8 things we now know about the toxicity of gadolinium to the brain

When it comes to imaging the nervous system, nothing but an MRI will do for the fastidious neurologist. CT has its uses, such as in detecting acute intracranial bleeding, but it lacks the sophistication to detect or differentiate between less glaring abnormalities. It also comes with a hefty radiation dose. MRI on the other hand, relying on powerful magnetic fields, is a ‘cleaner’ technology.

SLEIC 6. Penn State on Flickr. https://www.flickr.com/photos/pennstatelive/4946556307

MRI scans on their own are however often insufficient to sate the craving of the neurologist for precision. A plain MRI scan, for example, will not tell if a multiple sclerosis lesion is old or new, and it may fail to detect subtle but significant lesions such as low grade brain tumours or lymphoma. Many lesions on routine MRI scan are also ill-defined and non-specific, and could pass for abscesses, vasculitis, inflammation or just small vessel disease (wear and tear) changes.

The Brain. I has it. Deradrian on Flickr. https://www.flickr.com/photos/mgdtgd/3507973704

To silence the niggling doubts, the neurologist often requests an MRI scan with contrast. The idea is to use a dye to separate the wheat from the chaff, the active lesions from the silent ones. This works because sinister lesions have a bad and dangerous habit of disrupting the blood brain barrier. All such insurgencies across the hallowed BBB is sacrilege, a sign that something serious is afoot, (or is it underfoot?). Contrast dyes, on the other hand, are adept at detecting these breaches, traversing them, and staining the sinister lesion in the process. This stain appears on the MRI scan as contrast enhancement. MRI with contrast is therefore invaluable, and a positive study is a call to arms.

By © Nevit Dilmen, CC BY-SA 3.0, Link

Without any doubt, gadolinium is the favoured dye for contrast MRI scans. Gadolinium (Gd) is a lanthanide rare earth metal and it is one of the heavier elements of the periodic table with atomic number 64. It is named after the thrice-knighted Finnish chemist Johan Gadolin, who also discovered the first rare earth metal, yttrium.

Periodic table model. Canada Science and technology Museum on Flickr. https://www.flickr.com/photos/cstmweb/4888243867

We know a lot about some of the risks of injecting gadolinium into the body, such as its tendency to accumulate in people with kidney impairment (who cannot excrete it efficiently). We also know that it may cross the placenta to damage the developing baby. These are however hazards with simple and straight-forward solutions: avoid gadolinium in pregnancy, and don’t use it in people with poor renal function.

By Hi-Res Images ofChemical Elements – http://images-of-elements.com/gadolinium.php, CC BY 3.0, Link

Much more challenging is the problem of gadolinium deposition in the brain of people with normal renal function. This is concerning because it is unpredictable, and because it has the potential to compromise brain structure and function. This blog has previously asked the question, “Is gadolinium toxic?“. The question remains unanswered, and regulatory agencies are still studying the data to provide guidance to doctors. Patient groups on the other hand have been up in arms, as one would expect, impatiently waiting for answers. What then is the state of play with gadolinium? Should neurologists and their patients really be worried? Below are 8 things we now know about gadolinium and its potential brain toxicity.

By Peo at the Danish language Wikipedia, CC BY-SA 3.0, Link


1. Gadolinium deposition is related to its insolubility at physiological pH

The toxic potential of gadolinium is thought to be the result of its insolubility at physiological pH. Furthermore, gadolinium competes against calcium, an element fundamental to cellular existence. This competition is obviously detrimental to the body.

064 Gadolinium-Periodic Table of Elements. Science Activism on Flickr. https://www.flickr.com/photos/137789813@N06/22951789105

2. The less stable gadolinium agents are the most toxic

There are two forms of gadolinium based contrast agents (GBCAs): the less stable linear GBCAs, and the more stable macrocyclic GBCAs. The linear GBCAs are more toxic, of which Gadodiamide (Omniscan) stands out. Other linear agents are gadobenate dimeglumine (MultiHance), gadopentetate dimeglumine (Magnevist), gadoversetamide (OptiMARK), gadoxetate (Eovist), and gadofosveset (Ablavar). The macrocyclic GBCAs, even though safer, are not entirely blameless. They include gadobuterol (Gadavist), gadoterate meglumine (Dotarem), and gadoteridol (ProHance). Therefore, choose your ‘gad’ wisely.

