Thought-4-the-day – Prof G's MS Blog Archive

#T4TD: pneumonia

Barts-MS rose-tinted-odometer: zero-stars

#T4TD (thought for the day)

How bad is your breathing and lung function?

Every year a few of our patients with advanced MS die. During the first COVID-19 lockdown I received an email from the husband of one of my patients I had been looking after for over a decade. Thankfully she died peacefully in her sleep. Her MS had affected her swallowing to such an extent that she had to have a feeding tube inserted into her stomach for feeding. Prior to the feeding tube, she was getting recurrent chest infections. Her speech was also very poor and at times I couldn’t really understand what she was saying. Her other complications included intermittent pressure sores and frequent bladder infections.

A common cause of unscheduled hospital admissions and sadly death is aspiration pneumonia. This is when people with MS have poor coordination of their swallowing mechanism and instead of swallowing saliva and/or food properly some of it travels down the trachea or windpipe into their lungs and causes pneumonia.

At the same time, people with swallowing difficulties may have weakness of their muscles of respiration, in particular, the diaphragm. The cause of diaphragmatic weakness is usually lesions in the upper cervical spine. However, it is often made worse by poor posture. For the diaphragm to work properly it needs to be able to move downwards into the abdominal cavity without being impeded; sitting upright and not hunched over help. Seeing a physiotherapist is important to correct your posture and to make sure your wheelchair if you are using a wheelchair, has the correct postural supports. There has been a lot of wheelchair innovation recently with the production of bespoke moulded body supports to keep you sitting straight and upright.

When the diaphragm is weak the so-called accessory muscles of respiration help a person breath. The accessory muscles lift the thorax or chest as the weak diaphragm pushes downwards. The accessory muscles actually work as a pulley and then rely on gravity to lower the chest. So for the accessory muscles to work well you need to be sitting upright; as soon as you lean back or lay down you reduce the effect of gravity and the accessory muscles’ ability to function as a pulley.

When we look at how well your breathing capacity is we often measure your so-called vital capacity, i.e. how much air you can move in and out of your lungs. A normal vital capacity is around 60-70 mL/kg; so a 70kg person has a vital capacity of about 4.5-5.0 litres. When the vital capacity drops below about 20-30ml/kg it is associate with a reduced ability to cough and move mucus plugs out of your lungs. When your cough reflex is weak it puts you at risk of segments of the lung collapsing (atelectasis) and becoming infected.

When your vital capacity drops below 15mL/kg you are in serious trouble and are likely to be in or close to respiratory failure and your blood gases (oxygen and carbon dioxide) may be affected.

When I was a trainee neurologist in South Africa we used to carry around a vital capacity flow metre on our ward consult rounds. This was to assess respiratory function in patients admitted with paralysis from nerve or muscle disease. These vital capacity meters were expensive and in short supply and we didn’t own them and some hospitals didn’t have them. Nowadays you can purchase relatively cheap vital capacity meters that connect to a smartphone.

At Baragwanath hospital, now called the Chris Hani hospital, in Soweto (South Western Township) outside Johannesburg, we used to use low tech clinical signs. The first was how many numbers could someone count at a rate of one number per second on a single breath-hold, whilst sitting-up. If the person couldn’t get to 12 they needed to be seen by the respiratory intensive care team. The other test was whether or not the patient could blow out a lit match or candle held 30cm from their face. The use of a lit match or candle was not really allowed on the wards because of the fire risk, particularly if patients were on oxygen therapy, but the Baragwanath consultants ignored health and safety and used the test anyway. It is important to realise that if someone can’t blow out a lit match or candle at 30cm then their ability to cough is likely to be compromised and they are therefore likely to at risk of collapsing part of their lung and getting a serious lung infection.

Another important clinical sign is simply to listen to a person speak. If their speech is not smooth, but soft and broken up with frequent pauses to take a breath, also indicates a problem with their breathing. You can also ask the person to cough; if the quality of the cough is poor and weak that can also be taken as a sign of weak respiratory muscles.

A mistake that many people make is to use a so-called peak flow meter and pulse oximeter to monitor lung function. These two devices are not suitable for pwMS. The peak flow is really best for people with asthma and bronchospasm and the peripheral blood oxygenation as measured with a pulse oximeter only becomes abnormal very late. Although a pulse oximeter is good to monitor lung function when you have an infection, such as COVID-19 pneumonia, or when someone has a pulmonary embolus (blood clot in the arteries to the lung) it is not a good measure of your respiratory reserve.

