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Featured researches published by Markus Schmidt.


Neurobiology of Sleep and Circadian Rhythms | 2017

The role of sleep in recovery following ischemic stroke: A review of human and animal data

Simone Duss; Andrea Seiler; Markus Schmidt; Marta Pace; Antoine Roger Adamantidis; René Martin Müri; Claudio L. Bassetti

Despite advancements in understanding the pathophysiology of stroke and the state of the art in acute management of afflicted patients as well as in subsequent neurorehabilitation training, stroke remains the most common neurological cause of long-term disability in adulthood. To enhance stroke patients’ independence and well-being it is necessary, therefore, to consider and develop new therapeutic strategies and approaches. We postulate that sleep might play a pivotal role in neurorehabilitation following stroke. Over the last two decades compelling evidence for a major function of sleep in neuroplasticity and neural network reorganization underlying learning and memory has evolved. Training and learning of new motor skills and knowledge can modulate the characteristics of subsequent sleep, which additionally can improve memory performance. While healthy sleep appears to support neuroplasticity resulting in improved learning and memory, disturbed sleep following stroke in animals and humans can impair stroke outcome. In addition, sleep disorders such as sleep disordered breathing, insomnia, and restless legs syndrome are frequent in stroke patients and associated with worse recovery outcomes. Studies investigating the evolution of post-stroke sleep changes suggest that these changes might also reflect neural network reorganization underlying functional recovery. Experimental and clinical studies provide evidence that pharmacological sleep promotion in rodents and treatment of sleep disorders in humans improves functional outcome following stroke. Taken together, there is accumulating evidence that sleep represents a “plasticity state” in the process of recovery following ischemic stroke. However, to test the key role of sleep and sleep disorders for stroke recovery and to better understand the underlying molecular mechanisms, experimental research and large-scale prospective studies in humans are necessary. The effects of hospital conditions, such as adjusting light conditions according to the patients’ sleep-wake rhythms, or sleep promoting drugs and non-invasive brain stimulation to promote neuronal plasticity and recovery following stroke requires further investigation.


Swiss Medical Weekly | 2017

Sleep-disordered breathing: clinical features, pathophysiology and diagnosis.

Sebastian Robert Ott; Lyudmila Korostovtseva; Markus Schmidt; Thomas Horvath; Anne-Kathrin Brill; Claudio L. Bassetti

In recent decades, the association between sleep-disordered breathing (SDB) and cardio- and cerebrovascular diseases (including hypertension, coronary heart disease and stroke) has been the focus of interest of both clinicians and researchers. A growing concern is the increasing prevalence of SDB in the general population, which can be partly explained by the rise in obesity prevalence and population aging, as well as by the development of enhanced diagnostic tools and approaches. Because of evidence of adverse long-term effects of SDB on cardiovascular morbidity and overall mortality, systematic screening for SDB should be considered for populations at risk. The evidence of a long-term benefit of treatment for SDB, however, is still controversial and the best management approaches are still unclear. This article summarises available epidemiological data and focuses on the main pathophysiological mechanisms linking SDB to cardio- and cerebrovascular disorders. We will also give a critical overview of the current diagnostic procedures. The available treatment approaches and their prognostic effects on cardio- and cerebrovascular health will be discussed in a second paper.


PLOS ONE | 2017

State-dependent metabolic partitioning and energy conservation: A theoretical framework for understanding the function of sleep

