind when interpreting the results of this written report. Outset, our conclusions are based on a sample of l children with ADHD and 50 of their unaffected siblings. This is of course a small sample for gamble studies. These results need to be confirmed in a larger grouping in order to ensure their validity. 2d, comorbidity is very high in ADHD; information technology would have been very informative to study PLDNC co-ordinate to comorbid disorders. However, the small-scale sample precluded this analysis. Another limitation of this study is that boys were overrepresented in the ADHD group. However, given that girls may be more resilient to developing the disorder, it is expected that some girls may have a high level of PLDNC and yet do not express the illness. This bias may therefore be conservative, that is, unlikely to outcome in false-positive findings. In this study, we also observed that unaffected siblings experienced more forceps interventions. Although this difference may be related to the fact that unaffected siblings were on average more likely to be get-go-born children compared with their afflicted siblings, its estimation is difficult because of the difference in sex between the 2 groups. A further limitation of this study is the departure in age and birth rank. Here over again, most of the affected children were younger and resulted from a 2nd pregnancy, which is usually considered to be at lower risk than a starting time pregnancy. Some other limitation of this pattern is its reliance on a maternal retrospective interview, which is the case for almost all studies of maternal lifestyle during pregnancy.17 In order to have information most the validity of the maternal written report, we compared the maternal reports with the data derived from the medical files for threescore% of the patients. Every bit reported in the literature,49 we found that mothers tended to underreport PLDNC. Finally, although using siblings equally controls reduces a large number of potential biases, it does not control for 50% of the genes that differ betwixt siblings, making this pattern more than robust than case–control studies just less so than twin studies, which are difficult to comport.
Determination
To our noesis, this is the starting time study to utilize an intrafamilial design to address the implication of PLDNC in ADHD. This design has the important advantage of controlling for many confounding factors, including, to a certain extent, the genetic background. Information technology might be a useful intermediate tool between unrelated case–control and twin run a risk studies. In addition, this type of design may assistance to delineate the nature of ecology run a risk factors and to empathize the role of the different factors in the expression of ADHD. The results of this study propose that neonatal complications are more frequent in children with ADHD compared with their unaffected relatives. The severity of these complications, their prolonged character, their association with clinical dimensions and their possible nonshared nature suggest that these factors may play a function in the crusade of ADHD and may help to delineate relevant subgroups in this disorder.
Acknowledgments
We would like to thank Julian Doan for his contribution.
Footnotes
Nosotros would like to thank the Fonds de la recherche en santé du Québec and the Roaster Foundation for grants to Drs. Joober and Grizenko, and we would similar to thank Pfizer Canada for a support grant to Dr. Ben Amor.
Competing interests: None alleged.
Correspondence to: Dr. Ridha Joober, Douglas Hospital Inquiry Heart, 6875 LaSalle Blvd., Montréal QC H4H 1R3; fax 514 888-4064; air conditioning.lligcm@rebooj.ahdir
Submitted Sept. xix, 2003; Revised Mar. 16, 2004; Accepted Mar. 29, 2004
References
1. Paule MG, Rowland As, Ferguson SA, Chelonis JJ, Tannock R, Swanson JM, et al. Attention arrears/hyperactivity disorder: characteristics, interventions and models. Neurotoxicol Teratol 2000; 22:631-51. [PubMed]
2. Faraone SV, Biederman J, Milberger S. An exploratory report of ADHD amidst second-degree relatives of ADHD children. Biol Psychiatry 1994;35:398-402. [PubMed]
iii. Hechtman L. Families of children with attention deficit hyperactivity disorder: a review. Tin J Psychiatry 1996;41:350-60. [PubMed]
4. Samuel VJ, George P, Thornell A, Curtis Southward, Taylor A, Brome D, et al. A pilot controlled family study of DSM-Iii-R and DSM-IV ADHD in African-American children. J Am Acad Kid Adolesc Psychiatry 1999;38:34-9. [PubMed]
5. Eaves LJ, Silberg JL, Meyer JM, Maes HH, Simonoff East, Pickles A, et al. Genetics and developmental psychopathology: 2. The main effects of genes and environment on behavioral bug in the Virginia Twin Study of Adolescent Behavioral Development. J Child Psychol Psychiatry 1997;38:965-fourscore. [PubMed]
