The blogger that can’t write, the artist that can’t create & the Pilates advocate that can’t practice


This is where I am now but I can’t walk well and definitely show the pain!

I’m quiet because it hurts. Everywhere hurts so much, it’s a pain like no other and nothing stops it completely.
My mood is the lowest it has been in a long time, it’s expected when I’m struggling to manage my pain.

Normally I would be using exercise to help with my pain but I’m having to take some time off that.
I started to experience funny sensations in my feet which, over 2 weeks have crept up both of my legs.
Around the same time this happened I found my legs were getting weaker, I have now adapted my walking ‘gait’ to suit how my legs feel. My feet are now wider apart for stability & my legs although weak are also a lot like I imagine wooden legs to be, stiff!

So after speaking with my Neurological Physiotherapist I have been advised not to exercise at the gym & no pilates classes for a while.
It’s time to give my body a rest & not make it harder for it to recover. It seems more & more likely that this is a relapse!
Like my Big Sistaaah of the MegaSpecial variety says: just when we get our lives back on track our MS flares up & reminds us it’s still there!

The 'Foot ups'
The ‘Foot ups’

I have to wear my ‘foot ups’ full time now as well, even in doors! They help me to lift my toes when I walk, this problem that I am having is called ‘Dropped foot’

Foot drop

Foot drop, or dropped foot, is a symptom experienced by some people with multiple sclerosis. It is caused by weakness in the ankle that means the foot drags along the ground or hangs down when walking. People with MS with foot drop are more vulnerable to tripping and falling. Walking also uses more energy and people may alter their gait to compensate, commonly lifting their leg higher.

Foot drop can be treated using functional electrical stimulation (FES). This uses small electrical charges to force the foot into a more natural position for walking. An ankle splint (orthosis) can also be used to hold the foot in a rigid position.

These are the days that are the longest! I can’t exercise, blogging is extremely hard as I’m lacking concentration & can’t do my art without falling asleep!
It’s a good job my artwork is digital otherwise I’d be waking up with paint all over my face! Instead I just wake up with ‘qwerty’ across my forehead!

I’m the blogger that can’t write, the artist that can’t create & the Pilates advocate that can’t practice.

*It has taken me literally all day to do this short blog!*


Constraints of my MS: Fatigue

Constraints of my MS

The last part of ‘Constraints of my MS’ was

about PAIN & all the medication I take!

With that in mind, my next part talks about…




Fatigue is one of the commonest symptoms of multiple sclerosis and can often have a major impact on people’s lives. The level of fatigue does not reflect the severity of someone’s MS and people can experience fatigue that interrupts their daily life or that prevents them from working, whilst having no other symptoms.

Fatigue is very different from the tiredness or exhaustion that people without MS experience following strenuous exercise or a busy day at work. Fatigue is described as interfering with normal activity and being out of all proportion to any activity undertaken. It is often involves the sudden loss of energy and the inability to continue an activity. MS fatigue can not be worked through, as can sometimes be done with non MS fatigue, and recovery time also tends to be much longer.

Fatigue does not relate to relapses, nor to any permanent increase in disability. Previously experienced MS symptoms may get worse during fatigue but reduce again after rest. Fatigue can also affect cognitive symptoms such as short term memory, concentration or word finding. People report that it is harder to ‘think straight’ when they are fatigued.

As an ‘invisible’ symptom of MS, fatigue is sometimes not properly understood by family, friends or colleagues, who assume that the person with MS is depressed or just not trying hard enough. Fatigue is a major cause of early departure from the workforce.

Once again, I take medication for my fatigue which help by keeping my MS’y symptoms from getting worse throughout the day and help to keep me awake past 7pm!

Now, my fatigue is not only a symptom of my MS but it is also a cause from the cocktail of medication that I take!

I recently reduced the amount of Pregabalin from the highest amount of 600mg a day to 400mg day. I decided to do this so I could try & get a bit of brain function back instead of feeling as though I am in a daze 24/7 with my head in the clouds – also known as ‘Cog fog’…..

Innovative research tool pinpoints potential therapies for multiple sclerosis

Shared on Facebook yesterday by an inspirational Mega Special lady & 5 x Paralympic medalist! Stephanie Millward.

I haven’t read this yet but I bet it is great news! Anything that will repair the nervous system must be amazing for us!!!

Innovative research tool pinpoints potential therapies for multiple sclerosis

by Pete Farley
multiple sclerosis
Demyelination by MS. The CD68 colored tissue shows several macrophages in the area of the lesion. Original scale 1:100. Credit: Marvin 101/Wikipedia
Using a novel screening platform to rapidly evaluate the cellular effects of 1,000 chemical compounds, a team led by UC San Francisco scientists has identified eight drugs that may stimulate nervous system repair in multiple sclerosis (MS).

All eight compounds have previously been approved by the U.S. Food and Drug Administration (FDA) for the treatment of other conditions. One of the most promising agents is an antihistamine, though the scientists caution that MS patients should not use the drug until clinical trials have established whether it can safely and effectively treat MS, and if it does, what the proper dosages and treatment regimens would be. Because of the drug’s emergence as a clear front-runner in the new study, a Phase 2 clinical trial to evaluate its effectiveness in MS is already underway at UCSF.

“A major unmet need in the development of therapeutics for repair in MS has been the ability to screen compounds in a high-throughput manner,” said Jonah Chan, PhD, the Debbie and Andy Rachleff Distinguished Professor of Neurology at UCSF and senior author of the new study. “Through a great deal of serendipity, combined with the hard work of outstanding students and colleagues, we have been able to address this need, and I am happy that we are already testing one compound in the clinic.”

