RESUMEN
We compared diagnoses made blindly by experienced clinicians from interview records with diagnoses obtained by computer pooling and scoring of relatives' information on the same persons. For major affective disorder diagnosed by interview, the relatives' information agreed on presence of affective illness for 96% of 159 probands and 48% of 195 relatives of affectively ill and control probands. In 1,093 relatives of affectively ill and control probands, the k values for diagnostic agreement were as follows: any major affective disorder, 51; bipolar I disorder, .61; and unipolar disorder, .42. Schizoaffective and bipolar II diagnoses did not show significant agreement. Only 15% of interview-diagnosed relatives were identified as having a major affective disorder by one informant alone, going up to 64% agreement with four or more informants. Final diagnostic estimate from all available information, including medical records, generally followed the interview diagnosis rather than the relatives' information.
Asunto(s)
Familia , Trastornos del Humor/diagnóstico , Adulto , Trastorno Bipolar/diagnóstico , Trastorno Bipolar/genética , Computadores , Trastorno Ciclotímico/diagnóstico , Trastorno Ciclotímico/genética , Trastorno Depresivo/diagnóstico , Trastorno Depresivo/genética , Humanos , Registros Médicos , Trastornos del Humor/genética , Escalas de Valoración Psiquiátrica , Trastornos Psicóticos/diagnóstico , Trastornos Psicóticos/genéticaRESUMEN
Linkage between protanopia and deuteranopia and bipolar manic-depressive illness is demonstrated in a sample of eight informative families ascertained in Brussels. Genetic heterogeneity of bipolar affective disorders is also shown in the present study. These results add new evidence to the hypothesis of X-linked dominant genetic transmission of affective liability in a subgroup of patients with bipolar affective disorders.
Asunto(s)
Trastorno Bipolar/genética , Defectos de la Visión Cromática/genética , Ligamiento Genético , Adulto , Anciano , Femenino , Genes Dominantes , Tamización de Portadores Genéticos , Humanos , Masculino , Persona de Mediana Edad , Linaje , Cromosoma XRESUMEN
Eight hundred twenty-three relatives of bipolar and schizoaffective patients were divided into groups of birth cohorts. The rates of bipolar, schizoaffective, and unipolar disorders were higher in the cohorts born after 1940 than in the cohorts born earlier. Life-table analysis of the cumulative hazard of illness in the different cohorts revealed significant differences among them, implying that the cumulative hazard of developing any affective disorder by a given age was greater in the post-1940 cohorts. When these data are combined with other reports, an ominous trend may be present, leading to an increase in prevalence of a broad spectrum of familial affective disorders in the coming decades.
Asunto(s)
Trastorno Bipolar/genética , Trastorno Depresivo/genética , Trastornos Psicóticos/genética , Análisis Actuarial , Adulto , Factores de Edad , Trastorno Bipolar/epidemiología , Trastorno Depresivo/epidemiología , Femenino , Humanos , Masculino , Persona de Mediana Edad , Riesgo , Factores de TiempoRESUMEN
Two hundred thirty-seven relatives of 48 patients with chronic psychosis, diagnosed as either schizophrenia or schizoaffective disorder, along with 380 relatives of psychiatrically normal controls, were studied using systematic diagnostic interviews, information from relatives, and review of medical records where appropriate. A variety of nonbipolar psychotic disorders was found in the relatives of the patients. Comparing relatives of patients with schizophrenia with relatives of patients with schizoaffective disorder, there was no tendency for schizoaffective diagnosis or acute psychoses to aggregate separately from schizophrenia. Increased incidence of bipolar disorder was found in relatives of patients with schizoaffective disorder but not in relatives of patients with schizophrenia. Incidence of major affective disorder (bipolar and unipolar) was increased in relatives of probands with both types of psychoses. If we subdivide the ill probands according to whether or not they had a history of substance abuse, relatives of probands with substance abuse had greater frequency of affective disorder and substance abuse, but there were not significant differences in the number of relatives with nonbipolar psychoses.
