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Making new brain cells: how mice could help astronauts and DCM patients

By M Stewart
Editor: B Davies

It’s a commonly held belief that you can’t grow new brain cells as adult; you’re born with one hundred billion neurons and that’s as many as you’re getting. However, this isn’t quite the case. While new neurons don’t form in most parts of the human central nervous system (the brain and spinal cord), there are two special areas where new neurons do indeed arise after birth. These areas are found in specific parts of the brain with rather complicated names: the subgranular zone of the dentate gyrus  and the subventricular zone of the lateral ventricle. These two areas (which we call the ‘SGZ’ and ‘SVZ’ for short) contain what we call ‘neural stem cells’ (NSCs), which are able to produce new neurons throughout adult life. This production of new neurons from stem cells is called ‘neurogenesis’. 

Figure 1: Neurogenesis in the rodent (A) and human (B) brains. The final destinations of newly born neurons are shown in green. In both man and rodent one site is the dentate gyrus (DG). Neurons from the subventricular zone of the lateral ventricle (LV) end up in the olfactory bulb (OB) in rodents and in a part of the brain called the striatum in man. From Ernst et al 20153.

Interestingly, there’s a link between neural stem cell activity and exercise. Increased levels of physical activity have been shown to increase neurogenesis, and even restore it in mice who have stopped producing new neurons due to genetic manipulation1. Importantly, this increased neurogenesis has been associated with increased learning ability2. While we know quite a lot about what happens to neural stem cells when we move more, we don’t know much about what happens to neurogenesis when we move less. This gap in our knowledge actually rather important when we consider that prolonged reductions in movement are increasingly common. Lack of muscle activity occurs inn prolonged bed rest or neurological diseases which affect motor function, like spinal cord injury, multiple sclerosis or potentially DCM. Alternatively, effects equivalent to reduced movement can occur in prolonged stays in space, where there the reduced gravity means that muscles aren’t placed under load. 

As patients survive longer with neurological diseases and as we expect longer stays in space, it becomes more and more important to understand any links between immobility and neurogenesis for two reasons. Firstly, changes to neurogenesis could affect brain health – it may be that changes to neural stem cells following reduced mobility feed back into disease like MS or DCM and actually become part of the cause. Adult neurogenesis is greatly decreased in Huntington’s disease patients when compared to healthy people, suggesting that there could be a link between reduced neurogenesis may play a role in the disease3. Secondly, exploring the link may help us understand the effects of exercise on the brain. Reduced movement has been shown to impair memory function and learning4 and to change the chemical environment of the brain5. We may also be able to better understand the link between exercise and prevention of neurodegenerative conditions like Alzheimer’s disease, which is associated with degeneration in neurogenic areas6.

For all the above reasons, a team from Italy lead by Rafaella Adami recently set out to explore whether reduced movement lead to changes in neural stem cells7.
The study was done in mice. While mice do have some notable differences to humans in terms of the neural stem cells (see below), these experiments require the dissection of large amounts of brain tissue and immediately after death and so are practically impossible to do in humans. 

PictureFigure 2: Diagram of the HU mouse model. From Barbosa et al 20118

How was this study done?
The researchers wanted to recreate the conditions seen in situations (e.g. neurological diseases) where people can’t move very much. In these situations limbs are ‘unloaded’ – people aren’t using their arms or legs to move their weight around. in something called the ‘hindlimb unloading model’8 (HU) mouse model. Mice are suspended by their tales from the ceiling of a cage, taking the load off their hind legs, but leaving them free to walk on their front legs. Thus the hind legs don’t bear the mouse’s weight and are ‘unloaded’ (see figure 2). Adami et al put a group of mice in this position for 14 days, over which time their back leg muscles shrank significantly, as they would if they were unable to move them due to neurological disease (or if they were in space and carrying no weight!). After 14 days the mice were killed and their brains where dissected to examine the neural stem cells in the SVZ. Brains from mice which had been allowed to run around their cages freely where used for comparison (control). 

It’s important to stress that the mice were well looked after during the experiment. They always had access to as much food and water as the wanted and were visited by a vet 3 times during the 14 days of suspension. The showed the same key mouse behaviours as the free (control) mice and showed no increased levels of stress hormones. Taken together, all these factors strongly suggest that the mice suffered “little” stress during the experiment.

What were the results of the study?
Firstly the researchers looked at the number of proliferating (dviding/reproducing) cells found in the SVZ. In this case, proliferating cells were the stem cells that were dividing to make neurons, so more proliferation suggests more neurogenesis. Adami et al found that there were 70% fewer proliferating cells in the HU mice compared to controls – so neurogenesis was reduced. 

