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S V Faraone

Publications and source records attributed to S V Faraone.

At least 181 records · Page 10Linked to original sources

Is maternal smoking during pregnancy a risk factor for attention deficit hyperactivity disorder in children?

OBJECTIVE: This study investigated the role of maternal smoking during pregnancy in the etiology of attention deficit hyperactivity disorder (ADHD). METHOD: Subjects were 6-17-year-old boys with DSM-III-R ADHD (N = 140) and normal comparison subjects (N = 120) and their first-degree biological relatives. Information on maternal smoking was obtained from mothers in a standardized manner by raters who were blind to the proband's clinical status. RESULTS: Twenty-two percent of the ADHD children had a maternal history of smoking during pregnancy, compared with 8% of the normal subjects. This positive association remained significant after adjustment for socioeconomic status, parental IQ, and parental ADHD status. Significant differences in IQ were found between those children whose mothers smoked during pregnancy and those whose mothers did not smoke (mean IQ = 104.9, SD = 12.3, and mean = 115.4, SD = 12.2, respectively). CONCLUSIONS: These findings suggest that maternal smoking during pregnancy is a risk factor for ADHD. If confirmed, these findings will stress the importance of programs aimed at smoking prevention in nonsmoking women and smoking cessation in smoking women of childbearing age.

Adolescent↗

Six-week, double-blind, placebo-controlled study of desipramine for adult attention deficit hyperactivity disorder.

OBJECTIVE: Despite the increasing awareness of attention deficit hyperactivity disorder (ADHD) in adults, there are a limited number of controlled pharmacologic studies of this disorder; most of the trials have focused on the psychostimulants. Because the tricyclic anti-depressant desipramine has been found to be effective in treating ADHD in pediatric groups, the authors tested its efficacy in adults with ADHD. METHOD: The authors conducted a randomized, 6-week, placebo-controlled, parallel-design study of desipramine at a target daily dose of 200 mg in 41 adult patients with DSM-III-R ADHD. They used standardized structured psychiatric instruments for diagnosis and, as the dependent variables (outcome), used separate assessments of ADHD, depressive, and anxiety symptoms at baseline and at each biweekly visit. RESULTS: There were highly significant differences in the reduction of ADHD symptoms between adults receiving desipramine and placebo. Within the desipramine-treated group, there were clinically and statistically significant differences between baseline and the week 6 end point for 1) reduction of 12 of 14 symptoms of ADHD and 2) decreases in the broad categories of hyperactivity, impulsivity, and inattentiveness. In contrast, placebo-treated patients showed no differences between baseline and end point for any of the ADHD symptoms assessed. According to strict, predefined criteria for response, 68% of desipramine-treated subjects and no subjects in the placebo group were considered positive responders. Response to desipramine was independent of dose, level of impairment, gender, or lifetime psychiatric comorbidity with anxiety or depressive disorders. CONCLUSIONS: These results, similar to findings in children and adolescents with ADHD, indicate that desipramine is effective in the treatment of ADHD in adults.

Adolescent↗

Genetics of Alzheimer's disease.

We briefly reviewed methods of psychiatric genetics and showed how these have elucidated genetic aspects of Alzheimer's disease. Although some cases of Alzheimer's disease are not familial, clinicians and researchers have identified many families in which the disease occurs in multiple generations in approximately 50% of family members. Linkage analyses have implicated several genes as causes or risk factors for Alzheimer's disease in different families: the amyloid precursor protein gene, the apolipoprotein-E gene (E4 subtype) on chromosome 19, the S182 gene on chromosome 14 and the STM2 gene on chromosome 1. These linkage findings have been replicated in independent laboratories and, thus, provide strong evidence for genetic heterogeneity of this disease. The discovery of these genes may lead to a better understanding of the etiology and pathophysiology of Alzheimer's disease and also raises the possibility of genetic counseling for patients with familial Alzheimer's disease.

Alzheimer Disease↗

Genetic heterogeneity may in part explain sex differences in the familial risk for schizophrenia.