Asunto(s)
Trastorno Depresivo/genética , Trastornos Psicóticos/genética , Esquizofrenia/genética , Adolescente , Adulto , Trastorno Bipolar/genética , Femenino , Humanos , MasculinoRESUMEN
In a family study of 1,254 adult relatives of patients and controls, lifetime prevalences of major affective disorder (including schizoaffective) were 37%, 24%, 25%, 20% and 7% in relatives of probands with schizoaffective, bipolar I, bipolar II, and unipolar disease, and normal controls. These data were compatible with the different affective disorders representing thresholds on a continuum of underlying multifactorial vulnerability. In this model, schizoaffective illness represents greatest vulnerability, followed by bipolar I and bipolar II, then unipolar illnesses. Alcoholism, drug abuse, and sociopathy were not more frequent in relatives of patients v relatives of controls. Sex-related transmission of morbid risk was not present. Morbid risk was 74% to offspring of two III parents, and 27% to offspring of one III parent. Nationality and age at time of interview seem to be nongenetic factors that affect frequency of diagnosis.
Asunto(s)
Trastorno Bipolar/genética , Trastorno Depresivo/genética , Trastornos Psicóticos/genética , Adulto , Factores de Edad , Alcoholismo/genética , Trastorno de Personalidad Antisocial/genética , Femenino , Humanos , Masculino , Persona de Mediana Edad , Modelos Genéticos , Linaje , Riesgo , Factores Sexuales , Trastornos Relacionados con Sustancias/genéticaRESUMEN
A family study of psychiatric disorders in 2,003 first-degree relatives of 335 probands found increased rates of bipolar I disorder and major depression (MD) in the relatives of probands with bipolar disorder and increased rates of MD in the relatives of probands with MD. There was a similarity in rates of affective disorders in the relatives of ambulatory and of hospitalized depressed probands (suggesting that ambulatory depressed patients may be as suitable as hospitalized ones for biological studies) and a comparability of rates of illness in relatives between centers for most disorders when comparable diagnostic criteria and procedures were used.
Asunto(s)
Trastorno Bipolar/genética , Trastorno Depresivo/genética , Adulto , Factores de Edad , Atención Ambulatoria , Trastorno Bipolar/diagnóstico , Connecticut , Trastorno Depresivo/diagnóstico , Femenino , Hospitalización , Humanos , Masculino , Trastornos Mentales/diagnóstico , Trastornos Mentales/genética , Persona de Mediana Edad , National Institute of Mental Health (U.S.) , Escalas de Valoración Psiquiátrica , Proyectos de Investigación , Riesgo , Factores Sexuales , Estados UnidosRESUMEN
BACKGROUND: Although genetic epidemiological studies of bipolar (BP) illness are consistent with a heritable component, inherited risk factors remain unknown. The goal of the present study is to describe the localization of BP susceptibility loci through linkage strategies, including a genome-wide search. METHODS: A linkage study of 22 BP families has been performed. These BP families include almost 400 persons, 173 of whom have been diagnosed as having BP I, schizoaffective, BP II with major depression, or recurrent unipolar illness. Using an autosomal dominant disease model with 85% or 50% age-dependent penetrance, and a recessive model with 85% penetrance, linkage analyses were performed assuming a narrow (BP and schizoaffective) or a broad (BP, schizoaffective, or unipolar) definition of the BP spectrum. Affected sibling pairs and affected pedigree member analyses were performed when positive lod scores were observed in multiple pedigrees. The present article describes linkage analysis of 310 DNA markers on chromosomes 1, 5p, 6, 8, 10q, 11q, and 12 to 18. RESULTS: None of the loci examined disclosed compelling evidence for linkage using lod score analyses. Model-independent analysis by multilocus affected pedigree member method in the pericentromeric chromosome 18 region disclosed statistically significant evidence (P < .0001) for a BP susceptibility gene in this region. Multilocus analysis by affected sibling pair method also disclosed evidence for linkage (P < .00008). CONCLUSIONS: Our results imply that a BP susceptibility gene exists near the centromere of chromosome 18. Confirmation of this finding (by independent investigators studying different pedigrees) has been published, suggesting that a valid BP disease linkage may have been discovered.
Asunto(s)
Trastorno Bipolar/genética , Ligamiento Genético , Trastorno Bipolar/epidemiología , Cromosomas Humanos Par 18/genética , Femenino , Marcadores Genéticos , Predisposición Genética a la Enfermedad , Genotipo , Humanos , Escala de Lod , Masculino , Modelos Genéticos , Linaje , Factores de RiesgoRESUMEN
Data from a family study of psychiatric disorders showed higher rates of major affective disorders, eating disorders, and alcoholism in first-degree relatives of 40 bulimic probands than in first-degree relatives of 24 control subjects. More importantly, the data showed higher rates of major affective disorders in relatives of bulimic probands who themselves had no history of major affective disorders than in relatives of control subjects. This significant finding indicates a familial relationship between bulimia nervosa and major affective disorders, which suggests the possibility of a common diathesis.
