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When the mind can’t visualise



It’s nearly three years since Professor Adam Zeman helped to introduce the world to a new species of brain condition. Yet the letters and emails from people who believe they have aphantasia – an inability to summon images to the mind’s eye – have barely stopped arriving since.

Sack-loads of mail, amounting to some 12,000 reported cases, have built up at his University of Exeter Medical School base.

This is despite there previously being only sporadic published examples from history of people unable to voluntarily picture things in their mind.

Zeman, a professor of cognitive and behavioural neurology, is now investigating various avenues related to the phenomenon, including a possible link to brain injuries and neurological conditions.

“The most common cause for not having a mind’s eye is being born that way, but there are examples in literature describing people losing it through some form of brain injury,” he says.

The first reported case of visual imagery loss due to brain injury was publicised in 1883 (Charcot & Bernard). A much later study (Farah, 1984) concluded that the vividness of self-reported visual imagery can be dimmed by a brain injury.

It can also vary widely among healthy individuals (McKelvie 1995), and be affected 
by depression, anxiety and “depersonalisation”
(Sierra, 2009).

Zeman says: “I’m keen to revisit Farah’s work in particular to assess what is happening in brains that have been damaged in such a way that they can no longer visualise.

“We want to work out whether there
are common areas of the brain or processes affected. We don’t yet know what the proportion of people with brain injuries with aphantasia is, but it would need to be a moderately bad brain injury to either cause focal brain damage or damage to some connections.

“On the other hand, it obviously couldn’t be so severe that the person can’t notice or describe what has happened.”

Studies into mental imagery were pioneered by
Francis Galton who, in 1880, published evidence of a wide variation in subjective vividness among survey respondents; some participants described no power of visualising, he reported.

Over a century later, a study showed that 2.1 to 2.7 per cent of general population participants claimed no visual imagination (Faw, 2009).

Zeman and fellow researchers coined the term aphantasia based on the classical Greek word for imagination, phantasia, defined by Aristotle as the faculty/power by which a phantasm, is presented to us.

In 2010 they reported a particularly pure case of imagery generation disorder
(Zeman et al., 2010). A 65-year-old man had become unable to summon images to his mind’s eye following a coronary angioplasty.

The subsequent paper was picked up by the popular science periodical Discover, prompting people with similar experiences to make contact.

These 21 individuals had a lifelong reduction 
of visual imagery and were analysed via a questionnaire (Zeman, Dewa & Della Sala, 2015).

The results, published in 2015, delivered several interesting findings. While respondents could not visualise when prompted by the questionnaire, most reported that they experienced involuntary imagery.

These usually occurred in dreams or in the form of ‘flashes’ during sleep onset. Most respondents didn’t become aware of their condition until their teens or 20s; it was only 
in conversation or through reading that they’d stumbled upon the fact that most people can visualise in their minds eye.

This new proof of an inability to voluntarily visualise caught the world’s attention and triggered a fresh wave of letters and emails from hundreds, and then thousands, of people with potential aphantasia.

Work is now underway to gain deeper insights into the condition. Questionnaire responses have been elicited from 2,000 more cases, while a separate study involves brain imaging and neuropsychology comparisons between groups with low, moderate and very vivid mind’s eye imagery.

The results of both aspects of the research are expected to be published later this year.

“We have a mountain of data and are trying 
to work out whether aphantasia comes in different shapes and sizes, which we think it
does. It’s associated with problems related to autobiographical memory and, in some cases, with autistic spectrum disorder. So there are lots of subgroups.

“Of course, prosopagnosia [an inability to recognise faces] and autobiographical memory problems can occur through brain injury, and we’ve had around 50 individuals contact us whose aphantasia was seemingly caused by brain injury, stroke or meningitis, and we want to look at them more closely.”

Investigations into the root causes of aphantasia, and how it impacts on individuals, require the factoring in of multiple regions of the brain.

“Visualising involves a network of brain regions. To visualise you have to make a conscious decision to do so. This involves the decision-making regions
in the front and parietal lobes. Visualisation 
also involves memory-related regions if you are visualising something you encountered in the past which is stored in your memory.

“Then you also activate visual areas; we know from functional imaging that people do use visual areas of the brain to visualise.”

While acquired aphantasia may be thought of as a condition, causing various challenges such as facial recognition problems, for people with lifelong aphantasia it is merely considered a different way of experiencing life.

“Lifelong aphantasia is not a disorder. People’s experience may be different from the rest of us but it is not an illness. You can lead a completely normal, fulfilling, productive life without having imagery. If you have a mind’s eye and you lose it, that’s different and it seems natural in that case to call it a disorder.”

Aphantasia may even help, rather than hinder, some people, with a strange correlation existing between a lack of mental imagery and high achievement.

Oliver Sacks, the late neurologist, naturalist
and author whose bestselling case histories on disorders were adapted for the stage, big screen and fine art exhibitions, had no mind’s eye.

Nor does Craig Venter, who pioneered the decoding of the human genome. Famously, Blake Ross, co-creator of the Firefox web browser, had an aphantasia-infused awakening in 2016 and documented it on Facebook.