The purpose of this study was to attempt, in part, to explain significant sex differences in the familial risk (FMR) for schizophrenia found in previous studies. We hypothesized that, like probands, relatives of male vs. female probands may express different forms or subsyndromal symptoms of schizophrenia, i.e., differential expression of flat affect. Studied were 332 schizophrenic probands defined by Diagnostic and Statistical Manual of Mental Disorders, 3rd ed. (DSM-III), criteria and 725 first-degree relatives from well-known retrospective cohort family studies. Results showed that relatives of male probands were at significantly higher risk for expressing flat affect than relatives of female probands, which did not hold for relatives of normal controls. Logistic regression was used to show that when flat affect was incorporated into the definition of affected among relatives, sex differences in FMR disappeared.

Adult↗

The '3 Rs' and neuropsychological function in schizophrenia: a test of the matching fallacy in biological relatives.

The 'matching fallacy' suggests that matching schizophrenic patients and normal control subjects on education or IQ may cause systematic mismatching of theoretically expected ability. This study supports a modest version of the matching fallacy effect in nonpsychotic biological relatives of schizophrenic patients. At equivalent levels of education, relatives and control subjects had similar Reading and Spelling scores on the Wide Range Achievement Test-Revised--measures that are largely unimpaired by schizophrenia-related processes. However, relatives showed a deficit in IQ (primarily verbal IQ) compared with what would be predicted from their Reading scores. A similar deficit in Arithmetic scores was found in non-college-educated relatives, but college-educated relatives showed an advantage. We discuss possible implications of the findings with regard to genetic and environmental factors.

Adult↗

A double-blind, crossover comparison of methylphenidate and placebo in adults with childhood-onset attention-deficit hyperactivity disorder.

BACKGROUND: There are few controlled studies of methylphenidate hydrochloride in adults with attention-deficit hyperactivity disorder (ADHD), and their results have been equivocal. The discrepancies among these studies may be related to low doses, diagnostic uncertainties, and lack of attention to comorbid disorders. METHODS: We conducted a randomized, 7-week, placebo-controlled, crossover study of methylphenidate in 23 adult patients with DSM-III-R ADHD using standardized instruments for diagnosis, separate assessments of ADHD and depressive and anxiety symptoms, and a robust daily dose of methylphenidate hydrochloride, 1.0 mg/kg per day. RESULTS: We found a marked therapeutic response for methylphenidate treatment of ADHD symptoms that exceeded the placebo response (78% vs 4%, P < .0001). Response to methylphenidate was independent of gender, psychiatric comorbidity with anxiety or moderate depression, or family history of psychiatric disorders. CONCLUSION: Robust doses of methylphenidate are effective in the treatment of adult ADHD.

Adolescent↗

Family-environment risk factors for attention-deficit hyperactivity disorder. A test of Rutter's indicators of adversity.

BACKGROUND: This study investigated whether family-environment risk factors are associated with attention-deficit hyperactivity disorder (ADHD). Compelling work by Rutter and coworkers revealed that it was the aggregate of adversity factors (severe marital discord, low social class, large family size, paternal criminality, maternal mental disorder, and foster care placement) rather than the presence of any single factor that led to impaired development. Based on the work of Rutter, we hypothesized a positive association between indicators of adversity and the diagnosis of ADHD and ADHD-associated impairments. METHODS: We studied 140 ADHD and 120 normal control probands. Subjects were non-Hispanic white boys between the ages of 6 and 17 years. Rutter's indicators of adversity were used to predict ADHD-related psychopathology as well as impaired cognitive and psychosocial functioning. RESULTS: The odds ratio for the diagnosis of ADHD increased as the number of Rutter's adversity index predicted ADHD-related psychopathology (depression, anxiety, and conduct disorder), learning disabilities, cognitive impairment, and psychosocial dysfunction. CONCLUSIONS: A positive association appears to exist between adversity indicators and the risk for ADHD as well as for its associated psychiatric, cognitive, and psychosocial impairments. These findings support the work of Rutter and stress the importance of adverse family-environment variables as risk factors for children with ADHD.

