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Delayed diagnosis in myelopathy, common to many neurological diseases

By Max Butler Edited by Ben Davies

Delayed diagnosis is a major issue for myelopathy patients (Davies et al, 2018) as delays can be distressing for sufferers, and the condition is likely to worsen without treatment. On top of this, surgical treatment becomes less effective the longer the delay (Tetreault et al., 2013). However, these experiences are not unique to myelopathy.

The 2018/19 National Neurological Patient Experience Survey shows that diagnostic delays are the norm for many with neurological diseases. These findings suggest a need for large-scale change in how neurological conditions are approached on the ‘front-line’ of care.

Why was this study conducted?

The survey, run by The Neurological Alliance, asks patients with neurological diseases
about their experiences. It covers a broad range of topics, such as diagnosis,
communication, hospital care, support for mental wellbeing, and access to social care,
welfare and employment. It is an important tool for establishing the quality of
neurological care in England, and for providing an evidence-base for the need for
improvement.

How was the study conducted?

A questionnaire was completed by patients online and in neurology clinics between
October 2018 and March 2019. 10,339 patients responded to the survey, making it the
largest ever survey of people with neurological conditions in England. Previous surveys
were taken in 2014 and 2016, but this is the first time this survey has been conducted in
clinics, meaning a greater number of patients could be reached. It is also the first-time
regional differences in care have been studied.

What was discovered?

The survey shows many patients with neurological conditions are experiencing large
delays in referral to a neurologist, and therefore in diagnosis and treatment. Some key facts from the survey: 

  • 39% of survey respondents reported that they saw their GP five or more times
    before being told they needed to see a neurologist
  • 29% of survey respondents who needed to see a neurologist waited more than
    12 months (from first seeing the GP)
  • Over a fifth (21%) waited over 12 months for a confirmed and accurate diagnosis, after their first visit to a neurologist.
  • Over half (55%) of respondents said they have experienced delays in accessing
    healthcare in general
  • The survey also found wide regional variation in waiting times. The longest waits are experienced by people with neurological conditions living in the most deprived areas.

Why is this important?

The survey shows that delays to diagnosis are experienced by many patients with
neurological diseases, suggesting a need for change.

As patients are visiting the GP multiple times before diagnosis, clinician training
focussed on neurological diseases may be needed. Indeed, research carried out by The Neurological Alliance in 2016 showed 84% of GP respondents felt they could benefit from further training on identifying and managing people presenting with neurological conditions. The survey also revealed inequalities in the services provided, suggesting a ‘post-code’ lottery in the care neurological patients receive.

The Neurological Alliance, in response to the survey, has said that a National Plan for Neurology in England must be urgently developed to address the range of problems found. The Neurological Alliance is also encouraging people to write to their MP about these important issues.

Further information can be found in Neuro-Patience, which presents the findings of the 2018/19 National Neurology Patient Experience Survey.

References

  1. Davies, B.M., Mowforth, O.D., Smith, E.K., and Kotter, M.R. (2018).
    Degenerative cervical myelopathy. BMJ 360, k186.
  2. Tetreault LA, Kopjar B, Vaccaro A, Yoon ST, Arnold PM, Massicotte
    EM, Fehlings MG. (2013). A clinical prediction model to determine outcomes in
    patients with cervical spondylotic myelopathy undergoing surgical treatment: data from the prospective, multi-center AOSpine North America study. J Bone Joint Surg Am. 18;95(18):1659-66.

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  

Spinal Cord Stem Cell Transplantation for Spinal Cord Injury

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By A.Willison
Reviewed by B.Davies

​Humans require many different repair and renewal strategies. At the earliest point in life, we need these pathways to grow and develop but in later life, we use these pathways to recover from disease and injury. For this, our bodies activate a unique type of cell known as a stem cell. Stem cells are a special form of cell, as they can make any cell type in the body, and so can provide building blocks for our organs and tissues.  

Over the past 20 years, researchers have been trying to harness the power of stem cells to guide damaged nerves in spinal cord injury (SCI) towards repair, or to grow new nerve cells altogether. By doing so, it is hoped that the damage can be undone, and a more effective treatment can be offered to those living with SCI. 

Recently, a Californian group led by Dr.Joseph Ciacci, has released an exciting clinical study where, for the first time in humans, four patients had a special preparation of foetal spinal cord stem cells (called Neuralstem) transplanted directly into their spinal cord at the site of injury. After following the patients’ recovery for over two years, they discovered that 3 of the 4 patients had made some improvements. Two patients recovered sensory and motor function, with a third patient showing an improvement in motor activity.  Whilst these changes were measured, it is noted that this did not lead to a change in the patient’s quality of life.  Importantly, the researchers also found no concerns about the safety or side effect profile of stem cell transplant. 

Strategies to repair the spinal cord are sorely needed, and whilst these findings must be treated with significant caution (as there was no group of patients to compare to and the improvements did not reach statistical significance), they are promising as typically for this group of patients, so far down the line after injury, no improvement would be expected. 


Much more work is required before this could lead to real world treatments, and we look forward to follow this story. 

References

  1. Curtis, E et al. 2018 A First-in-Human, Phase I Study of Neural Stem Cell Transplantation for Chronic Spinal Cord Injury Cell Stem Cell  Jun 1;22(6):941-950.e6. doi: 10.1016/j.stem.2018.05.014

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 


Community Champion Frank Dutton shares his top fundraising tips

As a Myelopathy.org Community Champion, I had the honour of holding the charity’s first fundraiser at my local football club.

PictureCommunity Champion Frank Dutton

Myelopathy.org and Myelopathy Support on Facebook have been a great help for both me and my wife since my diagnosis in 2016. Since then, life has been difficult to say the least. Cervical myelopathy, and the accidents it has caused, have led to me going under the knife for no less than six major surgeries. These have significantly affected my body and its ability to cope with everyday life.

I created a ‘lucky numbers’ board featuring 1-100. I then made a list of those numbers with spaces next to them for people to write down their names and telephone numbers. It cost £1 per number and I decided on a winning pay-out of £25 which, if all the numbers had been taken, would deliver a tidy profit of £75 for Myelopathy.org. 

I set my table up in the club room. I took along some laminated photos of people’s CT scans, including my own, as visual aids. I also made copies of one of the charity’s media releases about the condition and the need for early diagnosis, and the basic facts about myelopathy. These are part of the Myelopathy.org fundraising pack. 

It was very interesting to see how people reacted to the photographs and then responded to the information in the leaflets and that I was able to supply about myelopathy. 

The fundraising experience was a positive one and the fact that I was able to raise £71.10 (no idea where the 10p came from) was a bonus. I am now really looking forward to taking part in the next fundraising event. So, if you have any ideas or want to hold a fundraiser yourself, please let me or one of the Myelopathy.org team know.

My top five tips for fundraising.
1) Plan where you want to hold your fundraiser and contact relevant authority/fête organiser/owner etc for permission

2) Share, share, share. Use social media, such as Facebook, WhatsApp, Instagram etc, to gain maximum promotion and coverage for your fundraising activity.

3) Make it personal. Tell your own story so that people can understand more about your experiences and your reasons for fundraising. Sometimes that personal touch/story can elicit donations.

4) Remember your inspiration. There’s a reason why you are supporting this cause. Hold on to your inspiration and bring all that enthusiasm to your fundraising activities.

5) Have fun. If you are not enjoying yourself, you will give off all the wrong vibes. So, smile and perhaps rope in a friend or two to help so that you can jolly each other along.


    If you would like to organise your own fundraising even then please leave your details below