Background Disclosure of items used in multiple-choice-question (MCQ) exams may decrease student anxiety and improve transparency, feedback, and test-enhanced learning but potentially compromises the reliability and fairness of exams if items are eventually reused. Evidence regarding whether disclosure and reuse of test items change item psychometrics is scarce and inconclusive. Methods We retrospectively analysed difficulty and discrimination coefficients of 10,148 MCQ items used between fall 2017 and fall 2019 in a large European medical school in which items were disclosed from fall 2017 onwards. We categorised items as 'new'; 'reused, not disclosed'; or 'reused, disclosed'. For reused items, we calculated the difference from their first ever use, that is, when they were new. Differences between categories and terms were analysed with one-way analyses of variance and independent-samples t tests. Results The proportion of reused, disclosed items grew from 0% to 48.4%; mean difficulty coefficients increased from 0.70 to 0.76; that is, items became easier, P < .001, eta(p) (2) = 0.011. On average, reused, disclosed items were significantly easier (M = 0.83) than reused, not disclosed items (M = 0.71) and entirely new items (M = 0.66), P < .001, eta(p) (2) = 0.087. Mean discrimination coefficients increased from 0.21 to 0.23; that is, item became slightly more discriminating, P = .002, eta(p) (2) = 0.002. Conclusions Disclosing test items provides the opportunity to enhance feedback and transparency in MCQ exams but potentially at the expense of decreased item reliability. Discrimination was positively affected. Our study may help weigh advantages and disadvantages of using previously disclosed items.

BackgroundDiagnostic accuracy is one of the major cornerstones of appropriate and successful medical decision-making. Clinical decision support systems (CDSSs) have recently been used to facilitate physician's diagnostic considerations. However, to date, little is known about the potential assets of CDSS for medical students in an educational setting. The purpose of our study was to explore the usefulness of CDSSs for medical students assessing their diagnostic performances and the influence of such software on students' trust in their own diagnostic abilities.MethodsBased on paper cases students had to diagnose two different patients using a CDSS and conventional methods such as e.g. textbooks, respectively. Both patients had a common disease, in one setting the clinical presentation was a typical one (tonsillitis), in the other setting (pulmonary embolism), however, the patient presented atypically. We used a 2x2x2 between- and within-subjects cluster-randomised controlled trial to assess the diagnostic accuracy in medical students, also by changing the order of the used resources (CDSS first or second).ResultsMedical students in their 4(th) and 5(th) year performed equally well using conventional methods or the CDSS across the two cases (t(164) = 1,30; p = 0.197). Diagnostic accuracy and trust in the correct diagnosis were higher in the typical presentation condition than in the atypical presentation condition (t(85) = 19.97; p < .0001 and t(150) = 7.67; p < .0001).These results refute our main hypothesis that students diagnose more accurately when using conventional methods compared to the CDSS.ConclusionsMedical students in their 4(th) and 5(th) year performed equally well in diagnosing two cases of common diseases with typical or atypical clinical presentations using conventional methods or a CDSS. Students were proficient in diagnosing a common disease with a typical presentation but underestimated their own factual knowledge in this scenario. Also, students were aware of their own diagnostic limitations when presented with a challenging case with an atypical presentation for which the use of a CDSS seemingly provided no additional insights.

Recently, representatives of politics, health officials and academia in Germany have advocated a greater role for Germany in matters concerning global health. However, health professionals in Germany are rarely taught about global health topics and accordingly real expertise in this field is lacking. To advance knowledge and competencies at German universities and adequately equip health professionals to achieve Germany's political goals, global health curricula must be developed at medical schools and other institutions. Such ambitions raise questions about the required content and dimensions of global health curricula as the field is currently highly heterogeneous and ill defined. To systematically identify strengths and shortcomings of current curricula, we scrutinised the global health curriculum at our institution, Charité-Universitätsmedizin Berlin, using an analytical framework that integrates the various approaches of global health. Our analysis identified that four (technical, social justice, security and humanitarian) of five approaches are present in our core global health curriculum. Local and global aspects of the field are equally represented. We propose that the use of such a structured analytical framework can support the development of GH curricula for all health professionals-in Germany and elsewhere. But it can also help to evaluate existing curricula like ours at Charité. This framework has the potential to support the design of comprehensive GH trainings, serving German aspirations in politics and academia to promote health worldwide.