The team then wondered if this reduced proliferation meant that the stem cells themselves had changed in some way. To explore this possibility, they then took NSCs out of the HU and control mouse brains and grew them in a dish, to form a ball of stem cells and neurons. They saw that stem cells from HU mice divded more slowly than in controls, taking 7 days to double in number (the controls only took 2 days). They also checked that this slower rate of growth wasn’t due to cells dying.

Overall, these findings led the team to their first key result: reducing movement reduces the proliferative capacity of neural stem cells. 
Adami et al then wondered what caused this reduced proliferation. They discovered that it was because the more of the HU mouse stem cells appeared to have become stuck in the ‘resting state’ when compared to the control mouse stem cells. 69%  of HU stem cells were found to be in a resting state, compared to 57% of controls. Far more of the control cells were in a very active, dividing state (21% vs 13% of HU mice).
The researchers then looked at whether the neural stem cells were able to form mature neurons. They found that 6.8% of control stem cells could form mature neurons, whereas only 0.5% of HU stem cells could. 

This lead the team to their second key result: reducing movement reduces the maturation capabilities of neural stem cells. 
Next, Adami  et al explored whether the metabolism (energy production) of neural stem cells in HU mice had changed. Most neural stem cells produce energy by a process called glycolysis, which by produces a byproduct known as lactate. HU stem cells produced significantly less lactate than controls cells, suggesting that reduced movement gives neural stem cells an abnormal metabolism. 

Finally, to try and understand what could be underlying these changes, the researchers looked at gene expression in the neural stem cells. They found that expression of 2 genes were significantly different between HU and control samples. A gene known as CDKrap1 was 3.5x lower in HU stem cells than in controls, while a gene known as cdk6 was 2.3x high in HU stem cells. Overall, it appears that reduced movement changes the genes expressed in neural stem cells. Adami et al haven’t commented on what these different levels of cdkrap5 might mean, but they think that the higher levels of cdk6, which helps keep cells in the resting state rather than dividing, could explain the reduced neurogenesis seen in HU mice.

What do these results mean for DCM?
Right now, not a great deal. This work is still very much ‘blue sky research’ intended to see if the neural stem cells are worth further study for neurological disease (or space travel!). While its fascinating to see that that restricting movement leads to change in neural stem, we have to be cautious in how far we extrapolate the results to humans. Firstly, while mice and humans may be similar, they aren’t the same (newly born neurons rom the SVZ actually end up in a totally different places in mice and people). Secondly, while DCM can involve reduction in movement if nerve damage progresses to an extreme stage or pain becomes debilitating, it’s not quite as clear cut as in this mouse model. Therefore it’s hard to say if neural stem cells would undergo the same changes in DCM patients as they do here. Thirdly, it’s difficult to understand the implications of the results when we don’t fully understand how/if reduced neurogenesis contributes to neurological diseases. Furthermore, the consequences of reduced neurogenesis are likely to vary across conditions – changes to neurogenesis might be completely in DCM than they are for something like Huntington’s. 
The next step will be to explore the nature of neural stem cells in other mouse models of reduced movement, such as multiple sclerosis, spinal cord injury and DCM to see if neural stem cells undergo similar reductions in neurogenesis. Then we’ll need to determine how/if reduced neurogenesis might contribute to the problems we see in these conditions. If such a contribution was confirmed, this could be a breakthrough in our understanding of how DCM develops. We might even then be able to developing new treatments which target the neural stem cells themselves. However, there are many steps we must take before we reach that stage – for now we’ll have to move slowly. Watch this space for more!


1.    Farioli-Vecchioli, S. et al. Running Rescues Defective Adult Neurogenesis by Shortening the Length of the Cell Cycle of Neural Stem and Progenitor Cells. Stem Cells 32, 1968–1982 (2014).
2.    van Praag, H., Shubert, T., Zhao, C. & Gage, F. H. Exercise Enhances Learning and Hippocampal Neurogenesis in Aged Mice. J. Neurosci. 25, 8680–8685 (2005).
3.    Ernst, A. & Frisén, J. Adult Neurogenesis in Humans- Common and Unique Traits in Mammals. PLOS Biol. 13, e1002045 (2015).
4.    Wang, T. et al. iTRAQ-based proteomics analysis of hippocampus in spatial memory deficiency rats induced by simulated microgravity. J. Proteomics 160, 64–73 (2017).
5.    Dupont, E., Canu, M.-H., Stevens, L. & Falempin, M. Effects of a 14-day period of hindpaw sensory restriction on mRNA and protein levels of NGF and BDNF in the hindpaw primary somatosensory cortex. Brain Res. Mol. Brain Res. 133, 78–86 (2005).
6.    Guure, C. B., Ibrahim, N. A., Adam, M. B. & Said, S. M. Impact of Physical Activity on Cognitive Decline, Dementia, and Its Subtypes: Meta-Analysis of Prospective Studies. Biomed Res. Int. 2017, 1–13 (2017).
7.    Adami, R. et al. Reduction of Movement in Neurological Diseases: Effects on Neural Stem Cells Characteristics. Front. Neurosci. 12, 336 (2018).
8.    Barbosa, A. A. et al. Bone mineral density of rat femurs after hindlimb unloading and different physical rehabilitation programs. Rev. Ceres 58, 407–412 (2011).


