10 catchy neurology headlines to bid farewell to 2021

Carrying on with my tradition of highlighting the most captivating neurology headlines, here again is a selection of 10 neurology articles with catchy titles. Each headline is a carefully crafted piece of work created with striking phrases which efficiently convey the key messages of the articles. So go ahead and savour these 10 catchy neurology titles as you bid farewell to 2021.

Catchy colours. ૐ Didi ૐ on Flickr. https://www.flickr.com/photos/dey/98655234/

A Broken Heart

Myasthenia gravis and cardiac arrest are not phrases that often occur together in the same headline. Indeed, they are probably phrases that have never occurred together before. That is, until this arresting headline (pardon the pun) which is the title of a case report published in 2020 in the journal Cereus. The authors of the paper, full title being A broken heart: cardiac arrest as the initial presentation of myasthenic crisis, reported the case of a 61-year-old man who sustained a cardiac arrest shortly before he was admitted to their emergency department. He had presented with symptoms of an upper respiratory tract infection, and myasthenia gravis was the only stain in his otherwise unsullied past medical history. With no other suspects, the authors concluded that the cardiac arrest was a manifestation of myasthenic crisis. They felt further justified in their diagnosis when the man’s short PR interval resolved on treatment with steroids and plasmapheresis. The authors made the important point that some myasthenia gravis antibodies, such as Titin, RYR and Kv1.4, may “trigger inflammation in cardiac muscle and cause conduction abnormalities“. There was however no indication that they tested for these antibodies in their own subject; the case report therefore has a few ‘asystolic gaps‘ of its own that make the accolade of “first ever case of” perhaps a tad too premature. But the paper rightly emphasises the definite links between myasthenia gravis and the heart…along with generating a catchy headline.

Inferior-lateral MI> Popfossa on Flickr. https://www.flickr.com/photos/popfossa/3992534762

When Does a Heap Become a Heap?

If this sounds like one of those philosophical paradoxes that turn logic on its head, well it is, and it does. This headline is the title of an editorial published in 2021 in the journal Multiple Sclerosis, and at its heart is the philosophical conundrum of how many grains of sand must be added to other grains of sand to make a heap. This metaphysical rumination is however not an exercise in futility because the author of the editorial has a neurological corollary in mind: at what point does relapsing remitting multiple sclerosis (RRMS) transition into secondary progressive multiple sclerosis (SPMS). And an extension of this puzzle is, how can two disorders be considered distinct entities if there is a “continuum of states” between them? This is a practical problem neurologists face all the time, especially when they have to determine whether and when to discontinue disease modifying therapy in people with RRMS. To complicate matters further, the paper which the editorial was commenting on had shown that, compared to a data-driven algorithm (DDA), neurologists are not that good at recognising SPMS; the study had reported that neurologists make the diagnosis of SPMS in much younger patients with less disability, then the DDA diagnosis. After picking apart these observations, the editorialist reassuringly concluded that neurologists and algorithm at least agree that disease modifying therapies slow down the rate of progression to SPMS. That’s uncontroversial enough.

Pile of sand. Demmer S on Flickr. https://www.flickr.com/photos/kre8ivps/8055350928

To Bee or Not To Bee

This headline which alludes to the contemplations of the murderous Hamlet, refers to an equally unorthodox subject – bee venom acupuncture. The idea of using a venom as a therapeutic agent also stands in stark contrast to the fact that Hamlet died from a poisoned knife. It is therefore most helpful that the article from which the headline above is sourced explores the logic, the efficacy, and the downsides of using a toxic substance as a panacea. The article, published in 2018 in the journal Toxicon, has the full title, “To bee or not to bee: the potential efficacy and safety of bee venom acupuncture in humans“. Perhaps the most enlightening information in the paper is the range of disorders that are amenable to treatment with bee venom acupuncture – including, of interest to neurology, peripheral neuropathy and Parkinson’s disease. And why does bee venom work? The secret seems to be in the anti-inflammatory substances it contains. The authors however pointed out that bee venom is dangerous (as if we needed reminding of that), and they noted that it may result in anaphylactic reaction and potential death. They therefore advocated a strategy of “refining bee venom to remove harmful substances that may potentially limit its toxicity“. That will be a good start.

