Sarah Garside

Internet-based learning in the health professions:a meta-analysis

CONTEXT The increasing use of Internet-based learning in health professions education may be informed by a timely, comprehensive synthesis of evidence of effectiveness. OBJECTIVES To summarize the effect of Internet-based instruction for health professions learners compared with no intervention and with non-Internet interventions. DATA SOURCES Systematic search of MEDLINE, Scopus, CINAHL, EMBASE, ERIC, TimeLit, Web of Science, Dissertation Abstracts, and the University of Toronto Research and Development Resource Base from 1990 through 2007. STUDY SELECTION Studies in any language quantifying the association of Internet-based instruction and educational outcomes for practicing and student physicians, nurses, pharmacists, dentists, and other health care professionals compared with a no-intervention or non-Internet control group or a preintervention assessment. DATA EXTRACTION Two reviewers independently evaluated study quality and abstracted information including characteristics of learners, learning setting, and intervention (including level of interactivity, practice exercises, online discussion, and duration). DATA SYNTHESIS There were 201 eligible studies. Heterogeneity in results across studies was large (I(2) > or = 79%) in all analyses. Effect sizes were pooled using a random effects model. The pooled effect size in comparison to no intervention favored Internet-based interventions and was 1.00 (95% confidence interval [CI], 0.90-1.10; P < .001; n = 126 studies) for knowledge outcomes, 0.85 (95% CI, 0.49-1.20; P < .001; n = 16) for skills, and 0.82 (95% CI, 0.63-1.02; P < .001; n = 32) for learner behaviors and patient effects. Compared with non-Internet formats, the pooled effect sizes (positive numbers favoring Internet) were 0.10 (95% CI, -0.12 to 0.32; P = .37; n = 43) for satisfaction, 0.12 (95% CI, 0.003 to 0.24; P = .045; n = 63) for knowledge, 0.09 (95% CI, -0.26 to 0.44; P = .61; n = 12) for skills, and 0.51 (95% CI, -0.24 to 1.25; P = .18; n = 6) for behaviors or patient effects. No important treatment-subgroup interactions were identified. CONCLUSIONS Internet-based learning is associated with large positive effects compared with no intervention. In contrast, effects compared with non-Internet instructional methods are heterogeneous and generally small, suggesting effectiveness similar to traditional methods. Future research should directly compare different Internet-based interventions.

Instructional design variations in internet-based learning for health professions education: A systematic review and meta-analysis

Purpose A recent systematic review (2008) described the effectiveness of Internet-based learning (IBL) in health professions education. A comprehensive synthesis of research investigating how to improve IBL is needed. This systematic review sought to provide such a synthesis. Method The authors searched MEDLINE, CINAHL, EMBASE, Web of Science, Scopus, ERIC, TimeLit, and the University of Toronto Research and Development Resource Base for articles published from 1990 through November 2008. They included all studies quantifying the effect of IBL compared with another Internet-based or computer-assisted instructional intervention on practicing and student physicians, nurses, pharmacists, dentists, and other health professionals. Reviewers working independently and in duplicate abstracted information, coded study quality, and grouped studies according to inductively identified themes. Results From 2,705 articles, the authors identified 51 eligible studies, including 30 randomized trials. The pooled effect size (ES) for learning outcomes in 15 studies investigating high versus low interactivity was 0.27 (95% confidence interval, 0.08–0.46; P = .006). Also associated with higher learning were practice exercises (ES 0.40 [0.08–0.71; P = .01]; 10 studies), feedback (ES 0.68 [0.01–1.35; P = .047]; 2 studies), and repetition of study material (ES 0.19 [0.09–0.30; P < .001]; 2 studies). The ES was 0.26 (−0.62 to 1.13; P = .57) for three studies examining online discussion. Inconsistency was large (I2 ≥89%) in most analyses. Meta-analyses for other themes generally yielded imprecise results. Conclusions Interactivity, practice exercises, repetition, and feedback seem to be associated with improved learning outcomes, although inconsistency across studies tempers conclusions. Evidence for other instructional variations remains inconclusive.

What do we mean by web‐based learning? A systematic review of the variability of interventions

Medical Education 2010: 44: 765–774

Virtual reality and brain anatomy: a randomised trial of e-learning instructional designs

Context  Computer‐aided instruction is used increasingly in medical education and anatomy instruction with limited research evidence to guide its design and deployment.

