A Note on the "One Case per Stagger Position" Character of Common Multiple-Baseline Intervention Designs.

PURPOSE: To overcome the constraint of common multiple-baseline designs that only one case per stagger position is permitted. METHODS: Three alternative strategies for assigning more than one case to each stagger position are examined. RESULTS: The three recommended strategies achieve the objective while maintaining the study's internal and statistical-conclusion validities. CONCLUSIONS: ExPRT, a freely available Excel-based randomization-test package, can be used to assist in both the design and statistical analysis associated with each of the strategies.

Comparison of randomization-test procedures for single-case multiple-baseline designs.

In three simulation investigations, we examined the statistical properties of several different randomization-test procedures for analyzing the data from single-case multiple-baseline intervention studies. Two procedures (Wampold-Worsham and Revusky) are associated with single fixed intervention start points and three are associated with randomly determined intervention start points. Of the latter three, one (Koehler-Levin) is an existing procedure that has been previously examined and the other two (modified Revusky and restricted Marascuilo-Busk) are modifications and extensions of existing procedures. All five procedures were found to maintain their Type I error probabilities at acceptable levels. In most of the conditions investigated here, two of the random start-point procedures (Koehler-Levin and restricted Marascuilo-Busk) were more powerful than the others with respect to detecting immediate abrupt intervention effects. For designs in which it is not possible to include the same series lengths for all cases, either the modified Revusky or restricted Marascuilo-Busk procedure is recommended.

Additional comparisons of randomization-test procedures for single-case multiple-baseline designs: Alternative effect types.

A number of randomization statistical procedures have been developed to analyze the results from single-case multiple-baseline intervention investigations. In a previous simulation study, comparisons of the various procedures revealed distinct differences among them in their ability to detect immediate abrupt intervention effects of moderate size, with some procedures (typically those with randomized intervention start points) exhibiting power that was both respectable and superior to other procedures (typically those with single fixed intervention start points). In Investigation 1 of the present follow-up simulation study, we found that when the same randomization-test procedures were applied to either delayed abrupt or immediate gradual intervention effects: (1) the powers of all of the procedures were severely diminished; and (2) in contrast to the previous study's results, the single fixed intervention start-point procedures generally outperformed those with randomized intervention start points. In Investigation 2 we additionally demonstrated that if researchers are able to successfully anticipate the specific alternative effect types, it is possible for them to formulate adjusted versions of the original randomization-test procedures that can recapture substantial proportions of the lost powers.

Mechanism of NMDA receptor contribution to axon-to-glia signaling in the crayfish medial giant nerve fiber.

Electrical stimulation of crayfish giant axons at high frequency activates group II metabotropic and NMDA glutamate receptors on adjacent glial cells via release of N-acetylaspartylglutamate and glutamate formed upon its hydrolysis. This produces a transient depolarization followed by a prolonged hyperpolarization of glial cells that involves nicotinic acetylcholine receptor activation. The hyperpolarization is nearly completely blocked by antagonists of metabotropic glutamate receptors but only slightly reduced by inhibition of NMDA receptors. We report that the NMDA-induced hyperpolarization of glial cells is reduced by decreased calcium in the solution bathing the giant nerve fiber, while removal of sodium ions or block of voltage-dependent calcium channels completely prevents the glial response to NMDA. Inhibition of nicotinic acetylcholine receptors or removal of extracellular Cl(-) converts the glial response from a hyperpolarization to a depolarization that is sensitive to NMDA receptor antagonist. We propose that NMDA receptor activation by glutamate, formed from extracellular N-acetylaspartylglutamate during nerve stimulation, contributes to glial hyperpolarization by increasing intracellular Ca(2+) via opening of voltage-sensitive Ca(2+) channels. Based on our previous work, we propose further that the added Ca(2+) supplements that produced by N-acetylaspartylglutamate and glutamate acting on group II metabotropic glutamate receptors to cause an increased release of acetylcholine and a larger hyperpolarization.