The Teenage Brain – Charlie Delilkan

We’ve all been there. “I’m leaving home and I’m never coming back!” “It’s not just a phase, Mum.” Slammed doors. Smashed plates. My Chemical Romance t-shirts and “bold” eyeliner. If you haven’t guessed already, I’m referring to those golden teenage years. Whilst we may have given our parents a hard time, we may not be completely responsible for that increased phone bill.

When we’re born, our brains aren’t fully formed so the first few years of our existence involve an expansion of connections – synapses – between cells. Approximately 10,000 different connections are made between the hundred billion brain cells you were born with by the time you are six-years-old!

But during our teenage years, these numerous connections are trimmed down; the brain decides which connections are important enough to keep, and which can be let go, depending on how frequently each neural link is used. This process is called synaptic pruning. This process actually continues well after we stop calling people “teenagers” – some researchers believe this only ceases in our mid twenties, sometimes later! But sometimes this process can go wrong, leading to important connections being lost which could lead to psychiatric disorders such as schizophrenia.

The synapses that are kept are then subjected to a process called myelination, where the synapse is given a sheath that helps them transmit signals more quickly. That is why the teenage years are so critical to your future development! Skills and habits laid down at this point are likely to stay in the long run.

Interestingly, the prefrontal cortex is the last part of the brain to fully mature (or finish pruning). However, this is the part that allows us to be an adult – it controls our emotions and helps us to empathise with others. Therefore, if your prefrontal cortex isn’t functioning fully, you tend to be impulsive and insensitive to other people’s feelings. Sound familiar? Don’t worry though – as teenagers mature, the prefrontal cortex is used a lot more when making decisions, showing that they start to consider others when making choices.

What about that stereotype that teenagers are “hormonal”? Well stereotypes usually come from some truth! Teenagers are hypersensitive to pleasure; rewards such as the neurotransmitter dopamine release is at its peak during adolescence. Any action that causes dopamine release is positively reinforced, but the actions that cause the most dopamine release are usually associated with a stereotypical teenager – reckless driving, drug taking, and/or risk taking. Or in my case, 7 hours of dungeons and dragons on a Friday night – please don’t judge. This reward system is also closely harmonious with the brain’s social network, which uses oxytocin, a neurotransmitter that strengthens bonding between mammals. This causes teenagers to strongly associate social interactions with happiness  and so constantly seek out social situations. This explains why we usually see a dynamic shift from kids being close to parents to teenagers having friends being their emotional centres.

So the next time the teenager in your life is threatening to throw a chair at you, just remember that parts of their brain are literally being destroyed. Cut them some slack, bro.

What Causes Alzheimer’s? Emma Pallen

Alzheimer’s disease is a chronic neurodegenerative disorder with a wide range of emotional, behavioural, and cognitive symptoms. It is the most common cause of dementia, causing around 60-70% of dementias and is primarily associated with older age, with around 6% of the global population over 65 being affected and risk increasing with age. This is especially concerning considering our ageing population and, by 2040, it is expected that there will be 81.1 million people suffering with Alzheimer’s worldwide. It is also one of the costliest conditions to society, costing the US $259 billion in 2017.

Symptoms of Alzheimer’s can be grouped into three categories. Perhaps the most recognisable category is cognitive dysfunction, which includes symptoms such as memory loss, difficulties with language, and executive dysfunction. Another category of Alzheimer’s symptoms is known as disruption to activities of daily living (ADLs). Initially this can be difficulty performing complex tasks such as driving and shopping, later developing to needing assistance with basic tasks such as dressing oneself and eating. A third category of AD symptoms are related to emotional and behavioural disturbances. This can range from depression and agitation in earlier stages of the disease to hallucinations and delusions as the disease progresses.

What causes Alzheimer’s Disease?

We know that the symptoms of Alzheimer’s are caused by a gross loss of brain volume, also known as atrophy, in a number of regions that progress as the disease develops. As brain tissue is lost, symptoms associated with the function of the lost area emerge, such as personality changes developing as tissue is lost in the prefrontal cortex.

We also know that this brain atrophy is caused by a loss of neurons and synapses in the brain. However, what we don’t know is exactly why this neuronal loss occurs. One way to attempt to solve this question is to compare the brains of Alzheimer’s patients to normally ageing brains. This has led to the observation that the brains of Alzheimer’s patients have two distinct biochemical markers: amyloid plaques and neurofibrillary tangles, which are both abnormal bundles of proteins. While these features are often present to some degree in normal ageing and are not always observed in Alzheimer’s, they are often more associated with specific brain regions, such as the temporal lobe, in Alzheimer’s than in regular ageing. There are a number of theories as to how these biochemical markers may be linked to neuronal and synaptic loss, however none are fully conclusive.