“I just learned something about you and it’s blowing my goddamned mind,” he wrote.

“This is not a joke…It is as close to an honest to goodness revelation as I will ever live in the flesh. Here it is: You can visualise things in your mind.”

Zeman says: “There seems to be a relationship between aphantasia and being involved in mathematical, computational and scientific types of activity. Perhaps this is an interesting way of putting it, but maybe not having your head cluttered by visual images is helpful if you want to think in an abstract way.

“It’s a bit of an open question whether it can help creativity. Certainly, it does seem that not having much visual imagery biases people towards becoming involved in abstract mathematical and computational professions. That is an empirical fact from our survey data.

“We’ve found that people with low imagery are likely to be in those sorts of roles, whereas people with high imagery are more likely to be in what are typically regarded as creative pursuits, such as painting or writing a novel.”

At the same time, people considered creative appear to be more prone to being affected by the acquired version of the condition – or at least noticing the limitations it can cause.

“It is generally true among those who have lost their mind’s eye, perhaps following stroke, brain injury or meningitis, that they were very visual to start with. Artists and other people who take a particular interest in the visual world and visual experience are clearly going to notice if something changes.

“For example, a chap came to see me who had gradually lost his mind’s eye over two to three years, possibly as part of the start of a neurological degenerative disorder. He was a photographer and spent a lot of time visualising things in his mind’s eye, so he noticed the change.”

Loss of mental imagery does not equate to loss of imagination, however.
“It’s hard to define imagination, but it involves being able to detach yourself from the here and now and things that aren’t present in a more or less creative way.

“For most of us, visualisation is an important part of the imagination because most of us think visually to some degree. But there are other ways of thinking, for example you can use language very imaginatively without being able to visualise or you can use your auditory imagination – things in your mind’s ear – and imagine movements, such as dancing.

“So, visual imagination is important to most of
us because vision is pretty important, but it is certainly not the only way to represent things that are not present to us.”

Read more about aphantasia

Professor Zeman is pursuing the study of aphantasia through an interdisciplinary project. Click here for more

Read his initial blog article about the subject here

Here’s how Firefox founder Blake Ross shared his discovery of aphantasia

The Discover magazine article which helped to bring the world’s attention to aphantasia.

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Light therapy could stop epileptic seizures – study



The researchers were able to activate the brains of mice using light rather than an electrical current

Deep brain stimulation could prevent epileptic seizures, a new study has found.

Research in mice has revealed that low-frequency stimulation of specific brain areas, using light rather than electric current, could completely stop epileptic activity.

Traditionally, epileptic activity originating from one or more diseased brain regions in the temporal lobe is difficult to contain.

Many patients with temporal lobe epilepsy often do not respond to treatment with anti-epileptic drugs, and the affected brain areas must therefore be surgically removed – although this only gives freedom from seizures to around a third of patients.

Now, this new light-based therapeutic approach, investigated by scientists at the University of Freiburg, could yield a significant breakthrough for patients.

“As soon as we stimulated the brain region with a frequency of one hertz, the epileptic seizures disappeared. This effect was stable over several weeks,” says Professor Carola Haas, head of the research group at the department of neurosurgery at the University of Freiburg.

In the study, habituation, which can occur with drug therapy, did not take place. The brain region was stimulated for one hour daily.

In temporal lobe epilepsy, the hippocampus is often pathologically altered and usually represents the so-called focus of epileptic activity.

Previous studies have used precise genetic labelling techniques to map the fibre system and its synaptic contacts between the temporal lobe and hippocampus, which are typically preserved in temporal lobe epilepsy.

The researchers used this fibre system to manipulate hippocampal activity in a specific and temporally precise manner using light-dependent proteins.

Measuring brain waves showed that rhythmic activation of the diseased hippocampus at a low frequency of one hertz suppressed epileptic activity and prevented it from spreading.

Professor Haas and her team demonstrated that the anti-epileptic effect is largely due to the repeated activation of surviving granule cells in the seizure focus.

Single cell studies confirmed the assumption that the granule cells are less excitable due to the stimulation, making the epileptic seizure less likely to spread.

“It’s also possible that we have a widespread network effect because the stimulation can spread through the hippocampal circuitry,” Professor Haas adds.

In the future, the team, along with the medical physics department at the Medical Center – University of Freiburg, have plans to use magnetic resonance imaging to observe the entire brain during stimulation.

This technique could be used to identify additional brain regions that are affected by the stimulation. Corresponding findings on these could provide information on how they are connected and what further consequences stimulation has.

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Gene linked to long lifespans can protect from stress



"Without SAM, lamin can't form this strong barrier and DNA starts leaking out."

A gene linked to unusually long lifespans in humans protects brain stem cells from the harmful effects of stress, a new study has found.

Studies of humans who live longer than 100 years have shown that many share an unusual version of a gene called Forkhead box protein O3 (FOXO3).

That discovery led Dr Jihye Paik, associate professor of pathology and laboratory medicine at Weill Cornell Medicine, and her colleagues to investigate how this gene contributes to brain health during ageing.