The Power of the Word

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​By Iwan Sadler

​Words can be powerful when spoken or in thought. Words are used on so many different levels from the expression of your thoughts to the decision you will make within the moment.Peace is delivered with words but also wars are started by the spoken or written word.

We choose our life choices on words. The average person can speak between 125 and 150 words a minute, but the rate of “expanded inner speech! (word-for-word) is slightly faster than verbal speech. That puts into perspective how many words enter our train of thought on a daily basis. Some decisions can sometimes be made in seconds – other decisions take a lot longer. One thing is for certain: they are all decided with words. 

With the technological development of the internet and mobile phones, words are used more now than ever. The average person uses their mobile phone for approximately four hours per day and around 18.7 billion text messages are sent around the world on a daily basis. And we can’t forget the amount of words we use on our social media platforms. I think you’ll agree that’s a great quantity of words.

This just shows how important words are for our social integration and how powerful words can be. They say that concurring thoughts will eventually become your actions so should we be careful at what we think? Many people think that words, once spoken, cannot be taken back and the action of those words, even if they were delivered within seconds, will last and echo for a lot longer. 
So should we be more careful with what we choose to say? Do words really cut deeper than a knife and leave longer lasting invisible scars? Could our words to a situation decide the overall reactive decision to a situation? Can our words totally change a decision within a scenario? The answer is “Yes!” Our action will always lead to a reaction and the outcome will always depend on our words.

“Where are you going with all this?” you may ask and “What has this got to do with living with a chronic condition?” Could the words we think and use every day help us deal with our condition? Remember that the actual words you say matter, not just the thoughts you convey. Try to use more positive words on a daily basis even if you are unable to replace negative words with positive ones, try replacing them with more accurate neutral ones. Instead of, “This chair is horrible”, try“This chair is not for me.”

Try not to use absolutes, especially in relation to your goals, where falling short of your expectations can be particularly depressing. These words and phrases include: “always”, “never”, “nothing” – the list goes on. Replace them with nuance. Instead of, “I can walk that far”, try “Sometimes I can’t walk that far”.

So the key is to think and speak in a more positive manner. Positive thinking often starts with self-talk. Self-talk is the endless stream of unspoken thoughts that run through your head. These automatic thoughts can be positive or negative. Some of your self-talk comes from logic and reason. Other self-talk may arise from misconceptions that you create because of lack of information.

Positive thinking doesn’t mean that you keep your head in the sand and ignore life’s less pleasant situations. Positive thinking just means that you approach unpleasantness in a more positive and productive way. You think the best is going to happen, not the worst.

The Health Benefits of Positive Thinking
Researchers continue to explore the effects of positive thinking and optimism on health. Health benefits that positive thinking may provide include:

  • Increased life span
  • Lower rates of depression
  • Lower levels of distress
  • Greater resistance to the common cold
  • Better psychological and physical well-being
  • Better cardiovascular health and reduced risk of death from cardiovascular disease
  • Better coping skills during hardships and times of stress

You can learn to turn negative thinking into positive thinking. The process is simple, but it does take time and practice – you’re creating a new habit, after all.

If you are looking for another way to relieve discomfort that doesn’t involve drugs, some age-old techniques – including meditation and yoga as well as newer variations, may help reduce your need for pain medication.
Research suggests that because pain involves both the mind and the body, mind-body therapies may have the capacity to alleviate pain by changing the way you perceive it. How you feel pain is influenced by your genetic makeup, emotions, personality, and lifestyle. It’s also influenced by past experience. If you’ve been in pain for a while, your brain may have rewired itself to perceive pain signals even after the signals aren’t being sent any more. Stress and pain are tightly connected and can have a strong influence on each other. Therefore, if positive thinking is able to counter some of the effects of chronic stress, it could also help lower pain levels.


Practising  Positive Thinking Every Day
If you tend to have a negative outlook, don’t expect to become an optimist overnight. But with practice, eventually your self-talk will contain less self-criticism and more self-acceptance. You may also become less critical of the world around you.