One such theory is the amyloid cascade hypothesis. This hypothesis suggests that amyloid plaques, which are made up of a protein known as amyloid beta, are the primary cause of the disease and that all other pathological features of Alzheimer’s are as a consequence. This theory suggests that the accumulation of amyloid beta into plaques leads to disrupted calcium homeostasis in the cells, which can lead to excitotoxicity and ultimately cell death. Evidence in support of this theory comes from the fact that Down’s Syndrome, a condition in which almost all sufferers display some degree of Alzheimer’s disease by age 40, is associated with a mutation on chromosome 21 which is also the location for the gene coding for Amyloid Precursor Protein (APP), a precursor protein that leads to the formation of amyloid beta.

However, if the buildup of amyloid plaques are the cause of cell death in Alzheimer’s disease, it stands to reason that the removal of these plaques should at the very least stop the progression of the disease, which has not been found to be the case. Furthermore, whilst APP producing transgenic mice do end up having more amyloid beta and amyloid plaques, this does not lead to other features of the disease such as neurofibrillary tangles and most importantly, no neuronal loss. This suggests that there may be some other cause for the neuronal loss seen in Alzheimer’s.

Another theory about the cause of neuronal loss in Alzheimer’s focuses on hyperphosphorylated tau, a protein that is the main component of neurofibrillary tangles. The tau hypothesis suggests that the hyperphosphorylation of tau leads to the formation of these neurofibrillary tangles which can result in depleted axonal transport, a potential cause of cell death. This idea is supported by the fact that the number of neurofibrillary tangles is linked to the degree of observed cognitive impairment. Additionally the progression of where tangles are found is similar to the known progression of atrophy observed in Alzheimer’s. Dysfunction of tau is also known to be linked to another type of dementia, frontotemporal dementia, so it seems plausible that similar mechanisms may be at work in Alzheimer’s.

Whilst these are the two of the most prominent explanations for neuronal death in Alzheimer’s, there are a multitude of other potential explanations, and it is likely that no single explanation will capture all facets of the disease. Rather, it is more likely that there is a complex interplay of biochemical reactions along multiple pathways that lead to the clinical features we see in Alzheimer’s disease. These are likely affected by many other risk factors, such as genetics, or environmental factors such as smoking or head trauma.

A, T, C, G… and more? Adding Letters to Life’s Genetic Code – Alex Marks

Scientists have created bacteria that carries two extra synthetic ‘letters’ of the genetic code.

The genetic code is made from four bases, more commonly known as the ‘letters’, A, T, C and G. It is the order of these ‘letters’ that create the genetic blueprint for all life: DNA. Scientists have modified the bacteria, E. coli, so that it can carry two unnatural ‘letters’ in its DNA.

By adding the extra two ‘letters’, which are named X and Y, scientists have increased the number of combinations that the ‘letters’ could make. These additional combinations could potentially increase the number of biological functions this bacterium could do. The international team of scientists hope that this can lead to the creation of new classes of drugs to treat diseases.

In a standard cell, the four ‘letters’ of the genetic code tell the cell how to make proteins. Proteins are responsible for almost every function and structure within a cell. They repair and maintain the cell; they transport atoms and small molecules; and they make up an important part of your immune system.

By expanding the genetic alphabet from four to six ‘letters’ the potential number of proteins that could be synthesised dramatically increases, allowing for semisynthetic organisms that have new qualities not found anywhere in nature.

It had already been shown that semisynthetic organisms could be created. However, the ones that had been made were slow to replicate and regularly lost their unnatural ‘letters’. The new study has “made this semisynthetic organism more life-like,” according to Prof Romesberg, senior author of the study.

By modifying the existing version of the genetic ‘letter’ Y, the team created a semisynthetic organism that could hold on to the unnatural ‘letters’ X and Y for 60 generations. The scientists believe that the bacterium will keep the letters indefinitely.  Making the DNA is still stable, even with the extra ‘letters’ in it.

“Your genome isn’t just stable for a day,” said Prof Romesberg. “Your genome has to be stable for the scale of your lifetime. If the semisynthetic organism is going to really be an organism, it has to be able to stably maintain that information.”

