Janis L. Anderson

Testing the testing effect in the classroom

Laboratory studies show that taking a test on studied material promotes subsequent learning and retention of that material on a final test (termed the testing effect). Educational research has virtually ignored testing as a technique to improve classroom learning. We investigated the testing effect in a college course. Students took weekly quizzes followed by multiple choice criterial tests (unit tests and a cumulative final). Weekly quizzes included multiple choice or short answer questions, after which feedback was provided. As an exposure control, in some weeks students were presented target material for additional reading. Quizzing, but not additional reading, improved performance on the criterial tests relative to material not targeted by quizzes. Further, short answer quizzes produced more robust benefits than multiple choice quizzes. This pattern converges with laboratory findings showing that recall tests are more beneficial than recognition tests for subsequent memory performance. We conclude that in the classroom testing can be used to promote learning, not just to evaluate learning.

Biologic rhythm disorders, depression, and phototherapy. A new hypothesis.

Disturbances of the circadian timing system are implicated in the pathogenesis of numerous clinical syndromes, including sleep and affective disorders. Abnormalities of circadian rhythms can now be directly measured in the clinical laboratory and potentially corrected. Sleep scheduling disorders are most commonly due to phase misalignments between the endogenous circadian pacemaker and the socioenvironmental schedule. Current research is increasing our understanding of the influence of bright light exposure on the circadian timing system and has begun to be used successfully in the management of these conditions. There is substantial evidence that abnormalities of the circadian timing system are associated with depression. However, the application of new biologic rhythm diagnostic techniques would be required to establish whether circadian dysfunction is involved in the pathogenesis of these conditions. We propose a new hypothesis that phototherapy for seasonal depression may act by increasing an abnormally low circadian amplitude in those patients, such as that reported in endogenously depressed patients. The powerful effect of light on the circadian system indicates that phototherapy may become an important tool in the management of disorders of circadian etiology.

Effects of Bright Incandescent Light on Seasonal and Nonseasonal Major Depressive Disorder

Previous research has indicated that exposure to bright fluorescent light can benefit clinically depressed individuals. The present study, a 1- to 2-week open trial of bright (greater than or equal to 2,000 lux) incandescent light with seasonal (fall/winter) and nonseasonal depressives, produced a therapeutic effect on seasonal depression, as measured by three criteria for recovery: final score on the Hamilton Rating Scale for Depression (HRSD) less than 10; final HRSD score less than or equal to 50% of pretreatment HRSD score; no longer meets DSM-III criteria for major depressive disorder. Phototherapy was not effective in the nonseasonal patients, whose functioning was more impaired than that of the seasonal subjects even before the trial. No adverse effects were observed in any patient.

Lux vs. wavelength in light treatment of Seasonal Affective Disorder

Objective:  Published dosing guidelines for treatment of Seasonal Affective Disorder (SAD) refer to photopic lux, which is not appropriate for short‐wavelength light. Short wavelengths are most potent for many non‐visual responses to light. If SAD therapy were similarly mediated, standards utilizing lux risk overestimating necessary dose. We investigated antidepressant responses to light using two light‐emitting diode (LED) sources, each emitting substantial short‐wavelength light, but <2500 lux.

Sleep in fall/winter seasonal affective disorder: effects of light and changing seasons.

Disturbances of sleep are a hallmark of seasonal affective disorders (SAD), as they are of other mood disorders. Fall/winter SAD patients most often report hypersomnia. Among responses of 293 SAD patients on a symptom questionnaire, complaints of winter hypersomnia (80%) greatly exceeded insomnia (10%), hypersomnia plus insomnia (5%), or no sleep difficulty (5%). Increased sleep length in fall/winter is not unique to SAD. Among 1571 individuals across four latitudes surveyed at random from the general population, winter sleep increases of < or = 2 hr/day relative to summer were reported by nearly half. However, hypersomnia had a low correlation (r = 0.29) with the total number of other SAD symptoms that were reported in this sample. Ten SAD patients kept daily sleep logs across 1 yr that showed increases in fall and winter (sleeping most in October; least in May) whose maximum averaged 2.7 hr per day more weekend sleep than in spring and summer. These winter increases might have been somewhat attenuated since most received light therapy during part of the winter. Nocturnal EEG recordings of depressed SAD patients in winter showed decreased sleep efficiency, decreased delta sleep percentage, and increased REM density (but normal REM latency) in comparison with recordings: (1) from themselves in summer; (2) from themselves after > or = 9 days of light therapy; or (3) from age- and gender-matched healthy controls. Thus, the extent of fall/winter oversleeping recorded by our SAD patients did not differ dramatically from that reported by the general population, but sleep complaints of our SAD patients have been accompanied by features of sleep architecture that are different from healthy controls and are reversed by summer or by bright-light therapy.

Serotonin receptor changes after chronic antidepressant treatments: Ligand binding, electrophysiological, and behavioral studies

Early biochemical research on antidepressant treatments provided evidence that the treatments alter catecholaminergic and serotonergic activity. The mechanisms of action proposed by the resulting biogenic amine hypotheses of affective disorders, however, are not consistent with the delayed onset of therapeutic effects of antidepressant treatments nor with the acute effects of more recently developed antidepressant drugs. Recent investigation of chronic antidepressant treatments using ligand binding, electrophysiological, and behavioral techniques have attempted to identify subgroups of receptors that might be affected uniquely and specifically by chronic antidepressant treatments. Such receptor changes have been suggested to form a basis for the mechanism of action of antidepressants. At the present time, however, the data produced by ligand binding experiments and electrophysiological experiments investigating serotonergic functioning do not fit together. In addition, interpretational problems and internal contradictions exist within each of the three bodies of data when straightforward hypotheses regarding a serotonergic role in antidepressant treatment are formulated. In order to clarify the serotonergic role in antidepressant drug and ECS effects the functional significance of observed changes in putative serotonergic receptors must be discovered. Unfortunately, putative receptors identified by ligand binding cannot be directly compared to those identified by electrophysiological techniques, because these two methods require the disassembly of the organism in mutually incompatible ways. In order to prove that either or both techniques do in fact identify functional serotonin receptors, investigators need to proceed both more microscopically and also more globally. Further anatomical and physiological studies are necessary to locate putative receptors and to demonstrate their place in existing serotonergic networks. Further behavioral studies must be done to relate alterations in receptor characteristics to the functioning of the intact organism.