Method and reporting quality in health professions education research: a systematic review

Medical Education 2011: 45: 227–238

The Psychiatric Manifestations of Mitochondrial Disorders: A Case and Review of the Literature

OBJECTIVE Mitochondrial disorders are caused by gene mutations in mitochondrial or nuclear DNA and affect energy-dependent organs such as the brain. Patients with psychiatric illness, particularly those with medical comorbidities, may have primary mitochondrial disorders. To date, this issue has received little attention in the literature, and mitochondrial disorders are likely underdiagnosed in psychiatric patients. DATA SOURCES This article describes a patient who presented with borderline personality disorder and treatment-resistant depression and was ultimately diagnosed with mitochondrial encephalomyopathy with lactic acidosis and stroke-like episodes (MELAS) 3271. We also searched the literature for all case reports of patients with mitochondrial disorders who initially present with prominent psychiatric symptoms by using MEDLINE (from 1948-February 2011), Embase (from 1980-February 2011), PsycINFO (from 1806-February 2011), and the search terms mitochondrial disorder, mitochondria, psychiatry, mental disorders, major depression, anxiety, schizophrenia, and psychosis. STUDY SELECTION Fifty cases of mitochondrial disorders with prominent psychiatric symptomatology were identified. DATA EXTRACTION Information about the psychiatric presentation of the cases was extracted. This information was combined with our case, the most common psychiatric manifestations of mitochondrial disorders were identified, and the important diagnostic and treatment implications for patients with psychiatric illness were reviewed. RESULTS The most common psychiatric presentations in the cases of mitochondrial disorders included mood disorder, cognitive deterioration, psychosis, and anxiety. The most common diagnosis (52% of cases) was a MELAS mutation. Other genetic mitochondrial diagnoses included polymerase gamma mutations, Kearns-Sayre syndrome, mitochondrial DNA deletions, point mutations, twinkle mutations, and novel mutations. CONCLUSIONS Patients with mitochondrial disorders can present with primary psychiatric symptomatology, including mood disorder, cognitive impairment, psychosis, and anxiety. Psychiatrists need to be aware of the clinical features that are indicative of a mitochondrial disorder, investigate patients with suggestive presentations, and be knowledgeable about the treatment implications of the diagnosis.

Dopamine–glutamate interactions in the striatum: behaviourally relevant modification of excitotoxicity by dopamine receptor-mediated mechanisms

The two most important afferent projections to the striatum contain glutamate and dopamine, respectively. Excitotoxic damage resulting from excessive stimulation of the N-methyl-D-aspartate subtype of glutamate receptor has been implicated in pathophysiology of ischaemic stroke, hypoglycaemic brain damage and Huntingtons disease. We studied the ability of the dopamine system to modify the anatomical, neurochemical and behavioural consequences of glutamatergic toxicity in the striatum. In a first set of experiments, the specific N-methyl-D-aspartate receptor agonist quinolinate was injected unilaterally into the striatum of rats pretreated with one of (i) intraperitoneal (i.p.) saline (controls); (ii) i.p. haloperidol, a D2 dopamine receptor agonist; or (iii) 6-hydroxydopamine lesion of the ipsilateral nigrostriatal tract. Quinolinate-induced striatal damage, as assessed by morphometric and neurochemical criteria, was significantly attenuated in the animals with 6-hydroxydopamine lesions and in those pretreated with haloperidol, compared with saline-pretreated controls. There were no significant differences between the 6-OHDA and haloperidol groups. In a second set of experiments, animals received (i) bilateral intrastriatal quinolinate plus perioperative i.p. saline; (ii) bilateral intrastriatal quinolinate plus i.p. haloperidol; or (iii) bilateral intrastriatal saline. Again, the quinolinate-lesioned animals treated with perioperative haloperidol had significantly less striatal damage than the bilateral quinolinate rats. Behavioural assessment in the Morris Water Maze showed the bilateral quinolinate+haloperidol group to be significantly less impaired on a spatial acquisition task than the bilateral quinolinate animals. Measures of spontaneous daytime motor activity showed significant differences in average speed and rest time between the bilateral quinolinate+haloperidol rats and the bilateral quinolinate group. The performance of the bilateral quinolinate+haloperidol group was not significantly different from that of controls on any of the behavioural tasks. These results indicate an important role for D2 dopamine receptor-mediated mechanisms in striatal excitotoxicity. Since the excitotoxic process involves the same fundamental signalling mechanism that is involved in normal glutamatergic transmission, these findings imply an ability of D2 receptor blockade to modify glutamate signalling in the striatum. These results may have implications for treatment strategies in ischaemic stroke, hypoglycaemic brain damage and schizophrenia.

