Pediatric Cardiology Fellowship Standards for Training in Exercise Medicine and Curriculum Outline.

Over the past 2 decades, fundamentals of exercise medicine, including clinical exercise testing, assessment and promotion of physical activity, exercise prescription, and supervised exercise training/rehabilitation programming have demonstrated considerable clinical value in the management of children and adolescents with congenital and acquired heart disease. Although the principles of exercise medicine have become an integral component in pediatric cardiology, there are no standardized training recommendations for exercise physiology during pediatric cardiology fellowship at this time. Thus, the Pediatric Cardiology Exercise Medicine Curriculum Committee (PCEMCC) was formed to establish core and advanced exercise physiology training recommendations for pediatric cardiology trainees. The PCEMCC includes a diverse group of pediatric cardiologists, exercise physiologists, and fellowship program directors. The expert consensus training recommendations are by no means a mandate and are summarized herein, including suggestions for achieving the minimum knowledge and training needed for general pediatric cardiology practice.

Clinicians' judgement of capacity of nursing home patients to give informed consent.

OBJECTIVE: The study determined the rate of incapacity to give informed consent for medical treatment among patients admitted to a nursing home and assessed whether clinical staff members recognized this incapacity and whether they used alternative means to provide surrogate decision making for their patients' treatment. METHODS: After 44 patients admitted to a nursing home affiliated with a major teaching hospital gave oral consent, two standardized tests, the Hopkins Competency Assessment Test (HCAT) and the Mini Mental State Examination (MMSE) were administered to them. Later a researcher blind to the test results reviewed subjects' clinical records to determine whether staff recognized any incapacity in giving informed consent for medical treatment. RESULTS: Twenty of 44 subjects were identified by the HCAT as incompetent to give informed consent for medical treatment. Clinical staff had identified 13 of those subjects as clinically incompetent. None of the subjects whom clinical staff identified as clinically incompetent was provided with surrogate decision makers in accordance with procedures outlined in state law. CONCLUSIONS: The prevalence of incapacity to give informed consent in the nursing home population was high. Clinical screening by staff did not identify all clinically incompetent patients, and staff had unresolved conflicting opinions about individual patients' capacity to give informed consent. Even when staff recognized a patient's incapacity to give informed consent, proper legal procedures for appointing surrogate decision makers were not followed.

Evidence for two functionally distinct subpopulations of neurons within the rat striatum.

Type I and Type II extracellular action potential waveforms were recorded from the rat striatum and studied with respect to their dependence on recording conditions, response to paired impulse stimulation of the corticostriatal pathway, and iontophoretic application of dopamine (DA). Results showed that the distinguishing characteristics of Type I and Type II waveforms are relatively independent of the degree of filtering, distance of the electrode tip from the target neuron, type of recording electrode, and firing rate of the neuron. Very low impedance electrodes, however, were found to mask the difference in spike shape. Electrical stimulation of cortical afferents results in excitation of both action potential waveforms, though the Type II class exhibits a significantly shorter latency than the Type I class. Paired impulse analyses revealed that both waveforms exhibit variation in the probability of discharge (facilitation or inhibition) to the second impulse of each impulse pair that are a function of the interimpulse interval. Most importantly, however, the probabilities of discharge of Type I and Type II neurons to the second impulse are inversely related, i.e., when one cell type exhibits facilitation, the other displays inhibition. These data demonstrate that Type I and Type II waveforms represent the activity of functionally different subpopulations of striatal neurons. Moreover, Type II neurons are found much more often than Type I cells, suggesting that the 2 cell classes may be represented with different frequencies within striatum. Finally, Type II neurons display at least a 5 times greater sensitivity to iontophoretically applied DA than Type I cells, suggesting that the 2 cell populations also are affected differentially by dopaminergic input from the substantia nigra.

Effects of dopamine depletion on the spontaneous activity of type I striatal neurons: relation to local dopamine concentration and motor behavior.

The relation between the electrophysiological activity of Type I striatal neurons, local dopamine (DA) concentration, and motor behavior in rats was investigated using intraventricular administration of the neurotoxin 6-hydroxydopamine (6-HDA) and extracellular single-unit recording. Results are compared with findings of past experiments in which the activity of Type II striatal neurons was examined after comparable 6-HDA-induced lesions. Several differences between the present observations and the earlier results were found. First, although large depletions (greater than 50%) of DA local to the site of the recording were required before the spontaneous firing rate of either cell type was increased, the levels necessary for this effect were found to be less for Type I cells than for Type II neurons. Second, although DA depletions of greater than 50% always were associated with increased Type I cell activity, depletions of greater than 95% resulted in spontaneous firing rates that were lower than those observed after depletions of approximately 90%. Thus, the relation between extent of dopaminergic depletion and Type I cell firing rate was biphasic, whereas that relation previously was found to be monophasic for Type II neurons. Finally, whereas increased Type I cell activity in the lateral striatum was associated with the aphagia, adipsia, and akinesia induced by large DA-depleting brain lesions, increased Type II cell activity in the medial striatum was found to be associated with these impairments. Because accumulating evidence suggests that the functioning of the lateral striatum is more critical for these behaviors, however, it is proposed that the substrate of the behavioral dysfunctions resulting from DA depletion is the Type I cell population in lateral striatum.