They managed to make the DNA stable by destroying the bacteria that lost the unnatural ‘letters’. Using CRISPR-Cas9 genome editing tool, the scientist could check the bacteria to see if they had retained X and Y. This tool can read specific parts of the DNA and can also add tags. If the bacteria had not kept X and Y, CRISPR-Cas9 marked them for destruction.

By destroying the unstable bacteria, only the stable bacteria could go on and replicate. By doing this, the scientist’s increased the chance that the replicated bacteria was stable.

“This science suggests that all of life’s processes can be subject to manipulation.” Said Prof Romesberg.

Being able to manipulate processes within cells will help us understand these processes and might be able to help cure diseases.

Natural Cycles – Rhiannon Lyon

Contraception can be a pain. From the long list of side-effects associated with hormonal pills, to the painful and invasive nature of implants and IUDs, women put up with a lot to avoid getting pregnant. And with the search for a male contraceptive pill that lacks undesirable side-effects (the type that women have put up with for decades) still unfruitful, things look set to stay this way for a while.

Or do they? As the first and only app to become certified as a contraceptive in Europe, Natural Cycles promises a hormone-free, non-invasive alternative to traditional forms of birth control.

Natural Cycles was developed by physicist Dr Elina Berglund, who works at CERN and was part of the team responsible for confirming the existence of the Higgs boson.  The app started out as an algorithm Berglund developed after deciding to stop taking hormonal contraceptives. She started looking into the biology of the menstrual cycle and found that ovulation can be accurately predicted by small changes in body temperature, and this data can be used to calculate when an individual is and is not fertile. Berglund began to monitor her own cycle using the algorithm, along with some of her colleagues at CERN. This ended up working so well that her Berglund and her husband decided to develop the algorithm into an app, so that more people could benefit from it. The latest study shows that the app is 99% effective when used perfectly, or 93% effective with typical use (for comparison, the pill is 91% effective with typical use).

So how does a simple fertility awareness method manage to have such success in preventing pregnancy? To answer this, we first need to understand a bit of the biology of the menstrual cycle.

nat cycles graphPhoto source: https://www.naturalcycles.com/en/science/menstrual-cycle

The menstrual cycle can be roughly divided into three stages: the follicular (pre-ovulatory) phase, ovulation, and the luteal (post-ovulatory) phase. The levels of the hormones oestrogen, progesterone and LH vary over these stages, as shown in the diagram above, with the body’s basal body temperature (temperature at rest) changing as a result of these different levels. This is how Natural Cycles detects where the user is in their menstrual cycle: a temperature taken each morning with a two decimal place thermometer.

During the follicular phase oestrogen levels are high, and progesterone levels low, leading to a lower body temperature. At the end of the follicular phase is the fertile window. This is approximately six days long – starting five days before ovulation occurs. This is because sperm can survive in the uterus and fallopian tubes for up to five days waiting for an egg to fertilise.

At ovulation an egg is released by one of the ovaries, and travels through the fallopian tube, where it can be fertilised if it encounters a sperm (which could have been hanging around in the tube for several days).

After ovulation the luteal phase starts. Progesterone levels increase in order to aid the foetus’s development if fertilisation has occurred. The rise in progesterone causes the basal body temperature to go up an average of 0.3°C. If fertilisation has not occurred the progesterone levels then fall again, and the uterine wall begins to shed with the beginning of menstruation, which starts a new cycle.

From this we can see that there is actually only a window of around 6 days each cycle where fertilisation could actually occur, on all the other days of the cycle intercourse will not result in a pregnancy. The Natural Cycles app uses this logic to assign ‘red’ and ‘green’ days – those on which you do and do not need to use protection, respectively. Of course an app that accurately tracks fertility can also be used to increase chances of pregnancy, and around 20% of Natural Cycles users are in fact using it to aid in becoming pregnant.

However, the app may not be for everyone. Success depends on users strictly abstaining or using barrier protection such as condoms on red days, and making sure to take their temperature each morning, having had a decent amount of sleep (as sleep deprivation can cause fluctuations in the basal body temperature). Those who have irregular menstrual cycles, such as people with PCOS (polycystic ovarian syndrome), which affects around 10% of women, may not benefit so much from Natural Cycles, as the algorithm is likely to give them many more red days per cycle. A subscription to the app also costs around £40 per year, which is pretty pricey considering that all other birth control is free on the NHS (although you do get a thermometer thrown in). Whether that is value for money for a side-effect-free form of contraception is down to the individual.