When your state of mind is generally optimistic, you’re better able to handle everyday stress in a more constructive way. That ability may contribute to the widely observed health benefits of positive thinking.

​Final Thought
Being careful with our self talk is essential for our own. wellbeing. And we can also take care to avoid ill-considered words that could damage the wellbeing of others. 
Our minds too often seem to be programmed to keep recalling and dwelling on negative comments which drown out or dismiss any positive feedback we have received. 

The tongue is the strongest muscle in the human body so be careful on how you use it may it be online by txt or word of mouth because “words can only be forgiven not forgotten”.

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​   JOIN OUR INSIGHT TIMER CERVICAL MYELOPATHY
   MEDITATION GROUP


Broken bones more likely following a Cervical Myelopathy fall.

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By T.Boerger
Reviewed by. BM Davies

Reason for the Study
Walking impairments are a common feature of cervical myelopathy and can lead to falls.  In elderly individuals such falls, even if minor, can lead to injuries, such as broken bones.  Broken bones (‘fractures’) are more common as we get older, as aging affects bone strength, including conditions such as osteoporosis.  Such fractures generally occur in stereotyped locations such as the wrist, shoulder, hip, and low back and therefore termed ‘fragility fractures’. These secondary injuries are associated with a significant impact on life, including in some cases death.  In 2015, a group from the USA showed that 18% of patients with a hip fracture had undiagnosed myelopathy [1].  However the overall rate of fragility fractures (a fall related injury also associated with fragile bones) amongst elderly individuals with cervical myelopathy has not yet been investigated [2]


How was this study done?
This study was conducted by searching a database of Medicare patients (meaning previously collected anonymous medical data from individuals in the United States age 65+). This study included 24,439 patients with cervical myelopathy who had undergone surgery, 35,893 patients with cervical myelopathy who had not undergone surgery, and 831,532 patients without myelopathy who had a general medical appointment during the study timeframe of 2008-2011. 
For this study, the researchers excluded patients who might confuse the data (e.g. those who had a neck surgery unrelated to cervical myelopathy or history of cancer, infection, or trauma to the spine, but also those with a history of fragility fractures). The researchers then tracked the occurrence of fractures over the next 3 years and used statistical tests to account for differences in study groups which could influence the results (e.g. age, sex or diagnosis of osteoporosis). 

What did they find?
There were some differences in the characteristics of the study groups:

  1. The cervical myelopathy surgical group was more likely to be male and younger, than the non-operative cervical myelopathy group. 
  2. Both cervical myelopathy groups tended to have higher rates of additional diseases than controls
  3. The non-operative cervical myelopathy had higher rates of osteoporosis, dementia and cerebrovascular disease than the surgical cervical myelopathy group.

At 12 months follow up, both non-operative and surgical cervical myelopathy groups were more likely to sustain fragility fractures than controls. The odds ratios were 1.59 and 1.48 respectively (odds ratios indicate relative odds of a diagnosis or injury with a value closer to 1 indicating no difference). Further, the odds of fracture were higher in both groups than controls at 36 months as well, however, at 36 months the surgical group was lower than the non-operative group.

Why is this important?
There are some limitations to this study; first, because this was a search of a Medicare database it is most applicable to patients with cervical myelopathy 65 and older, but also due to the type of data recorded, there are some possible factors related to falls the researchers were unable to account for such as BMI or physical activity.
However, this is an extremely large study which gives us confidence the results are real, and not simply a coincidence.  
Hopefully these findings will help to raise the profile of myelopathy; as 1) the impact and cost of fragility fractures is significant for healthcare providers, 2) myelopathy is not routinely considered as part of managing a patient’s falls risk and 3) falls assessments are carried out by general professionals. 
Whilst surgery did not eliminate the risk of fragility fractures, they were reduced in those that had surgery.  It would appear from the characteristics of the study groups, that age and ill-health were more likely to lead to conservative management of cervical myelopathy and whether or not this is appropriate, given the potential significance of fragility fractures will need further investigation.   

​​References
[1] Radcliff et al (2015). High Incidence of Undiagnosed Cervical Myelopathy in Patients with Hip Fracture Compared to Controls. Journal of Orthopaedic Traumahttp://doi.org/10.1097/BOT.0000000000000485
[2] Horowitz JA, et al (2018). Fragility Fracture Risk in Elderly Patients with Cervical Myelopathy. Spine.
(3) Can Cervical Myelopathy cause hip fractures 

We welcome Frank Dutton to our fundraising  team

PictureFrank Dutton Charity Ambassador

We are very happy to welcome Frank Dutton to our team,Frank was diagnosed with cervical myelopathy in  2015 and is currently leading our fundraising efforts as  a Charity Ambassador.If you have any fundraising ideas or want to raise money for our cause you can email Frank directly at the bottom of the page.

