Association between idiopathic intracranial hypertension and risk of cardiovascular diseases in women in the United Kingdom. Adderley NJ, Subramanian A, Nirantharakumar K, et al. JAMA Neurol 2019 (Epub ahead of print). Abstract BACKGROUND: Cardiovascular disease (CVD) risk has not been previously evaluated in a large matched cohort study in idiopathic intracranial hypertension (IIH). OBJECTIVES: To […]
Hand posture as localizing sign in adult focal epileptic seizures. Ferando I, Soss JR, Elder C, et al. Ann Neurol 2019; 86:793-800. Abstract OBJECTIVE: The aim of this study was to identify specific ictal hand postures (HPs) as localizing signs of the epileptogenic zone (EZ) in patients with frontal or temporal lobe epilepsy. METHODS: In this study, we retrospectively […]
It’s that time of the year again… When we look back and reflect… Over how many visitors took a peek… And what most piqued their interest. *** >10,000 people visited our blog in 2019… They viewed >300 abstracts… Of which >70 were freshly minted in 2019. *** Our visitors favoured some abstracts over others, So we […]
The brain is the most enigmatic structure in the universe. But every now and then, the brain malfunctions. And just like Humpty Dumpty, we struggle to put it back together again…at least not to its previous level of complex organisation. But we are remarkably ingenious creatures, obviously because we possess great brains, and we are ever-inventing brilliant schemes to fix the brain (or at least our brains are). And we, or our brains, often conjure up unthinkable technologies (pardon the intended pun!) Over the years this blog has tried to keep up with these improbable schemes, and you can check the veracity of this claim by looking up two of my very old blog posts on this:
But the developments keep rolling in, so here are 7 remarkable technologies shaping the future of the brain.
What if you could just replace your damaged nerves with spare neurones-just as you would replace a faulty spark plug in your car (OK, wrong analogy for many people I know). Well, this may not be a fantasy for too long. This comes from a piece in Popular Science titled Artificial neurones could replace some real ones in your brain. The article says “Swedish researchers have developed a synthetic neuron that is able to communicate chemically with organic neurones, which could change the neural pathways and better treat neurological disorders”. This is just understandable enough for most people and I will go no further. But if you desire the hard science version, with references to biomimetic neurones, (or is it neurons?), you may check out the original study in the journal Biosensors and Bioelectronics ; it does come with a slightly shorter and less convoluted, but totally undecipherable title, An organic electronic biomimetic neuron enables auto-regulated neuromodulation. I will stick to the Popular Science version.
One major disorder everyone fears is dementia. The concept of forgetting, not just your experiences but family, friends, and eventually yourself, is frightening. But what if you could rely on an electronic memory. A start in this direction was a report that researchers have built a nano memory cell that mimics the way humans lay down memory. At 10,000 sizes smaller than a human hair, such an external memory will surely prove useful. But just take a breath and imagine what it will be like to be incapable of forgetting! Solomon Shereshevsky on my mind. Some way to go yet. This story is sourced from the website Mashable but the research itself is published in the journal Advanced Functional Materials with the, again, cryptic title Donor‐induced performance tuning of amorphous SrTiO3 memristive nanodevices: multistate resistive switching and mechanical tunability. Stick to the translated version in Mashable.
Most people do not want extraordinary memories and would just want to access the ones they have laid down. Some of these are however buried so deep in the crypts of their brains, they have become inaccessible. Again, technology may have something to promise them. And this comes in the form of a memory boosting brain implant. This device, developed by US Defence scientists, can detect how we retrieve memory, and predict when this will fail, and kick in to action to save the day. A sort of brain pacemaker you may say. The potential benefit is in head injury, but we can all do with a little help every now and then, when the ‘uhms’ and the ‘aahs’ kick in. This piece comes from Science Alert but the original article is on the website of the Defence Advanced Research Project Agency (DARPA), and it is titled Targeted Electrical Stimulation of the Brain Shows Promise as a Memory Aid. Not a bad one this time.
