Some effects of congenital spasticity on fundamental frequency

5 normal speakers and 5 speakers with congenital upper motor-neuron damage repeatedly spoke a three-work sentence stressing the first, second, or third words. Fundamental frequency was measured for each word and over each sentence. Analysis showed that the spastics' mean fundamental frequency was significantly higher than the normals', regardless of utterance. Also, spastics were more restricted in their prosodic maneuvering above this average fundamental frequency. Despite this finding, the spastics were capable of producing consistent stress patterns with normal variability.     

A nonsequential approach to the study of operant renewal: a reverse translation

ABA renewal is a model of treatment relapse that describes the recurrence of severe problem behavior when behavior learned in one context (e.g., home; A) and treated in a separate context (e.g., clinic; B) reemerges when the original context is reintroduced (A). However, in the typical environment and during the usual course of treatment for severe problem behavior, the target behavior is exposed to the baseline context periodically (e.g., the child returns home after several hours in a clinic setting). Due to the difficulty of studying what effect this may have on treatment relapse during ABA renewal in a strictly applied investigation, we developed a human‐laboratory translation to study renewal in a nonsequential manner. Using undergraduate students as subjects, we directly compared levels of recurrence using the standard ABA renewal procedure and a modified nonsequential ACA procedure, one modeled from the typical course of treatment for problem behavior. Both methods produced renewal at comparable levels, and patterns during nonsequential ACA renewal were similar to those during sequential ABA renewal. We discuss the implications of these findings in the framework of treatment for severe problem behavior.     

Parental Opioid Abuse: A Review of Child Outcomes,Parenting, and Parenting Interventions

Opioid abuse is now considered an epidemic, and many of the adults using this substance are parents. The purpose of the current paper is twofold: (1) to review rigorously conducted studies (e.g., included a comparison group; utilized inferential statistics) examining the association of opioid abuse with parenting and child outcomes, and (2) to review parenting intervention programs with these caregivers. Findings indicate that there are very few rigorously conducted studies examining children and parenting when parents abuse opioids. Furthermore, only four intervention programs have been conducted using randomized control trials and inferential statistics. We conclude that there is limited research that can be labeled as a rigorous science currently addressing this aspect of the opioid epidemic. Recommendations for further research are delineated.     

Follow-up evaluation of 55 child guidance cases

Parents coming to a child guidance clinic reported behaviour in their children which they (parents) viewed as problems or symptoms. The first 55 families coming to a new clinic were selected as part of a programme to evaluate the effects of the clinic's services on its total caseload. A follow-up inquiry was made about the presenting symptoms six months after the family ceased attending the Center. The parental reports of improvement in the child's symptoms appeared to be related to the extent to which both parents participated in coming to the clinic: the child's age also had some relationship to reported improvement. The kind of service provided, and the number of contacts with the Center appeared to be unrelated to reported improvement.     

Cellular and molecular mechanisms underlying learning and memory impairments produced by cannabinoids

Why does smoking marijuana impair learning and memory? Behavioral studies suggest that a disruption of normal hippocampal function contributes to these deficits. In vitro experiments find that cannabinoid receptor activation reduces neurotransmitter release below the levels required to trigger long-term changes in synaptic strength in the hippocampus. Cannabinoids reduce glutamate release through a G-protein-mediated inhibition of the calcium channels responsible for neurotransmitter release from hippocampal neurons. These mechanisms likely play a role in the learning and memory impairments produced by cannabinoids and by endogenous cannabinoid receptor ligands.