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In search of Myelopathy man

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By Delphine Houlton 
Our Facebook Myelopathy Support group, founded by Iwan Sadler, now has more than 1,000 members worldwide.
A great success story which is set to grow as awareness of Degenerative Cervical Myelopathy (DCM) increases. 
There is little doubt that social media is revolutionizing health care. A US study by Pricewaterhouse Cooper in 2012 showed that one third of US consumers use social space as a natural habitat for health discussions. Meanwhile a 2010 report by the Pew Internet and American Life Project showed one half of e-patients living with chronic diseases take advantage of user generated information.

Using this research and more, Pius Boachie writing for http://www.adweek.com/digital/ demonstrates the importance of Facebook groups for people with health issues sharing experiences, offering support and raising awareness and funds.
Social media has also given patients opportunities to vent their frustrations and anger as well as following up issues keeping healthcare providers on their toes.
But it is not just of benefit to the patients. Pius Boachie claims 88% of doctors use social media to research pharmaceutical, biotech and medical devices, and 60% of doctors say social media improves the quality of care delivered to patients.
However, at Myelopathy Support we are facing a challenge and one that not only Iwan has noticed. Our Facebook group has attracted many more women than men. In fact, 76.7% of Myelopathy Support members are women and just 23.2% men!
The specialists tell us that DCM does not discriminate between the sexes, so what is going on?
According to research by Statista, women have been leading the way on the major social media platforms, such as Facebook, for a long time but the gap is narrowing. Now the USA has 230 million Facebook users of which 52% are women and 48% are men. 
So, men are aware of Facebook and interacting but there is a possibility they are using it differently. At least this is an argument presented in www.socialmediatoday.com in 2016.
The authors say research reveals men are more likely to use social media to seek information or new relationships while women use platforms such as Facebook to connect with people and nurture existing relationships. 
Women are more likely to share personal issues while men prefer more abstract topics. On a more negative note, men were much more commonly trolling on social media or engaging in aggressive and even abusive language. In conclusion, they accept that men and women communicate differently.
This sort of argument can be compelling along the lines of the popular Men are from Mars, Women are from Venus theses. I’m not a huge fan not least because I favour nurture over nature and see most styles of communications as culturally constructed with culture very clearly an ongoing process – a verb and not a noun.
Irrespective of my preferences, we do face the challenge of attracting more men to join and to benefit from the information, support and expertise available at Myelopathy Support on Facebook.
Should we be doing more on YouTube (54% male users) who spend, on average, twice as much time as women do on the site per week? Should we signpost the vast amount of detailed information available at Myelopathy Support more clearly? Should we run an invite-a-man initiative or offer a prize to the 500th man to sign up?
All suggestions gratefully received!  Email: info@myelopathy.org



Investigating exercise after anterior cervical discectomy: what should we advise?

My name is Dr Teena Fernandez. I am a GP in North Wales currently undertaking research as part of my Masters in Sports and Exercise Medicine at Nottingham University. During my studies my husband sustained a cervical spine injury resulting in a 2 level anterior cervical discectomy and fusion and we found little advice or evidence on returning to sport following such surgery.

Can you help researchers from the University of Nottingham?


We did not know if he could go dog walking, do martial arts or do manual labour for 2 hours a day? I subsequently undertook research which only identified expert opinion on returning to sport. I have now (with the help of a neurosurgery consultant) decided to find out how people return to sport following 2 level anterior cervical discectomy and fusion.

I plan to undertake a qualitative project interviewing approximately 8-16 participants to find out whether they have returned to at least 2 hours of exercise a day following the surgery. I would like to know whether they developed problems such as neck pain or pain or loss of function of the arms and legs with exercise.

Being a GP, I hope I can interpret the interviews and help people who require advice on getting fit after surgery. 

Please have a look at my advert and get in touch if you would like to be involved.