This paper examines the history of the clinical trials conducted in the German Democratic Republic (GDR) mandated by Western pharmaceutical companies between 1983 and 1990. Beginning in 2010, that history was hotly debated in the German media. The paper argues that a centralised state health care system like that in the GDR corresponded better to the requirements of the international pharmaceutical industry for clinical trials than did a privately organised and more decentralised health care system. It was perhaps less the coercive nature of the Eastern German State that was attractive to Western companies, than an effectively centralised health care system. Whatever the case, the arrangement permitted a win-win situation for both partners during the times of the "Cold War."

A 52-year-old man with recently diagnosed HIV infection (CD4 count 105/µL; normal range 700–1,200/µL) presented with a 5-week history of irregular shaking of his left hand triggered by lifting his arm accompanied by “feeling of stiffness and clumsiness.” On clinical examination, focal myoclonus with positive and negative components affecting the left upper limb with distal predominance was detected (see video on the Neurology® Web site at Neurology.org). Cerebral MRI revealed a demyelinating lesion affecting the juxtacortical white matter of the precentral gyrus (figure). The CSF PCR for JC virus was strongly positive, confirming the diagnosis of progressive multifocal leukoencephalopathy.1

Cataplexy is one of the hallmark symptoms of patients diagnosed with narcolepsy type 1 (N1 = narcolepsy with cataplexy). Our pathophysiologic understanding of cataplexy has been based on the hypothesis that the loss of muscle tone characteristic for cataplectic attacks (CA) is identical to muscle atonia in REM sleep.(1) However, this hypothesis has not been proved in humans since cataplexy can hardly be provoked experimentally. Recently, F-waves have been shown to be a valuable marker for spinal inhibition in REM sleep.(2) We present F-wave recordings in 3 patients with N1 before, during, and after a CA (figure) to test whether the level of spinal excitability in cataplexy equals that in REM sleep.

This study examines the excitability and recruitment of spinal motoneurons in human sleep. The main objective was to assess whether supraspinal inhibition affects the different subpopulations of the compound spinal motoneuron pool in the same way or rather in a selective fashion in the various sleep stages. To this end, we studied F-conduction velocities (FCV) and F-tacheodispersion alongside F-amplitudes and F-persistence in 22 healthy subjects in sleep stages N2, N3 (slow-wave sleep), REM and in wakefulness. Stimuli were delivered on the ulnar nerve, and F-waves were recorded from the first dorsal interosseus muscle. Repeated sets of stimuli were stored to obtain at least 15 F-waves for each state of vigilance. F-tacheodispersion was calculated based on FCVs using the modified Kimura formula. Confirming the only previous study, excitability of spinal motoneurons was generally decreased in all sleep stages compared with wakefulness as indicated by significantly reduced F-persistence and F-amplitudes. More importantly, F-tacheodispersion showed a narrowed range of FCV in all sleep stages, most prominently in REM. In non-REM, this narrowed range was associated with a shift towards significantly decreased maximal FCV and mean FCV as well as with a trend towards lower minimal FCV. In REM, the lowering of mean FCV was even more pronounced, but contrary to non-REM sleep without a shift of minimal and maximal FCV. Variations in F-tacheodispersion between sleep stages suggest that different supraspinal inhibitory neuronal circuits acting on the spinal motoneuron pool may contribute to muscle hypotonia in human non-REM sleep and to atonia in REM sleep.