 

Sources:

https://www.naturalcycles.com/en

http://nordic.businessinsider.com/birth-control-app-as-effective-as-the-pill-2017-2/

http://www.vogue.co.uk/article/natural-cycles-app-hormone-free-non-intrusive-contraceptive-method

http://www.wired.co.uk/article/natural-cycles-as-effective-as-traditional-contraceptives

https://www.theguardian.com/lifeandstyle/2016/nov/07/natural-cycles-fertility-app-algorithm-replace-pill-contraception

 

Dyslexia: In the eye of the Beholder?

Dyslexia Word Cloud

Bethany Firmin

Dyslexia is a specific learning difficulty (SpLD) affecting between 5-10% of people. The disorder is characterised by difficulties in phonological awareness (this refers to the ability to focus on and manipulate individual sounds in spoken words), verbal memory and verbal processing speed.

As well as difficulties with spelling and reading, there are a broad range of other symptoms – this can include concentration issues, trouble understanding certain jokes/expressions and difficulties with time management. Dyslexia is a broad spectrum, with some individuals experiencing some of the associated difficulties but not others, and with varying levels of severity. While some may have mild dyslexia, which can (personally, I was only diagnosed in my first year of university) be managed, others may always struggle significantly with reading and spelling. Intelligence is not affected.

For someone to be diagnosed with dyslexia, diagnostic tests are carried out, the content of which varies depending on the age of the individual. While these tests are very useful in giving information about an individual’s specific strengths and weaknesses, they can be very time-consuming.

Currently, there is no cure for dyslexia, but there are many strategies to help people, such as alternative exam arrangements and extra tutoring. With adequate support, many people with dyslexia go on to be very successful in life. The importance of early intervention is emphasised.

Dyslexia is widely believed to be a neurological problem, but a recent study suggests they may have found a possible cause of dyslexia – not in the brain, but the eyes!

Photoreceptors in the eye

In the eye, there are two types of photoreceptor (structures that respond to light) – the rod and cone cells. Rod cells, the more plentiful (around 120 million), respond to low levels of light but do not detect colour, which allows you to see in the dark. There is only one type of rod cell, and they are absent from the fovea (the region of the retina responsible for the highest visual acuity) but concentrated elsewhere. Cone cells (6-7 million) are only activated at higher concentrations of light, but detect colour. There are three types of cone cell – blue, red and green. There is a ‘blind spot’ in the fovea of about 0.1-0.15 millimetres, in which there are no blue cone cells.

Eye Dominance and Dyslexia

Similarly to the way in which most people have a dominant hand (apart from those who are ambidextrous), most people have a dominant eye. Both eyes record slightly different versions of the same image, so the brain decides which one is likely to be the most accurate. Signals from this dominant can override signals from the other. Lots more people are right-eyed than left.

This study investigated the presence or absence of eye dominance in 30 non-dyslexic students and 30 dyslexic students, using a method called the afterimage test. For the non-dyslexic participants, 19 were right-eye dominant and 11 were left-eye dominant – therefore, all had a dominant eye. On the other hand, 27/30 of the dyslexic participants had no dominant eye.

Furthermore, there were correlations between lack of eye dominant and apparent physical differences in eye. In the dominant eye, the shape of the blind spot is circular, while the shape in the non-dominant eye is elliptical. In the dyslexic participants with no eye dominance, however, the shape was circular in both eyes. For one of these participants, five family members who also had dyslexia were studied – there was no asymmetry in the arrangement of cone cells, as well as no eye dominance. This suggests a possible genetic cause of dyslexia, and could lead to new diagnostic strategies for dyslexia

Lack of asymmetry would mean the brain has to process two slightly different ‘mirror images’, which researchers believe would confuse the brain. Perhaps this could explain why dyslexic people commonly make ‘mirror image errors’ – for example, mistaking ‘b’ and ‘d’, or ‘3’ and ‘E’ – and often get confused between left and right.

So, what else does this study mean for dyslexic people? Firstly, lack of afterimage dominance could lead to a potential new, quicker way to diagnose the condition. In addition, researchers were able to use an LED lamp to “cancel” one of the images in the brains of the dyslexic participants, which reduced reading difficulty. Some participants referred to this as the “magic lamp”.