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Peppering the Pons

One of the prominent disorders that neurologists associate with pepper is CLIPPERS, the neuro-inflammatory disorder whose acronym stands for chronic lymphocytic inflammation with pontine perivascular enhancement responsive to steroids. A descriptive name no doubt, even if it is a bit of a mouthful. The unique thing about CLIPPERS is its radiological appearance – minuscule lesions in the pons which display a salt and pepper pattern of enhancement or brightening up on MRI scans when a contrast dye is injected. But, as with almost all things neurological, no clinical or radiological feature is the sole province of any disease, and the paper from which the headline above comes from illustrates this graphically with its full title, “Peppering the pons”: CLIPPERS or myelin oligodendrocyte glycoprotein associated disease?“. And to prove its point that CLIPPERS has no monopoly over pepper (or any other spice for that matter), the paper, published in 2021 in the journal Multiple Sclerosis and Related Disorders, presents three cases of anti MOG antibody disease with radiological features that would pass for CLIPPERS. The authors of the paper therefore sagely advised that “when CLIPPERS is observed, it is crucial to test for mimickers“. Wise and savoury words.

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Laughter isn’t Always the Best Medicine

This headline is not only a targeted attack on the popular aphorism that mirth is better than medicines, it is also a creative strategy of ensuring that those who frivolously inhale nitrous oxide (N2O) are not left in real stitches. The headline is the full title of an editorial published in 2018 in the British Medical Journal, and the editorialist was warning that the recreational use of nitrous oxide was becoming “an emerging public health problem“. The author pointed out that, whilst the the immediate effect of inhaling nitrous oxide is relatively innocuous – “a short lived, rapid onset euphoria and a dissociative effect“, what follows in anything but benign: from dizziness, vomiting, and fainting, to asphyxia, megaloblastic aneamia, and peripheral neuropathy. And as if those are not enough, the cherry on top is the dreaded subacute combined degeneration of the spinal cord. Laughter is still probably the best medicine, but it is far merrier when dispensed by a competent anaesthetist…or a professional comedian.

Laughing Men. Per Olsen on Flickr. https://www.flickr.com/photos/polesen/4879085978

The Neurologist’s Troponin?

Serum troponin is perhaps the best-known disease biomarker in medicine, on the ready at the slightest cardiac perturbation to rapidly confirm or exclude the presence of heart muscle damage. A positive troponin test triggers aggressive life-saving interventions, and a negative test is a source of huge sighs of relief all round. Neurologists, ever-envious of cardiologists in this regard, have been fighting to get out of the wilderness and into the limelight of biomarkers. And this headline suggests that their dreams are starting to come true. Published in 2020 in the journal Biomedicines, the full title of the paper lets the cat out of the bag: “Blood neurofilament light chain: the neurologist’s troponin?” The rhetorical question mark at the end of the title is however an indicator that neurofilament light protein is still falling short of the mark; the authors of the paper made the disturbing observation that, unlike the disease-specific troponin, neurofilament light protein is elevated in almost any disorder that causes neuronal damage – from ischaemia to inflammation. They therefore dropped the dampener that neurofilament light protein will make for a very poor diagnostic marker. But they however reassure the neurologist, emerald green with envy by now, that neurofilament will have a place in the monitoring of the progression of disorders such as multiple sclerosis. I however doubt that this will go far enough to console the broken-hearted neurologist.

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In the Air

No, Phil Collins and John Paul Young, this headline is not about your love songs at all. Rather, it is a call to recognise the risks posed by pollutants circulating in the air we breathe every day. The headline comes from a paper published in 2019 in the journal Revue Neurologique (Paris), and its full title is “Air pollution and stroke. A new modifiable risk factor is in the air“. The authors describe the paper as a “narrative literature review” which sets out how air pollution has emerged as a “silent killer” by virtue (or is it by vice) of its potential to trigger stroke. After reviewing 21 relevant studies, the authors concluded that air pollution now “contributes to about one-third of the global burden of stroke”. They also explored the “biological mechanisms” by which air pollution has become such a major modifiable stroke risk factor. This headline is therefore a warning against the dangers of the small particulate matter which are blowing in the wind (no Bob Dylan, this has nothing to do with you either).

Air pollution in the City. 君勇 林 on Flickr. https://www.flickr.com/photos/cslmedia888/22029186835

A Cup of Coffee a Day Keeps the Dyskinesia Away?

Now, this is a headline to gladden the heart of every coffee addict out there, whether or not they suffer from dyskinesias. It is the title of an editorial published in 2013 in the journal Movement Disorders, and it is itself a commentary on a study published in the same journal which had reported that people with Parkinson’s disease who consumed more than 12 ounces of coffee a day were significantly less likely to develop dyskinesias than those who drank less the 4 ounces a day (sorry, but some are still very traditionally pounds and ounces). The editorial writer was however rather sceptical of this beneficial effect of caffeine, and this is reflected in the question mark at the end of the title. He was particularly doubtful that caffeine has dyskinesia-alleviating qualities, or that this works via the mechanism the authors of the study had proposed – the A2a adenosine receptor pathway. He also picked holes in the study’s methodology, noting the relatively small number of subjects, and the limited duration of the trial. Sorry coffee lovers, it is not yet Utopia.

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