Objective: Over the past year a variety of sleep disorders have been associated with idiopathic Parkinson's disease (IPS). While there is agreement that REM-sleep behavioural disorder (RBD) is an early clinical manifestation of IPS, it has been controversially debated whether patients with idiopathic Parkinson's disease (IPS) are prone to develop obstructive sleep apnea (OSA). A recently published study in IPS patients with and without disturbed sleep (Cochen de Cock, 2009) found a higher apnea-hypopnea-index (AHI) – as an expression of OSA – in IPS patients with RBD than in those IPS patients without RBD. In line with this observation we are examining the prevalence of OSA in insomniac IPS patients with and without RBD to compare both groups regarding further clinical and polysomnographic parameters as well as regarding the echogenicity of the substantia nigra (SN).

Objective: Deep brain stimulation (DBS) as a treatment option for various neurological disorders also allows to record local field potentials (LFP) from subcortical regions. Using coherence analysis between surface-EEG and LFPs from Globus pallidus in dystonia patients we recently characterized an alpha-activity in sleep stages N2 and N3 (Salih et al., 2009). Based on our findings we discussed whether this alpha-activity could act as a specific signature of the motor system in human non-REM sleep. Here we test whether patients with idiopathic Parkinson's disease (PD) show alterations of this alpha-activity. Methods: So far, nine PD patients were investigated (age: 44–71 years; m=5, f=4). DBS target was the subthalamic nucleus (STN). Coherence analysis was performed between surface-EEG and LFPs from STN using sequences for N2 and N3 in the frequency band between 0.5–40Hz. For all patients the Parkinson Disease Sleep Scale (PDSS), the Unified Parkinson Disease Rating Scale part III (UPDRS) and the clinical DBS outcome (i.e., improvement rate) were evaluated. Results: In 4 patients (44.4%) coherent alpha-activity was found between motor cortex and STN during non-REM sleep (N3>N2). These patients had lower UPDRS III scores compared to those patients who showed no alpha-activity (36.5 vs. 53.0). Mean PDSS scores were not different (113.5 vs. 111.0). Mean DBS outcome was 68% in patients with alpha-activity (vs. 62%). Discussion: The preliminary results of this study support the hypothesis that alpha-activity could be a signature of the motor system during non-REM sleep. The loss of alpha-activity in patients with higher UPDRS III scores indicates the physiologic nature of this activity as progressing neurodegeneration may lead to a decrease of non-REM specific alpha-activity.

Recent evidence suggests that the motor system undergoes very specific modulation in its functional state during the different sleep stages. Here we test the hypothesis that changes in the functional organization of the motor system involve both cortical and subcortical levels and that these distributed changes are interrelated in defined frequency bands. To this end we evaluated functional connectivity between motor and non‐motor cortical sites (fronto‐central, parieto‐occipital) and the globus pallidus (GP) in human non‐REM sleep in seven patients undergoing deep brain stimulation (DBS) for dystonia using a variety of spectral measures (power, coherence, partial coherence and directed transfer function (DTF)). We found significant coherence between GP and fronto‐central cortex as well as between GP and parieto‐occipital cortex in circumscribed frequency bands that correlated with sleep specific oscillations in ‘light sleep’ (N2) and ‘slow‐wave sleep’ (N3). These sleep specific oscillations were also reflected in significant coherence between the two cortical sites corroborating previous studies. Importantly, we found two different physiological activities represented within the broad band of significant coherence between 9.5 and 17 Hz. One component occurred in the frequency range of sleep spindles (12.5–17 Hz) and was maximal in the coherence between fronto‐central and parieto‐occipital cortex as well as between GP and both cortical sites during N2. This component was still present between fronto‐central and parieto‐occipital cortex in N3. Functional connectivity in this frequency band may be due to a common input to both GP and cortex. The second component consisted of a spectral peak over 9.5–12.5 Hz. Coherence was elevated in this band for all topographical constellations in both N2 and N3, but especially between GP and fronto‐central cortex. The DTF suggested that the 9.5–12.5 Hz activity consisted of a preferential drive from GP to the fronto‐central cortex in N2, whereas in N3 the DTF between GP and fronto‐central cortex was symmetrical. Partial coherence supported distinctive patterns for the 9.5–12.5 and 12.5 and 17 Hz component, so that only coherence in the 9.5–12.5 Hz band was reduced when the effects of GP were removed from the coherence between the two cortical sites. The data suggest that activities in the GP and fronto‐central cortex are functionally connected over 9.5–12.5 Hz, possibly as a specific signature of the motor system in human non‐REM sleep. This finding is pertinent to the longstanding debate about the nature of alpha–delta sleep as a physiological or pathological feature of non‐REM sleep.