Dr Teena Fernandez
MBBS MRCGP DFFP DRCOG BMEDSCI PGCE

Why does this matter? A word from the director

The role of exercise after surgery in CSM is largely unexplored.  However there is much to suggest that it can enhance recovery; indeed this is well demonstrated in animal studies of spinal cord injury, underpins the basis for spinal cord injury rehabilitation centres and is starting to be evidence based in traumatic spinal cord injury.  So at Myelopathy.org, we are pleased to support this research study.   It should be noted, that this study is not just for CSM and looks in particular at higher performance athletes (exercising more than 2 hours per day), but no doubt this will have some relevance and we look forward to seeing the results.    Ben Davies, Director Myelopathy.org  

Worried about participating in research?

Myelopathy.org ensures all affiliated research meets UK Research Standards.  A useful video has been prepared by  Connected Health Cities and The Farr Institute to provide an overview of how health research is conducted and overseen in the UK, including how your data is looked after and used.  If you have any further questions or concerns, please get in touch. 

Headaches more common in CSM

​Cervical spondylosis, more than a pain in the neck?

by J.Hamilton

For some migraines is just another word for headache, but in medicine it refers to a specific type of headache characterised by severe head pain that can last from 2-72 hours, are a common disorder and can be incapacitating to people who suffer them. Migraines are common, with estimates suggesting up to one billion people are affected worldwide. Various triggers may cause migraines, causing a sequence of events that lead to head pain. It has been suggested that cervical spondylosis, the degeneration of the bones of the neck, may initiate migraines, but little research has been done on the topic.

With this in mind, a group at the China Medical University wanted to determine if there was an association between cervical spondylosis and the likelihood of suffering from migraines. 

​How was it done?

​The group used a health insurance research database in Taiwan.  From this database,  a group patients with and without cervical spondylosis were selected.  The group without spondylosis were matched, such that they had similarly ages, genders and presence of other illnesses such as diabetes.  Over the next 10 years, between 2000-2010, the patients who developed migraine were noted. At the end of the study, the group looked at the relative risk of getting migraines and compared them between the groups.

Do you suffer from headaches or pain and have CSM?
Researchers from the University of Cambridge what to hear about your experience


​What were the results? 

​The group of Spondylosis sufferers numbered at 27,000, compared to 111,000 without spondylosis. When they looked at the rate of people acquiring migraines each year, they found that out of those with Spondylosis, 5.16 people out of 1000 per year acquired migraine, compared to 2.09 per 1000 people per year in people without spondylosis. When they looked at the risk of getting migraine, using a statistical method known as “hazard ratios”, which compares the relative risk of getting a migraine between two groups, it was found that comparing patients with and without spondylosis patients gave a risk of 2.03. This means that people with Spondylosis are twice as likely to develop migraines as those without. When looking at the data more closely, the researchers found that this risk was further increased in patients with myelopathy and spondylosis as opposed to spondylosis patients with no myelopathy.  As expected, they also found that women and younger individuals were more likely to develop migraines, a well described association.

​How could this happen?

​Although headache has not been considered a ‘classical’ feature of neck disorders, it has been proposed for many decades that neck disorders can cause headaches.  This led to the creation of a condition called ‘Cervicogenic’ Headache (literally ‘neck generated headache’).  For some professionals this remains a controversial condition, as how a neck condition can cause a headache remains unclear.  The proposed mechanism is based on something called ‘sensitization’, a well described pain process by which the regular perception of pain can alter the ‘wiring’ of the brain and spinal cord, make them more sensitive: so what once felt like a tickle, could become more like a stab.  For Cervciogenic headaches, the theory is the neck pain from spondylosis is the regular pain, and because the pain pathways from the neck are shared with some of those of the head, these wires can cross and lead to headaches.  This has previously been discussed by Dr Lavin, Neurologist for Myelopathy.org, including an alternative theory related to altered blood flow.  

​What does this mean for Myelopathy sufferers? 