Adolescent↗

Differential heritability of adult and juvenile antisocial traits.

BACKGROUND: Studies of adult antisocial behavior or criminality usually find genetic factors to be more important than the family environment, whereas studies of delinquency find the family environment to be more important. We compared DSM-III-R antisocial personality disorder symptoms before vs after the age of 15 years within a sample of twins, rather than comparing across studies. METHODS: We administered the Diagnostic Interview Schedule Version III-revised by telephone to 3226 pairs of male twins from the Vietnam Era Twin Registry. Biometrical modeling was applied to each symptom of antisocial personality disorder and summary measures of juvenile and adult symptoms. RESULTS: Five juvenile symptoms were significantly heritable, and five were significantly influenced by the shared environment. Eight adult symptoms were significantly heritable, and one was significantly influenced by the shared environment. The shared environment explained about six times more variance in juvenile anti-social traits than in adult traits. Shared environmental influences on adult antisocial traits overlapped entirely with those on juvenile traits. Additive genetic factors explained about six times more variance in adult vs juvenile traits. The juvenile genetic determinants overlapped completely with genetic influences on adult traits. The unique environment (plus measurement error) explained the largest proportion of variance in both juvenile and adult antisocial traits. CONCLUSIONS: Characteristics of the shared or family environment that promote antisocial behavior during childhood and early adolescence also promote later antisocial behavior, but to a much lesser extent. Genetic causal factors are much more prominent for adult than for juvenile antisocial traits.

Adolescent↗

No confirmation of Geschwind's hypothesis of associations between reading disability, immune disorders, and motor preference in ADHD.

Geschwind and colleagues have proposed an association among reading disability, immune disorder, and motor preference. Although reading disability commonly overlaps with attention deficit hyperactivity disorder (ADHD), ADHD has not been previously examined in studies evaluating Geschwind's hypothesis. In this paper we evaluate whether ADHD is associated with either asthma or left motor preference and whether asthma and left motor preference are associated with each other. Subjects were 6- to 17-year-old boys with DSM-III-R ADHD (n = 140) and normal controls (n = 120). Information on reading disability, asthma, and motor preference was obtained in a standardized manner blind to the proband's clinical status. Neither ADHD nor reading disability was associated with either asthma or left motor preference nor was asthma and left motor preference associated with one another. Our results are not consistent with Geschwind's hypothesis linking reading disability, immune disorder, and left motor preference.

Adolescent↗

The case for heterogeneity in the etiology of schizophrenia.

To confirm etiological heterogeneity, it is required that schizophrenic patients may be separated into at least two classes having different known etiologies and, perhaps, different pathophysiological signatures. In contrast, the homogeneity hypothesis asserts that there is a single necessary and sufficient cause or configuration of causes of schizophrenia. Because the link between phenotypic heterogeneity and etiological heterogeneity is tenuous, attempts to use purely phenotypic data to infer etiologic heterogeneity must be viewed cautiously. We examined three candidate causes for schizophrenia: genes, obstetric complications and viral infection. Cytogenetic studies show that some rare cases of schizophrenia are due to gross abnormalities of chromosomes. As for the large majority of schizophrenic patients, the candidate cause data most certainly reject the most parsimonious version of the hypothesis of etiological homogeneity: that all schizophrenia is caused by exactly the same pattern of genetic mutations, birth related complications and exposure to the same viral infections. We conclude that the heterogeneity debate should consider the possibility of rewording the question: 'Heterogeneity: yes or no?' to 'Heterogeneity: how much?'

Chromosome Aberrations↗

Neuropsychological functioning among the nonpsychotic relatives of schizophrenic patients: a diagnostic efficiency analysis.