By زرشکOwn work, CC BY-SA 3.0, Link


3. Gadolinium deposits in favoured sites in the brain

It is now established that gadolinium deposits in three main brain areas. The most favoured site is the dentate nucleus of the cerebellum. Other popular regions are the globus pallidus and the pulvinar. This deposition is, paradoxically, visible on plain T1-weighted MRI scans where it shows as high signal intensity.

By Polygon data were generated by Database Center for Life Science(DBCLS)[2]. – Polygon data are from BodyParts3D[1], CC BY-SA 2.1 jp, Link

4. The risk of deposition depends on the number of injections

The risk of gadolinium deposition in the brain is higher with multiple administrations. Stated another way, and to stretch this paragraph out a bit longer, the more frequently contrast injections are given, the higher the chances gadolinium will stick to the brain. The possible risk threshold is 4 injections of gadolinium. The fewer the better…obviously!

Number-04. StefanSzczelkun on Flickr. https://www.flickr.com/photos/stefan-szczelkun/3931901057

5. Gadolinium also deposits outside the brain

The favoured site of gadolinium deposition outside the brain is the kidney, where it causes nephrogenic systemic fibrosis, a scleroderma-like disorder. This however occurs mostly in people with renal impairment. Gadolinium also deposits in other organs outside the brain including bone, skin, and liver. (Strictly speaking, this item has nothing to do with the brain, but it helped to tot up the number to 8 in the title of this blog post, avoiding the use of the more sinister se7en).

By JudgefloroOwn work, CC BY-SA 4.0, Link

 6. Harm from gadolinium brain deposition has not been established

Whilst we know for sure that gadolinium deposits in the nervous system, harm from deposition has not been definitively established. There are, however, reports that gadolinium deposition may produce muscle and eye symptoms, and chronic pain. There are also reports of cognitive impairment manifesting as reduced verbal fluency.

Words words words. Chris Blakeley on Flickr. https://www.flickr.com/photos/csb13/4276731632

7. Precautions may reduce the risk of gadolinium brain deposition

The current recommendation is not to withhold the appropriate use of gadolinium, but to observe simple precautions. Sensibly, use GBCAs only when absolutely necessary. Also consider preferentially using macrocyclic GBCAs and evaluate the necessity for giving repeated GBCA administrations.


By IntropinOwn work, CC BY-SA 3.0, Link


8. There are emerging ways to avoid gadolinium toxicity

The safest use of gadolinium is not to use it at all. There are some developments in the pipeline to achieve this, although probably not in the very near future. Such developments include manganese based contrast agents such as Mn-PyC3A. A less definitive option is to mitigate the effects of gadolinium by using chelating agents; two such potential agents are nanoparticles and 3,4,3-LI(1,2-HOPO).


Why not get the snapshot view of gadolinium toxicity in the neurochecklist:

Gadolinium-based contrast agent (GBCA) toxicity

…and leave a comment!


MRI scan. NIH Image Gallery on Flikr. https://www.flickr.com/photos/nihgov/30805879596

What is the impact of Vitamin D on the complicated course of MS?

Some general neurologists get away with not having to think too much about multiple sclerosis (MS). This is because they have an ‘MSologist‘ at hand to refer all their patients with ‘demyelination‘. Many general neurologists however care for people with MS because they do not have a ‘fallback guy‘ to do the heavy lifting for them. This therefore makes it imperative for neurologists to keep up with everything about this often disabling and distressing disorder.

MS prevalence map. By AdertOwn work and [1], CC BY-SA 3.0, Link
The management of MS is however very tricky, and it is challenging to get a grip of it all. This is partly because the clinical course is varied, and the diagnostic process tortuous. The patient first goes through an onerous retinue of tests which include an MRI, a lumbar puncture, evoked potentials, and a shedload of blood tests. This is all in a bid to secure the diagnosis and to exclude all possible MS mimics.

MRI scan. NIH Image Galley on Flikr. https://www.flickr.com/photos/nihgov/30805879596

Then comes the head-scratching phase of determining if the patient actually fulfils the diagnostic criteria for MS, or if they just have clinically isolated syndrome (CIS) and radiologically isolated syndrome (RIS). To secure the diagnosis of MS, the neurologist turns to the McDonald criteria which stipulate dissemination in time and place of inflammatory events. As simple as this should be, this is no easy task at all. This is because, at different times, the criteria have meant different things to different people. The guidelines have also gone through several painful, and often confusing, iterations. Indeed the McDonald criteria have only recently been re-revised-to the delight of MSologists but the chagrin of the general neurologist!

