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Learn more about two issues that can have a profound impact on quality of life – pain and sleep disorders in MS – and about managing these problems, available treatment options, and research to identify the cause of pain and sleep disorders.
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Sativex (nabiximols) is the first cannabis-based medicine to be licensed in the UK. The drug can prescribed for the treatment for MS-related spasticity when a person has shown inadequate response to other symptomatic treatments or found their side effects intolerable. Sativex can be used in addition to a person's current anti-spasticity medication.
Prior to gaining a licence for use in MS-related spasticity, Sativex had been studied for its effects on a number of MS related symptoms including: spasticity and spasms, pain, bladder symptoms, tremor, and sleep disturbance.
How is Sativex given?
Sativex is a mouth (oromucosal) spray containing two chemical extracts derived from the cannabis plant: delta-9 tetrahydrocannabinol (THC) and cannabidiol (CBD). The number of sprays is gradually increased each day until the optimum dose is reached.
MS Views and News Providing educational information, resources and services for those affected by MS
For true marijuana connoisseurs, tetrahydrocannabinol (THC) isn’t the only thing in marijuana about which to rave. There’s also the increasingly popular cannabidiol (CBD) part of the plant. CBD is a compound in marijuana with mild to no psychoactive effect. It is frequently used to prevent seizures and there also have been some promising studies regarding its ability to treat brain injuries. CBD’s market potential is growing rapidly, but its legal status is uncertain.
Many companies claim to be able to sell and ship medical-grade CBD anywhere in the U.S. via the internet. For more on this, go here, here, and here. But is CBD actually legal under federal law so as to allow for what otherwise appears to be interstate drug trafficking? It all depends on where the CBD originates.
Marijuana is currently listed as a Schedule I narcotic under the federal Controlled Substances Act, meaning the federal government believes it to be a dangerous drug with no recognized medical benefit. Consequently, any CBD derived from marijuana violates the federal Controlled Substances Act, and the Drug Enforcement Administration has already stated that it believes CBD to be a marijuana derivative and, therefore, a Schedule I drug.
Hemp, on the other hand, is more complicated. The DEA defines hemp as the parts of the cannabis plant excluded from the Controlled Substances Act, namely the mature stalks and seeds. To legally grow cannabis in the U.S. — hemp or not — you must possess a permit from the DEA, which the DEA typically never issues. Consequently, cultivating hemp without a permit remains a federal crime. The only exception is the 2014 federal Farm Bill, which defines “industrial hemp” as cannabis that contains less than 0.3 percent THC by weight, and which allows state departments of agriculture, universities, and colleges to cultivate industrial hemp for educational and research purposes without a DEA permit. Despite the prohibition on hemp cultivation without a DEA-issued permit, it is not a violation of the federal Controlled Substances Act to purchase, sell, and possess processed hemp products.
Click here to receive MS news via e-mail 2016 MS Symposium - South Florida - 11.12.16 With over 200 attending Live and another 50+ watching via webcast to listen with our MS Neurology Panel (Energizer Bunnies 20:49) consisting of Doctors: Aaron Boster, MD, Brian Steingo, MD and Christopher LaGanke, MD - 1st neurologist (Boster) begins at 23:20 into this video. -.. Q&A began at 2:14:56
This event began with a warm-up from Jeffrey A. Segal, BS, NSCA-CPT, CSCS, CPTS, CPR/AED- a personal trainer who speaks at many MS Events.