​This study is part of a number of recent articles helping to shine the spotlight on headaches and CSM.  Whilst it cannot show exactly why it happens, the association is becoming harder to ignore and makes it less likely to be simply a coincidence.    Hopefully these studies will help to raise the profile of headaches in CSM, to trigger the research necessary to further understanding and develop treatments – watch this space!
 
In the meantime, some small things that can minimize your risk of migraine include: remain well hydrated, reducing your caffeine intake (although some people find caffeine helpful), as well as ensuring a regular sleeping habit. 

Ageing increases impact of spinal cord compression

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FEM (Finite Element Method) analyses the impact of mechanical loads e.g. ‘stress’. It was principally used in engineering (for example aerospace), but increasingly also medical research

At the moment, we do not have medical investigations which are able to represent accurately the significance of spinal cord injury.  For example, you could have two patients with exactly the same MRI changes, one who is without symptoms and the other who is severely affected. 

This is a major challenge for researchers, with many exploring new tools to provide better assessment methods

However, amongst this confusion, age seems to be important as the number of people with symptomatic cord compression increases with age.  Moreover, some have shown that age can affect response to surgery.  

A group from Japan have been experimenting using a preclinical (animal) model, to investigate how spinal cords of different ages react to the same compression force.  Using a technique called Finite Element Method, more typically used in engineering, they have shown that in an older spinal cord the same amount of compression causes a much higher stress to the spinal cord tissue, than in a younger spinal cord.  This was the same for sudden or slow compressive forces. 

​ Of course this experiment has not been conducted on human spinal cords, but the findings are in keeping with a wider experience of aging and CSM and is a further reminder of the need for more sophisticated tools to represent the extent of spinal cord injury in CSM.  

Reference

1. Okazaki et al. Age‐related changes of the spinal cord: A biomechanical studyExperimental and Therapeutic Medicine 2018

Addressing recent concerns about Myelopathy.org and affiliated surveys

A message from the director

Concerns have recently been raised with regards the legitimacy of the Health Surveys hosted by Myelopathy.org and I would like to address these directly.
 
As you are only too aware, Myelopathy is a condition which faces a number of significant challenges including lifelong disability, widespread misunderstanding and under-recognition, and a lack of clear information or support.   Myelopathy.org was founded to address these issues and become a rallying point for change. 
 
We see research as an important part of delivering change and support projects that can advance our understanding.  As the largest ever Myelopathy community, your shared experiences have a lot to offer researchers, and therefore health surveys have been a prominent part of our research arm.  So far, more than 2000 people have shared their experiences, making these some of the largest ever studies in Myelopathy.  That data is still being processed, and we look forward to seeing the results soon, but this in itself is a testament to what we can achieve together.
 
As an organisation we recognise the power of this community and are committed to its responsible management.  In this respect, all research associations and projects have been and are expected to meet our ethical standards.  This includes adhering to our code of conduct, providing appropriate regulatory approval and practicing safe management of personal data.  All proposed surveys are first piloted and approved internally.
 
Looking through our research section today, I can see that this oversight is not as explicit as it should be, and we will be introducing clearer documentation to correct this.
 
We are a very young organisation, developing and learning as we go along but in a short time we have made great in roads; I remember when we first launched, canine myelopathy was the prominent feature of google search results, but now our myelopathy has come to the forefront.    
 
There is still a long way to go, but it will be together that we can drive change and not as individuals.  The internet has provided a platform for us to come together, but we must remember that it can also have the potential to divide us: both as an organisation and as individual members we all must act responsibly.  In that regard, if you feel any of our actions or the actions of our members questionable, please get in touch directly.
 
Thank you for your ongoing support.
 
 
Benjamin Davies
Director Myelopathy.org  

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 

Myelopathy Research Struggling To Gain Attention

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By Timothy Boerger
Reviewed by B.Davies

Reason for the study
The number of times a paper is cited is a common metric of how meaningful that paper is to the scientific community. Generally, papers that are highly cited have a profound impact on their field. If scientists look at the trends of which papers are most cited, it can give us an idea of what topics within a scientific discipline are experiencing the most interest over time.