The pathophysiological mechanisms of primary dystonia have largely remained obscure. Yet there is one undeniable observation: lesioning or high-frequency stimulation of the internal segment of the globus pallidus (GP) ameliorates dystonic symptoms. The latter observation implicates abnormal pallidal activity in the genesis of primary dystonia. Recently, excessive oscillatory pallidal activity in the 3-10 Hz frequency range, synchronized with dystonic EMG, has been related to the occurrence of involuntary muscle activity in these patients. However, it is unclear whether this pathological synchronization is driven by GP, caused by re-afference from dystonic muscle, or due to a combination of these two processes. Here we used the Directed Transfer Function as a spectral measure to identify the degree and direction of coupling across time between GP and muscle in seven patients with primary dystonia. We show that pallidal local field potential activity <or= 10 Hz is coherent with dystonic movements, and that although the coupling between GP and activity in the sternocleidomastoid muscle is bidirectional, the drive from GP to muscle significantly outweighs that from muscle to GP. In addition, the net GP drive to muscle is not stable but fluctuates across time, in keeping with the dynamic nature of dystonic muscle activity.

Sensory sleep starts are variants of the more common motor sleep starts (hypnic jerks).1 Though sensory sleep starts may lead to repeated awakenings resulting in sleep-onset insomnia, their course is usually benign and no cerebral lesion has yet been described as being pathogenetically involved. Here we report a case of acoustic sleep starts (“exploding head syndrome”) which contests this latter assertion because their onset coincided with the occurrence of a brainstem lesion. ### Case report. A 64-year-old woman reported on problems initiating sleep related to the impression of a cracking sound of average loudness. Up to 15 times during the first hours after going to bed this sound occurred shortly after losing full consciousness, followed by an experience of jerking in all four limbs and a brief sensation of fear leading to full wakefulness. The patient, who had been healthy until then, noticed her sleep problem for the first time 12 years ago, coinciding with the diagnosis of pulmonary and extrapulmonary sarcoidosis. Corticosteroids were instituted under which no further progression of sarcoidosis occurred, even when steroids were tapered. Over this period the patient’s sleep problem was waxing and waning in intensity. Treatment with doxepin, citalopram, trimipramine, and amitriptyline led to no improvement. Only bromazepam (6 mg/day, 8 weeks) instantly led to unhampered sleep. Successive MRI scans of the brain (figure, A and B) revealed an unchanging, nonenhancing, singular, symmetric T2-hyperintense pontomesencephalic lesion around the periaquaductal gray reaching into the tegmentum. Figure MRI …

PURPOSE:To investigate alterations of inhibitory and excitatory cortical circuits during non-rapid eye movement (NREM) sleep in drug-naive patients with partial epilepsies and sleep-bound seizures only.METHODS:A paired-pulse TMS paradigm was used to test intracortical inhibition (ICI) and facilitation (ICF) in the hemisphere of the epileptic focus in three untreated patients with nonlesional, nongenetic frontal lobe epilepsy in NREM2 (three patients), NREM3/4 (one patient), and wakefulness (three patients).RESULTS:All three patients exhibited a major decrease of ICI in NREM sleep as opposed to the physiological enhancement of ICI with the progression of NREM sleep.CONCLUSIONS:Decreased ICI might reflect a substrate for the association of epileptic processes with thalamocortical networks that propagate sleep. Thus our findings contribute to a hypothesis of how NREM sleep could promote seizures.