If you have advanced MS with swallowing or breathing problems you may want to self-monitor yourself. You need to see a speech therapist to have your swallowing assessed. If your swallowing is compromised you may need to change your diet; for example, if you are choking or coughing when drinking liquids you may need to use thickened liquids. It is also important to have regular home chest physiotherapy to prevent sections of your lung collapsing and to lung muscle exercises. The physiotherapists use so-called incentive spirometers to make the lung exercises fun. I know all about these devices; I had to do incentive spirometry four times a day in the first few weeks after my accident to prevent lung atelectasis.

It is also important that your family and carers have basic first aid training and can do a pharyngeal sweep and/or Heimlich manoeuvre to dislodge food stuck in your throat. Portable pharyngeal suction or vacuum devices can also be purchased and kept at home to clear the throat. If you go this route then your carers and family will need to be trained in how to use them.

If this post is relevant to you because you have advanced MS or you have a family member or patient with advanced MS it is important to ask them if they have an advanced directive. An advanced directive is a legally binding document setting-out how you want to be managed if you ever end up with life-threatening medical complications of having MS. For example, do you want advanced life support or not? It is important that your family doctor, hospital team, family members and carers have a copy of this directive so that they can ensure your wishes are carried out if ever the need arises.

Finally, please make sure you have had your vaccine requirements reviewed. You need your annual flu vaccine, the pneumococcal vaccine if you have not had one on the last 5 years and a COVID-19 vaccine.

CoI: multiple

Twitter: @gavinGiovannoni Medium: @gavin_24211

#T4DT: Do you have a sleep disorder?

Over 70% of pwMS have a sleep disorder with about 40-45% having obstructive sleep apnoea. The latter is massively underdiagnosed and needs to be actively screened for to be detected. I suspect having MS increases one’s chances of developing OSA by affecting the tone and function of the so called bulbar or throat muscles. This problem is that OSA affects quality of sleep and leaves most people with daytime sleepiness, which exacerbates MS-related fatigue and cognitive impairment. This is why if you have daytime sleepiness, fatigue or cognition problems you need to be screened for one of the many sleep disorders that affect pwMS.

The simplest screen for OSA is the Epworth Sleepiness Scale, which takes about 2 minutes to complete. The following symptoms are also clues to having OSA:

Snoring
Stopping breathing or struggling to breathe
Feeling of choking
Tossing and turning
Sudden jerky body movements
Needing to go to the toilet in the night

Sometimes your partner might be more aware of your snoring and pauses in your breathing than you are. If you don’t have a partner you can download one the many sleep apps that monitors your sleep and records snoring. Some of my patients are surprised when they actually hear how bad their snoring is at night.

The good news is that OSA is treatable and many patients come back and say that their lives are transformed after getting a good night’s sleep. The study below documents that pwMS with OSA also improve their cognitive function when their OSA is treated.

McNicholas et al. Impact of obstructive sleep apnoea on cognitive function in multiple sclerosis: A longitudinal study. J Sleep Res. 2020 Aug 13;e13159. doi: 10.1111/jsr.13159.

Cognitive impairment (CI) and fatigue are common in people with multiple sclerosis (MS), with well-known profound effects on quality of life. Sleep disorders, including obstructive sleep apnoea (OSA), are also common in MS patients. The presence of CI has previously been shown to strongly correlate with OSA diagnosed using polysomnography in MS. Treatment of OSA has not previously been investigated as a potential modality to improve cognition in MS patients. Therefore, we sought to investigate the potential effects of OSA treatment on both cognitive function and fatigue in MS patients. Twenty-three participants with MS reporting significant fatigue were enrolled. CI was assessed by the Brief International Cognitive Assessment in MS and the 3-second Paced Auditory Serial Addition Test. All participants underwent overnight polysomnography to assess for possible OSA. Cognitive and fatigue measures were repeated in those subsequently treated for OSA and in a comparative untreated sample. Seven participants (30%) had a diagnosis of OSA based on an apnoea-hypopnea index greater than 5 per hour, with no correlation between the presence of CI and OSA. Verbal learning at follow-up assessment was seen to improve significantly in those treated for OSA, compared with those who were not treated for a sleep disorder. This small study demonstrates the potential for OSA treatment to improve verbal learning in people with MS, larger studies are indicated to further investigate the potential for cognitive and fatigue improvement in people with MS through treatment of comorbid OSA.