Considerations & Limitations

While this study seems very promising, it is important to remember that only 30 dyslexic participants were studied – this sample size is too small to draw any absolute conclusions. Also, all participants were students, so these would not have been representative of the whole dyslexic population.

A further problem is that the study cannot establish cause-effect relationships. It cannot be said whether the visual differences are the trigger of dyslexia, or simply a consequence.

As well as that, the findings from the study may explain some people’s dyslexia symptoms, but may not necessarily explain the symptoms of other people. As mentioned before, dyslexia has many symptoms and manifestations, which this study does not necessarily explain. For me, I don’t experience ‘mirror image’ distortions when reading, but the words sometimes start to go wobbly after I’ve been reading for a while. There are a range of other distortions experienced by other dyslexic people too, such size distortions of letters/words or gaps between words appearing narrower/wider.

In conclusion, while the study seems promising, significantly more work is needed before any proper conclusions about the cause of dyslexia can be drawn.

Using Cancer to treat Diabetes? Sort of…

Vanessa Kam

Tumour.  The word immediately summons negative connotations, embedded in the general fear surrounding cancer and impounded by the Daily Mail’s endless crusade to classify everything into cancer causes or cures.

While ‘tumour’ is often used as a synonym for ‘cancer’, in science, the two are not quite the same.  ‘Tumour’ is derived from the Latin word for ‘swelling’, and originally referred to any swelling, like a pooling of fluid in inflammation.  Nowadays it is used to refer to ‘neoplasms’ which form a mass, an abnormal growth of cells appearing bigger in size.  These masses can be benign, sticking to one location and easier to treat, or malignant, invading into other tissues and spreading around the body.  Cancer, derived from the Latin word for crab, refers to the malignant tumours, which extend out from their original site like a crab’s legs from its body.

 

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(Cancer Cells:  Image source: National Cancer Institute)

Now that it’s clear benign tumours are not cancerous, we move on to a diabetes discovery, lest getting tied down by etymology.

In a study published in October, researchers at the Icahn School of Medicine at Mount Sinai, New York, harnessed critical information from the genomes and expression patterns of insulinoma cells.

Insulinomas are rare, small, benign tumours of pancreatic beta cells.  The pancreas is a pivotal organ in regulating blood sugar, and its beta cells secrete insulin to capture excess glucose from the bloodstream for storage.

In diabetes, beta cells are either destroyed by the patient’s own immune system (type I) or cease to function, with type II diabetes seeing a reduction in working beta cell numbers, often alongside insulin resistance.  Much work has been invested into inducing beta cells from stem cells to transplant into patients with type I diabetes, effectively replacing the destroyed cells, but what about inducing beta cells to regenerate in situ?

This is notoriously difficult, in part due to the normal development of beta cells.  Beta cell proliferation occurs shortly after birth, continues for about a year, then rapidly declines in early childhood.  In adults, the increase in beta cells is virtually zero, bad news for diabetics.  Even at its highest rate, beta cell proliferation is relatively low, with about 2% of cells dividing versus up to 50% in other cell types.  With normal proliferation rates so low in later life, there’s a particularly high barrier to promoting regeneration in adult beta cells.

This is where insulinoma comes in.  In insulinomas, beta cells proliferate.  While this generates tumours which overproduce insulin, causing patients to display symptoms of low blood sugar, identifying the mechanisms by which insulinoma cells overcome division dormancy can be applied therapeutically to diabetics, re-expanding their beta cell populations.

In fact many cancers are undergoing genomic scrutiny under various projects, including the Cancer Genome Atlas and the International Cancer Genome Consortium.  But seeing as insulinoma has a low incidence rate of two in every one million people worldwide and is largely benign—only 10% is cancerous,—insulinoma slipped through the net.

Until now.  Wang and his team at Icahn conducted whole exome sequencing and RNA sequencing on 38 benign human insulinoma samples, analysing the DNA sequence for all the protein-coding genes (exons) in the cells and the transcriptome, the variable, actively expressed portion of exons in those particular cells at that specific point in time, comparing them to normal beta cells.

They found insulinomas to display mutations and differing expression of epigenetic modifying genes—genes coding for proteins which alter the expression of other genes without changing their DNA sequence—and their targets.

One such example is a new potential drug target KDM6A.  KDM6A supports the cell cycle inhibitor CDK1NC, a protein only expressed in pancreatic beta cells and prompts their inability to divide.  CDK1NC is reduced in insulinoma, and allows beta cell proliferation when turned off.