Markus Schmidt; Theodore W. Swang; Ian M. Hamilton; Janet Best

Metabolic rate reduction has been considered the mechanism by which sleep conserves energy, similar to torpor or hibernation. This mechanism of energy savings is in conflict with the known upregulation (compared to wake) of diverse functions during sleep and neglects a potential role in energy conservation for partitioning of biological operations by behavioral state. Indeed, energy savings as derived from state-dependent resource allocations have yet to be examined. A mathematical model is presented based on relative rates of energy deployment for biological processes upregulated during either wake or sleep. Using this model, energy savings from sleep-wake cycling over constant wakefulness is computed by comparing stable limit cycles for systems of differential equations. A primary objective is to compare potential energy savings derived from state-dependent metabolic partitioning versus metabolic rate reduction. Additionally, energy conservation from sleep quota and the circadian system are also quantified in relation to a continuous wake condition. As a function of metabolic partitioning, our calculations show that coupling of metabolic operations with behavioral state may provide comparatively greater energy savings than the measured decrease in metabolic rate, suggesting that actual energy savings derived from sleep may be more than 4-fold greater than previous estimates. A combination of state-dependent metabolic partitioning and modest metabolic rate reduction during sleep may enhance energy savings beyond what is achievable through metabolic partitioning alone; however, the relative contribution from metabolic partitioning diminishes as metabolic rate is decreased during the rest phase. Sleep quota and the circadian system further augment energy savings in the model. Finally, we propose that state-dependent resource allocation underpins both sleep homeostasis and the optimization of daily energy conservation across species. This new paradigm identifies an evolutionary selective advantage for the upregulation of central and peripheral biological processes during sleep, presenting a unifying construct to understand sleep function.


Journal of Clinical Sleep Medicine | 2017

Patient-Reported Measures of Narcolepsy: The Need for Better Assessment.

Ulf Kallweit; Markus Schmidt; Claudio L. Bassetti

STUDY OBJECTIVES Narcolepsy, a chronic disorder of the central nervous system, is clinically characterized by a symptom pentad that includes excessive daytime sleepiness, cataplexy, sleep paralysis, hypnopompic/hypnagogic hallucinations, and disrupted nighttime sleep. Ideally, screening and diagnosis instruments that assist physicians in evaluating a patient for type 1 or type 2 narcolepsy would be brief, easy for patients to understand and physicians to score, and would identify or rule out the need for electrophysiological testing. METHODS A search of the literature was conducted to review patient-reported measures used for the assessment of narcolepsy, mainly in clinical trials, with the goal of summarizing existing scales and identifying areas that may require additional screening questions and clinical practice scales. RESULTS Of the seven scales reviewed, the Epworth Sleepiness Scale continues to be an important outcome measure to screen adults for excessive daytime sleepiness, which may be associated with narcolepsy. Several narcolepsy-specific scales have demonstrated utility, such as the Ullanlinna Narcolepsy Scale, Swiss Narcolepsy Scale, and Narcolepsy Symptom Assessment Questionnaire, but further validation is required. CONCLUSIONS Although the narcolepsy-specific scales currently in use may identify type 1 narcolepsy, there are no validated questionnaires to identify type 2 narcolepsy. Thus, there remains a need for short, easily understood, and well-validated instruments that can be readily used in clinical practice to distinguish narcolepsy subtypes, as well as other hypersomnias, and for assessing symptoms of these conditions during treatment.


Sleep Medicine | 2018

The unfinished journey with modafinil and discovery of a novel population of modafinil-immunoreactive neurons

Jian-Sheng Lin; Bernard Roussel; Alexandre Gaspar; Yan Zhao; Yiping Hou; Markus Schmidt; Anne Jouvet; Michel Jouvet

Modafinil, a wake-promoting compound now used worldwide in sleep medicine, was initially regarded as a sedative compound because mice were so quiet with respect to locomotion after receiving it that this behavioral state was qualified as sedation. In the early 1980s when modafinil was first assessed by polysomnography in a cat in our laboratory, surprisingly, the cat spent the whole night awake without even one minute of sleep! This initial observation resulted subsequently in a series of basic and clinical studies in order to define the pharmacological profile of modafinil and its mode of action and, notably, to identify the brain targets by which modafinil acts to promote wakefulness. These studies were undertaken using pharmacologic approach coupled with the Cerveau isolé (brain transection) preparation, c-fos labelling and knockout mouse models. It was also in this context that we have developed a purified polyclonal antibody against modafinil. We expected that using immunohistochemistry with this antibody would allow us to localize the brain distribution of modafinil dosing. Surprisingly, we found discrete modafinil immunoreactive neuronal populations in several brain areas of modafinil-naive cats, rodents and humans. The most numerous and intensely labeled modafinil-immunoreactive neurons characterized by granular staining were found in the basal forebrain. They shared the regional location with cholinergic and aspartate-containing neurons but did not colocalize with them. In summary, we here present a newly identified neuronal population located in the basal forebrain that has never previously been published and suggests that these modafinil-immunoreactive neurons might be involved in forebrain functions such as sleep-wake control and cognition. This paper briefly reviews our journey with modafinil research and presents new unpublished experimental data.


