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Subsequent to EMA approval of tetrahydrocannabinol (THC): cannabidiol (CBD) oromucosal spray based on results of various studies, including an enriched-design clinical trial, two newer postapproval randomized trials have confirmed its efficacy and safety for treating resistant multiple sclerosis spasticity, while simultaneously addressing specific authorities' concerns.
A double-blind, placebo-controlled, Phase IV trial, conducted as part of the EMA's risk management plan, found no effect of THC:CBD spray on cognition and mood after 50 weeks of treatment. In the Sativex® as add-on therapy versus further optimized first-line ANTispastics (SAVANT) study, add-on THC:CBD spray was significantly more effective than readjusting standard antispasticity therapy and provided new evidence of efficacy as requested by German authorities. SAVANT results support practical recommendations for treating resistant multiple sclerosis spasticity in daily practice.
When I first met Stephanie in March, she was like any healthy 28-year-old coming in to see me for a nutrition consult. Her positive attitude and bright smile filled the room as she told me about her job as a grade school teacher and the new apartment she just moved into with her boyfriend of seven years.
“We are a great team,” she said. “Little did he know that his law school wouldn’t be the biggest challenge we’d face as a couple.”
Stephanie was diagnosed about a year ago with multiple sclerosis (MS), and behind her beautiful eyes and strong spirit, I could sense her pain at the discovery of the most recent spinal cord lesions after she complained to her doctors of new nerve pain in her feet. She will be starting steroid infusions in a few weeks, and together we hope to design a nutrition and lifestyle plan that will support her health and healing, and preserve her quality of life.
Nerve pain is hard to grasp and relentless in its unpredictability. The nerve damage associated with MS has been linked to causative factors including dysbiosis of the gut microbe, autoimmune responses, and increased inflammation, all leading to an attack on the nervous system by the body’s own immune cells.
One of the hardest things I’ve had to accept with MS is the necessity of asking for help.
Pride and self-reliance dissipate remarkably quickly when you find yourself splayed on the floor and you no longer have the capacity to get up.
In extremis, I then ask for help. But if I’d asked earlier, the whole farrago probably could have been avoided. This lesson took a while to sink in; indeed, I’m not sure I’ve made it out of kindergarten yet!
Kindergarten. Yes, this disease does infantilize.
I can no longer put on my shoes. Each new strategy to do so worked for a while, but eventually, they all failed. I suppose that if I started the day before, I’d have a chance. I’d forget why I was putting them on, but by then the challenge would be enough.
I still find it weird as a 61-year-old bloke to watch my 22-year-old son slapping them on in seconds.
Hey, I used to beat him at tennis. He was only 8, and I didn’t have MS yet. Give me a break; it was still becoming increasingly difficult!
So, yes, I’ve become more receptive of asking for help and not feeling guilty. It’s not any fault of ours, we’re just dealing with the cards that life has dealt.
Blood infection with the yeast Candida albicans,a type of fungus, can reach the brain and trigger an immune response, a new mouse study shows. Although the fungus can be cleared within 10 days, it affects the spatial memory of mice.
These findings are the first evidence that a blood infection with a fungus may have a role in diseases linked with a deregulated immune response in the central nervous system, like multiple sclerosis (MS).
Can you use your mind to attack your MS, just as you use things such as medications and physical therapy? Some people who believe in the benefits of mindfulness think you can, at least to some extent.
Mindfulness is defined as “the basic human ability to be fully present, aware of where we are and what we’re doing, and not overly reactive or overwhelmed by what’s going on around us,” according to mindful.org. It uses a combination of things like yoga, meditation, music, stretching, and group support to reduce stress.
For a number of years, Maryanna Klatt, PhD, and others at The Ohio State University have been using mindfulness techniques to help people with MS. The idea is that by lowering a person’s stress, their quality of life will be raised. The Mindfulness in Motion program was first tried several years ago on a group of surgical intensive care nurses. (There’s plenty of stress in that line of work.) An article in NARCOMS Now magazine reported that following the eight-week program, “nurses who participated had lower levels of salivary amylase, an enzyme in the saliva associated with prolonged stress. Along with lower levels of these stress chemicals, the nurses had increased job satisfaction and less ’emotional exhaustion.’”
MS is thought to be caused by immune-mediated inflammation that damages the myelin — an insulating sheath around nerve cells. For this reason, current MS disease-modifying treatments focus on immune-mediated inflammation. Although these treatments moderate disease relapses, their impact on disease progression is unclear.