CoI: multiple

#T4TD colour vision

When your neurologist looks in your eyes with an ophthalmoscope he/she is looking for the telltale signs of previous damage to the optic nerve. The sign we look for is optic disc pallor. The optic disc is made up of nerve fibres from the retina, which then pass out of the back of the eye to form the optic nerve. If you have had optic neuritis in the past and have lost nerve fibres this can be detected with an ophthalmoscope, OCT (optical coherence tomography) or with retinal photography. Nerve fibre loss from optic neuritis makes the optic disc look pale (see figure below).

The optic disc receives its blood supply from small arteries from the back of the eye; the amount of blood is proportional to the number of nerve fibres in the optic disc. The lower the number of nerve fibres the fewer blood vessels there are the paler the disc looks. Please remember red blood cells are red and give a health optic disc a pinkish colour (see top images above).

Did you know that with a typical attack of optic neuritis you lose about 20% of the nerve fibres in the eye? If you lose so many nerve fibres why isn’t your vision so badly affected in that eye? That is simply because your visual system is able to compensate for the damage; it has spare capacity. Despite this most pwMS who have optic neuritis will know that although their visual acuity, or gross vision, may have recovered they have subtle deficits that we don’t routinely test for. For example, colour vision is often abnormal; colours appear washed out. Contrast sensitivity is abnormal; you may have difficulty distinguishing between shades of grey. Depth perception is all over the place; you need binocular (both eyes) vision for accurate depth perception. If you have poor depth perception you may see things in 3D when they should be in 2D and you may have difficulty judging distances. You may also find that you are hypersensitive to bright lights or lights with certain wavelengths; I find a lot of pwMS become intolerant of fluorescent lights after an attack of optic neuritis.

The problem with the COVID-19 induced changes in our MS service is that with remote consultations I can do this aspect of the neurological examination. Is it important? Yes, firstly it allows one to determine what neuronal systems have been affected by MS, which is required for diagnosis, i.e. dissemination of disease in space, and secondly for assessing your EDSS or Expanded Disability Status Scale.

I am telling you all this as we developed a web-EDSS that requires you to know if your neurological examination is normal or abnormal. Having optic disc pallor is one clinical sign that may affect the EDSS. If you can’t get this information from your neurologist you can get a reasonable idea if your optic nerve has been affected by MS by downloading and using one of the many colour vision applications on your smartphone; we recommend using ‘eye handbook’ as it is free. So before completing your webEDSS you will need to know if you have abnormal colour vision in your left or right eye; this could be used as a proxy for optic nerve involvement. Please note if you have congenital colour blindness, which is more common in males, you can’t use this sign as a proxy for optic nerve involvement.

#T4TD = Thought for the Day

CoI: nil in relation to this post

#T4TD Anticholinergics

Are you taking anticholinergics?

It is clear that centrally acting anticholinergic drugs, which block so-called muscarinic receptors, are being used by many people with multiple sclerosis as DIY agents to promote remyelination. The scientific rationale for this practice is based on preclinical work in cell culture systems and animal models and one proof-of-concept study of clemastine in pwMS with previous optic neuropathy.

Is this practice wise? I say no. We need properly controlled large studies to confirm the results and show that clemastine and other drugs in this class are remyelinating, have a clinical effect that is meaningful and improve quality of life.

Why am I being so pessimistic? The problem is centrally-acting anticholinergic affect cognition. Oxybutynin, a first-generation CNS-penetrant anticholinergic, which is commonly prescribed for urinary frequency, reduces the average IQ of someone with MS by 7 points or half a standard deviation. This is a massive drop in cognitive function particularly if you already have cognitive impairment, which may be overt or hidden and is very common in pwMS.

I have been waging a war with many continence services who look after my patients who still use oxybutynin because it is cheap. There are many alternative newer anticholinergic agents that don’t penetrate the CNS or work on a different mechanism. So if you are on oxybutynin you need to switch drugs.

Lessons from the opicinumab phase 2 remyelination trial suggests that only a subset of pwMS are likely to benefit from a remyelinating agent. This is because not everyone with MS has demyelinated axons or nerve fibres that need remyelination. The estimate is that in pwMS with moderate disability (EDSS 2.0-5.5) only a third will benefit from a remyelinating agent. So if you are taking clemastine you may be taking a hit on your cognition when you don’t even know if you are one of those people who has a population of nerve fibres that are ready to be remyelinated.