Lesions of the retrosplenial cortex produce deficits in reversal learning of the rabbit nictitating membrane response: implications for potential interactions between hippocampal and cerebellar brain systems.

The effect of bilateral lesions of the retrosplenial cortex on discrimination reversal learning of the rabbit nictitating membrane response was examined. Results showed that animals with such lesions were not impaired in their ability to acquire a cross-modality discrimination, but were severely impaired in their ability to reverse the discrimination once it was learned. All animals failed at the reversal phase of the task because they displayed high levels of conditioned responding to both the CS+ and the CS-. Thus bilateral damage to the retrosplenial cortex results in deficits in reversal learning that are highly similar to those observed after bilateral hippocampectomy. These findings are interpreted within a conceptual framework that characterizes multisynaptic projections from the hippocampus to the retrosplenial cortex, and ultimately to the cerebellum, as responsible for the behavioral expression of learning-related changes in hippocampal pyramidal cell activity.

Short-term effects of dopamine-depleting brain lesions on spontaneous activity of striatal neurons: relation to local dopamine concentration and behavior.

The spontaneous activity of striatal neurons was measured after dopamine (DA)-depleting brain lesions were produced in rats by the neurotoxin 6-hydroxydopamine. The extent of DA depletion was determined using tissue punches from the same regions of striatum in which cell activity was recorded. Results showed that the spontaneous activity of Type II neurons in either the medial or lateral striatum increased only when local DA depletions exceeded 90%; when local depletions were less than 90%, spontaneous firing rates of Type II neurons were equivalent to control values. This finding was consistent with additional observations that ingestive and motor behaviors of the same animals were not disrupted until striatal DA depletions exceeded 90%. It also was found that spontaneous firing rates of neurons in the lateral but not the medial striatum could be at control levels in animals clearly exhibiting aphagia, adipsia and akinesia.

Hippocampectomy disrupts the topography of conditioned nictitating membrane responses during reversal learning.

The effects of bilateral hippocampectomy on the topography, or shape, of conditioned nictitating membrane (NM) responses were examined during four learning tasks: one-tone delay conditioning, unpaired extinction, two-tone discrimination, and reversal of two-tone discrimination. Results showed that hippocampal ablation altered conditioned NM response topography only during reversal learning and not during the other training paradigms. In addition, the shapes of learning curves for hippocampectomized animals were different from those of control animals during reversal conditioning but not during the other paradigms. The implications of these findings with respect to unit-recording studies of hippocampal cellular activity during classical conditioning of the NM response are discussed.

Hippocampectomy disrupts acquisition and retention of learned conditional responding.

The effects of bilateral hippocampal and neocortical lesions were examined on acquisition and retention of classically conditioned responses based on (a) simple associations, (b) a nonconditional discrimination, and (c) a conditional discrimination in the same subjects. Results showed that combined hippocampal and neocortical damage permanently prevented (within the limits tested) both acquisition and retention of learned behavior based on the conditional discrimination but had no effect on behaviors based on the nonconditional discrimination or simple associations. Neocortical lesions alone had no effect on either conditional or nonconditional discriminative responding, but they did temporarily disrupt acquisition and retention of behavior dependent on CS-CS (two conditioned stimuli) associations. Neither lesion affected learned behaviors mediated by CS-US (conditioned stimulus and unconditioned stimulus) associations. Thus, results showed that hippocampal damage selectively disrupted learned conditional behaviors and also revealed that central nervous system control of conditional discrimination performance, within-compound associations, and CS-US associations is mediated by different neural mechanisms.

Hippocampectomy selectively disrupts discrimination reversal conditioning of the rabbit nictitating membrane response.

The effects of hippocampal lesions were tested on two-tone discrimination reversal conditioning of the rabbit nictitating membrane response. Results showed that hippocampectomized animals learned the initial two-tone discrimination at rates equivalent to operated control animals and animals with neocortical lesions. During reversal conditioning, however, animals with hippocampal lesions were severely impaired relative to both other groups. Neocortical lesions were without effect on reversal learning. An additional study revealed that the hippocampectomized animals' failure at reversal could not be attributed to a lesion-induced increased resistance to extinction. Results are discussed with respect to several theories of hippocampal function, and with respect to changes in the activity of hippocampal pyramidal neurons which occur during classical conditioning of the nictitating membrane response.