Previous studies have demonstrated that oligodendrocytes — cells that produce myelin — are critical in protecting against neuron demyelination and axon (nerve fiber) damage. As a result, researchers have been keen to develop alternative therapeutic approaches that protect oligodendrocytes, and ultimately limit disease progression.
A signaling pathway called integrated stress response that acts as a natural defense system to protect cells has been shown to reduce the inflammatory impact on oligodendrocytes. This response is triggered by phosphorylation (a chemical reaction) of a protein called eukaryotic initiation factor 2 alpha (eIF2α), and reduces the total production of proteins, instead promoting the synthesis of protective proteins in the cells.
Autologous hematopoietic stem cell transplant is better than disease-modifying therapies (DMT) at reducing the risk of disease progression in patients with relapsing-remitting multiple sclerosis (RRMS), results from the MIST clinical trial show.
While RRMS patients may respond to immune suppressive therapies, in order to be effective these need to be applied early in the disease course, i.e., while MS is mainly an immune-mediated and inflammatory disease.
A type of immune cell from the gut can reduce brain inflammation in people with multiple sclerosis (MS), and increasing the numbers of these cells in a mouse model of the disease halts inflammation completely, new research reports.
In MS, immune cells in the central nervous system attack myelin — the protective sheath around nerve fibers that is critical to an efficient conduction of electrical impulses between the brain and other parts of the body.
SECONDARY PROGRESSIVE MULTIPLE SCLEROSIS: WHEN MS ADVANCES
If your doctor says you have secondary progressive multiple sclerosis (SPMS), it means you're in a different stage of your disease. Most folks get it after living for a while with relapsing-remitting MS (RRMS).
In SPMS, you may not get any break in your symptoms, unlike RRMS, when you had flare-ups that came and went. But your doctor can suggest medicine to help manage them.
Secondary vs. Relapsing-Remitting MS
About 85% of people with MS start with the relapsing-remitting form. They get attacks of symptoms called relapses, followed by symptom-free periods called remissions.
During relapses, your immune system -- your body's defense against germs -- causes inflammation that damages the protective coating around nerve fibers. This disrupts the flow of nerve signals to and from the brain and spinal cord. It leads to symptoms like tiredness, numbness, and weakness.
Then the immune system stops attacking. Your symptoms improve or disappear, and you go into remission. Relapses and remissions alternate over time.
In SPMS, your symptoms steadily get worse instead of coming and going. You might still have relapses, but they don't happen as often.
What Causes SPMS?
It's not clear exactly why RRMS changes to SPMS. Some researchers think it happens because of nerve damage that occurred earlier in the disease.
Not everyone with the relapsing-remitting form of the disease will get SPMS. Doctors don't know for sure who will and who won't, and how quickly it will happen.
You're more likely to change to SPMS if:
You've lived with MS for a long time
You have a lot of nerve damage in your brain and spinal cord
You have frequent and severe relapses
When Do People Change to SPMS?
A small number of people start out with SPMS. They may have had RRMS first, but it wasn't diagnosed or their symptoms were too mild to notice.
Before disease-modifying drugs were available, half of people with RRMS changed to SPMS within 10 years.
New treatments have altered the course of MS. Today these drugs can slow MS and delay the move towards SPMS, although doctors don't know how much they delay it.
Relapses and progression contribute to multiple sclerosis (MS) disease course, but neither the relationship between them nor the spectrum of clinical heterogeneity has been fully characterized. A hypothesis-driven, biologically informed model could build on the clinical phenotypes to encompass the dynamic admixture of factors underlying MS disease course. In this medical hypothesis, we put forth a dynamic model of MS disease course that incorporates localization and other drivers of disability to propose a clinical manifestation framework that visualizes MS in a clinically individualized way. The topographical model encapsulates 5 factors (localization of relapses and causative lesions; relapse frequency, severity, and recovery; and progression rate), visualized utilizing dynamic 3-dimensional renderings. The central hypothesis is that, like symptom recrudescence in Uhthoff phenomenon and pseudoexacerbations, progression clinically recapitulates prior relapse symptoms and unmasks previously silent lesions, incrementally revealing underlying lesion topography. The model uses real-time simulation software to depict disease course archetypes and illuminate several well-described but poorly reconciled phenomena including the clinical/MRI paradox and prognostic significance of lesion location and burden on disease outcomes. Utilization of this model could allow for earlier and more clinically precise identification of progressive MS and predictive implications can be empirically tested.
