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Dive into the research topics where Ralph E. Tarter is active.

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Featured researches published by Ralph E. Tarter.


American Journal of Drug and Alcohol Abuse | 1990

Evaluation and Treatment of Adolescent Substance Abuse: A Decision Tree Method

Ralph E. Tarter

A procedure for systematically evaluating and treating adolescents with known or suspected substance abuse is described. Integrating assessment with intervention affords the opportunity to comprehensively characterize the adolescents problems and to quantitatively monitor treatment progress and outcome.


Development and Psychopathology | 1999

Etiology of early age onset substance use disorder: A maturational perspective

Ralph E. Tarter; Michael Vanyukov; Peter R. Giancola; Michael A. Dawes; Timothy C. Blackson; Ada C. Mezzich; Duncan B. Clark

The etiology of early age onset substance use disorder (SUD), an Axis I psychiatric illness, is examined from the perspective of the multifactorial model of complex disorders. Beginning at conception, genetic and environment interactions produce a sequence of biobehavioral phenotypes during development which bias the ontogenetic pathway toward SUD. One pathway to SUD is theorized to emanate from a deviation in somatic and neurological maturation, which, in the context of adverse environments, predisposes to affective and behavioral dysregulation as the cardinal SUD liability-contributing phenotype. Dysregulation progresses via epigenesis from difficult temperament in infancy to conduct problems in childhood to substance use by early adolescence and to severe SUD by young adulthood.


Drug and Alcohol Dependence | 1998

Adolescent versus adult onset and the development of substance use disorders in males.

Duncan B. Clark; Levent Kirisci; Ralph E. Tarter

This study examines the influence of adolescent age of onset on the development of substance use disorders (SUD) by comparing adult males (n = 181) with SUD categorized into adolescent-onset, early-adult onset and late-adult onset groups on patterns of substance use and related disorders, time course of the development of substance dependence and rates of comorbid mental disorders. A sample of male adolescents (n = 81) with SUD was also included as a comparison group. The subjects were recruited from intervention programs in the community and participated in semistructured interviews with diagnoses determined by the best estimate method. Adolescent-onset adults, compared with other adult-onset groups, had higher lifetime rates of cannabis and hallucinogen use disorders, shorter times from first exposure to dependence, shorter times between the development of their first and second dependence diagnoses and higher rates of disruptive behavior disorders and major depression. Adolescents were similar to adolescent-onset adults. While the findings must be interpreted in light of methodological limitations, these results suggest that adolescent-onset SUD is a distinct subtype involving different substances and more rapid development than adult-onset SUD.


Journal of Consulting and Clinical Psychology | 1994

Alcoholism: a developmental disorder.

Ralph E. Tarter; Michael Vanyukov

Alcoholism etiology is discussed from a developmental behavior genetic perspective. At the outset point, temperament characteristics, by means of ongoing and reciprocal interaction with the social environment, shape the course of behavioral development. The behavioral characteristics successively acquired during development are vectors that determine the ontogenetic trajectory that culminates ultimately in the clinical disorder of alcoholism. The temperament features that appear to be associated with a heightened risk for alcoholism are examined. Their interactions with the environment during the course of development are considered within an epigenetic framework and, as discussed, have important ramification for improving the prevention and treatment of alcoholism.


Clinical Psychology Review | 2002

Origins and consequences of child neglect in substance abuse families.

Marija G. Dunn; Ralph E. Tarter; Ada C. Mezzich; Michael Vanyukov; Levent Kirisci; Galina P. Kirillova

The empirical literature pertaining to the prevalence, origins, and consequences of neglectful parenting as it relates to substance abuse is critically reviewed. Available evidence indicates that children who experience parental neglect, with or without parental alcohol or drug abuse, are at high risk for substance use disorder (SUD). The effects of parental substance abuse on substance abuse outcome of their children appear to be partly mediated by their neglectful parenting. The discussion concludes with presentation of a developmental multifactorial model in which neglect, in conjunction with other individual and environmental factors, can be integratively investigated to quantify the childs overall liability across successive stages of development as well as to map the trajectory toward good and poor outcomes.


Substance Use & Misuse | 1975

Psychological Deficit in Chronic Alcoholics: A Review

Ralph E. Tarter

Chronic alcoholics exhibit impaired performance on a variety of psychological measures. While no generalized intellectual deterioration is evident, specific deficits on spatial, cognitive, learning, and motor tasks are observed. The manifest pattern of deficits is amenable to a neuropsychological interpretation, of which the presently most comprehensive hypothesis asserts that alcoholics suffer from a neurological disorder that is primarily localized to the anterior-basal region of the brain.