For how long do you have to take a remyelination drug to achieve maximum benefit? Provided your MS is under control with an anti-inflammatory DMT and you are not demyelinating new axons you may only need a remyelination agent for a few weeks or months. Once you have stimulated remyelination and all the naked axons are remyelinated there is no need to continue taking the remyelination agent.

Please note these concepts about remyelination are based on animal models and early trials and are mostly hypothetical when it comes to pwMS.

Another worrying observation about anticholinergic drugs is that the impact on cognition may be irreversible and reduce your brain reserve. Several epidemiological studies have shown that in the general population 2-3 years of continuous anticholinergic exposure increases your risk of getting dementia by ~30%. Whether this is applicable to pwMS is at present unknown, but I can’t think of any reason why the MS brain would be less susceptible to anticholinergics; in fact, I suspect the MS brain may be more susceptible as pwMS have reduced brain and cognitive reserve.

So if you are taking off-label clemastine for its unconfirmed benefits in MS or another anticholinergic that is CNS penetrant my advice would be to stop taking them and to seek alternative cognition-friendly medication.

Please be aware that there are many drugs that have anticholinergic effects; the following website lists them. In addition, apart from blunting cognition the list of side effects attributable to anticholinergics includes the following:

Dry mouth
Difficulty in swallowing
Constipation
Paralytic ileus (paralysis of the bowl)
Nausea or vomiting
Increased heart rate
Urinary retention
Difficulty in urinating
Blurred vision
Dry eyes
Exacerbation or precipitation of acute angle-closure glaucoma
Decreased sweating
Drowsiness or sedation
Dizziness
Hallucinations
Deliriums
Restlessness
Irritability
Nervousness
Slurred speech
Impaired concentration
Confusion
Memory impairment

Postscript 1: I have been asked which of the anticholinergics used for MS-related bladder dysfunction are the safest. The table below indicates that Trospium is by far the least CNS penetrant; is the least lipid-soluble and the most positively charged. It is clear that oxybutynin is the worst. Tolterodine, darifenacin and solifenacin are in between.

Source: Chancellor M, Boone T. Anticholinergics for overactive bladder therapy: central nervous system effects. CNS Neurosci Ther. 2012;18(2):167-174. doi:10.1111/j.1755-5949.2011.00248.x

Postscript 2: I have also been asked about what dose of drug X or drug Y is sufficient to cause anticholinergic cognitive effects. A good example on this list is Amitriptyline; just 10mg of Amitriptyline per day is sufficient.

Source: Gray SL, Anderson ML, Dublin S, et al. Cumulative use of strong anticholinergics and incident dementia: a prospective cohort study. JAMA Intern Med. 2015;175(3):401-407. doi:10.1001/jamainternmed.2014.7663

#T4TD = Thought for the Day

CoI: nil in relation to this post

#T4TD onychogryphosis

When last did you cut your toenails?

In patients who I think are vulnerable, I always try to take the time to look at their feet. Unfortunately, because of COVID-19-induced NHS service changes, this is very difficult using telemedicine.

Poor foot hygiene and uncut toenails are in my experience an integrator of neglect. As the feet are generally hidden from view people with MS often neglect their foot hygiene more than other aspects of their grooming. Poor foot hygiene is not intentional, but simply represents the reality of living with a disability. Poor eyesight, double vision, oscillopsia, weakness, tremor, loss of feeling in the hands, slow movement, incoordination, obesity, etc. are all more common in pwMS and make cutting your own toenails difficult.

During COVID-19 lockdown nail bars have been closed and podiatrists have not been seeing patients; therefore, I suspect general foot hygiene may have deteriorated in many people with more advanced MS.

There is little doubt that MS or physical disability is a risk factor for onychogryphosis; in plain English overgrown and neglected toenails. Onychogryphosis makes it difficult to wear shoes, causes pain and may even put mobile patients at risk of falls. So if you can’t manage to look after your own feet I suggest post-lockdown setting-up regular appointments to have your toenails cut and your feet examined by a podiatrist. Please note in the UK podiatry is an NHS service.

Marginal gains, i.e. focusing on small differences which add up can make big differences to the quality of life and health outcome for people with MS, and this should include foot hygiene and taking care of your toenails. This is just another factor that HCPs need to consider if they want to manage MS holistically.