CONTEMPORARY CONCEPTUALIZATION OF MS DISEASE COURSE
Multiple Sclerosis (MS) is a disease characterized by both relapses and insidious progression, and is notably heterogeneous in clinical course, symptomatology, and severity. The accepted MS clinical course phenotypes1 have been foundational in clinical practice and are utilized to inform the eligibility requirements and outcomes of clinical trials, which shape regulatory approvals and indications for MS therapeutics.
While relapsing and progressive processes contribute to MS disease course,1,2 neither the relationship between them3,4 nor the spectrum of clinical heterogeneity has been fully characterized.2,3 Although the contemporary phenotypes, revised in 2013,5 have been refined with subdescriptors based on the presence or absence of inflammatory activity and disease progression, they maintain distinctions between relapsing and progressive disease as separate core disease subtypes at a given time point. These phenotypes have focused on clinical manifestations, yet by design, they do not directly represent the diversity of symptoms, relapse severity, and the pattern and manner of accumulation of disability.
Furthermore, uncertainties remain regarding the biological underpinnings of the disease. Perhaps relapsing-remitting MS (RRMS) is also progressive from onset, as atrophy is known to begin early in the disease.2,6 Perhaps progressive MS is inflammatory throughout the course, as there is evidence of inflammation even late in progressive disease.7 A contemporary view is that MS is a single disorder with an intermingling of acute focal recurrent inflammation and diffuse chronic neurodegeneration from the outset of the disease.3 In clinical practice, the line between relapsing and progressive MS is not always discrete. In one study, we found a mean period of diagnostic uncertainty of 4.3 years during the transition from RRMS to secondary progressive MS (SPMS), highlighting that there is no way to clinically determine a precise moment of transition between these 2 categories.8 A dynamic model of MS disease course must visualize this admixture of relapsing and progressive aspects of the disease in a way that remains true to MS clinical phenomenology, while also capturing the clinical variability manifested by individual patients.
THE TOPOGRAPHICAL MODEL OF MS AND THE RECAPITULATION HYPOTHESIS
The topographical model of MS described in this medical hypothesis builds directly on the 2013 clinical course revisions' delineation of relapse activity and progression as distinct processes coexisting in parallel.5 As a unified visualization of disease course, this new model illustrates the interplay of relapses and progression in MS across the entire range of disease course depictions, including the transitions between clinical phenotypes. The model provides a clinical manifestation frameworkthrough which disease course may be better understood.
Central to this model is the observation that progression clinically recapitulates a patient's prior relapse symptoms and unmasks previously clinically silent lesions, incrementally manifesting above the clinical threshold a patient's underlying “disease topography.” The recapitulation hypothesis central to this new clinical framework may better elucidate the drivers of disability accumulation and could allow for earlier and more clinically precise identification of progressive MS. A novel contribution of this model is to depict both the location and severity of an individual patient's lesions in the form of a topographical map of MS disease burden, explicating the clinical heterogeneity inherent to the disease. It is important to acknowledge that this model does not attempt to address or answer unresolved questions about the underlying immunologic or pathologic bases of the disease. Indeed, the model is designed to encapsulate and depict clinical course while remaining agnostic to, and not predicated on assumptions regarding, currently unreconciled questions2 of MS pathogenesis and etiology.
Fundamental assumptions and variables.
The topographical model of MS visualizes the CNS as a pool divided into 3 basic anatomical regions with increasing amounts of functional reserve. MS lesions are represented as topographical peaks that rise up from the pool base. Localization of lesions is visualized by plotting lesions on an anatomical grid with lateralization grouped across the 3 key regions: (1) the spinal cord and optic nerves occupy the shallow end, (2) the brainstem and cerebellum comprise the middle; and (3) the cerebral hemispheres constitute the deep end of the pool.
The water itself represents neurologic functional capacity: in essence, the compensatory ability of the nervous system that keeps regions of damage “submerged.” Functional reserve is thus a “fluid” construct, variable over time, and subject to periods of depletion (during fever or concurrent illness), renewal, and decline over the long-term disease course to a variable degree. The water's surface depicts the clinical threshold: those peaks that cross above the threshold upon formation cause clinical relapses; those topographical peaks below the surface are seen as clinically silent lesions on MRI. Depending on extent of relapse recovery, a topographical peak that crosses the threshold may recede again beneath the water's surface, or remain above the clinical threshold, leaving residual deficits. Progression is depicted as the slowly declining water level, representing a gradual depletion of functional capacity, and revealing clinical symptoms referable to the underlying disease topography.
To express the heterogeneity of clinical course and varied prognostic outcomes, the model design encapsulates 5 variable factors: localization of relapses and causative lesions; relapse frequency, severity, and recovery; and progression rate (table).