The Effects of Two Taped-Words Interventions on Sight-Word Reading in Students with Mental Retardation

Multiple-baseline and alternating treatments design elements were combined to evaluate the effects of two taped-words (TW) interventions (rapid-paced and slow-paced) on sight-word reading accuracy levels in elementary students with mental retardation. During rapid TW, one word was presented every second via tape recorder and students were instructed to read aloud along with the tape. During slow TW, words were presented every 5s. Both TW interventions increased word reading accuracy but differences in learning rates between the two TW interventions were inconsistent across participants. Although no firm conclusions can be drawn regarding which pace is more effective, results show that regardless of pace, this efficient, self-managed intervention can be used to increase sight-word reading in students with mental retardation.     

The personal inventory as a psychotherapeutic technique in treating a person with AIDS

The use of a personal inventory, an adaptation of the moral inventory used in Twelve Step programs, is discussed as a psychotherapeutic tool in providing treatment to persons with AIDS. Clinical application of this technique can facilitate progress toward achieving a sense of integrity prior to death by addressing a client's feelings of guilt and shame. The authors describe the use of this technique in working with a young adult African-American female diagnosed with AIDS and discuss appropriate and inappropriate applications of this approach.     

Interrupting neural pathways that transduce stressful information into physiological responses.

Stressor-stimuli evoke a noradrenergic process in the frontal lobes, the amplitude of which depends on both the individual's experience with the stimulus and his or her genetic background. Novel and noxious stimuli evoke large frontocortical responses and benign ones evoke relatively larger reactions in persons with a family history of cardiovascular disease. Blockade of neural projections from the frontal cortex and amygdala to the brainstem cardiovascular centers will normalize blood-pressure elevations in experimental hypertension and prevent lethal arrhythmias in animals with a myocardial infarction. The anti-mortality effect of the cardiac drugs known as beta-blockers is exerted by inhibition of cerebral beta-receptors, not peripheral ones. A new putative neuropeptide, NLX, may have the same desirable cardiovascular effects, but without the side-effects that limit clinical usefulness. The neural regulation of the heart during stress can be detected by a new deterministic measure of low-dimensional chaos in heartbeat intervals. In both animals and humans undergoing myocardial infarction, this deterministic measure correctly predicts lethal arrhythmogenesis, minutes to hours prior to the event. Thus an approach combining both brain and heart studies (i.e., "neurocardiology") has led to an understanding of how stressor-stimuli evoke autonomic reactions. This, in turn, has led to new methods in the diagnosis and treatment of cardiovascular disorders.     

Neurocardiology shows that the central, not peripheral, action of propranolol reduces mortality following acute coronary artery occlusion in the conscious pig.

Neurocardiology emphasizes the role of the higher cerebral mechanisms in cardiovascular disorders. Several large clinical trials (BHAT, MIAMI, and ISIS) have consistently shown that treatment with a beta-receptor blocker (propranolol, metoprolol, or atenolol) will produce a 26% to 29% reduction in mortality in high-risk survivors of acute myocardial infarction. Because all beta-blockers cross the blood-brain barrier, it is not clear whether the salutary action is on the central or peripheral receptors. Therefore the effects of intracerebral versus intravenous propranolol were observed in 30 conscious pigs following complete occlusion of the left anterior descending coronary artery. Controls showed the propranolol to remain confined throughout the experiment to the central or peripheral compartment into which it was injected. To assure the occurrence of ventricular fibrillation (VF), each pig was psychologically stressed by being unconditioned to the laboratory. Intracerebral propranolol (0.05 mg/kg) prevented VF within a 20 min period of reversible ischemia in 6 of 9 pigs, whereas VF was prevented in 0 of 11 controls injected intravenously with either dextro-propranolol (2 pigs) or vehicle (9 pigs) (P less than .0006, binomial probability ratio). In some pigs in which VF was not manifested by 20 min, the ischemia was reversed and additional control observations were achieved; a total of 10 counter-balanced within-subjects experiments confirmed the between-subjects result (P less than .01, paired-t test). In contrast intravenous propranolol (0.2 to 2.0 mg/kg) in 7 pigs had no effect on VF latency compared to 7 vehicle controls. It is concluded that beta-receptor antagonists prevent VF in the ischemic myocardium by their effect on the brain and not the heart.     

Methylphenidate and stimulus control of avoidance behavior

The introduction of a warning signal that preceded a scheduled shock modified the temporal distribution of free-operant avoidance responses. With response-shock and shock-shock intervals held constant, response rates increased only slightly when the response-signal interval was reduced. The result is consistent with Sidman's (1955) findings under different conditions, but at variance with Ulrich, Holz, and Azrin's (1964) findings under similar conditions. Methylphenidate in graded doses increased response rates, modifying frequency distributions of interresponse times. Drug treatment may have disrupted a "temporal discrimination" formed within the signal-shock interval. More simply, methylphenidate influenced response rates by increasing short response latencies after signal onset; this effect was more prominent than the drug's tendency to increase the frequency of pre-signal responses. When signal-onset preceded shock by 2 sec, individual differences in performance were marked; methylphenidate suppressed responding in one rat as a function of increasing dose levels to a greater degree than in a second animal, but both subjects received more shocks than under control conditions.