RESUMO
The Personality Assessment Inventory (PAI; Morey, 1991) contains scales that were designed to make predictions about how an individual might respond to treatment, thereby allowing clinicians to attune treatment plans to a client's specific needs. The present study utilized two features of the PAI as predictors of treatment process and outcome in a sample of 47 outpatient veterans: the Treatment Rejection (RXR) scale and the Treatment Process Index (TPI). Data were collected for three treatment process and outcome measures: treatment utilization (ratio of appointments attended to appointments scheduled), therapist-rated therapeutic alliance, and symptom change over time. Results indicated that RXR significantly predicted utilization over and above the TPI. The TPI significantly predicted the rate of distress symptom decline over time, but RXR did not. Lastly, neither RXR nor the TPI were significant predictors of therapist-rated alliance.
Assuntos
Avaliação de Resultados em Cuidados de Saúde/métodos , Pacientes Ambulatoriais/psicologia , Determinação da Personalidade/estatística & dados numéricos , Cooperação e Adesão ao Tratamento/psicologia , Veteranos/psicologia , Adulto , Feminino , Humanos , Masculino , Pessoa de Meia-Idade , Valor Preditivo dos Testes , Relações Profissional-Paciente , PsicoterapiaRESUMO
Random-interval reinforcement was arranged for a sequence of pigeon first-key pecks followed by second-key pecks. First-key pecks, separated from reinforcers by delays that included number of second-key pecks and time, decreased in rate as delays increased. Delay functions, or gradients, were obtained in one experiment with reinforced sequences consisting of M first-key pecks followed by N second-key pecks (M + N = 16), in a second where required first-key pecks were held constant (M = 8), and in a third where minimum delay between most recent first-key pecks and reinforcers varied. In each, gradients were equally well fitted by exponential, hyperbolic and logarithmic functions. Performances were insensitive to reinforcer duration and functions were consistent across varied random-interval values. In one more experiment, time and number delays were independently varied using differential reinforcement of rate of second-key pecks. Delay gradients depended primarily on time rather than on number of second-key pecks. Thus, reinforcers have effects based on earlier responses, not just the ones that produced them, with the contribution of each response weighted by the time separating it from the reinforcer rather than by intervening behavior. Situations where unwanted responses (e.g., errors) often precede reinforced corrects can maintain them unless designed to avoid such effects of delay.
Assuntos
Esquema de Reforço , Animais , Columbidae , Condicionamento Operante , Feminino , Generalização Psicológica , Masculino , Reforço Psicológico , Fatores de TempoRESUMO
Schizophrenia is hypothesized to be the result of an interaction between specific genetic factors and nonspecific insults during embryonic development. Dermatoglyphic abnormalities appear to mark these putative insults--providing information about the temporal sequence of aberrant developmental events as well as the organism's vulnerability to their adverse effects. In the present study, dermatoglyphic measures thought to mark first and second trimester development were examined in patients with schizophrenia and first degree relatives and compared with those of healthy controls to examine whether genetic factors may mediate this vulnerability. Both patients with schizophrenia and relatives exhibited dermatoglyphic abnormalities compared with controls. Patients were more likely to exhibit dermatoglyphic abnormalities indicative of early second trimester development, which suggests that vulnerability interacts with the timing of insults to produce overt disease. These findings indicate that the two-hit model, in which schizophrenia-specific genetic factors combine in an additive fashion with environmental insults to produce the illness, may be oversimplified. Rather, the data are consistent with a more complex model in which nonspecific genetic factors that increase susceptibility to developmental abnormalities interact with insults and specific genetic factors.