​Frank’s Background Story 
My whole life was driven by sport, mainly encouraged by my Granddad, and I played both football and Ice-hockey at an early age, the latter for a living. A severe knee injury forced me to hang my boots up but I continued being involved in sport only this time I took on the role of a goalkeeping coach in football, working with all age groups in both Milton Keynes and Bedford. An innocuous dive for a ball during a coaching session on the 27th September 2008 was to change my life drastically. I landed awkwardly on my arm and the elbow dug into my lower abdomen. A few hours later I was rushed into A&E and despite breaking bones and tearing ligaments during my career this was at a level I had never truly experienced before.

Roughly a year and half later I was referred to Addenbrookes hospital pain management team, and they diagnosed I had torn a stomach muscle, for the second time in my life, but had also damaged nerve endings and I was now suffering from Chronic Pain Syndrome and due to the damage done to my nerve endings, I would probably suffer from that for the rest of my life. To go from being so physically active to not being able to move without causing any pain was very hard to accept and then having to endure things such as having to be pushed around in a wheelchair where I had become so weak was tough and mentally I have constantly struggled to come to terms with it. Thankfully my partner Lucy has helped me to learn to deal with these emotions and in 2010 she encouraged me to enrol on an Access Course at Bedford College with a view to going to University and begin training as a Primary School Teacher. For someone who had left school with no qualifications to speak of, and to go to college was really scary but I enjoyed my time there, and I even wrote an article for the college paper about being a mature student struggling with a disability. I passed the course with merits and distinctions and gained a triple distinction for my final dissertation. I was speechless at how well things had gone and I was even more amazed when the University of Bedfordshire accepted me onto their Early Years Education, 3 year BA Hons degree. Whilst at Uni I knew the typical student nightlife was never going to be an option however I wanted to get involved as much as I could and so I became a Course Rep, a PAL leader during my 2nd and 3rd years, which involved helping first year students negotiate their first two terms on campus, and I also volunteered as a Student Ambassador, which involved helping out on Open Days showing prospective students around the campus and giving talks both on campus and in local colleges and schools about my experiences of being a student as well. This all helped me to gain confidence in myself and I found myself being asked to become a mentor to disabled students who were finding it difficult to adjust to university life. As I had done at college, I also found myself writing an article for the university magazine about how I’d gone from playing hockey to being a student wanting to work with children. My health continued to make things difficult but the university were superb and with an added year I eventually graduated in the July of 2015. Despite the issues I had endured, I enrolled onto the PGCE course to gain my teachers qualification. My health unfortunately took a turn for the worse, and I began to have constant tingling in my left arm and I had started to pass out with an alarming frequency.

Eventually I had to accept things were not getting better and I withdrew from the course on the 17th November which was one of the lowest points in my life. In January 2016 I applied for a job at the university working with the Dean of Student Experience and was offered the job on a 6 month contract. The role meant talking to students and finding out what issues they had experienced as well as contacting other universities to see what things they were initiating to get students involved more. During my time in this role I was instrumental in the starting of a student society called PAMMS, which was for parents and mature students, a student group I felt were regularly missed during student life and events. I was still passing out regularly and in late May 2016 that problem eventually caught up with me. I was in the garden playing with my dogs when I passed out, and upon coming round I was surrounded by broken wood and a concerned dog licking my face, it became clear I had gone through a small garden table and had badly bruised my left arm. A trip to A&E showed I hadn’t broken any bones but my arm was still extremely sore and had swollen quite alarmingly. The arm continued to swell and a few days later the whole forearm was black with bruising and was so painful I couldn’t bear anything touching my arm, leading to another trip up to A&E. A succession of specialists and nurses took it in turns to look at my arm and I was eventually taken to a ward before having surgery to repair the Compartment Syndrome which I was now suffering from. A CT and an MRI scan back in February of 2016 had already shown I had issues with 5 discs in my neck and that these were pressing on my spinal cord. In the August 2016 after seeing the neurology department at Cambridge hospital I had an ACDF to repair my C4/5 discs, however the surgeon stated I would need further surgery to repair the other levels. Another knock to my left hand caused my arm to swell again, and another trip to A&E led to me being rushed to surgery in late November 2016 to repair a second Compartment Syndrome, this time on the inner half of my left arm. I have been left with two 7* inch long scars on my left arm, and I was still continuing to pass out on a regular basis, and a further MRI scan in March of 2017 showed the discs in the neck had got worse and I needed major surgery to repair things. Lucy and I got married in late July and enjoyed a superb Honeymoon in Wales later on in September. My surgery was scheduled for 11th December and unfortunately was postponed three times, however, I reported to Addenbrookes on the 24th January 2018 for surgery the day after.