Another technology promising to help memory is neural prosthetics. These serve to directly send our short-term memories into long-term storage, bypassing the hippocampus when it is too defective to do the job properly. This comes from a piece in Science Daily titled Scientists to bypass brain damage by re-encoding memories. What the prosthesis does is “to bypass a damaged hippocampal section and provide the next region with the correctly translated memory”. In effect it will make the hippocampus redundant. I’m sure the hippocampus does other things apart from encode memories… but we don’t want to think of that now.
Imagine being able to move a robotic limb by just thinking about it. No, not telepathy, but with your brain wired to the limb. This is what a prosthetic technology promises for people with brain damage who are unable to move. The prosthetic is implanted in the part of the brain that initiates our intention to move. The source for this story comes from USC News, and it is titled Neural prosthetic device yields fluid motions by robotic arm. In the example cited in the piece, the surgeons “implanted a pair of small electrode arrays in two parts of the posterior parietal cortex-one that controls reach and another that controls grasp“. You have to see the robotic arm in action. Sci-fi is becoming reality in a brain lab near you soon.
Behavioural remote control
Press a button and alter behaviour. Exciting and scary at the same time. But this is what chemogenetics promises, or threatens, depending on your point of view. This one comes from a piece on the website Neuroscience News titled Chemogenetics technique turns mouse behaviour on and off. The technique “achieves remote control by introducing a synthetic brain chemical messenger system that integrates with the workings of naturally-occurring systems”. ‘Integrate’ feels a tad extreme, almost like being assimilated by the Borg. But I suppose it will be no worse than the antipsychotics and sedatives we currently use to control the behaviour of people with schizophrenia and addictive disorders. It surely looks like it has potential, at least in mice for now.
This technology goes beyond just increasing the ability to preserve or retrieve memory. It sets out to make the brain smarter. This piece comes from The Atlantic and is titled Why cognitive enhancement is in your future (and your past). The technology is transcranial direct current stimulation (TDCS) of the deeper reaches of the brain, using electrodes to send small and painless electrical currents. The currents are thought to increase neuroplasticity, and this enables neurons (or perhaps neurones?) to form the connections necessary for learning.
It is mind-boggling enough just thinking that people out there are thinking of stuff like these! But it is equally reassuring that the future of the brain is bright.
Neurochecklists is continuously pushing the limits. This is why it remains comprehensive and topical Why not confirm this for yourself. Below are just 12 completely new checklists. *** Cannabidiol (CBD) Visual snow syndrome Cryptogenic stroke Insular seizures Decompression sickness Hereditary haemochromatosis Essential thrombocythemia Topographical disorientation SYNGAP1 epileptic encephalopathy Neuroparacoccidiodomycosis Gadolinium contrast enhancement patterns Neuronal intranuclear […]
Randomized, controlled crossover study of IVIg for demyelinating polyneuropathy and diabetes. Breiner A, Tapia CB, Lovblom LE, Perkins BA, Katzberg HD, Bril V. Neurol Neuroimmunol Neuroinflamm 2019 (Epub ahead of print). Abstract Objective: To determine whether IV immunoglobulin (IVIg) is more effective than placebo at reducing disability in patients with diabetes and demyelinating polyneuropathy features. […]
In medicine, microbes are notorious for causing disease. In neurology particularly, infection is the direct cause of serious diseases such as meningitis and encephalitis. Infections may also act as catalysts for neurological disorders, for example when they trigger Guillain Barre syndrome (GBS). Infection is therefore a villain, a scoundrel to be apprehended and disarmed whenever it rears its head. But this picture may not hold true when it comes to multiple sclerosis (MS) where a contrary story is emerging, a narrative which holds infection as the hero, the daredevil that will save the day. The premise is simple: MS has very little presence in the regions of the world where infections reign supreme. Just look at any world prevalence map of MS to be convinced.