Use of a supplementary internet based education program improves sleep literacy in college psychology students

INTRODUCTION Knowledge regarding the importance of sleep in health and performance and good sleep hygiene practices is low, especially among adolescents and young adults. It is important to improve sleep literacy. Introductory psychology is one of the most highly enrolled courses at colleges and universities. This study tested the impact of an Internet-based learning module on improving sleep literacy in this venue. METHODS An Internet-based supplementary learning module containing sleep physiology and hygiene information was developed using content from the Harvard Medical School sleep educational website http://www.understandingsleep.org. Access to the module was provided as an extra credit activity for 2 of 4 sections (Supplemental Sleep, SS, N = 889) of an introductory college psychology course during their standard instruction on sleep and dreaming. The remaining 2 sections (Standard Instruction, SI, N = 878) only were encouraged to visit the website without further direction. Level of knowledge was assessed before and after availability to the module/website and at the end of the semester. Students were asked to complete a survey at the end of the semester inquiring whether they made any changes in their sleep behaviors. RESULTS Two hundred fifty students participated in the extra credit activity and had data available at all testing points. Students in the SS Group had a significant improvement in sleep knowledge test scores after interacting with the website in comparison to the SI group (19.41 ± 3.15 vs. 17.94 ± 3.08, p < 0.001). This difference persisted, although at a lower level, at the end of the semester. In addition, 55.9% of the SS group versus 45.1% of the SI group indicated that they made changes in their sleep habits after participation in the extra credit sleep activity (p < 0.01). The most common change was a more consistent wake time. CONCLUSION Use of a supplementary internet-based sleep learning module has the potential to enhance sleep literacy and change behavior among students enrolled in an introductory college psychology course.

The immune system and major depression.

This paper reviews research literature on the links between human immune functioning and mood disorders. It summarizes the initial steps of this fledgling research area since its inception in the late 1970s, and outlines a range of studies that are needed to increase our neuroimmunological sophistication. Future investigations will require greater specificity in several interrelated realms of inquiry: diagnostic, epidemiologic, and physiologic. In particular, this paper highlights basic physiological studies needed in both neurophysiology and immunology to provide a foundation for meaningful examination of their interface. Among the areas that require more specific investigation in both immunologic and mood disorders research is that of temporal organization. Just as psychiatric researchers have begun to scrutinize temporal cycles of mood, behavior, and neurophysiology, so too exploration of immune functioning must take into account predictable temporal cycles such as circadian and ultradian rhythms, as they shape responses to unanticipated external perturbations. Clarification of the temporal dimension will add significantly to our analysis of the links between immune functioning and mood disorders. The basic science of psychoneuroimmunology continues to mature, bringing new discoveries and revealing hitherto unknown mechanisms and interactions. This is a field of study in many ways still on the frontier, and explication of the long suspected links between mood disorders and immune functioning continues to beckon.

Changes in Regional Cerebral Blood Flow following Light Treatment for Seasonal Affective Disorder: Responders versus Nonresponders

BACKGROUND Several brain imaging studies of antidepressant pharmacologic treatment utilizing single photon emission computed tomography (SPECT) have reported a normalization of deficits in cerebral blood flow (CBF) associated with recovery; other studies report no change, or a reduction in CBF following successful treatment. There have been no published SPECT studies of seasonal affective disorder (SAD) assessing response to light treatment in relation to changes in regional CBF (rCBF). In this study, we sought to test the hypothesis that increases in rCBF would be observed in SAD patients who responded to light treatment. METHODS Ten depressed patients with SAD underwent functional brain imaging studies with 99mTc-hexamethylpropyleneamine oxime SPECT before and after light treatment. RESULTS Relative increases in rCBF were observed in all brain regions compared to cerebellum in treatment responders, whereas nonresponders showed no change or decreases in rCBF relative to cerebellum. Significant differences in mean percentage change in rCBF between responders (n = 5) and nonresponders (n = 5) were detected in frontal and cingulate cortex, and thalamus. CONCLUSIONS These findings provide preliminary support for the hypothesis that an increase in rCBF is associated with recovery from depression in SAD.

BIOLOGICAL RHYTHMS IN THE PATHOPHYSIOLOGY AND TREATMENT OF AFFECTIVE DISORDERS

Publisher Summary This chapter discusses the biological rhythms in the pathophysiology and treatment of affective disorders. It presents the pharmacological agents used in the treatment of depression that have been prominent among the substances found to affect biological rhythmicity.. Speculations about biological rhythm disturbances in affective disorders have been made repeatedly over the years because these disorders have temporal features, such as diurnal mood variation, changes in sleep architecture and timing, periodicity in the occurrence of episodes, and anomalies in patterns of hormone secretion. The chronobiological approach has also revived intriguing questions regarding the role of inefficiencies and defects in physiological systems for energy metabolism and thermoregulation in the pathophysiology of affective disorders and related conditions. In this way, studies of circadian rhythms have fostered a type of physiological approach to the biology of affective disorders in which larger physiological systems provide a conceptual bridge between events at the synaptic level and actual symptoms experienced by individuals.