Posts tagged medication
Articles and news from the latest research reports.
Sleep Disturbances, Common in Parkinson’s Disease, Can Be Early Indicator of Disease Onset
Up to 70% of Parkinson’s disease (PD) patients experience sleep problems that negatively impact their quality of life. Some patients have disturbed sleep/wake patterns such as difficulty falling asleep or staying asleep, while other patients may be subject to sudden and involuntary daytime sleep “attacks.” In the extreme, PD patients may exhibit REM-sleep behavior disorder (RBD), characterized by vivid, violent dreams or dream re-enactment, even before motor symptoms appear. A review in the Journal of Parkinson’s Disease discusses the underlying causes of sleep problems in PD, as well as medications, disease pathology, and comorbidities, and describes the most appropriate diagnostic tools and treatment options.
Sleep problems in PD patients can have wide-ranging adverse effects and can worsen in later stages of the disease. Sleepiness socially isolates patients and excessive sleepiness can put patients at risk of falls or injury, and can mean patients must give up driving. Sleepiness can impair cognition and concentration, exacerbate depression, and interfere with employment. Wakefulness at night impairs daytime wakefulness and may also cause mood instabilities and can exhaust caregivers.
“Diagnosis and effective treatment and management of these problems are essential for improving the quality of life and reducing institutionalization of these patients,” says lead author Wiebke Schrempf, MD, Technische Universität Dresden, Faculty of Medicine Carl Gustav Carus, Department of Neurology, Division of Neurodegenerative Diseases, Dresden, Germany.
Dr. Schrempf and colleagues describe some of the complexities associated with treating sleep problems in PD patients, such as the worsening of sleep problems by dopaminergic medications used to treat motor symptoms. Lower doses of levodopa or dopamine agonists are able to improve sleep quality partly by reducing motor symptoms such as nighttime hypokinesia (decreased body movement), dyskinesia (abnormal voluntary movements), or tremor (involuntary shaking), which interfere with normal sleep. However, the same medications may also cause excessive daytime sleepiness. The report describes how changing medication, dose, duration of treatment, or timing of administration can improve outcomes.
The presence of other conditions common in PD patients such as depression, dementia, hallucinations, and psychosis may interfere with sleep. Unfortunately, some antidepressants can also impair sleep.
Sleep problems may also be harbingers of future neurodegenerative disease. Patients with RBD exhibit intermittent loss of normal muscle relaxation during REM sleep and engage in dream enactment behavior during which they may shout, laugh, or exhibit movements like kicking and boxing. “RBD seems to be a good clinical predictor of emerging neurodegenerative diseases with a high specificity and low sensitivity, whereas other early clinical features of PD, such as olfactory dysfunction and constipation, are less specific,” says Dr. Schrempf. “These early clues may help identify PD patients before motor symptoms appear, when disease-modifying therapies may be most beneficial.”
PD is the second most common neurodegenerative disorder in the United States, affecting approximately one million Americans and five million people worldwide. Its prevalence is projected to double by 2030. The most characteristic symptoms are movement-related, such as involuntary shaking and muscle stiffness. Non-motor symptoms, such as worsening depression, cognition, and anxiety, olfactory dysfunction, and sleep disturbances, can appear prior to the onset of motor symptoms.
(Source: alphagalileo.org)
Cannabis-based medications have been proved to relieve pain. This is the conclusion drawn by Franjo Grotenhermen and Kirsten Müller-Vahl in issue 29–30 of Deutsches Ärzteblatt International.
Cannabis medications can be used in patients whose symptoms are not adequately alleviated by conventional treatment. The indications are muscle spasms, nausea and vomiting as a result of chemotherapy, loss of appetite in HIV/Aids, and neuropathic pain.
The clinical effect of the various cannabis-based medications rests primarily on activation of endogenous cannabinoid receptors. Consumption of therapeutic amounts by adults does not lead to irreversible cognitive impairment. The risk is much greater, however, in children and adolescents (particularly before puberty), even at therapeutic doses.
Over 100 controlled trials of the effects of cannabinoids in various indications have been carried out since 1975. The positive results have led to official licensing of cannabis-based medications in many countries. In Germany, a cannabis extract was approved in 2011 for treatment of spasticity in multiple sclerosis. In June 2012 the Federal Joint Committee (the highest decision-making body for the joint self-government of physicians, dentists, hospitals and health insurance funds in Germany) pronounced that the cannabis extract showed a slight additional benefit for this indication and granted a temporary license until 2015.
