Evaluation of Patient-Friendly Diagnosis Clarifications in a Hospital Patient Portal.

Background: Medical data can be difficult to comprehend for patients, but only a limited number of patient-friendly terms and definitions are available to clarify medical concepts. Therefore, we developed an algorithm that generalizes diagnoses to more general concepts that do have patient-friendly terms and definitions in SNOMED CT. We implemented the generalizations, and diagnosis clarifications with synonyms and definitions that were already available, in the problem list of a hospital patient portal.

Diagnosis clarification by generalization to patient-friendly terms and definitions: Validation study.

Background: Now that patients increasingly get access to their healthcare records, its contents require clarification. The use of patient-friendly terms and definitions can help patients and their significant others understand their medical data. However, it is costly to make patient-friendly descriptions for the myriad of terms used in the medical domain.

Evaluation of lexical clarification by patients reading their clinical notes: a quasi-experimental interview study.

Background: Patients benefit from access to their medical records. However, clinical notes and letters are often difficult to comprehend for most lay people. Therefore, functionality was implemented in the patient portal of a Dutch university medical centre (UMC) to clarify medical terms in free-text data.

Towards an Adoption Framework for Patient Access to Electronic Health Records: Systematic Literature Mapping Study.

Background: Patient access to electronic health records (EHRs) is associated with increased patient engagement and health care quality outcomes. However, the adoption of patient portals and personal health records (PHRs) that facilitate this access is impeded by barriers. The Clinical Adoption Framework (CAF) has been developed to analyze EHR adoption, but this framework does not consider the patient as an end-user.

Determinants and outcomes of patient access to medical records: Systematic review of systematic reviews.

Background: Patient access to electronic health records (EHRs) is associated with several determinants and outcomes, which are interrelated. However, individual studies and the reviews summarizing them have only addressed particular aspects, such as policy, usability or health outcomes of adoption. Therefore, no comprehensive overview exists.

Clarifying Diagnoses to Laymen by Employing the SNOMED CT Hierarchy.

Patient access to electronic health records (EHRs) is associated with improved efficiency, self-management, and patient engagement. However, the EHR contains medical language that can be difficult to comprehend by patients. In Dutch hospitals, the Diagnosethesaurus (DT) is used as an interface terminology to register diagnoses, but it does not contain patient-friendly terms.

Are validated outcome measures used in distal radial fractures truly valid? A critical assessment using the COnsensus-based Standards for the selection of health Measurement INstruments (COSMIN) checklist.

Objectives: Patient-reported outcome measures (PROMs) are often used to evaluate the outcome of treatment in patients with distal radial fractures. Which PROM to select is often based on assessment of measurement properties, such as validity and reliability. Measurement properties are assessed in clinimetric studies, and results are often reviewed without considering the methodological quality of these studies.

Cumulated Ambulation Score to evaluate mobility is feasible in geriatric patients and in patients with hip fracture.

Introduction: Regaining basic mobility independence is considered important for elderly hospitalised patients. The Cumulated Ambulation Score (CAS) is a valid tool for evaluating these patients' basic mobility (getting in and out of bed, sit-to-stand from a chair and walking) in orthopaedic wards, and its use is recommended in Denmark for patients with hip fracture. The aims of the present study were to evaluate the feasibility of the CAS in a geriatric ward and to describe its use after hip fracture in Denmark.

Cerebrospinal fluid hypocretin (orexin) levels are elevated by play but are not raised by exercise and its associated heart rate, blood pressure, respiration or body temperature changes.

Hypocretin (Hcrt) has been implicated in the control of motor activity and in respiration and cardiovascular changes. Loss of Hcrt in narcolepsy is linked to sleepiness and to cataplexy, a sudden loss of muscle tone which is triggered by sudden strong emotions. In the current study we have compared the effects of treadmill running, to yard play on cerebrospinal fluid (CSF) Hcrt level in normal dogs.

Role of the hypocretin (orexin) receptor 2 (Hcrt-r2) in the regulation of hypocretin level and cataplexy.

Hypocretin receptor-2 (Hcrt-r2)-mutated dogs exhibit all the major symptoms of human narcolepsy and respond to drugs that increase or decrease cataplexy as do narcoleptic humans; yet, unlike narcoleptic humans, the narcoleptic dogs have normal hypocretin levels. We find that drugs that reduce or increase cataplexy in the narcoleptic dogs, greatly increase and decrease, respectively, hypocretin levels in normal dogs. The effects of these drugs on heart rate and blood pressure, which were considerable, were not correlated with their effects on cataplexy.

Localized loss of hypocretin (orexin) cells in narcolepsy without cataplexy.

Study Objectives: Narcolepsy with cataplexy is characterized by a loss of approximately 90% of hypocretin (Hcrt) neurons. However, more than a quarter of narcoleptics do not have cataplexy and have normal levels of hypocretin in their cerebrospinal fluid, raising the possibility that their disease is caused by unrelated abnormalities. In this study we examined hypocretin pathology in narcolepsy without cataplexy.

Rapid eye movement sleep deprivation contributes to reduction of neurogenesis in the hippocampal dentate gyrus of the adult rat.

Study Objectives: The dentate gyrus (DG) of the adult hippocampus contains progenitor cells, which have potential to differentiate into neurons. Previously we reported that 96 hours of total sleep deprivation reduces neurogenesis in the DG of adult rats. Loss of either non-rapid eye movement (NREM) or rapid eye movement (REM) sleep could have contributed to the effect of total sleep deprivation.

Pattern of hypocretin (orexin) soma and axon loss, and gliosis, in human narcolepsy.