Asunto(s)
Bulimia/genética , Trastornos Mentales/genética , Adulto , Alcoholismo/genética , Trastorno de Personalidad Antisocial/genética , Bulimia/complicaciones , Trastornos de Alimentación y de la Ingestión de Alimentos/genética , Femenino , Humanos , Trastornos Mentales/complicaciones , Trastornos del Humor/genética , Trastornos Relacionados con Sustancias/genéticaRESUMEN
A region between D13S71 and D13S274 on 13q32 showed linkage to bipolar disorder (BP) based on a genome scan using markers with an average spacing of approximately 6 cM and an average heterozygosity of approximately 60% [Detera-Wadleigh et al., 1999: Proc Natl Acad Sci USA 96:5604-5609]. In an attempt to confirm this finding and achieve fine mapping of the susceptibility region, nine additional microsatellite markers with average heterozygosity of approximately 86%, located between D13S71 and D13S274, were typed in the same sample. The strongest linkage evidence was detected by multipoint linkage analysis (ASPEX program) around D13S779-D13S225 with maximum LOD score of 3.25 under Affection Status Model II (ASM II; P = 0.0000546). Data from additional nine markers resulted in a decrease of the 95% confidence interval of the linkage region. Association analyses with GASSOC TDT and ASPEX/sib_tdt detect potential linkage disequilibrium with several markers, including D13S280 (ASPEX TDT P = 0.0033, ASM I). These data generated using a higher marker density within the proposed susceptibility region strengthen the validity of our previous findings and suggest a finer localization of the susceptibility gene(s) on 13q32.
Asunto(s)
Trastorno Bipolar/genética , Cromosomas Humanos Par 13/genética , Predisposición Genética a la Enfermedad/genética , Mapeo Cromosómico , Salud de la Familia , Femenino , Ligamiento Genético , Humanos , Escala de Lod , Masculino , Repeticiones de MicrosatéliteRESUMEN
In an effort to identify features indicative of underlying bipolarity within the unipolar relatives of bipolar probands, we compared unipolar relatives of bipolars with unipolar relatives of controls. Using data from the Yale-NIMH Collaborative Study of Depression, we compared a number of demographic and clinical features individually, and then developed a logistic regression model for the differences found. Unipolar relatives of bipolars were generally similar to relatives of controls, but they were older and more likely to suffer from more severe, even psychotic, depression, and somewhat less likely to report a brief transition into their illness. A multiple logistic regression model for observed differences was highly statistically significant, but had limited ability to discriminate effectively between the two groups. These findings suggest that more stringent diagnostic criteria might be beneficial if unipolar relatives are counted as affected in linkage studies of bipolar disorder. The ability of this strategy to improve the "clinical phenotype" is limited, however, and other approaches may be needed to identify features of underlying bipolarity and thus to define "caseness" for unipolar relatives in linkage analyses of bipolar disorder.
Asunto(s)
Trastorno Bipolar/genética , Ligamiento Genético , Adulto , Edad de Inicio , Alcoholismo/complicaciones , Alcoholismo/epidemiología , Trastorno Bipolar/complicaciones , Trastorno Bipolar/psicología , Demografía , Depresión/psicología , Trastorno Distímico/complicaciones , Trastorno Distímico/epidemiología , Familia , Femenino , Marcadores Genéticos , Humanos , Masculino , Morbilidad , Análisis Multivariante , Oportunidad Relativa , Trastorno de Pánico/complicaciones , Trastorno de Pánico/epidemiología , Linaje , Fenotipo , Análisis de Regresión , Caracteres SexualesRESUMEN
We are conducting a genome search for a predisposing locus to bipolar (manic-depressive) illness by genotyping 21 moderate-sized pedigrees. We report linkage data derived from screening marker loci on chromosomes 2, 3, 4, 7, 9, 10p, 11p, 22, and the pseudoautosomal region at Xpter. To analyze for linkage, two-point marker to illness lod scores were calculated under a dominant model with either 85% or 50% maximum penetrance and a recessive model with 85% maximum penetrance, and two affection status models. Under the dominant high penetrance model the cumulative lod scores in the pedigree series were less than -2 at theta = 0.01 in 134 of 142 loci examined, indicating that if the disease is genetically homogeneous linkage could be excluded in these marker regions. Similar results were obtained using the other genetic models. Heterogeneity analysis was conducted when indicated, but no evidence for linkage was found. In the course of mapping we found a positive total lod score greater than +3 at the D7S78 locus at theta = 0.01 under a dominant, 50% penetrance model. The lod scores for additional markers within the D7S78 region failed to support the initial finding, implying that this was a spurious positive. Analysis with affected pedigree member method for COL1A2 and D7S78 showed no significance for linkage but for PLANH1, at the weighting functions f(p) = 1 and f(p) = 1/sqrt(p) borderline P values of 0.036 and 0.047 were obtained. We also detected new polymorphisms at the mineralocorticoid receptor (MLR) and calmodulin II (CALMII) genes. These genes were genetically mapped and under affection status model 2 and a dominant, high penetrance mode of transmission the lod scores of < -2 at theta = 0.01 were found.