Journal of Clinical Sleep Medicine | 2018

Stevens-Johnson Syndrome After Armodafinil Use

Steven Holfinger; Asim Roy; Markus Schmidt

ABSTRACT We present the case of a 21-year-old woman in whom Stevens-Johnson syndrome (SJS) developed after initiation of armodafinil. Although this rare and life-threatening reaction is listed on armodafinils label, no cases have been reported in the literature. This case, in addition to an update of the drugs label after post-marketing research, both support the link between armodafinil and SJS. Providers should maintain a high clinical suspicion for SJS when starting therapy to minimize associated morbidity and mortality by discontinuing armodafinil at the onset of first symptoms.


Frontiers in Neurology | 2018

Sleep-Wake Cycling and Energy Conservation: Role of Hypocretin and the Lateral Hypothalamus in Dynamic State-Dependent Resource Optimization.

Blerina Latifi; Antoine Roger Adamantidis; Claudio L. Bassetti; Markus Schmidt

The hypocretin (Hcrt) system has been implicated in a wide range of physiological functions from sleep-wake regulation to cardiovascular, behavioral, metabolic, and thermoregulagtory control. These wide-ranging physiological effects have challenged the identification of a parsimonious function for Hcrt. A compelling hypothesis suggests that Hcrt plays a role in the integration of sleep-wake neurophysiology with energy metabolism. For example, Hcrt neurons promote waking and feeding, but are also sensors of energy balance. Loss of Hcrt function leads to an increase in REM sleep propensity, but a potential role for Hcrt linking energy balance with REM sleep expression has not been addressed. Here we examine a potential role for Hcrt and the lateral hypothalamus (LH) in state-dependent resource allocation as a means of optimizing resource utilization and, as a result, energy conservation. We review the energy allocation hypothesis of sleep and how state-dependent metabolic partitioning may contribute toward energy conservation, but with additional examination of how the loss of thermoregulatory function during REM sleep may impact resource optimization. Optimization of energy expenditures at the whole organism level necessitates a top-down network responsible for coordinating metabolic operations in a state-dependent manner across organ systems. In this context, we then specifically examine the potential role of the LH in regulating this output control, including the contribution from both Hcrt and melanin concentrating hormone (MCH) neurons among a diverse LH cell population. We propose that this hypothalamic integration system is responsible for global shifts in state-dependent resource allocations, ultimately promoting resource optimization and an energy conservation function of sleep-wake cycling.


Archive | 2015

Effects of Thermoregulation on Human Sleep Patterns: A Mathematical Model of Sleep–Wake Cycles with REM–NREM Subcircuit

Selenne Bañuelos; Janet Best; Gemma Huguet; Alicia Prieto-Langarica; Pamela B. Pyzza; Markus Schmidt; Shelby Wilson

In this paper we construct a mathematical model of human sleep–wake regulation with thermoregulation and temperature effects. Simulations of this model show features previously presented in experimental data such as elongation of duration and number of REM bouts across the night as well as the appearance of awakenings due to deviations in body temperature from thermoneutrality. This model helps to demonstrate the importance of temperature in the sleep cycle. Further modifications of the model to include more temperature effects on other aspects of sleep regulation such as sleep and REM latency are discussed.


Sleep Medicine | 2006

Use of pramipexole in REM sleep behavior disorder: Results from a case series

Markus Schmidt; Vipin B. Koshal; Helmut S. Schmidt


Sleep | 2018

0064 Lateral Hypothalamic Control of REM Sleep Expression During Ambient Temperature Warming

Markus Schmidt; N Komagata; B Latifi

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