Steampunk Time and Space Machine. Don Urban on Flikr. https://www.flickr.com/photos/donpezzano/3230179951

Once the diagnosis of relapsing remitting MS (RRMS) is reasonably established, the patient is taken through a guided tour of the ever-expanding available treatment options. These are typically to prevent relapses, but more recently to prevent disease progression as well. People with mild to moderate MS are nudged towards interferons, glatiramer acetate, dimethylfumarate, or terifluonamide. Those with more aggressive disease, on the other hand, are offered a menu of fingolimod, natalizumab, or alemtuzumab. Other newer agents include daclizumab and cladribine. And, just stepping into the arena, there is ocrelizumab for primary progressive (PPMS). Whichever option is chosen, the course of treatment is long, and it is fraught with risks such as infections and immune suppression.


Once the bigger questions have been settled, the neurologist then braces for the ‘minor’ questions her enlightened patients will ask. The easier questions relate to the treatment of symptoms, and some of the most vexing concern the role of Vitamin D deficiency. Such questions include, ‘Is vitamin D deficiency a cause of MS?‘, ‘Do people who are vitamin D deficient experience a worse outcome?‘, and ‘Should patients with MS be on Vitamin D supplementation?‘.

Pandora’s box. Michael Hensman on Flikr. https://www.flickr.com/photos/mycael/3664900435

To attempt to resolve these questions I plunged into some of the literature on Vitamin D and MS. And this is like opening Pandora’s box. Here are some of the things I found.


Is MS associated with Vitamin D deficiency?

It therefore appears that there is an association of vitamin D deficiency with MS, but it is far from certain that this is a causative relationship. One hypothesis is that vitamin D deficiency is the outcome, rather than the cause, of MS. The deficiency presumably results becuase the very active immune system in people with MS mops up the body’s Vitamin D. This so-called reverse causation hypothesis asserts that vitamin D deficiency is a consumptive vitaminopathy

Sunshine Falls. Dawn Ellner on Flikr. https://www.flickr.com/photos/naturesdawn/4299041739

Does Vitamin D deficiency worsen MS progression?

There is therefore no single answer to this question, but the emerging consensus is that Vitamin D deficiency adversely affects the course of MS. 

Milk splash experiment. Endre majoros on Flikr. https://www.flickr.com/photos/boneball/24597145866

Should people with MS be on Vitamin D supplementation?

Even if Vitamin D deficiency doesn’t cause MS, the evidence suggests that it negatively influences the course of the disease.

Salmon salad nicoise. Keith McDuffee on Flikr. https://www.flickr.com/photos/gudlyf/3609052894

What to do?

This is the million dollar question eloquently posed by a recent editorial in the journal Neurology titled Preventing multiple sclerosis: to (takevitamin D or not to (takevitamin D? The reasonable consensus is to encourage vitamin D replenishment to prevent MS, starting from preconception. It is also generally agreed that people with MS should be on vitamin D supplementation in the expectation that it will slow the disease activity.

A practical approach to Vitamin D replacement is the Barts MS team vitamin D supplementation recommendation. This is to start with 5,000IU/day vitamin D, and aim for a plasma level of 100-250 nmol/L. Depending on the level, the dose is then adjusted, up or down, to between 2-10,000IU/day. They also advise against giving calcium supplementation unless there is associated osteoporosis.

What is a general neurologist to do? To follow the prevailing trend, and hope it doesn’t change direction too soon!

Vitamin D Pills. Essgee51 on Flikr. https://www.flickr.com/photos/sg51/5224823967


What is the value of temporal artery biopsy in the diagnosis of GCA?

Giant cell arteritis (GCA) is a nasty inflammatory disorder that affects the large arteries. Because it characteristically involves the temporal artery, this form of vasculitis is also referred to as temporal arteritis. It usually affects people over the age of 50 years and manifests with sudden onset headache, scalp pain, and a thick, tender temporal artery. GCA is often accompanied by polymyalgia rheumatica (PMR) , a painful condition of the joints and muscles. The active systemic inflammation in GCA is often detected by the erythrocyte sedimentation rate (ESR) or C-reactive protein (CRP) tests. These distinguishing features constitute most of the diagnostic criteria for GCA.