KDM6A was mutated in several insulinoma samples in this study, prompting the team to interfere with it by inhibition using both a drug and a virus.  This resulted in lower levels of CDK1NC, which will allow beta cells to re-enter the cell cycle and proliferate, exciting news for diabetes therapy.  Future work screening for molecules which inhibit KDM6A may identify drugs promoting beta cell regeneration.

In fact, this study reaffirmed the presence of targets of a novel drug another team at Mount Sinai identified.  In 2015, after screening through 100,000 compounds, only one, harmine, was found to drive human beta cell replication in culture.  This was unheard of, with all previous attempts seeing beta cells resist pushes to multiply.

Harmine is derived from the plant harmal, which due to its psychoactive properties, is used in many spiritual rituals, hung around to protect from the ‘evil eye’ in Turkey, for example.  When used to treat mice mimicking human diabetes, harmine tripled beta cell numbers and improved blood sugar control, and is now under early development for diabetes treatment.

However even with harmine, the induced proliferation rates of beta cells are modest.  With new information about beta cell replication gathered from insulinomas, more novel drug targets can be identified and promising compounds highlighted.  This goes to show that studying rare diseases like insulinoma can bring about medical advances for the masses, with beta cell regeneration therapy now an increasing reality for the millions of diabetics worldwide.

Regaining signs of consciousness after 15 years in a vegetative state!

brainscancoma_web_1024

Emma Hazelwood.

A man in France has regained some signs of consciousness after being in a vegetative state for fifteen years.

A vegetative state is defined as the absence of responsiveness and awareness due to brain damage, although some motor reflexes are maintained as normal. The issue of consciousness has baffled humans for centuries – there is no one test to determine whether someone is conscious. Instead, there is a scale known as the Coma Recovery Scale, which looks at various aspects of consciousness (including communication and auditory and visual functions).

The 35-year-old went into a coma after being involved in a car accident in 2001, and had shown no signs of improvement since. That is, until scientists tried a new treatment, involving using electricity to stimulate a nerve in the man’s body, known as the vagus nerve. This nerve runs from the brain to several areas of the body, including areas involved in emotion, alertness and memories. It was thought that after this treatment the patient may be able to regain some consciousness, without the risk of side effects from medication.

Improvements in the subject’s condition could be seen within a month of treatment. At first, this just meant being able to open his eyes more often. His brain showed activity in areas which had previously been quiet, and eventually he was able to follow an object around the room with his eyes, and even respond to requests to turn his head from one side to the other. He reacted with surprise when the examiner’s head suddenly approached his face. Amazingly, he shed tears and could smile with the left side of his face when he was played his favourite music.

According to medical professionals, this is known as a “minimally conscious state” – the man has not fully regained consciousness to the extent he had before the accident, but he is able to show some self and environmental awareness.

Although the test needs to be repeated in other patients, the results have neurologists very excited for future potential treatments involving this technique.

However, this experiment further demonstrates how little we know about consciousness, and brings into question the ethics surrounding treatment of people in vegetative states. Recently, the Court of Protection in England and Wales ruled that if doctors agree it is in the patient’s best interests, families of people in vegetative states no longer need the court’s permission to let their loved one die.

We do not have a perfect way of deciding whether someone is conscious or not. A 2010 study by the New England Journal of Medicine found that 40% of patients who had been assumed to be completely vegetative were actually able to communicate, even if it was just through yes or no questions.

If someone can “wake up” after fifteen years of no environmental awareness, this may complicate the already complex issue of whether it is right to decide to stop artificially feeding people in vegetative states. This could add to the guilt and emotional distress of families trying to decide whether or not to keep their loved one alive through machines, not knowing whether or not they are in pain or will ever wake up; or letting them die, never knowing whether they would have recovered.

The process may also be emotionally distressing for the patient. In this example, doctors have not yet asked the man whether he is in pain. Furthermore, doctors agree that he has such severe brain damage that it is unlikely he will ever be able to walk or talk again – even if he is eventually able to fully regain consciousness. This brings into light concerns around whether it is right to bring back someone who has been unconscious for so long (so many things have changed since he went into a coma in 2001), and to a lower quality of life than before, especially when we do not fully understand the process.

This treatment has been a breakthrough discovery for neurologists, and opens up a new world of possible treatments. However, it is essential that as we discover more about consciousness and how it is regained, we continue to consider the ethical consequences of our actions.