Asunto(s)
Trastorno Bipolar/genética , Mapeo Cromosómico , Cromosomas Humanos , Ligamiento Genético , Southern Blotting , Cromosomas Humanos Par 10 , Cromosomas Humanos Par 11 , Cromosomas Humanos Par 2 , Cromosomas Humanos Par 22 , Cromosomas Humanos Par 3 , Cromosomas Humanos Par 4 , Cromosomas Humanos Par 7 , Cromosomas Humanos Par 9 , Femenino , Genotipo , Humanos , Escala de Lod , Masculino , Linaje , Reacción en Cadena de la Polimerasa , Cromosoma XRESUMEN
A report on an initial genome screen on 540 individuals in 97 families was collected as part of the NIMH Genetics Initiative on Bipolar Disorder. Families were ascertained to be informative for genetic linkage and underwent a common ascertainment and assessment protocol at four clinical sites. The sample was genotyped for 65 highly polymorphic markers from chromosomes 1, 6, 8, 10, and 12. The average intermarker interval was 16 cM. Genotypic data was analyzed using affected sib pair, multipoint affected sib pair, and pedigree analysis methods. Multipoint methods gave lod scores of approximately two on chromosomes 1, 6, and 10. The peak lod score on chromosome 6 occurred at the end of the q-arm, at some distance from the 6p24-22 area previously implicated for schizophrenia. We are currently genotyping additional markers to reduce the intermarker interval around the signals. The interpretation of results from a genome screen of a complex disorder and the problem of achieving a balance between detecting false positive results and the ability to detect genes of modest effect are discussed.
Asunto(s)
Trastorno Bipolar/genética , Ligamiento Genético , Marcadores Genéticos , Cromosomas Humanos Par 1 , Cromosomas Humanos Par 10 , Cromosomas Humanos Par 12 , Cromosomas Humanos Par 6 , Cromosomas Humanos Par 8 , Femenino , Genoma Humano , Genotipo , Humanos , Escala de Lod , Masculino , National Institute of Mental Health (U.S.) , Núcleo Familiar , Linaje , Polimorfismo Genético , Programas Informáticos , Estados UnidosRESUMEN
An initial genome scan was performed on 540 individuals from 97 families segregating bipolar disorder, collected through the National Institutes of Mental Health Genetics Initiative. We report here affected-sib-pair (ASP) data on 126 marker loci (approximately 68,000 genotypes) mapping to chromosomes 4, 7, 9, 18, 19, 20, and 21q, under three affection status models. Modest increases in identical-by-descent (IBD) allele sharing were found at the following loci: D4S2397 and D4S391 (P < 0.05) on 4p, D4S1647 (P < 0.05) on 4q, D7S1802 and D7S1869 (low P = 0.01) on 7p, D9S302 (P = 0.004) on 9q, and D20S604 on 20p and D20S173 on 20q (P < 0.05). In addition, five markers on 7q displayed increased IBD sharing (P = 0.046-0.002). Additional ASP analyses on chromosomes 18 and 21q marker data were performed using disease phenotype models defined previously. On chromosome 18, only D18S40 on 18p and D18S70 on 18q yielded a slight elevation in allele sharing (P = 0.02), implying that the reported linkages in these regions were not confirmed. On chromosome 21q, a cluster of markers within an approximately 9 cM interval: D21S1254, D21S65, D21S1440, and D21S1255 exhibited excess allele sharing (P = 0.041-0.008). Multilocus data on overlapping marker quartets, from D21S1265 to D21S1255, which were consistent with increased IBD sharing (P < 0.01, with a low of 0.0009), overlapped a broad interval of excess allele sharing reported previously, increasing support for a susceptibility locus for bipolar disorder on 21q.