Methods
The prominent journals publishing research related to the spine were first identified from a database of journals. This list of journals including: Spine, Journal of Spinal Disorders, European Spine Journal, Journal of Spinal Cord Medicine, Spinal Cord, Spine Journal, Journal of Spinal Disorders & Techniques, and Journal of Neurosurgery: Spine were searched using the database Web of Science which provides all articles ever published from the selected journals. Articles were then sorted by most citations and the top 100 cited articles were analysed. Articles were then sorted by topic including, 

  1. Biomechanics 
  2. Cervical myelopathy/Cervical fusion 
  3. Degenerative disc disease, deformity 
  4. Iliac bone graft morbidity 
  5. Low back pain 
  6. Lumbar spinal stenosis/Lumbar fusion 
  7. Neck pain 
  8. Osteoporotic compression fractures 
  9. Psychosocial aspects of neck and low back pain 
  10. Tesearch methodology 
  11. Spinal fusion/implantants and rhBMP-2
  12. Spinal metasteses (cancer)
  13. Thoracic fusion 
  14. Trauma/spinal cord injury.

Results
By far the most articles were published in the journal Spine (84/100 articles). This suggests that the journal is publishing a substantial body of the spine research which is both impactful and broadly of-interest to clinicians and researchers of spinal conditions. Ranked according to most articles by topic, low back pain was 1st and had over 2x as many articles represented as any other topic area (22/100 articles). Ranked according to most articles by topic, Cervical myelopathy/Cervical fusion was tied-9th with 3/100 articles. Of these 3, all were on operative techniques for different aspects of cervical myelopathy. The most recent of these 3 articles was published in 2001 (the other 2 were published in 1983 and 1981). Neck pain was 12th.

Why is this important?
The number of times an article was cited is often an indicator of how popular a topic is. This suggests that cervical myelopathy, despite its prevalence and impact upon a person, has received relatively little impactful research. Impactful is an important caveat here; a terrible study, or one that only marginally advances the field, will probably not receive a lot of citations in the future. This means that researchers that look at myelopathy need to produce impactful research that helps us understand mechanisms of the disease, its impact, etc. that may help drive more interest and produce more highly impactful work and better treatments.

It isn’t all doom and gloom, however. On Aug 1, 2018 I searched pubmed (another database of research articles) for all research containing the keywords

  1. cervical myelopathy 
  2. cervical Spondylotic myelopathy 
  3. degenerative cervical myelopathy 
  4. cervical laminectomy 
  5. anterior discectomy and fusion 
  6. cervical disc replacement 
  7. cervical corpectomy
  8. posterior cervical discectomy


and got 24,107 results. Similarly if you search “low back pain, one would get 34,002 results in the same database. This suggests that there is a decent amount of research compared to low back pain, but not nearly in the ball park as other disabling conditions such as multiple sclerosis (~80,000 articles). This suggests that more research is needed in all facets of the disease, but this research also needs to be well designed, rigorous, and impactful. It also means that more publicity is needed for this disease to generate more interest in the scientific community.

References

  1. Badhiwala JH et al., Highly cited works in spinal disorders: the top 100 most cited papers published in spine journals. Spine. Epub ahead of print Jun 8, 2018

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).


My Island

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BY Alison Murphy  MY…Hell…opathy Laughing & living with Cervical Myelopathy

Yesterday, my husband dropped me off at the swimming baths.  The large float around my waist and my cycling style of swimming does raise a smile or two. Some call me a ninja turtle, some the barnacle woman.  Today my predicament was in the changing room.  With my combination lock.  I tried it, retried it, again and again to no avail.  It wasn’t the wrong combination; it’s my date of birth but the lock is old and sometimes you have to press it together for it to open.  I could see my issue was attracting the attention of others. So in my swimming costume, dripping, I went to reception.  A female employee, with bolt cutters came to my rescue.  She struggled a little until suddenly the lock exploded apart.I opened the locker.  Opps.  Someone else’s clothes.  I used the ‘f’ word; it was called for.The leisure centre girl was laughing. The audience of women changing was lapping it up.  I said this has probably happened to other people.  No, she said.  What an idiot.