Numerous studies suggest that the relatives of schizophrenic patients exhibit neuropsychological impairments that are milder yet similar to those seen among schizophrenic patients. The authors assessed 35 nonpsychotic relatives of schizophrenic patients and 72 normal controls using a clinical and experimental neuropsychological test battery. Three neuropsychological functions met criteria for risk indicators of the schizophrenia genotype: abstraction, verbal memory, and auditory attention. These findings could not be attributed to parental socioeconomic status, education, general visual-spatial ability, or psychopathology. Furthermore, exploratory analyses were performed to determine whether the diagnostic efficiency of the indicators could be adjusted to meet the needs of genetic linkage analyses. These analyses suggest that psychometric considerations may help to create measures for genetic linkage studies.

Adolescent↗

Correlates of psychosis proneness in relatives of schizophrenic patients.

The Magical Ideation Scale (MIS), Perceptual Aberration Scale (PABS), Social Anhedonia Scale (SAS), and Physical Anhedonia Scale (PAS) were administered to 98 relatives of schizophrenic patients along with a measure of personality disorders (the Personality Diagnostic Questionnaire--Revised). Hierarchical regression analysis indicated that the schizotypal and borderline personality disorder (PD) scales explained significant variance in both the MIS and PABS; the avoidant PD scale also explained significant variance in the PABS. The schizoid, paranoid, and avoidant PD scales explained significant variance in the SAS. Sibling intraclass correlations indicated a significant heritability of 0.62 for the PABS.

Adult↗

Mania-like symptoms suggestive of childhood-onset bipolar disorder in clinically referred children.

OBJECTIVE: To examine the prevalence, characteristics, and correlates of mania among referred children aged 12 or younger. Many case reports challenge the widely accepted belief that childhood-onset mania is rare. Sources of diagnostic confusion include the variable developmental expression of mania and its symptomatic overlap with attention-deficit hyperactivity disorder (ADHD). METHOD: The authors compared 43 children aged 12 years or younger who satisfied criteria for mania, 164 ADHD children without mania, and 84 non-ADHD control children. RESULTS: The clinical picture was fully compatible with the DSM-III-R diagnosis of mania in 16% (n = 43) of referred children. All but one of the children meeting criteria for mania also met criteria for ADHD. Compared with ADHD children without mania, manic children had significantly higher rates of major depression, psychosis, multiple anxiety disorders, conduct disorder, and oppositional defiant disorder as well as evidence of significantly more impaired psychosocial functioning. In addition, 21% (n = 9) of manic children had had at least one previous psychiatric hospitalization. CONCLUSIONS: Mania may be relatively common among psychiatrically referred children. The clinical picture of childhood-onset mania is very severe and frequently comorbid with ADHD and other psychiatric disorders. Because of the high comorbidity with ADHD, more work is needed to clarify whether these children have ADHD, bipolar disorder, or both.

Attention Deficit Disorder with Hyperactivity↗

How reliable are maternal reports of their children's psychopathology? One-year recall of psychiatric diagnoses of ADHD children.

OBJECTIVE: Although childhood psychiatric diagnoses often rely on maternal reports, little is known about their long-term reliability and diagnostic accuracy. Thus, the authors sought to examine these psychometric features in a cohort of ADHD and control children. METHOD: The sample consisted of 140 referred children with ADHD and 120 normal controls. The authors compared childhood diagnoses based on maternal reports of their children's psychopathology at this baseline assessment with those collected 1 year later. RESULTS: Both reliability and accuracy were excellent for ADHD. Reliability and specificity were also excellent for conduct disorder, oppositional defiant disorder, major depression, bipolar disorder, separation anxiety, and multiple anxiety disorders. Reliability and sensitivity were relatively low for simple phobia, social phobia, agoraphobia, and overanxious disorder. CONCLUSIONS: With some exceptions, maternal reports of their children's psychopathology provided a reliable and accurate means of assessment. Generally, maternally derived diagnoses were less accurate for internalizing compared with externalizing disorders. However, specificity was high for all diagnoses, suggesting that mothers were not biased to report symptoms that had not occurred.

Adolescent↗

Effects of family history and comorbidity on the neuropsychological performance of children with ADHD: preliminary findings.