6. Martin N, Scourfield J, McGuffin P. Observer effects and heritability of childhood attention-deficit hyperactivity disorder symptoms. Br J Psychiatry 1997;180:260-5. [PubMed]
7. Cadoret RJ, Stewart MA. An adoption study of attending deficit/hyperactivity/aggression and their relationship to adult antisocial personality. Compr Psychiatry 1991;32:73-82. [PubMed]
8. McGuffin P, Martin N. Science, medicine, and the time to come. Behaviour and genes. BMJ 1999;319:37-40. [PMC gratis article] [PubMed]
9. Astbury J, Orgill A, Bajuk B, Relationship betwixt two-yr behaviour and neuro-developmental issue at five years of very low-birthweight survivors. Dev Med Child Neurol 1987;29:370-9. [PubMed]
10. Kotimaa AJ, Moilanen I, Taanila A, Ebeling H, Smalley SL, McGough JJ, et al. Maternal smoking and hyperactivity in eight-year-old children. J Am Acad Child Adolesc Psychiatry 2003;42:826-33. [PubMed]
xi. Mick Eastward, Biederman J, Faraone SV, Sayer J, Kleinman Due south. Case- control study of attention-deficit hyperactivity disorder and maternal smoking, alcohol use, and drug use during pregnancy. J Am Acad Child Adolesc Psychiatry 2002;41:378-85. [PubMed]
12. Milberger Southward, Biederman J, Faraone SV, Guite J, Tsuang MT. Pregnancy, delivery and infancy complications and attention deficit hyperactivity disorder: issues of gene-environment interaction. Biol Psychiatry 1997;41:65-75. [PubMed]
13. McGrath MM, Sullivan MC, Lester BM, Oh Westward. Longitudinal neurologic follow-upwardly in neonatal intensive care unit survivors with various neonatal morbidities, Pediatrics 2000;106:1397-405. [PubMed]
14. Clayton D, McKeigue PM Epidemiological methods for studying genes and ecology factors in complex diseases. Lancet 2001;358:1356-sixty. [PubMed]
xv. Swanson JM, Flodman P, Kennedy J, Spence MA, Moyzis R, Schuck S, et al. Dopamine genes and ADHD. Neurosci Biobehav Rev 2000;24:21-v. [PubMed]
16. Faraone SV, Doyle AE, Mick East, Biederman J. Meta-analysis of the clan between the 7-repeat allele of the dopamine D (four) receptor gene and attention deficit hyperactivity disorder. Am J Psychiatry 2001;158:1052-vii. [PubMed]
17. Linnet KM, Dalsgaard S, Obel C, Wisborg K, Henriksen TB, Rodriguez A, et al. Maternal lifestyle factors in pregnancy risk of attention deficit hyperactivity disorder and associated behaviors: review of the current evidence. Am J Psychiatry 2003;160:1028-40. [PubMed]
eighteen. Milberger Due south, Biederman J, Faraone SV, Chen 50, Jones J. Is maternal smoking during pregnancy a take chances factor for attending deficit hyperactivity disorder in children? Am J Psychiatry 1996;153:1138-42. [PubMed]
19. Milberger Due south, Biederman J, Faraone SV, Jones J. Further testify of an clan between maternal smoking during pregnancy and attention deficit hyperactivity disorder: findings from a loftier-hazard sample of siblings. J Clin Kid Psychol 1998;27:352-8. [PubMed]
20. Milberger South, Biederman J, Faraone SV, Chen L, Jones J. ADHD is associated with early initiation of cigarette smoking in children and adolescents. J Am Acad Kid Adolesc Psychiatry 1997;36:37-44. [PubMed]
21. Milberger S, Biederman J, Faraone SV, Chen L, Jones J. Further evidence of an association between attention-deficit/hyperactivity disorder and cigarette smoking. Findings from a high-risk sample of siblings. Am J Addict 1997;6:205-17. [PubMed]
22. Brown RT, Coles CD, Smith IE, Platzman KA, Silverstein J, Erickson S, et al. Effects of prenatal alcohol exposure at school age. II. Attention and behavior. Neurotoxicol Teratol 1991;13:369-76. [PubMed]
23. Aronson M, Hagberg B, Gillberg C. Attending deficits and autistic spectrum issues in children exposed to alcohol during gestation: a follow-up study. Dev Med Child Neurol 1997;39:583-7. [PubMed]
24. Streissguth AP, Barr HM, Sampson PD, Bookstein FL. Prenatal booze and offspring development: the offset fourteen years. Drug Alcohol Depend 1994;36:89-99. [PubMed]
25. Hill SY, Lowers 50, Locke-Wellman J, Shen SA. Maternal smoking and drinking and the chance for child and adolescent psychiatric disorders. J Stud Alcohol 2000;61:661-8. [PMC gratuitous article] [PubMed]
26. American Psychiatric Association. Diagnostic and statistical manual of mental disorders. 4th ed. Washington: the Clan; 1994.
27. Shaffer D, Fisher P, Lucas CP, Dulcan M, Schwab-Rock Yard. NIMH Diagnostic Interview Schedule for Children Version Four (NIMH DISC-IV): description, differences from previous versions, and reliability of some common diagnoses. J Am Acad Kid Adolesc Psychiatry 2000;39(one):28-38. [PubMed]
28. Wechsler D. Manual for the Wechsler Intelligence Scale for Children. 3rd ed. Oxford (UK): the Psychological Corporation; 1991.