Spec Note: nice audience applause seeing Stuart's Handshake from Xavier at 19:00
This program was made possible with Support from: Sanofi-Genzyme, Teva Neuroscience, Novartis, Mallinckrodt, Biogen, Genentech,
IF You have general Questions for any of our presenters from the Neurology panel, please send an email to: firstname.lastname@example.org -- we will then send to the person whom you would like to answer your question and then we will ask that person to respond directly to you.. This program continued with the afternoon presentations on Social Security Disability Income (SSDI and Bladder-Bowel Care - Click hereto watch this video ~~~~~~~~~~~~~
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2016 MS Symposium from Davie, Florida Program Date: November 12, 2016
This video contains our afternoon session of topics: 1) Social Security Disability Law (SSDI) - Discussion & Q&A from Lisa Gonzalez-Goetz, P.A. 2_ Bladder & Bowel Care - Pelvic Floor Exercise -
Discussion and Q&A - from Carina Siracusa, PT, DPT, WCS
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Our sensation of pain is processed in the brain after neuronal circuits conduct the excitation of cells at the site of tissue damage to the spinal cord. This is where information is pre-processed and then transmitted to the brain, where the sensation of pain is finally produced. This process is controlled by nerve cells (also known as neurons).
Until now, this was the accepted hypothesis.
However, scientists at the Division of Neurophysiology at MedUni Vienna’s Center for Brain Research recently found that non-neuronal cells, called glial cells, may also participate in the process.
Glial cells are not neurons, but they also perform an important role. They maintain homeostasis, form myelin, and provide support and protection for neurons. Researchers are now reporting that glial cells are also activated in response to stimuli such as pain, and can contribute to cell signaling by releasing inflammatory cytokines, for example. Cytokines are small proteins that serve as molecular messengers between cells.
“The activation of glial cells results in a pain-amplifying effect, as well as spreading the pain to previously unaffected parts of the body. For the very first time, our study provides a biological explanation for this and for other hitherto unexplained pain phenomena in medicine,” Jürgen Sandkühler, the study’s lead author and head of the Division of Neurophysiology at MedUni Vienna’s Center for Brain Research, said in a press release.
In a large, international study, each 10-degree increase in distance from the equator was associated with a 10-month decrease in age at onset of MS symptoms. Led by researchers at the University of Tazmania, the MSBase study group (an international database of neurological records of people with MS worldwide) looked at the records of more than 22,000 people with MS from 21 countries. Previous studies had found that more people are at risk for getting MS in areas distant from the equator.
National MS Society-funded researchers have established and studied a new mouse model that mimics aspects of MS, especially MS in people who do not benefit from treatment with interferon beta.
Results suggest that the new subtype of the MS-like EAE which is resistant to interferon beta, and perhaps MS, has distinct features and may be treatable by targeting specific molecules.
Being able to detect interferon resistance in people with MS would allow the selection of more appropriate therapies sooner.
The study, by Drs. Makoto Inoue (University of Illinois at Urbana-Champaign), Mari Shinohara (Duke University School of Medicine) and colleagues, was published early online on November 7, 2016 in Nature Neuroscience.
Background: MS is an unpredictable disease that involves attacks on the brain and spinal cord by the person’s own immune system. There is currently no way to predict whether a person will respond to a particular therapy. Although many people with relapsing MS can be treated effectively with interferon beta (interferon beta-1a, peginterferon beta-1a, and interferon beta-1b), a proportion of people don’t benefit, and may be “interferon resistant.” The underlying biological reasons for interferon resistance are not clear; achieving a better understanding could lead to ways to predict an individual’s response to therapies and identify the best treatment option early in the course of the disease. To look at the question of interferon resistance, the researchers focused on EAE in mice. EAE is a laboratory-induced disease that mimics some aspects of human MS, and is an important research tool for gaining insights into specific disease mechanisms. The study: The researchers compared two variants of EAE in mice. The first type was the type commonly used in research, which is induced by weak immune activation. This type could be successfully treated with interferon-beta. The second type was a new approach, which was induced with a stronger immune activation that bypassed immune reactions typical in the more standard EAE. Mice with the second type showed more inflammation, resistance to interferon beta, and more damage to nerve fibers. They also showed involvement of two immune molecules: LTbR and CXCR2. The investigators also reported that they could improve the second type of EAE by blocking the activity of LTbR and CXCR2.
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