The new research was published online July 6, 2014 in Nature Medicine.

The decision to focus on compounds already approved by the FDA was driven by study co-author Stephen L. Hauser, MD, the Robert A. Fishman Professor and chair of the Department of Neurology at UCSF. As founder and director of UCSF’s interdisciplinary MS Research Group, Hauser has championed efforts to translate insights from basic neuroscience research into new therapies as quickly as possible. The new study is an exemplar of that strategy: only 14 months have elapsed since the team performed the first drug screen, and the Phase 2 trial is already at its halfway point.

Co-author Ari Green, MD, Debbie and Andy Rachleff Distinguished Professor of Neurology, is principal investigator on the Phase 2 trial at UCSF, which is known as the ReBUILD trial. According to Green, the trial was expedited by the FDA’s granting of a New Drug Application exemption, which allows clinical researchers to study drugs in conditions for which they were not originally approved. The trial is still enrolling MS patients and is expected to be completed by the end of 2014.

In MS, the immune system goes awry and attacks myelin, a fatty sheath covering the thin nerve-cell extensions called axons that transmit signals in the brain. Much like the plastic covering on electrical wiring, myelin provides insulation that is crucial to quick, efficient communication among neurons. Poor neural conduction leads to the range of progressively worsening symptoms of MS. Myelin degeneration damages axons and ultimately causes nerve cells to die off.

Myelin is formed by specialized cells called oligodendrocytes, which wrap themselves around axons in multiple layers. This wrapping process, known as myelination, has generally been studied in combined cultures of neurons and oligodendrocytes, and until recently it was widely believed that axons provide some chemical signal to oligodendrocytes that initiates myelination.

But in 2012, Chan and colleagues published studies showing that oligodendrocytes will myelinate synthetic “nanofibers” of approximately the same diameter as axons. Though this work showed that it was possible to study myelination in oligodendrocytes alone, the configuration of the fibers used in the experiments made it difficult to automate the detection and quantification of myelination, which are essential criteria to efficiently screen drugs that might stimulate remyelination to treat MS.

To address these problems, Chan’s research group designed a new system based around precisely fabricated conical “micropillars.” Each micropillar is only a few thousandths of an inch thick at its base, and 10,000 of them can fit within a 5-millimeter-square “well.” Chan’s team created plates of 96 micropillar wells and loaded up each well with 40,000 oligodendrocyte precursor cells (OPCs), the cells from which oligodendrocytes are derived in the brain and spinal cord.

OPCs do not always differentiate into myelin-forming oligodendrocytes, so the research team tagged the cells with fluorescent markers that would glow green if the cells remained OPCs, and glow red if they had become oligodendrocytes.

The group then systematically applied 1,000 compounds from a library of FDA-approved drugs to the wells with an automated screening platform. Using a confocal microscope to view the slides from below, the researchers could quickly determine from the color of the cells if they had differentiated into oligodendrocytes, and could also calculate how thoroughly any oligodendrocytes had wrapped the micropillars—from beneath the micropillars, myelination is seen in cross-section, and quantifying it is much like counting tree rings.

In 2013, Chan was the inaugural winner of the Barancik Prize for Innovation in MS Research from the National Multiple Sclerosis Society for his work on the new platform, which is known as BIMA (Binary Indicant for Myelination Using Micropillar Arrays).

The vast majority of the compounds tested with the BIMA platform in the new study killed the OPCs or were not beneficial to their development, and many prompted the OPCs to proliferate without transforming to oligodendrocytes. But eight drugs stood out on two counts: they successfully prompted OPCs to differentiate into oligodendrocytes, and the resulting  robustly wrapped the micropillars with layers of myelin.

Remarkably, all eight drugs share a common mechanism of action: they each block a particular receptor—called the muscarinic receptor—on a subset of OPCs that respond to the neurotransmitter acetylcholine.

The antihistamine clemastine was the most effective of all 1,000 compounds tested in promoting both oligodendrocyte production and myelination. The drug exerts some of its anti-allergy effects by blocking the actions of histamine in mucous membranes, but the drug also has an “off-target” effect, blocking muscarinic receptors in the brain and elsewhere in the body.

“It is imperative that we exploit and utilize the power of our screening platform to search for additional compounds, but another next step is to identify the receptor targets of these anti-muscarinic drugs so we can develop therapeutic compounds with minimal side effects,” said Chan. “There are five different muscarinic receptors expressed in the nervous system, and a major question is whether the effects we observed are the result of blocking a single receptor or a combination of multiple receptors. Understanding the molecular mechanisms responsible for oligodendrocyte differentiation and myelination will provide valuable insight into the repair process and guide the development of new effective therapeutics for remyelination.”

More information: Micropillar arrays as a high-throughput screening platform for therapeutics in multiple sclerosis, Nature… nt/full/nm.3618.html


Statins in neurological disorders: an overview and update


Shared on Facebook yesterday by an inspirational Mega Special lady & 5 x Paralympic medalist! Stephanie Millward.

This is pretty interesting from an MS point of view. They seem to be able to control/reduce new lesions!!

A critical review of the fundamental therapeutic effects of glatiramer acetate


Shared on Facebook yesterday by an inspirational Mega Special lady & 5 x Paralympic medalist!
Stephanie Millward.

This is so interesting from an MS point of view. It is more proof that people are trying their hardest to understand MS and therefore to find the Cure or at least a good treatment for us!