29. Achenbach TM. The child beliefs checklist/4-18. Burlington (VT): Academy of Vermont; 1991.
30. Kinney DK, Yurgelun-Todd DA, Tohen M, Tramer Due south. Pre- and perinatal complications and take a chance for bipolar disorder: a retrospective study. J Bear upon Disord 1998;fifty(ii-iii):117-24. [PubMed]
31. McNeil TF, Sjöstrom K. McNeil-Sjöstrom scale for obstetric complications. Malmo (Sweden): Section of Psychiatry, Lund University; 1995.
32. Conners CK. The computerized continuous operation test. Psychopharmacol Bull 1985;21:891-two. [PubMed]
33. Barkley RA. Tests and observational scales. In: Attending deficit hyperactivity disorder: a handbook for diagnosis and treatment. New York: The Guilford Press; 1990. p. 327-53.
34. Boksa P, El-Khodor BF. Birth insult interacts with stress at adulthood to alter dopaminergic office in animal models: possible implications for schizophrenia and other disorders. Neurosci Biobehav Rev 2003;27(i-2):91-101. [PubMed]
35. Botting N, Powls A, Cooke RW, Marlow N. Attending arrears hyperactivity disorders and other psychiatric outcomes in very depression nascence weight children at 12 years. J Kid Psychol Psychiatry 1997; 38:931-41. [PubMed]
36. Breslau N, Brown GG, DelDotto JE, Kumar S, Ezhuthachan S, Andreski P, et al. Psychiatric sequelae of low birth weight at 6 years of historic period. J Abnorm Kid Psychol 1996;24:385-400. [PubMed]
37. Breslau N, Chilcoat Hard disk drive. Psychiatric sequelae of low birth weight at eleven years of age. Biol Psychiatry 2000;47:1005-11. [PubMed]
38. Szatmari P, Saigal Southward, Rosenbaum P, Campbell D, Male monarch S. Psychiatric disorders at five years amongst children with birth weights less than 1000g: a regional perspective. Dev Med Child Neurol 1990; 32:954-62. [PubMed]
39. Hartsough CS, Lambert NM. Medical factors in hyperactive and normal children: prenatal, developmental, and wellness history findings. Am J Orthopsychiatry 1985;55:190-201. [PubMed]
twoscore. O'Callaghan MJ, Harvey JM. Biological predictors and co- morbidity of attention arrears and hyperactivity disorder in extremely low nascency weight infants at school. J Paediatr Kid Health 1997;33 491-half dozen. [PubMed]
41. Brake WG, Sullivan RM, Gratton A. Perinatal distress leads to lateralized medial prefrontal cortical dopamine hypofunction in developed rats. J Neurosci 2000;20:5538-43. [PMC complimentary article] [PubMed]
42. Davis JN, Giron LT Jr, Stanton E, Maury W. The consequence of hypoxia on encephalon neurotransmitter systems. Adv Neurol 1979;26:219-23. [PubMed]
43. Speiser Z, Korczyn Advertizement, Teplitzky I, Gitter S. Hyperactivity in rats following postnatal anoxia. Behav Brain Res 1983;7:379-82. [PubMed]
44. Badlissi D, Guillemette A, Fadin A. Prematurity and low birth weight: furnishings of active and passive smoking during pregnancy. Can J Public Health 2001;92:272-5. [PMC costless article] [PubMed]
45. Thapar A, Fowler T, Rice F, Scourfield J, van den Bree M, Thomas H, et al. Maternal smoking during pregnancy and attending deficit hyperactivity disorder symptoms in offspring. Am J Psychiatry 2003;160:1985-nine. [PubMed]
46. Biederman J, Faraone SV. Current concepts on the neurobiology of attention-arrears/hyperactivity disorder. J Atten Disord 2002;6 (Suppl 1):S7-16. [PubMed]
47. Castellanos FX, Giedd JN, Berquin PC, Walter JM, Precipitous Westward, Tran T, et al. Quantitative brain magnetic resonance imaging in girls with attention-deficit/hyperactivity disorder. Arch Gen Psychiatry 2001;58:289-95. [PubMed]
48. Hyman SE. Neuroscience, genetics, and the time to come of psychiatric diagnosis. Psychopathology 2002;35:139-44. [PubMed]
49. Buka SL, Goldstein JM, Seidman LJ, Tsuang MT. Maternal recall of pregnancy history: accuracy and bias in schizophrenia inquiry. Schizophr Bull 2000;26:335-50. [PubMed]
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Source: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC551167/
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