By National Institute of Standards and Technology – https://www.flickr.com/photos/usnistgov/5828207621/, Public Domain, Link

Most people with GCA however do not have all the ‘classical’ features of the disease. A high index of suspicion is therefore required to sniff out the duplicitous miscreant. It is particularly imperative to make the diagnosis as early as possible to prevent the dreaded complications of GCA, sudden blindness and stroke. The treatment of GCA, implemented according to established treatment guidelines, involves several months of oral steroids, drugs which cause immune suppression and a host of other side effects. It is therefore essential that the diagnosis of GCA is made correctly to avoid putting the patient on a long, risky, and unnecessary treatment.

By Henry Vandyke CarterHenry Gray (1918) Anatomy of the Human Body (See “Book” section below)Bartleby.com: Gray’s Anatomy, Plate 508, Public Domain, Link

The conventional method of establishing the definitive diagnosis of GCA is by performing a temporal artery biopsy. This involves taking a short segment of the temporal artery as it traverses the temple. This procedure however only confirms the diagnosis of GCA in 1335% of people with the condition. One reason the biopsy has such a poor sensitivity is that it is often performed after treatment has already commenced. Another reason the biopsy is often normal is that the inflammation in GCA occurs in patches, sparing large segments of the artery. Don’t even think about it-taking a longer biopsy segment does not increase the yield of temporal artery biopsy. Put another way, “specimen length is not associated with diagnostic yield of temporal artery biopsy.

By NephronOwn work, CC BY-SA 3.0, Link
What then is the value of the temporal artery biopsy in the diagnosis of GCA? This is the question posed by Bowling et al in their incisive paper titled Temporal artery biopsy in the diagnosis of giant cell arteritis: does the end justify the means? They reviewed 129 temporal artery biopsies and found that the clinical diagnosis of GCA was confirmed in only 13% of cases. Furthermore, the outcome of the biopsy rarely ever influenced the treatment; 87% of those with a normal biopsy result still continued their treatment. The miffed authors therefore rhetorically, and indignantly, asked: “can we justify invasive surgery to all patients on histological grounds when the results may not alter management?” 
Ipswich, Waterfront, Ipswich Campus, The Big Question Mark Sculpture. Martin Pettitt on Flikr. https://www.flickr.com/photos/mdpettitt/8671901426

This is an entirely reasonable question especially because there are other more accurate and less invasive ways of establishing the diagnosis of GCA. These include:

But the answer to the authors’ rhetorical question is anyones guess. It is a sad tradition of medicine that studies such as these take ages to change practice. Indeed I predict the the temporal artery biopsy will sidestep this minor hurdle and simply continue its long and agonising reign. Despair!
By No machine-readable author provided. Spekta assumed (based on copyright claims). – No machine-readable source provided. Own work assumed (based on copyright claims)., Public Domain, Link
You can at least read more on GCA in my previous blog post titled Advances in the management of giant cell arteritis. You may also explore these comprehensive neurochecklistsGiant cell arteritis (GCA): clinical featuresand Giant cell arteritis (GCA): diagnosis and management.


FDG. TRIUMF Lab on Flikr. https://www.flickr.com/photos/triumflab/8232448893


Do statins really increase the risk of Parkinson’s disease?

Statins are famous, and their fame lies in their ability to bust cholesterol, the villain in many medical disorders such as heart attack (myocardial infarction) and stroke. Some may add that statins are infamous, and this is partly because of their side effects such as muscle pain. Love them or hate them, we can’t get away from statins…even as the debate rages about their benefits and downsides.

By ChiltepinsterOwn work, CC BY-SA 3.0, Link

It is not surprising therefore that the statin debate will filter into neurology. The sticking point here however has nothing to do with cholesterol busting, but all to do with whether statins increase or reduce the risk of developing Parkinson’s disease (PD). Strange as it may seem, statins and PD have a long history. And a positive one generally, I hasten to add. There is a large body of evidence to suggest a protective effect of statins on PD as reflected in the following studies:

  1. Confounding of the association between statins and Parkinson disease: systematic review and meta-analysis 
  2. Statin therapy prevents the onset of Parkinson disease in patients with diabetes
  3. Statin use and risk of Parkinson’s disease: A meta-analysis 
  4. Statin use and its association with essential tremor and Parkinson’s disease
  5. Statin use and the risk of Parkinson’s disease: an updated meta-analysis
  6. Long-term statin use and the risk of Parkinson’s disease
  7. Discontinuation of statin therapy associated with Parkinson’s disease
Modeling the Molecular Basis of Parkinson’s Disease. Argonne National Laboratory on Flikr https://www.flickr.com/photos/argonne/4192798573

It was therefore with some consternation that a recent study, published in the journal Movement Disorders, really put the cat among the pigeons. The paper is titled:

Statins may facilitate Parkinson’s disease: insight gained from a large, national claims database,

The authors of this paper set out to investigate ‘the controversy surrounding the role of statins in Parkinson’s disease’. In this retrospective analysis of over 2,000 people with PD, and a similar number of control subjects, the authors found that statins significantly increased the risk of developing PD. This is clearly a conclusion looking for a fight!