How strong is this inverse relationship between infection and MS? It all boils down to the so-called hygeine hypothesis of autoimmune diseases. This suggests that the human immune system becomes dysregulated when it is not primed by infections, and this dysregulation results in autoimmune disorders. This point was strongly argued by Aakanksha Dixit and colleagues in their paper published in the International Journal of Molecular Science, titled Novel Therapeutics for Multiple Sclerosis Designed by Parasitic Worms. They contend that the relationship between parasitic infections and autoimmune diseases is “most compelling“, going on to assert that helminthic infections “may be the protective environmental factor against the development of MS”.
To support the hygiene theory of MS, that helminthic infections play a role in banishing MS, three levels of evidence are offered.
- The prevalence of MS steadily increases when the frequency of infections in a community is reduces.
- People with MS who also have helminthic infections have fewer relapses and slower disease progression.
- MS patients who are treated for their helminthic infections develop more relapses and have a more active disease course.
Toxoplasma gondii, the cause of toxoplasmosis, is perhaps the major parasite investigated in relation to MS. Asli Koskderelioglu and colleagues, for example, reported that exposure to T.gondii is less frequent in people with MS than in healthy control subjects. In their 2017 paper titled Is Toxoplasma gondii infection protective against multiple sclerosis risk?, published in Multiple Sclerosis and Related Disorders, they found that MS subjects who have higher toxoplasma antibody levels experience fewer relapses and less severe disease courses. This finding is corroborated by a 2015 paper in the Journal of Neuroimmunology titled Toxoplasma gondii seropositivity is negatively associated with multiple sclerosis.
Neurologists are however very cynical people, and they never believe what single trials tell them. After all, many microbes, such as Ebstein Barr virus (EBV), are touted as MS risk factors. For the sceptical neurologist, only systematic reviews and meta-analyses will do; these are the stuff of our dreams, the essence of our daily existence. So it is with a huge cheer that neurologists welcomed a 2018 systematic review and meta-analysis published in the Journal of Neuroimmunology and titled Is toxoplasma gondii playing a positive role in multiple sclerosis risk? The paper poured very cold water on the beautiful hygiene hypothesis. Whilst the authors, Reza Saberi and colleagues, confirmed that MS subjects had a lower risk of exposure to T. gondii, they found no relationship between this parasite and the development of MS. Wither a theory when it hits the reality of cold statistical analysis.
Notwithstanding the systematic review, the helminth hypothesis marches on. It has even reached the stage of therapeutic trials where, as distasteful as it sounds, subjects ingest parasites by mouth! And the fancied parasite is not Toxoplasma gondii but Trichuris suis ova (TSO). It all began with a small observational trial in 10 people which proved that TSO is safe and well-tolerated (phew), but it had no value whatsoever in treating MS. Not discouraged, the hypothesis entered the slightly larger HINT 2 trial; this again confirmed good tolerability in 16 subjects, but any benefit in reversing MS was questionable. Undeterred, the hypothesis has gone for a bigger study in the form of the TRIOMS trial. This is a randomized, placebo-controlled study of 50 people with MS or clinically isolated syndrome (CIS) in which subjects will be ingesting 2,500 Trichuris suis eggs every two weeks. We wait with bated breaths for the results.
Before leaving this subject, we must know that helminths are not the only game in town; they have strong competition from their cousins, bacteria. And the standout character in this arena is Helicobacter pylori. We learnt this from a study published in 2015 in the Journal of Neurology Neurosurgery and Psychiatry. Titled Helicobacter pylori infection as a protective factor against multiple sclerosis risk in females, the paper reported that people with MS were less likely than controls to have been exposed to H. pylori. Two meta-analyses have also reviewed the relationship of H. pylori and MS, arguing strongly that, in Western countries, there is an inverse relationship between H pylori and MS. And they assert that H. pylori may be protective against MS. If it feels like déjà vu, it is.
We have surely not heard the last of bugs and MS. However, for now, the foundations of the hygiene theory are a bit shaky, and the future rather hazy.