New drug could treat Alzheimer’s, multiple sclerosis and brain injury
July 24, 2012
A new class of drug developed at Northwestern University Feinberg School of Medicine shows early promise of being a one-size-fits-all therapy for Alzheimer’s disease, Parkinson’s disease, multiple sclerosis and traumatic brain injury by reducing inflammation in the brain.
Northwestern has recently been issued patents to cover this new drug class and has licensed the commercial development to a biotech company that has recently completed the first human Phase 1 clinical trial for the drug.
The drugs in this class target a particular type of brain inflammation, which is a common denominator in these neurological diseases and in traumatic brain injury and stroke. This brain inflammation, also called neuroinflammation, is increasingly believed to play a major role in the progressive damage characteristic of these chronic diseases and brain injuries.
By addressing brain inflammation, the new class of drugs — represented by MW151 and MW189 — offers an entirely different therapeutic approach to Alzheimer’s than current ones being tested to prevent the development of beta amyloid plaques in the brain. The plaques are an indicator of the disease but not a proven cause.
A new preclinical study published today in the Journal of Neuroscience, reports that when one of the new Northwestern drugs is given to a mouse genetically engineered to develop Alzheimer’s, it prevents the development of the full-blown disease. The study, from Northwestern’s Feinberg School and the University of Kentucky, identifies the optimal therapeutic time window for administering the drug, which is taken orally and easily crosses the blood-brain barrier.
"This could become part of a collection of drugs you could use to prevent the development of Alzheimer’s," said D. Martin Watterson, a professor of molecular pharmacology and biological chemistry at the Feinberg School, whose lab developed the drug. He is a coauthor of the study.
In previous animal studies, the same drug reduced the neurological damage caused by closed-head traumatic brain injury and inhibited the development of a multiple sclerosis-like disease. In these diseases as well as in Alzheimer’s, the studies show the therapy time window is critical.
Multiple sclerosis drug disappoints on disability
July 23, 2012 By David Orenstein
(Medical Xpress) — This week the Journal of the American Medical Association published a study with unfortuate news for the millions of people who suffer from multiple sclerosis. In the large study, a therapy known as interferon beta failed to stave off the progression of the incurable disease. Albert Lo, associate professor of neurology and epidemiology, comments on what the study means for patients, why it was well-designed, and how a new effort to support research on the disease in Rhode Island could help.
The results of this study with nearly 2,700 participants showed that treatment with interferon beta, which is a major class of disease-modifying therapy for multiple sclerosis, did not prevent progression of disability, which is very disappointing from a therapeutic perspective. Currently, there is no cure for MS, and as a lifelong disorder of the nervous system, MS is characterized by episodic relapses of neurological injury such as weakness or blindness. While in most cases, there is a varying degree of recovery after relapses, over time, disability accumulates. The accumulation of deficits and the loss of physical and mental function is a major concern for people with MS and their clinicians.
Currently, there is no medication on the market that is directed explicitly for neuroprotection and the prevention of disability. Many had hoped that the interferons, along with the other disease-modifying agents (which were developed to reduce relapse rates) would also have a significant effect on protecting patients from MS disability.
Although the results from this study were not as we would have hoped, they reflect a marked improvement over prior studies which used known methodologic flaws. The new results from the Tremlett group point to the importance of the research methodology used (prospectively collected longitudinal study data) and a well-controlled design to generate the results – approaches that we are using in our own research at Brown University.
A number of the early studies examining the effect of interferons on disability primarily used patient sample groups of convenience for post-marketing studies. They indicated that interferons were in fact preventing disability. However, using samples of convenience inherently includes a number of biases and problems. Dr. Tremlett’s results were generated from a more systematic longitudinal study in which biases and shortcomings can be better addressed. Therefore, making conclusions and clinical decisions from the results is more reliable. These data both will help in making clinical decisions on treating MS patients during the later course of their disease, when there are virtually no relapses, and will help to point more urgently toward the clinical need of an agent to prevent disability.
Provided by Brown University
Source: medicalxpress.com