In 2018, Dr Paik and her team showed that mice who lack the FOXO3 gene in their brain are unable to cope with stressful conditions in the brain, which leads to the progressive death of brain cells.

And their new study reveals that FOXO3 preserves the brain’s ability to regenerate by preventing stem cells from dividing until the environment will support the new cells’ survival.

Stem cells produce new brain cells, which are essential for learning and memory throughout our adult lives,” says Dr Paik.

“If stem cells divide without control, they get depleted. The FOXO3 gene appears to do its job by stopping the stem cells from dividing until after the stress has passed.”

Many challenges like inflammation, radiation or a lack of adequate nutrients can stress the brain. But Dr Paik and her colleagues looked specifically what happens when brain stem cells are exposed to oxidative stress, which occurs when harmful types of oxygen build up in the body.

“We learned that the FOXO3 protein is directly modified by oxidative stress,” she says.

This modification sends the protein into the nucleus of the stem cell where it turns on stress response genes.

The resulting stress response leads to the depletion of a nutrient called s-adenosylmethionine (SAM). This nutrient is needed to help a protein called lamin form a protective envelope around the DNA in the nucleus of the stem cell.

“Without SAM, lamin can’t form this strong barrier and DNA starts leaking out,” she says.

The cell mistakes this DNA for a virus infection, which triggers an immune response called the type-I interferon response. This causes the stem cell to go dormant and stop producing new neurons.

“This response is actually very good for the stem cells because the outside environment is not ideal for newly born neurons,” Dr Paik continues.

“If new cells were made in such stressful conditions they would be killed. It’s better for stem cells to remain dormant and wait until the stress is gone to produce neurons.”

The study may help explain why certain versions of the FOXO3 are linked to extraordinarily long and healthy lives – they may help people keep a good reserve of brain stem cells.

It may also help explain why regular exercise, which boosts FOXO3 helps preserve mental sharpness.

But Dr Paik cautions it is too early to know whether this new information could be used to create new therapies for brain diseases.

“It could be a double-edged sword,” Dr Paik adds.

“Over activating FOXO3 could be very harmful. We don’t want to keep this on all the time.”

To better understand the processes involved, she and her colleagues will continue to study how FOXO3 is regulated and whether briefly turning it on or off would be beneficial for health.

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Routine genetic tests ‘should be offered to all MND patients’



The Sheffield Institute for Translational Neuroscience made the conclusions from its research

Offering routine genetic testing for Motor Neurone Disease (MND) could improve knowledge of disease classification and impact clinical care, new research has concluded.

Routine testing may be appropriate for all MND patients – whether or not they have a family history of the disease – and could impact disease sub-classification and clinical care, the findings of the Sheffield Institute for Translational Neuroscience (SITraN) study revealed.

Currently only patients with a family history of MND, dementia, or who experience disease onset at a young age are routinely offered genetic screenings in the UK.

With the development of new therapies targeting specific genetic forms of the disease, researchers on the study – which was funded by the are recommending that all MND patients are offered a screening.

“Our study suggests that all patients with MND should, with careful counselling, be offered genetic testing,” says Professor Dame Pamela Shaw, Director of SITraN and the NIHR Sheffield Biomedical Research Centre.

“We hope that by screening all MND patients for gene mutations that are a known factor in MND, we can further our knowledge on subclassification of the disease, but also ensure that patients have access to clinical trials that are relevant for them personally.”

MND – also known as amyotrophic lateral sclerosis (ALS) – is an adult-onset neurodegenerative disease characterised by progressive injury and cell death of upper and lower motor neurons.

This leads to progressive failure of the neuromuscular system with death, usually from respiratory failure, within 2–5 years of symptoms in most cases.

Currently, there is no cure for MND – which affects 5,000 people in the UK and 450,000 people worldwide – and no effective treatments to halt or reverse the progression of this devastating disease.

Among the 100 patients who took part in the study, researchers found higher than expected genetic changes in the group of patients.

“Our study found that 42 per cent of patients involved in the screening showed variants in known MND-linked genes,” says Professor Janine Kirby, Professor of Neurogenetics at the University of Sheffield.

“This doesn’t mean that 42 per cent of MND cases are familial – but shows that some familial and sporadic cases can share the same genetic cause of disease.

“We found that 21 per cent of patients had a clinically reportable genetic alteration that has been proven to increase the likelihood of developing MND.

“Of these, 93 per cent had no family history of MND and 15 per cent met the inclusion criteria for a current MND gene therapy clinical trial.

“As future studies expand the number of verified genetic causes of MND, we will continue to see if they are also found in cases without a family history.

“This is increasingly important in light of the new personalised medicine treatments in development for MND that target a specific gene mutation to ensure that patients have access to potential treatments that could be beneficial to them.”

Dr Brian Dickie, director of research development at the MND Association, adds: “MND is a complex disease involving a complex mix of genetic and environmental factors.

“This latest research sheds more light on the genetic component and will hopefully lead to greater availability of genetic testing to aid earlier diagnosis and more tailored treatments in the future.

”This will provide an even clearer picture of the UK MND genetic landscape.’’

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