Asunto(s)
Trastorno Bipolar/genética , Ligamiento Genético , Marcadores Genéticos , Alelos , Mapeo Cromosómico , Cromosomas Humanos Par 18 , Cromosomas Humanos Par 19 , Cromosomas Humanos Par 20 , Cromosomas Humanos Par 21 , Cromosomas Humanos Par 4 , Cromosomas Humanos Par 7 , Cromosomas Humanos Par 9 , Femenino , Genoma Humano , Genotipo , Humanos , Masculino , National Institute of Mental Health (U.S.) , Núcleo Familiar , Linaje , Estados UnidosRESUMEN
We report on an initial genome screen of 540 individuals from 97 families collected as part of the NIMH Genetics Initiative Bipolar Group. Among the individuals studied, 232 were diagnosed with bipolar (BP) I, 72 with BPII, 88 with major depressive disorder-recurrent type (UPR), and 32 with schizoaffective disorder, bipolar type (SA/BP). A total of 53 markers on chromosomes 2, 11, 13, 14, and X (average spacing: 11.5 cM) were studied at Johns Hopkins University. Tests for linkage were performed using nonparametric affected sib-pair and whole pedigree methods with three definitions of affected status. Three regions of interest were identified (13q14-32, Xp22, and Xq26-28). On chromosomes 2, 11, and 14, a disease locus with relative risk lambda(i) = 1.5 could be excluded in <10% of the genetic distance studied, while a locus conferring lambda(i) = 3 or greater could be excluded across at least 96%. The autosomal region that could not be excluded even with lambda(i) = 5 was near 13q14-32. In this region, two-point affected sib-pair analyses revealed a pair of consecutive loci with excess sharing (P < 0.05) and a multipoint affected sib-pair LOD score of 1.12. On the X chromosome, nonparametric multipoint affected sib-pair analyses revealed peak total LOD scores of 0.94 on Xp22 and 1.34 on Xq26-28. A locus linked to the markers in Xp22 would have lambda(i) = 3.6 in affected brother-brother pairs, while a locus linked to the markers in Xq26-28 would have lambda(i) > 1.9 in affected sister-sister pairs. The results on 13q14-32, Xp22, and Xq26-28 suggest areas of interest for further studies.
Asunto(s)
Trastorno Bipolar/genética , Ligamiento Genético , Marcadores Genéticos , Cromosomas Humanos Par 11 , Cromosomas Humanos Par 13 , Cromosomas Humanos Par 14 , Cromosomas Humanos Par 2 , Femenino , Genoma Humano , Humanos , Escala de Lod , Masculino , National Institute of Mental Health (U.S.) , Núcleo Familiar , Linaje , Estadísticas no Paramétricas , Estados Unidos , Cromosoma XRESUMEN
As part of a four-center NIMH Genetics Initiative on Bipolar Disorder, a genome screen using 365 markers was performed on 540 DNAs from 97 families, enriched for affected relative pairs. This is the largest uniformly ascertained and assessed linkage sample for this disease, and includes 232 subjects diagnosed with bipolar I (BPI), 32 with schizo-affective, bipolar type (SABP), 72 with bipolar II (BPII), and 88 with unipolar recurrent depression (UPR). A hierarchical set of definitions of affected status was examined. Under Model I, affected individuals were those with a diagnosis of BPI or SABP, Model II included as affected those fitting Model I plus BPII, and Model III included those fitting Model II plus UPR. This data set was previously analyzed using primarily affected sib pair methods. We report the results of nonparametric linkage analyses of the extended pedigree structure using the program Genehunter Plus. The strongest finding was a lod score of 2.5 obtained on chromosome 10 near the marker D10S1423 with diagnosis as defined under Model II. This region has been previously implicated in genome-wide studies of schizophrenia and bipolar disorder. Other chromosomal regions with lod scores over 1.50 for at least one Model Included chromosomes 8 (Model III), 16 (Model III), and 20 (Model I). Am. J. Med. Genet. (Neuropsychiatr. Genet.) 96:18-23, 2000
Asunto(s)
Trastorno Bipolar/genética , Cromosomas Humanos Par 10 , Mapeo Cromosómico , Femenino , Genotipo , Humanos , Escala de Lod , Masculino , LinajeRESUMEN
An i.v. injection of dextroamphetamine (0.3 mgm/kg) was given to 13 pairs of normal monozygotic twins, three pairs of normal dizygotic twins and 11 patients with bipolar affective disorder in remission and off medications. Behavioral excitation in response to amphetamine was highly correlated in monozygotic twins; it was predicted by the baseline variables of high plasma MHPG, low serum prolactin and low pulse; it correlated with a rise in cortisol; and it was not correlated with plasma amphetamine level. Pre-infusion baseline MHPG and growth hormone and prolactin responses to amphetamine also were concordant in twins. Plasma amphetamine level, pulse and blood pressure and cortisol responses were not concordant, suggesting significant environmental influences. Haloperidol pretreatment in one pair of twins abolished the excitation response but did not reduce increases in cortisol and growth hormone. This suggests a role for dopamine in the excitation response but predominant serotonergic and noradrenergic mediation of the hormonal responses. None of the responses or baseline measures distinguished patients from controls. Thus, no consistently altered sensitivity to monoaminergic stimulation by amphetamine in bipolar affective disorder was demonstrated in this study. This is one of the first reports of familial (possibly genetic) variation in a psychostimulant drug response in man. The responses identified as concordant may be useful in characterizing other pathologic conditions.
