Family Therapy in Trouble: Psychoeducation as Solution and as Problem

The authors cite clinical literature attesting to the importance of recognizing the family, rather than the individual, as the proper locus of conceptualizing, diagnosing, and treating mental illnesses. Specifically with regard to severe psychiatric illnesses, in particular schizophrenia, family dysfunction contributes to the emergence of the illness, significantly affects its course, and strongly influences the achievement and maintenance of treatment gains. Currently, a movement is afoot to limit sharply the amount and kind of treatment offered to schizophrenic patients and their families. Rooted in a “medical model” or “biogenic” view of the etiology of schizophrenia, this school of thought prescribes psychoeducation as the family treatment of choice. The present article looks at some misconceptions regarding treatment that prompted a widespread turning away from psychoanalytically oriented family psychotherapy for schizophrenic patients and their families, examines the reductionism (biological and behavioral) inhering in the exclusive use of psychoeducation, and looks at the clinical dangers of such reductionism. Finally, it proposes that family psycho-therapists should not abandon a concern with the inner lives of severely ill patients and their families in the face of spuriously generalized claims made by reductionist researchers.     

Force variability in isometric responses

In the present study we examined the contribution of different impulse parameters to peak force variability in an isometric task. Five experiments are reported that each held constant a different impulse parameter while allowing the other impulse parameters to vary. The results indicate that change in force level is the parameter that has the greatest effect on peak force variability, although time to peak force and preload also systematically influence response variability. A formula that accommodates the relation between impulse parameters and force variability is proposed. The data suggest that even in isometric tasks, it is the force-time properties of the impulse, rather than discrete parameters such as peak force, that determine the outcome variability.     

Age-related changes in working and reference memory performance and locomotor activity in the Wistar rat

Wistar rats of three age groups were tested in an automated tunnel-maze system of variable geometry to investigate whether changes in spontaneous locomotor activity and in learning and memory develop differentially or in a correlated fashion as a function of age. Senescent (30 months) as well as mature-adult (17 months) rats showed an age-correlated decline of locomotor activity as compared to the mature-young (5 months) group. Both working-memory (measured as within-trial arm discrimination performance) and reference-memory (measured as avoidance of "blind alley" visits) were severely affected in the senescent group, whereas the middle-aged animals suffered only from a working-memory deficit. The findings provide evidence that locomotor deficits do not necessarily interfere in the assessment of age-related changes in cognitive performance. Furthermore the results support the hypothesis that working and reference memory have different underlying physiological correlates and that these neuronal systems are differentially affected by the aging process.     

Serotonergic and opiate interactions in the modulation of drug- and environmental-induced analgesia in the neonatal rat pup

Serotonergic and opiate interactions in the modulation of drug- and environmental-induced analgesia were assessed in 6-day-old Sprague-Dawley-derived rat pups using tail-flick testing procedures. In these experiments the serotonergic antagonist metergoline was observed to attenuate both the analgesia induced by the opiate agonist morphine and the analgesia induced by isolation from siblings and the dam, an environmental manipulation which has previously been shown to be associated with increases in opiate activity. In contrast, the opiate antagonist naloxone was observed to be ineffective in blocking not only analgesia induced by the serotonergic agonist quipazine, but also analgesia induced by long-term deprivation from the dam and food, a manipulation that has been previously reported to induce increases in serotonergic utilization. These results suggest that in the neonate, as in the adult, the serotonergic modulation of nociception appears to occur "downstream" from the opiate systems serving to regulate nociception following both drug- and environmental-induced alterations in pain sensitivity. Analgesia induced by long-term deprivation from food and the dam appears to be strongly related to increases in serotonergic activity and relatively unaffected by opiate antagonism, whereas analgesia induced by isolation from siblings and the dam may be related to increases in opiate activity, but modulated by serotonergic systems serving to regulate pain responsivity. Thus alterations in the environment, mediated at least in part by alterations in opiate and serotonergic activity, appear to play an important role in influencing the sensitivity of the neonate to pain stimuli.     

Comprehension of sentence structure in anomic and conduction aphasia

Picture-pointing auditory and reading comprehension tests were administered to anomic and conduction aphasics. Subjects responded to active sentences of the present progressive form. The possible errors which a subject could make on these experimental tasks included failure to correctly interpret noun order, number, or lexical meaning. Both groups made significantly more correct responses than error responses. Of their error responses, noun-order errors significantly exceeded number and lexical errors for which no differences were observed. When compared with results previously obtained for agrammatic Broca's aphasics, no differences in the pattern of errors were identified. These results are discussed relative to current theories of syntactic processing and for the mechanisms which account for these syntactic comprehension deficits following aphasia.