By Col. Albert S. Evans – internet archives, Public Domain, Link

I must admit I was totally unaware there was any controversy about statins and PD. I was therefore curious to find out what studies are out there fuelling it. Which other trials have bucked the trend and reported an increased risk of PD from statins? And where best to find the answers but in PubMed, the repository of all human knowledge! And I found that there were only a few studies that did not report a protective effect of statins on PD, and these studies concluded, quite reasonably, that they found no relationship between PD and statins. Here are a few of the studies:

  1. Statin adherence and the risk of Parkinson’s disease: A population-based cohort study. 
  2. Use of statins and the risk of Parkinson’s disease: a retrospective case-control study in the UK. 
  3. Statin use and the risk of Parkinson disease: a nested case control study. 

These papers reporting the absence of evidence seem happy to engage in an amicable debate to resolve the question.

By DavidKF1949Own work, CC BY-SA 3.0, Link

One study however stood out like a sore thumb because it positively reported a negative effect of statins on PD (try and work that out!). This 2015 study, also published in Movement Disorders, is titled Statins, plasma cholesterol, and risk of Parkinson’s disease: a prospective study. The paper concludes that “statin use may be associated with a higher PD risk, whereas higher total cholesterol may be associated with lower risk“. Not only are the authors arguing that statins are bad for PD, they are also suggesting that cholesterol is good! This is a paper that was itching for fisticuffs.

By Jan SteenWeb Gallery of Art:   Image  Info about artwork, Public Domain, Link

What is a jobbing neurologist to do? What are the millions of people on statins to do? Whilst awaiting further studies, I will say stay put. Go with the bulk of the evidence! And keep track of The Simvastatin Trial, funded by The Cure Parkinson’s Trust. This trial is looking at the benefit of statins in slowing down PD. And surely, very soon, the science will lead to a resolution of the argument-all you need to do is keep track of everything PD in Neurochecklists.

By Léon Augustin Lhermittehttp://wellcomeimages.org/indexplus/obf_images/fc/7f/643258ab30237374aaea5ac15757.jpgGallery: http://wellcomeimages.org/indexplus/image/L0006244.html, CC BY 4.0, Link


More activity on the fringes of gluten neurology

I have dabbled into gluten neurology before with my post gluten neurology-persisting and growing? 


Prophetic it seems, as I am here forced to revisit the topic because  I came across a few recent interesting reports on the neurology of gluten.

Gluten psychosis

By Vincent van Gogh - bgEuwDxel93-Pg at Google Cultural Institute, zoom level maximum, Public Domain, Link
By Vincent van GoghbgEuwDxel93-Pg at Google Cultural Institute, zoom level maximum, Public Domain, Link

Take this case report from Nutrients titled gluten psychosis: confirmation of a new clinical entity. The article comes with some good references that suggest it will do no harm to check anti-gliadin antibodies in people with unexplained psychosis. I do wonder how one case report would confirm an entity such as gluten psychosis, but there you are.

Gluten-induced visual impairment

By OpenStax College - Anatomy & Physiology, Connexions Web site. http://cnx.org/content/col11496/1.6/, Jun 19, 2013., CC BY 3.0, Link
By OpenStax College – Anatomy & Physiology, Connexions Web site. http://cnx.org/content/col11496/1.6/, Jun 19, 2013., CC BY 3.0, Link

The second item is another case report published in Journal of Neurology titled severe, persistent visual impairment associated with occipital calcification and coeliac disease. The subject of the case report has long-standing coeliac disease and visual impairment. Her brain MRI scan showed calcifications in the visual area, evidence the authors claim, of celiac disease causing brain calcifications …..and thereby causing the patients visual loss. Is it just a case of correlation rather than causation? But there you are.