Gastroenterology | 1984

Nonalcoholic Cirrhosis Associated With Neuropsychological Dysfunction in the Absence of Overt Evidence of Hepatic Encephalopathy

Ralph E. Tarter; Andrea M. Hegedus; David H. Van Thiel; Robert R. Schade; Judith S. Gavaler; Thomas E. Starzl

Although much is known about the neuropsychological functioning of cirrhotic individuals with Laennecs (alcohol associated) cirrhosis, little is known about the neuropsychological functioning of individuals with nonalcoholic cirrhosis. In the present investigation, we have determined that individuals suffering from chronic nonalcoholic cirrhosis, despite the absence of clinical signs of hepatic encephalopathy, are impaired on neuropsychological tests that measure visuopractic capacity, visual scanning, and perceptual-motor speed. In contrast, intellectual, language, memory, attentional, motor, and learning abilities are intact. In comparison with a chronically ill control group of patients suffering from Crohns disease, individuals with advanced nonalcoholic cirrhosis exhibit less emotional disturbance, but are more impaired in their daily activities. These findings indicate that individuals with nonalcoholic cirrhosis, even in the absence of overt clinical signs of encephalopathy, manifest neuropsychological impairments and experience significant disruption in the routines of everyday living.


Neuroscience & Biobehavioral Reviews | 2003

Liability to substance use disorders: 1. Common mechanisms and manifestations

Michael Vanyukov; Ralph E. Tarter; Levent Kirisci; Galina P. Kirillova; Brion S. Maher; Duncan B. Clark

Variation in the risk for and severity of substance use disorders (SUD) in the population is caused by multiple organismic (genetic, biochemical, psychological) and environmental factors. Whereas drug- or drug-class-specific liability mechanisms exist, a substantial proportion of variance in the risk is shared between specific liabilities, reflecting mechanisms that determine common liability to SUD. Data from epidemiologic, clinical, psychological, physiological, biochemical, and family and genetic studies reviewed in this paper indicate the existence of mechanisms and characteristics shared in common by liabilities to SUD related to different drugs. These mechanisms can be conceptualized as common liability to SUD, a latent trait accounting for a substantial portion of variation in SUD risk and severity and determined by all factors influencing the probability of SUD development. An accompanying paper describes an approach to the quantitative estimation of this trait.


Journal of Abnormal Child Psychology | 2002

Reactive aggression in boys with disruptive behavior disorders: behavior, physiology, and affect.

Daniel A. Waschbusch; William E. Pelham; J. Richard Jennings; Andrew R. Greiner; Ralph E. Tarter; Howard B. Moss

This study examined responses to peer provocation in boys ages 9–13 years who met symptomatic criteria for ADHD-only, ODD/CD-only, comorbid ADHD/ODD/CD, or no diagnosis. Boys participated in a reaction-time game that included standardized verbal and behavioral provocation. Their behavioral, physiological, and affective responses to this task were measured. Results showed that groups did not differ following high levels of provocation because all boys behaved aggressively. However, following low provocation boys with comorbid ADHD/ODD/CD had higher levels of behavioral aggression, had greater heart rate acceleration, and were rated as angrier than all other boys. In addition, boys with comorbid ADHD/ODD/CD held a grudge longer than other children. Results suggest that boys with comorbid ADHD/ODD/CD are especially reactive to provocation from their peers.


American Journal on Addictions | 2002

Etiology of adolescent substance abuse: A developmental perspective.

Ralph E. Tarter

Approximately 5% of adolescents in the U.S. qualify for a diagnosis of substance use disorder (SUD). Low affect and behavior self-regulation during child development interacting with family, peer and other ecological factors predisposes to substance use in adolescence. Maturational processes during adolescence, particularly involving the brain and reproductive system, exacerbate the low psychological self-regulation evidenced during childhood to promote initiation of alcohol, tobacco, and other drug (ATOD) consumption. This discussion examines the etiology of ATOD abuse and SUD from a developmental perspective. The ramifications of a developmental perspective for clinical practice and social policy are also considered.

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Levent Kirisci

University of Pittsburgh

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David H. Van Thiel

Rush University Medical Center

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Ada C. Mezzich

University of Pittsburgh

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Howard B. Moss

University of Pittsburgh

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Ty A. Ridenour

University of Pittsburgh

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