Asunto(s)
Trastorno Bipolar/fisiopatología , Dextroanfetamina , Gemelos Dicigóticos , Gemelos Monocigóticos , Gemelos , Adolescente , Adulto , Presión Sanguínea/efectos de los fármacos , Emociones/efectos de los fármacos , Femenino , Hormona del Crecimiento/sangre , Haloperidol/farmacología , Humanos , Hidrocortisona/sangre , Masculino , Embarazo , Prolactina/sangre , Pulso Arterial/efectos de los fármacos , Factores de TiempoRESUMEN
The clinical syndrome of multiple personality disorder (MPD) is an unusual dissociative condition that has been poorly characterized. In an attempt to better delineate the clinical phenomenology of MPD, 100 recent cases were collected on a 386-item questionnaire completed by clinicians involved in the treatment of MPD patients. This study documents the existence of a clinical syndrome characterized by a core of depressive and dissociative symptoms and a childhood history of significant trauma, primarily child abuse.
Asunto(s)
Trastorno Disociativo de Identidad/diagnóstico , Actuación (Psicología) , Adolescente , Adulto , Atención Ambulatoria , Niño , Maltrato a los Niños , Cognición , Conflicto Psicológico , Trastorno Depresivo/complicaciones , Trastorno Depresivo/diagnóstico , Trastorno Depresivo/psicología , Trastorno Disociativo de Identidad/complicaciones , Trastorno Disociativo de Identidad/psicología , Femenino , Humanos , Masculino , Manuales como Asunto , Trastornos Mentales/diagnóstico , Trastornos Mentales/genética , Trastornos Mentales/psicología , Persona de Mediana Edad , Modelos Psicológicos , Personalidad , Factores SexualesRESUMEN
Twenty-nine out of 195 bipolar/episodic schizoaffective patients were judged to be rapid-cyclers (15%). Twenty-five of the 29 were female (86%). The age-corrected morbid risk for major affective disorder was 23.5% in 179 relatives of rapid-cyclers and 31.0% in 189 relatives of matched non-rapid cyclers (chi 2 = 2.6, NS). The prevalence of rapid-cycling itself was also not different in the two groups of relatives. Rapid-cycling thus appears to arise from factors which are separable from the genetic vulnerability to bipolar illness and which do not lead to aggregation within families.
Asunto(s)
Trastorno Bipolar/genética , Trastornos Psicóticos/genética , Trastorno Depresivo/genética , Femenino , Humanos , Masculino , Factores de Riesgo , Factores Sexuales , Factores de TiempoRESUMEN
As compared with depressed relatives of normals, depressed relatives of affective patients are more likely to have severe impairment or incapacitation in their major life role when depressed, and more likely to suffer multiple episodes. These findings suggest that among major depressions, these clinical criteria may usefully identify cases with a familial, possibly genetic, vulnerability.
Asunto(s)
Trastorno Bipolar/genética , Trastorno Depresivo/genética , Trastornos Psicóticos/genética , Factores de Edad , Humanos , Factores SexualesRESUMEN
Seven persons (three normal volunteers and four euthymic bipolar patients) received one to four doses of gamma-aminobutyric acid (GABA) intravenously. All subjects reported dysphoria, and their mood disturbance scores on the Profile of Mood States were significantly increased in a dose-related fashion. Placebo infusions did not produce similar responses. Mood disturbance was accompanied by a dose-related increase in pulse and blood pressure.