#T4TD = Thought for the Day

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#T4TD Infected

Did you know that a third of relapses are triggered by infections, typically non-specific viral infections?

The observation that a relapse is more likely to occur in the so-called ‘at risk’ period, typically 5-6 weeks after infection than at other times predates the disease-modifying therapy era of MS. The mechanism is thought to be that infection boosts the immune system non-specifically, which then trigger relapses. This observation was extrapolated to vaccinations, but most vaccine studies now show that vaccines in general, with the possible exception of the yellow fever vaccine*, are safe and are not associated with an increased risk of relapses nor MRI activity.

* Please note recent data on the live yellow fever vaccine shows that it doesn’t trigger MS relapses.

Once people are on an effective DMT the link between infections and relapses is not observed. This is another, albeit minor, reason to be on a DMT. However, there is an emerging field in basic science and clinical evidence to support it that recurrent infections drive some of the pathological processes that are responsible for smouldering MS. Systemic inflammation activates CNS microglia that then produce cytokines and inflammatory mediators that have a negative effect on neuronal function. This is why people with MS handle infections so poorly and often don’t get back to baseline after a severe systemic infection.

Therefore as part of the holistic management of MS, it is a good idea to prevent chronic or recurrent infections. So if you have recurrent or chronic bladder infections, periodontitis (gum disease), chronic sinusitis or recurrent chest infections you need to do something about it. Don’t just accept recurrent infections as your lot in life ask your MS team for advice and help.

#T4TD = Thought for the Day

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#T4TD Driving at night

Did you know that more than half of people with established multiple sclerosis (pwMS) have had an episode of optic neuritis (an MS lesion in the optic nerve)? Not all episodes of optic neuritis cause symptoms and can be subclinical. We detect the latter using visual evoked potentials that show slowed conduction in a particular optic nerve.

When optic neuritis recovers the conduction speed of nerve impulses travelling through the recovered nerve rarely gets back to normal and is slower than the conduction speed in the unaffected eye. In addition, the conduction speed can change depending on fatigue or ambient temperature changes. The conduction in the affected, by remyelinated, nerves can even fail and this is can result in intermittent blurring or loss of vision called Uhthoff’s phenomenon.

The brain is usually quite good at compensating for the signals coming from the eyes at different speeds, but the one thing it is poor at doing is adjusting for depth perception. The reason we have two eyes with overlapping visual fields or binocular vision is for depth perception. This is why pwMS with previous optic neuritis may have poor depth perception, which affects their ability to judge where for example a cup or glass is on the table and as a result of this they often spill drinks. PwMS will also have difficulty playing ball sports such as tennis, table tennis or any sport that requires accurate depth perception.

One function that seems to very sensitive to this phenomenon is judging distances whilst driving at night; for example, estimating how far you are from the traffic intersection or a stop sign. Many of my patients don’t like driving at night because of this. Why? Well, the brain uses a process called parallax to compensate for the loss of depth perception; i.e. the brain uses the relative size of familiar objects to help make a judgment on how far something is away from you in the distance. By using parallax somebody who is blind in one eye can judge depth and distance relatively well. However, at night in the dark when images are not well illuminated and use of colour vision drops judgement by parallax fails and depth perception deteriorates.

I would be interested to know if any of you have any of these problems with depth perception and driving at night. If you do the chances are that you have had optic neuritis in the past.

Unfortunately, there is little we can do to treat this phenomenon, but knowing about and understanding why it occurs may help you compensate for this impairment, disability or handicap.

Parallax: Have you ever wondered why the setting-sun and full-moon on the horizon look so big compared to it being smaller when it above us in the sky? It is actually not bigger; simply having a reference on the horizon (trees, mountains, buildings, the sea, etc.) makes your brain perceive it as being larger, i.e. closer. This is how parallax affects how the brain works and judges distance from you to an object in the distance.

#T4TD = Thought for the Day

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#T4TD when it comes to Anti-CD20 therapy body size counts

Did you know that if you are a large person standard dose ocrelizumab is not as effective as it is in a small person?

When looking at the efficacy of anti-CD20 therapies such as ocrelizumab you shouldn’t bother looking at relapses and focal MRI activity (Gd-enhancing lesions or new T2 lesions) when comparing effectiveness between doses and competing products. Relapses and MRI lesions are ultrasensitive to the effects of anti-CD20 therapies and are suppressed, to almost zero, at relatively low doses. In scientific measurement-speak we refer to this as a floor effect; in other words, you can’t go lower than zero or near-zero.