​My locker was only three doors away and I didn’t even think to try it.  I was resolutely sure that the locker was mine.  I felt so sorry for whoever’s locker it was.  They came to the leisure centre to work out and relax.  I had to lock their locker with my lock.  I left an apologetic note on their door telling them the combination was at reception.  Then I went for a cappuccino.  With myelopathy you have to let these things wash over you.

​I’ve been a little Norman Bates lately; stable one day, struggling with my myelopathy persona the next but I’m quite proud of myself.  I’ve reached out to people to try to reconnect and everyone’s been so generous with their time and considerate of my condition. I’ve been going to events and sometimes only staying an hour; but enjoying that hour.I went to a lovely patisserie for coffee and cake this week but told Diane I could only stay an hour because I can’t stand independently, or straighten, if I sit over the hour. Also I’m learning how to be a bit precious. My husband calls me the princess and the pea because everything has to be just so.  If a chair is too soft my back spasms, if my shoe laces are too tight I can’t put shoes on, if my teacup is too full I can’t lift it, if there is spice in my food I get IBS.  I went from being totally laid back, able to eat street food cooked by greasy haired, uncompliant to hygiene standards, cooks to being very needy.  I don’t beat myself up about it.  I’m not elderly or frail or sick but titanium is holding my neck together and if I’m not careful my cervical spine might topple like Jenga bricks again.  So, when I’m chatting I need my friend opposite me, not beside.  I can get in a car, but I can’t get out without help.  I need to be front of the loo queue because I can’t hold it. If we can’t be fussy now, when can we?


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When the kids were little I would make up silly songs randomly about their activities and personalities.  I’d wake them up with a song, tuck them in with a song.  For a couple of years myelopathy stole my voice.  It truly is a challenging condition.  I wake up and feel how I image the wolf did in Red Riding Hood when his stomach was filled with stone.  My body is so uncomfortably heavy, my bones hurt, my head is constantly under a vice like pressure…and that’s at the start of the day!  Understanding cervical myelopathy has been an uphill struggle, health professionals are not up to speed with a condition whose numbers are constantly rising.   When my daughter was little she was given many Barbies and the first thing she’d do is cut Barbie’s hair off. Grace, I’d say, it won’t grow back, once it’s cut, it’s cut and that’s like the spinal cord, damage is unrepairable – for now anyway.  It’s through contact with fellow suffers at www.facebook.com/groups/myelopathy.support that has me bursting into song again.  Knowing that I haven’t got some one-off, obscure condition, that I’m not alone, is a huge deal.

My youngest daughter was eighteen yesterday.  When I think of Caitlan it’s like my heart bursts like a popping champagne bottle.  She was ten when I was first admitted to hospital with what doctors thought was a stroke. We’re throwing her a party.  If I thought too much about the organisation I’d feel overwhelmed.  I’ve called it a casual gathering, that way expectations aren’t so high.  I think if you have alcohol and food a party will run itself.  My brother and his family are over from Kilkenny, Caitlan’s godparents from Dublin, I can’t wait.  Having something to look forward to is paramount.  I look forward to coffee with my husband, I love going to M&S Food Hall, I have book club, I love Grace coming home for the weekend.  My four children are the painkiller that get my weak body out of bed.  They are the smile on my face.  They understand my condition better than neurologists, they live with my highs and lows and they pick me up.