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​The surgery:
My surgery was to be a posterior fusion from C2-T1 with a laminectomy of C3/4/5. Due to the issues with the arm I had been diagnosed with an Acquired Severe Bleeding Disorder and thus needed platelets and other blood cultures to try to ensure there were no complications during the surgery. Trust me to make it a problem as an issue with controlling the bleeding along with the intricate metal work being inserted into my neck meant I was in theatre for just over 8 hours before being taken to critical care to begin the recovery.


Post surgery:

I woke up and to be honest for the first 36 hours I felt pretty good, I think the copious amounts of Ketamine and morphine being pumped into my body may have had something to do with it. Lucy came to visit the day after surgery and couldn’t believe how coherent I was and in how little pain I appeared to be, this would definitely not be the case the day after, once I had been transferred to a Neuro ward and the Ketamine had worn off. I felt like I had been hit by a train and any movement sent fresh waves down my neck and back, and I couldn’t believe how uncomfortable the neck brace was either, even a morphine pump struggled to keep up with the need for pain relief as my body tried to cope with what had just happened. Over the next two weeks I gradually recovered and was allowed home, with the knowledge I had to keep the brace on for 24 hours a day and I would be seen in around 3 months time. The recovery process at home was hampered by an issue with sciatica which prevented me from laying in a reclined position in my bed forcing me to spend the first three months after the surgery sleeping on my sofa. This was really difficult to cope with but Lucy kept me going and I made sure the sympathy mode was kept up with wine gums and jelly babies being to the fore of my food intake. Lucy was able to take me out for a coffee on the odd occasion and my pain levels slowly reduced although even now 6 months down the line I am still having issues with the pain in the surgery site as the muscles begin to knit back together. My Chronic Pain has obviously not helped and has at times left me reaching for the oramorph as the pain relief I am already on had not controlled things. I have good and bad days and occasionally I have a very bad day which leaves me barely able to move. On a plus side I am no longer passing out 3-4 times a day, which when you think about it, I have been passing out for nearly 18 months, so at a best guess, I’ve zonked out over a 1,000 times.
I am now well on the road to recovery and despite still having issues with my shoulders and trying to get used to having a limited range of movement in my neck, having the surgery was worth it and indeed was necessary. My surgery was for prevention rather than cure and I know that whilst I wont ever score the winning goal in a Stanley Cup Final, I’m now looking forward to the future with confidence and this role is the perfect opportunity for me to continue with my recovery and make the most of the superb work done by my surgeon Dr Mark Kotter. It was Mark that explained myelopathy to me before I had my surgery and told me about the Facebook support group which I subsequently joined and that has been such a great support to myself and my wife. It has also helped me understand my condition more with the information available and accounts from others who suffer this tough condition.  When the group got the great news it was becoming a charity I really felt I wanted to be involved and to help spread he awareness of this condition and to raise funds. After speaking to the team I have been given the great opportunity to become the charity Ambassador for Myelopathy.org and hope that I can help to spread the word and begin to help people to understand the condition and thus give support to both sufferers and their loved ones. 


    If you want to raise money for myelopathy.org please enter your details below

Can a new MRI technique predict how you respond to surgery?

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By Timothy Boerger 
Edited by Benjamin Davies

Research Summary on MRI Methods for Predicting Functional Recovery from Surgery in Patients with Cervical Myelopathy.
Rao A et al., Diffusion Tensor Imaging in a Large Longitudinal Series of Patients With Cervical Spondylotic Myelopathy Correlated With Long-Term Functional Outcome. Neurosurgery. Epub ahead of print Feb 23, 2018
Reason for the study
Currently, the assessment of the impact of cervical myelopathy is based largely on patient reported symptoms and commonly quantified using an assessment scale called the mJOA. Patient reported symptoms are very important to take into account when discussing disease severity and function, but imaging measures which explain symptoms are also helpful. Currently there has been limited success in developing imaging measures which explain symptoms and, perhaps more importantly, predict future symptoms and potential recovery following surgery. This last part will be especially important for patients and surgeons determining who will benefit from surgery. 

This study examined a different magnetic resonance imaging (MRI) technique than normal, called diffusion tensor imaging. This technique quantifies how water naturally flows (diffuses). The specific measure they chose (fractional anisotropy) measures the degree to which water flows in a single direction on a scale of 0 to 1 with values closer to 1 indicating diffusion more strongly in 1 direction. In axons of the spinal cord, for example, it would be expected that water would flow consistently along the path of axons rather than perpendicular to the axons. If a group had a worse score, however, it might indicate that they had damage to the neurons allowing water to move more freely. So, the purpose of this study to use fractional anisotropy as a measure of integrity of neurons in the spinal cord and see if this correlated with function pre-surgically and change in function following surgery.