OBJECTIVE: Because ADHD is heterogeneous with respect to psychiatric comorbidity, familiality, and learning disabilities, it was hypothesized that such features might influence the severity and pattern of neuropsychological function in ADHD. METHOD: Subjects were 9- to 20-year-old males with DSM-III-R ADHD (n = 65) and normal controls (n = 45). Information on neuropsychological performance was obtained in a standardized manner, blind to the proband's clinical status. RESULTS: ADHD probands were significantly impaired on neuropsychological functions compared with controls irrespective of composite psychiatric comorbidity status, and those with a family history of ADHD were most impaired. ADHD probands with learning disabilities showed a pattern suggestive of reduced motor dominance and extremely slow reading speed. CONCLUSIONS: These results indicate that neuropsychological performance in ADHD is significantly affected by familial status and presence of learning disabilities. The similarity of findings between ADHD children with and without comorbid psychiatric disorders suggests that the neuropsychological impairments in our sample were associated with ADHD. These findings raise the possibility of alterations of cerebral dominance and of frontal networks in ADHD. Further research is needed to replicate these findings in larger samples, to clarify the role of specific comorbid psychiatric disorders, and to assess directly cerebral functioning in subjects with ADHD.

Adolescent↗

Impact of adversity on functioning and comorbidity in children with attention-deficit hyperactivity disorder.

OBJECTIVE: Prior research on risk factors for attention-deficit hyperactivity disorder (ADHD) has shown that familial risk factors play a role in the disorder's etiology. This study investigated whether features of the family environment were associated with ADHD. METHOD: One hundred forty children with ADHD and 120 normal control probands were studied. Subjects were Caucasian, non-Hispanic males between the ages of 6 and 17 years. Exposure to parental psychopathology and exposure to parental conflict were used as indicators of adversity, and their impact on ADHD and ADHD-related psychopathology and dysfunction in children was assessed. RESULTS: Increased levels of environmental adversity were found among ADHD compared with control probands. The analyses showed significant associations between the index of parental conflict and several of the measures of psychopathology and psychosocial functioning in the children. In contrast, the index of exposure to parental psychopathology had a much narrower impact, affecting primarily the child's use of leisure time and externalizing symptoms. CONCLUSIONS: A relationship appears to exist between adversity indicators and the risk for ADHD as well as for its associated impairments in multiple domains. These findings confirm previous work and stress the importance of adverse family-environment variables as risk factors for children who have ADHD.

Achievement↗

A pilot family study of childhood-onset mania.

OBJECTIVE: To investigate the familial association of attention-deficit hyperactivity disorder (ADHD) and bipolar disorder (BPD) among the first-degree relatives of children with comorbid ADHD and BPD. BACKGROUND: In contrast to a growing body of literature on childhood non-bipolar depression, little is known about childhood BPD. Among the explanations accounting for the lack of recognition and identification of these children is the symptomatic overlap of BPD with ADHD. Family-genetic studies provide information external to the clinical picture and thus are uniquely suited to clarify such issues of diagnostic comorbidity. METHOD: Structured diagnostic interviews were used to obtain DSM-III-R psychiatric diagnoses on first-degree relatives (n = 46) of referred children (aged < or = 12 years) satisfying diagnostic criteria for mania using the Schedule for Affective Disorders and Schizophrenia for School-Age Children-Epidemiologic Version (n = 16). For comparison, diagnostic information on the first-degree relatives of non-bipolar ADHD children and control children was examined. RESULTS: The results show high rates of comorbidity between BPD and ADHD in children and high rates of both BPD and ADHD in the first-degree relatives of these children. Moreover, ADHD and BPD cosegregated among the relatives of children with BPD. CONCLUSIONS: These findings, which are consistent with the authors' prior study of children with ADHD, provide family-genetic evidence for the validity of BPD and ADHD when they exist comorbidly in children. Moreover, they suggest that the comorbid condition of ADHD+BPD may be a distinct nosological entity.

Attention Deficit Disorder with Hyperactivity↗