However, when you look at disability progression (the real MS) there is clearly a dose effect, i.e. the higher the dose of ocrelizumab relative to body size, the greater the B-cell depletion and the less likely you are to progress. Most commentators miss this insight and are lulled into a false sense of security by seeing the relapse and MRI data when the real MS may be smouldering away and shredding your brain unabated.

For this reason, we really need to do studies with higher doses of ocrelizumab and almost certainly higher doses of rituximab and ofatumumab. The observation that rituximab, at relatively low doses, doesn’t prevent the majority of pwMS becoming secondary progress is not surprising when it seems we need more intensive and not less intensive B-cell depletion.

There are two hypotheses that could explain the dose-effect of ocrelizumab: (1) CNS penetration and the need to scrub the brain free of B-cells, or (2) really deep tissue B-cell depletion. Higher doses of ocrelizumab may achieve both of these. The real question is what is it about B-cells that is driving MS?

Those of you who are up to speed with safety and vaccine readiness data will argue that higher dose ocrelizumab will come with a price. Yes and no. Until we do the studies we won’t know. In relation to vaccine responses, I suspect there will be little difference between low and high dose ocrelizumab as both will almost certainly ablate germinal centre function.

In terms of long-term safety, I suspect we may not need to use high-dose or very high-dose anti-CD20 therapy long term; we may get away with using it as an induction therapy followed by a maintenance therapy.

Does this have implications for you as an individual? Yes, don’t accept your neurologist saying your disease is under control simply because you are relapse and MRI activity free; remember smouldering MS is the real disease. There are now compelling reasons why we need to do the double-dose ocrelizumab trial or DODO study and other add-on studies to target smouldering MS. Do you agree?

#T4TD = Thought for the Day

CoI: multiple

#T4TD falls and fractures

Did you know that people with MS have a six times higher risk than age-matched controls of having a long bone fracture of the lower limb?

The reason for this is that pwMS often have balance problems, unsteadiness of gait (ataxia), lower limb weakness (dropped foot) and are maybe excessively sedated from their medications. All these factors increase your chances of falling. In addition, pwMS are at high risk of poor bone health (osteopaenia or osteoporosis) due to inactivity, reduced outdoor activity, low vitamin D levels, steroid treatment and comorbidities such as smoking.

falls + poor bone health = increased long bone fractures

Why is this so important? A lower limb long bone fracture is one of the events that can tip someone with MS from being independent into becoming dependent and is often the trigger for needing a wheelchair. In addition, people with advanced MS don’t rehabilitate very well because they have reduced reserve and are usually quite disabled.

How do you know if you are at risk of falls and fractures? We have shown that the best predictor of falls is the need for a walking aid (splint, stick, crutch, frame, functional electrical stimulator, etc.). If you are using a walking aid and are having falls, or near falls, you need to see a physiotherapist to be enrolled in a falls prevention programme and you will also need to have your bone density checked. This latter can be assessed via several methods, but the commonest is called a DEXA scan (dual-energy X-ray absorptiometry scan). If you are found to be osteopaenic or osteoporotic you may need treatment.

Falls and fracture prevention is another self-management task; please don’t ignore it!

Prevention is better than treating the consequences of falls and fractures. For example, one of my patients with MS tragically fell going to the toilet at night. She crashed into a mirror that shattered and lacerated her arm and severed her brachial artery. She tragically bled to death as she lived alone, did not have an alert dongle around her neck and was unable to get herself up off the floor. Ever since she died I have taken falls prevention very seriously. Can you please do the same? You never know it may even save your life.

Long bones of the lower limbs = femur, tibia and fibula

#T4TD = Thought for the Day

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#T4TD vascular comorbidities

Did you know if you have MS and vascular comorbidity you are likely to need a walking stick approximately 6 years earlier than if you did not have vascular comorbidity? Importantly this 6-year difference in reaching EDSS 6.0 (requiring a walking stick) is larger than the treatment effect of a platform DMT.

As vascular comorbidities are largely preventable are you doing anything to prevent or optimally treat your own comorbidities? If not, you need to ask yourself why not? Self-management and taking responsibility for your own health is the order of the day; this has become the new normal.

Vascular comorbidities = diabetes, hypertension, heart disease, hypercholesterolemia, peripheral vascular disease and smoking.

#T4TD = Thought for the Day

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