Methods
​This study enrolled patients who were diagnosed with cervical myelopathy over a 5 year period (age range 33 – 81, 18 male, 26 female) and followed these patients for 2 years following surgery. They took their MRI scans and determined mJOA score pre-operatively. For this study they focused their imaging analysis at the spinal level with the greatest compression of the spinal cord. For this analysis they included the whole cord except for the border around the cord because the data they could gain from this area might be incorrect due to the surrounding cerebrospinal fluid. They then compared the MRI scans (fractional anisotropy) and mJOA pre-operatively, and 6-, 12-, and 24-months after surgery. They also compared fractional anisotropy values to those from a group of healthy control participants. 

Results
As expected fractional anisotropy (the MRI measure of neuron integrity) was lower in patients with cervical myelopathy than controls.  It was also associated with the severity of myelopathy before surgery, as assessed by the mJOA (a measure of patient function). 
Also, fractional anisotropy inversely predicted change in mJOA score at 12 months, but was less strongly predictive of change in mJOA at 6 and 24 months. Baseline mJOA also was inversely predictive of change in mJOA at 12 months. This means that in this study, those participants with lower fractional anisotropy (neural integrity) or mJOA (function) scores pre-operatively improved the most following surgery.

Why is this important?
At present, we are unable to predict accurately the response to surgery, and therefore markers which help this will be useful for doctors and patients.  Whilst fractional anisotropy, has been investigated before previous studies using this technique were less successful in drawing a relationship with function. This may be due to improving the methods of collecting and analyzing the MRI data. 
The identified relationship between baseline mJOA and change in mJOA with surgery are therefore promising, but require further research to understand the meaning for patients; for example it is recognized that patients with greater disability typically do improve more as measured by the mJOA, but that does not mean that they achieve a better functional outcome.The mJOA is not a linear scale, where each point gain is equally as important as the next.  
We look forward to watching our understanding of Fractional Anisotropy improve and if it can be of benefit to doctors and patients.


Spinal Cord Swelling: What is it?  Does it matter?

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By B.Samara 
Swelling is a common reaction of your body to any form of injury; remember the last time you banged your finger, or perhaps twisted your ankle?  So unsurprisingly, it can happen to the spinal cord and has been reported in patients with CSM.  However, it is not present in all patients and its significance is not certain.  In addition to this, some studies have now described that the spinal cord can swell after surgery.  The reason for this is unclear and equally what it means for patients is not clear. 
 

On basic MRI imaging, swelling is not that easy to detect; a doctor may look for a slight enlargement of the spinal cord or some signal change.  An alternative method is to inject a ‘contrast agent’ into the patient during the scan.  This is a special form of dye which highlights certain processes, and can be a indicator of swelling amongst other things.  We call this ‘highlighting’ enhancement.  

On this basis, a group from Japan have been looking at spinal cord swelling using contrast and what it means for patients. 

What did the study measure?​
The team from Japan performed ‘contrast MRI’ scans on patients with CSM due to undergo and operation, before and after their surgery.  They then compared what happened to patients who had enhancement and those that did not have enhancement. 

What were the results?
In the study they found that those with preoperative enhancement were more likely to have developed swelling at 1 month after the operation and the swelling was more likely to persist until 1 year post operation. Those who developed swelling had poorer outcomes as assed by a scoring system called the JOA that looks at movement skills as well as sensory loss (problems with feeling). 
What does this mean for those affected?
This sort of MRI imaging is not normally performed during the work up for CSM, but the potential to offer additional information into the severity of the disease and how patients are likely to respond to surgery would be helpful to doctors and sufferers alike. 
It is worth noting that the injection of dye can be harmful to some people, although this is uncommon. 

Therefore, for this technique to be adopted, healthcare providers are likely to need further information, such as:

  1. How does this change the management of patients?  This study only looked at patients who were due to undergo an operation anyway, is spinal cord swelling present in other forms of CSM?  Can it help decide when to perform an operation?

Of course a number of additional MRI techniques are being developed, and it is possible that the information that might be provided by this method, is superseded. 

References
Ozawa et al. Spinal Cord Swelling After Surgery in Cervical Spondylotic Myelopathy: Relationship With Intramedullary Gd-DTPA Enhancement on MRI. Clin Spine Surg. 2018 May 31. doi: 10.1097/BSD.0000000000000664
Cho et al.  https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3229731/


Heart Break for Myelopathy

Risk of acute coronary syndrome in patients with cervical spondylosis 
​J.Hamilton

What were the aims of the study?