Human narcolepsy is correlated with a greatly reduced number of hypocretin (orexin) containing neurons and axons, and an elevated level of hypothalamic gliosis. We now report that the percentage loss of Hcrt cells and percentage elevation of GFAP staining are variable across forebrain and brain-stem nuclei, and are maximal in the posterior and tuberomammillary hypothalamic region. Regional gliosis and percent loss of hypocretin axons in narcoleptics are not correlated with regional hypocretin cell soma density in normals or with regional percent soma loss in narcoleptics.

Sleep deprivation decreases superoxide dismutase activity in rat hippocampus and brainstem.

Sleep deprivation by the disk-over-water technique results in a predictable syndrome of physiological changes in rats. It has been proposed that reactive oxygen species (ROS) may be responsible for some of these effects. A variety of antioxidative enzymes such as superoxide dismutase (SOD) and glutathione peroxidase (GPx) help to regulate the level of ROS.

Cataplexy-related neurons in the amygdala of the narcoleptic dog.

The amygdala plays an important role in the interpretation of emotionally significant stimuli and has strong projections to brainstem regions regulating muscle tone and sleep. Cataplexy, a symptom of narcolepsy, is a loss of muscle tone usually triggered by sudden, strong emotions. Extracellular single-unit recordings were carried out in the amygdala of narcoleptic dogs to test the hypothesis that abnormal activity of a subpopulation of amygdala neurons is linked to cataplexy.

A brief history of hypocretin/orexin and narcolepsy.

The hypothalamic peptides named the orexins, or hypocretins, were discovered in 1998. In 1999 it was established that genetic narcolepsy could be caused by mutations in the genes synthesizing these peptides or their receptors. In September of 2000 it was found that most human narcolepsy is caused by loss of hypocretin cells, most likely as a result of a degenerative process.

Reduced number of hypocretin neurons in human narcolepsy.

Murine and canine narcolepsy can be caused by mutations of the hypocretin (Hcrt) (orexin) precursor or Hcrt receptor genes. In contrast to these animal models, most human narcolepsy is not familial, is discordant in identical twins, and has not been linked to mutations of the Hcrt system. Thus, the cause of human narcolepsy remains unknown.

Sleep in the platypus.

We have conducted the first study of sleep in the platypus Ornithorhynchus anatinus. Periods of quiet sleep, characterized by raised arousal thresholds, elevated electroencephalogram amplitude and motor and autonomic quiescence, occupied 6-8 h/day. The platypus also had rapid eye movement sleep as defined by atonia with rapid eye movements, twitching and the electrocardiogram pattern of rapid eye movement.

Neuronal degeneration in canine narcolepsy.

Narcolepsy is a lifelong illness characterized by persistent sleepiness, hypnagogic hallucinations, and episodes of motor paralysis called cataplexy. We have tested the hypothesis that a transient neurodegenerative process is linked to symptom onset. Using the amino-cupric silver stain on brain sections from canine narcoleptics, we found elevated levels of axonal degeneration in the amygdala, basal forebrain (including the nucleus of the diagonal band, substantia innominata, and preoptic region), entopeduncular nucleus, and medial septal region.

Monotremes and the evolution of rapid eye movement sleep.

Early studies of the echidna led to the conclusion that this monotreme did not have rapid eye movement (REM) sleep. Because the monotremes had diverged from the placental and marsupial lines very early in mammalian evolution, this finding was used to support the hypothesis that REM sleep evolved after the start of the mammalian line. The current paper summarizes our recent work on sleep in the echidna and platypus and leads to a very different interpretation.

The echidna Tachyglossus aculeatus combines REM and non-REM aspects in a single sleep state: implications for the evolution of sleep.

Placental and marsupial mammals exist in three states of consciousness: waking, non-REM sleep, and REM sleep. We now report that the echidna Tachyglossus aculeatus, a representative of the earliest branch of mammalian evolution (the monotremes), does not have the pattern of neuronal activity of either of the sleep states seen in nonmonotreme mammals. Echidna sleep was characterized by increased brainstem unit discharge variability, as in REM sleep.

Altered distribution of cholinergic cells in the narcoleptic dog.

Narcolepsy is characterized by excessive sleepiness and episodes of cataplexy brought on by emotional excitation. Cataplexy and sleep paralysis have been hypothesized to be produced by the triggering during waking of brain stem cholinergic mechanisms normally acting to induce atonia in REM sleep. We hypothesized that narcoleptics have an abnormal number of LDT and/or PPN cholinergic neurons.

Ontogeny of feline temporal lobe epilepsy, II: Stability of spontaneous sleep epilepsy in amygdala-kindled kittens.

We previously described a model of spontaneous "sleep epilepsy" in kindled kittens with temporal lobe epilepsy (TLE). We now describe the postkindling course of this model from preadolescence to maturity and suggest pathophysiologic mechanisms. Spontaneous epilepsy, particularly generalized tonic-clonic convulsions (GTCs), developed 1h to 4 months after amygdala kindling and persisted to adulthood.

Activity of medial mesopontine units during cataplexy and sleep-waking states in the narcoleptic dog.

Narcolepsy has been hypothesized to be a disease of rapid eye movement (REM) sleep. According to this hypothesis, cataplexy is a result of the triggering during waking of the mechanism that normally serves to suppress muscle tone in REM sleep. REM sleep control mechanisms have been localized to the pons.

Neuronal activity in narcolepsy: identification of cataplexy-related cells in the medial medulla.

Narcolepsy is a neurological disorder characterized by sleepiness and episodes of cataplexy. Cataplexy is an abrupt loss of muscle tone, most often triggered by sudden, strong emotions. A subset of cells in the medial medulla of the narcoleptic dog discharged at high rates only in cataplexy and rapid eye movement (REM) sleep.