Haloperidol induces persistent down-regulation of tyrosine hydroxylase immunoreactivity in substantia nigra but not ventral tegmental area in the rat.

The dopamine antagonist haloperidol can cause tardive side-effects that may persist after the drug is withdrawn. We studied the time course of changes in dopaminergic neurons of the substantia nigra and ventral tegmental area following withdrawal of haloperidol. Rats received daily intraperitoneal injections of saline or haloperidol for eight weeks and were killed at two, four or 12 weeks after the final injection. Sections of substantia nigra and ventral tegmental area were processed for tyrosine hydroxylase immunohistochemistry. Quantitative morphometric analysis was carried out blinded in order to determine the number, cell body size and topography of tyrosine hydroxylase-positive cells, and the immunoreactive area of the substantia nigra and ventral tegmental area. In haloperidol-treated rats, tyrosine hydroxylase-positive cell counts were normal in ventral tegmental area but were decreased in substantia nigra by 34% at two weeks withdrawal and by 52% at four weeks withdrawal; cell counts were almost fully recovered by 12 weeks withdrawal. Cross-sectional area of tyrosine hydroxylase immunoreactivity within the substantia nigra demonstrated a similar pattern of reduction, with full recovery by 12 weeks withdrawal. Mean cell size, by contrast, was essentially unchanged at two and four weeks withdrawal, but was significantly decreased in sub-regions of substantia nigra at 12 weeks withdrawal. These results indicate that haloperidol can produce selective changes in midbrain dopamine neurons that persist long after discontinuation of the drug. This decrease in tyrosine hydroxylase-immunoreactive cell counts may play a role in the neurobiology of the persistent tardive syndromes associated with the use of neuroleptics.

Persistent loss of tyrosine hydroxylase immunoreactivity in the substantia nigra after neuroleptic withdrawal

A 37 year woman developed neuroleptic induced parkinsonism that persisted long after the drug had been discontinued. This prompted a study of the effect of an eight week course of haloperidol (HAL) followed by two week withdrawal, on dopaminergic neurons of the substantia nigra in rats. Animals treated with HAL showed a highly significant 32%-46% loss of tyrosine hydroxylase (TH) immunoreactive neurons in the substantia nigra, and 20% contraction of the TH stained dendritic arbour. Neuroleptic drug induced downregulation of nigral dopaminergic neurons may help to explain the persistent parkinsonism found in many patients after withdrawal of medication.

Role of glutamate receptor subtypes in the differential release of somatostatin, neuropeptide Y, and substance P in primary serum-free cultures of striatal neurons

The spiny and aspiny neuronal populations of the striatum display differential vulnerability to the toxic effects of glutamatergic agonists. Substance P–containing spiny neurons appear to be more vulnerable to NMDA‐receptor–mediated toxicity and less susceptible to kainate toxicity than the somatostatin‐ and neuropeptide Y (NPY)‐containing aspiny population. We studied whether selective glutamatergic agonists might have similar differential effects on neuropeptide release from the substance P‐ and somatostatin/NPY‐containing neuronal populations. After collection of a baseline sample, striatal neurons in primary culture were treated with one of the following: phosphate‐buffered saline, 56 mM potassium chloride (KCl), 100 μM N‐methyl‐D‐aspartate (NMDA), 100 μM quisqualate, 100 μM kainate, or 100 μM glutamate. Baseline and treatment samples were measured by radioimmunoassay for somatostatin, NPY, and substance P. KCl and kainate provoked a selective release of somatostatin and NPY, whereas substance P measured in the same samples showed no response. By contrast, NMDA elicited a selective release of substance P without a similar increase of either somatostatin or NPY. Quisqualate evoked comparable responses in the three peptides. These results indicate that the glutamatergic regulation of somatostatin and NPY release from aspiny striatal neurons in primary culture is preferentially mediated by the kainate receptor, whereas substance P release is selectively mediated by the NMDA receptor. These findings suggest a preferential expression of functional kainate receptors on the aspiny somatostatin/NPY neurons and of NMDA receptors on the substance‐P–containing spiny neurons. Synapse 27:161–167, 1997.