Various studies in the past have described cervical spondylosis (CS), the degenerative changes in the cervical bones and ligaments contributing to degenerative cervical myelopathy, as associated with increased sympathetic nervous tone[1][2].

The sympathetic nervous system plays a role in controlling blood pressure, heart rate and various other aspects of our cardiovascular health.  But part of its control structure also lies in close proximity to the cervical spine. 

Increased sympathetic activity is known to contribute to increased atherosclerosis and cardiovascular events such as stroke, and myocardial infarction (heart attack)[3]

​The authors noted that no research had been done to link the above statements, if CS does cause increased sympathetic activity, does this logically follow that CS causes an increased incidence of cardiovascular events?
 
With this in mind, the aim of the study was to determine if cervical spondylosis increased the risk of cardiovascular health issues, specifically acute coronary syndrome (ACS), which in common terms is a heart attack.

Picture

The sympathetic nervous system is involved in controlling many of your bodies organ systems. Signals originate from ‘ganlgion’ that lie adjacent to the spine. The ganlgion in the cervical spine are involved in control of the cardiovascular system

How was the study performed?

The authors used a national insurance claims dataset of 22 million people in Taiwan and identified 27,947 patients with CS, they then matched this with a similar number of non-CS patients of a similar age and gender distribution, as well as matching numbers of patients with other health problems such as hypertension, diabetes, asthma and stroke. This was to allow them to compare the incidence of ACS between the groups without other diseases invalidating the comparison. 

All the patients were followed up until they had a diagnosis of ACS, died, or the end of the research period occurred at the end of 2011. After this, the number of ACS events in each group were measured as a rate over the number of “person years”. This being the number of times a diagnosis of ACS was made for every year a patient lived.
 
In this paper, the incidence of ACS was measured as number of ACS/1000-person years. These were then compared between various groups to obtain a ratio, to determine the relative risk of ACS occurring in a person with CS compared to someone without ACS in a similar state of health.


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What were the main findings?

Overall, the study showed that patients with CS were 13% more likely to have an ACS, than patients without CS. This was determined ‘statistically significant’, but in real terms this represents a very small increase from 3.9/1000-person years to 4.27/1000-person years in rates of ACS diagnosis. 

Looking in more detail at the patients with CS, for those with myelopathy the risk was slightly higher, increasing by 20% but interestingly, it seems treatment of CS has an effect in reducing ACS risk:
– 
Patients receiving spinal decompression surgery were less likely to have an ACS (27% reduction)
– Patients receiving rehabilitative therapy were less likely to have an ACS (33% reduction) 

The statistical difference between the form of treatment for CS and reducing ACS risk was not significant.  

​How could cervical spondylosis cause acute coronary syndrome?

This is a good question, and not entirely clear.  The researchers suggested that it may be to do with the sympathetic trunk. The cervical sympathetic trunk consists of collections of nerve cells bodies, called ganglia, aligned along the front of the spine.  The ganglion in the neck are involved in control of the cardiovascular system.  This special group of nerves also connect with the ligaments of the spinal column, such as the posterior longitudinal ligament, and the lining of the spinal cord. Irritation to these structures is thought to cause the sympathetic nervous system to increase its output, for example to fibers in blood vessels around the body, causing them to constrict and causing hypertension, which contributes to a diagnosis of ACS.

What can we take from this study?

This is not the first study to show a relationship between CSM and Cardiovascular health (we have previously described a study specifically looking at high blood pressure), however it is the first to show an increased risk of a heart attack.

There are a number of limitations to this study, and the actually increases in risk are relatively small.  But it adds to the research of CSM and Cardiovascular disease, and once again shows the far reaching impacts of CSM.    

References

Shih-Yi Lin et al. Risk of acute coronary syndrome in patients with cervical spondylosis ​Atherosclerosis 2018

[1]M. Singh, I. Khurana, Z. Kundu, A. Aggarwal, Link of sympathetic activity with cardiovascular risk in patients of cervical spondylosis, Int. J. Clin. Exp. Pathol. 3 (2016) 41e44 
[2]M. Singh, I. Khurana, Z.S. Kundu, A. Aggarwal, Galvanic skin response in pa- tients with cervical spondylosis, IJHSR 6 (2016) 148e152.
[3] N. Marina, A.G. Teschemacher, S. Kasparov, A.V. Gourine, Glia, sympathetic activity and cardiovascular disease, Exp. Physiol. 101 (2016) 565e576,