Gluten-induced motor neurone disease (MND)

Multiphoton microscopy of mouse motor neurons. ZEISS microscopy on Flikr. https://www.flickr.com/photos/zeissmicro/12174353194
Multiphoton microscopy of mouse motor neurons. ZEISS microscopy on Flikr. https://www.flickr.com/photos/zeissmicro/12174353194

The third report however pushes credulity to the limits. It is a review in Brain Blogger titled celiac disease and amyotrophic lateral sclerosis-is there a link? To its credit, the piece is heavily referenced; one such reference is from the American Journal of Neuroradiology  titled White Matter Lesions Suggestive of Amyotrophic Lateral Sclerosis Attributed to Celiac Disease. The thought is hard to bear, but there you are.


By Photograph by Pdeitiker - Transferred from en.wikipedia to Commons., Public Domain, Link
By Photograph by Pdeitiker – Transferred from en.wikipedia to Commons., Public Domain, Link

What are your thoughts on the neurology of gluten? Please leave a comment



Terminological exactitude: changing the names of established neurological disorders

This is a quick post to highlight changes and proposed changes to some neurological terms. It is not unusual for such changes to occur every now and then. We have, for example, seen benign intracranial hypertension (BIH) changed to idiopathic intracranial hypertension (IIH), and Hallavorden Spatz disease transformed into pantethonate kinase associated neurodegeneration (PKAN).

Names scratched into a wall. Evelyn Simak on Geograph. http://www.geograph.org.uk/photo/4681807
Names scratched into a wall. Evelyn Simak on Geograph. http://www.geograph.org.uk/photo/4681807

One recent important change in neurological terminology, starting tentatively but beginning to take hold, is of nocturnal frontal lobe epilepsy (NFLE) to sleep-related hypermotor epilepsy.

The second is the suggested change from exploding head syndrome to episodic cranial sensory shock. I am not quite sure it will take off, but time will tell!

The third, not too new but surprising non-the-less, is the change from primary dystonia to focal isolated dystonia

Are you aware of any other issues of terminological exactitude? Please leave a comment.



What is the relationship of MND and cancer?

There are many sources of neurology information, as I listed in my previous post titled what are the most reliable neurology reference sources? These sources let us know what is in and what is out; what is breaking and what has gone stale. Keeping on top of the ever-shifting information the journals churn out is challenging, but interesting. This information is the life blood of The Neurology Lounge, and keeps neurochecklists current and reliable.

Reference tracker icon. Berto on Flikr. https://www.flickr.com/photos/bertop/2485992973
Reference tracker icon. Berto on Flikr. https://www.flickr.com/photos/bertop/2485992973

In the task of keeping level with neurological developments, I first go to the journal Neurology, one of the clear leaders of the pack. Check it out on twitter under its handle, @GreenJournal. Browsing through a recent issue, I  was struck by a paper titled Population-based risks for cancer in patients with ALS. The authors of this paper report that people with motor neurone disease (MND) appear to be protected from developing many cancers, including the notorious lung cancer. In contrast, they are at a higher risk of testicular and salivary gland cancer.


Curious to know more, I looked for previous reports on this topic but I came out not any wiser. Older research have given conflicting results on the links between MND and cancer. Take this paper published in the International Journal of Cancer titled The risk of amyotrophic lateral sclerosis after cancer in U.S. elderly adults: a population-based prospective study. This found no links at all, as did another paper published in Journal of Neurology titled Prior medical conditions and the risk of amyotrophic lateral sclerosis. On the other hand, other researchers found that people with MND were at a higher risk of cancer. An example is this paper titled The association between cancer and amyotrophic lateral sclerosis, published in Cancer Causes and Control. This reported a link between MND and melanoma, and with tongue cancer. The bulk of the research before now however suggests that there is no link. Take this paper published in Amyotrophic Lateral Sclerosis & Frontotemporal Degeneration, and titled Amyotrophic lateral sclerosis and cancer: a register-based study in Sweden; the authors, led by Ammar al Chalabi, sounded an authoritative ring of finality when they said “our results provide no evidence for comorbidity of cancer and ALS“. Before now, that is!


So, is the latest study bucking the trend? Does MND really protect against some cancers and predispose to others? What does this all mean for people with MND? Or is all this just a quirk of the statistics? Questions, questions. I suspect this paper has just re-opened a can of worms, and more studies will surely follow. And they will refute and confirm the findings in equal measure.


For now, MND remains an enigma. You may explore it a bit more in my previous blog posts on the subject…and leave your thoughts behind in the comments box.