I am happy.   It’s a glorious feeling.  Once I get going I feel my life is full of possibility even though by four I will be totally slayed with pain and tiredness, my limbs will be unresponsive, and I will sway around the house, everything falling from my grip…I’ll end up in bed for a few hours but at nine I will be enjoying Love Island with my family. If I think of 2018 so far I’ve been part of a training video to help doctors diagnose myelopathy earlier, I’ve been skyped (never skyped before) by Dr Nidhi who is gathering info to support early diagnosis.  I’ve enjoyed two book club gatherings.  Met Sharon for a pub lunch.  Gone for innumerable coffees and cake and have the calories to prove it.

Caitlan recently returned from a geography trip to Iceland.  Putting on her crampons, about to step foot on a glacier she thought of me.  My mum will never do this, she’ll never see this powerful landscape with winds that take your breath away.   It’s true.  But it’s ok.  I’ve come a long way since my dramatic arrival at A&E.  I’m walking.  I’m sleeping.  I’m managing my pain.  I’m with my family.  I think of my life like Bear Grylls’ The Island.  Myelopathy is my island.  I’m not a giver upper and I’ve learnt to enjoy simple things.
Right now I’m sitting by the window, the sun is shining, a squirrel has just run the gauntlet across my garden fence while my two dogs are going bonkers.  Spanish rap is playing. I’m glad to be alive; the alternative is an eternity I’d like to avoid.  I’ve come to not expect too much of myself.  Myelopathy is the long game.

You can check out Alison’s blog My Hell opathy here 


More to Myelopathy than meets the eye

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By O.Mowforth
Edited by B.Davies

We don’t really know what symptoms a “typical” patient with myelopathy has. 
In fact, the huge number of often quite subtle and non-specific symptoms is probably one of the main reasons why early diagnosis is so challenging (Davies et al., 2018).
 
When medical students prepare for exams they tend to learn stereotypical descriptions of conditions. For myelopathy, this might be a patient with walking problems and clumsy hands.

However, increasingly symptoms that one might never consider could be linked with myelopathy are emerging from the shadows.

Depressed or anxious mood is one such symptom (Stoffman et al., 2005). 
In recent years we have realised that myelopathy patients suffer from high levels of depressed or anxious mood and that this often improves after spinal surgery. But we have had little understanding of why this is the case.

A recent study from Japan has provided a little more insight (Sawada et al., 2018). The Japanese team studied the activity levels of various sites in the brain in myelopathy patients before and after surgery. They also studied individuals without myelopathy as a control group for comparison.
To do this, the team asked participants to do a simple finger-tapping exercise whilst they observed activity levels in the brain using functional magnetic resonance imaging.

The team found that before surgery individuals in the myelopathy group had a significantly higher activation in an area of the brain called the supplementary motor area compared to individuals in the group without myelopathy.
Next the team found that activation of brain areas, including the anterior cingulate cortex, the supplementary motor area and the thalamus significantly correlated with depression. This meant that the greater a patient’s depression, the greater the activation they had in these brain areas.  
Finally, the team found that both depression and activity in the anterior cingulate cortex and supplementary motor area decreased following surgery for myelopathy. 
Interesting!

The team argue that up to now surgeons have focussed on the “typical” symptoms such as the clumsy hands and walking problems when deciding whether to operate. They believe that their work may lead to future surgical decisions taking more account of the psychological symptoms too!

Davies, B.M., Mowforth, O.D., Smith, E.K., and Kotter, M.R. (2018). Degenerative cervical myelopathy. BMJ 360, k186.
Sawada, M., Nakae, T., Munemitsu, T., and Hojo, M. (2018). Cortical Reorganizations for Recovery from Depressive State After Spinal Decompression Surgery. World Neurosurg. 112, e632–e639.
Stoffman, M.R., Roberts, M.S., and King, J.T. (2005). Cervical spondylotic myelopathy, depression, and anxiety: a cohort analysis of 89 patients. Neurosurgery 57, 307–313; discussion 307-313.