Tag Archives: #hallucinations

A Brain Mechanism Underlying “Vision” in the Blind is Revealed (Neuroscience)

Researchers observed slow spontaneous fluctuations in the brain’s visual centers that preceded visual hallucinations in blind people.

Some people have lost their eyesight, but they continue to “see.” This phenomenon, a kind of vivid visual hallucination, is named after the Swiss doctor, Charles Bonnet, who described in 1769 how his completely blind grandfather experienced vivid, detailed visions of people, animals and objects. Charles Bonnet syndrome, which appears in those who have lost their eyesight, was investigated in a study led by scientists at the Weizmann Institute of Science. The findings, published today in Brain, suggest a mechanism by which normal, spontaneous activity in the visual centers of the brain can trigger visual hallucinations in the blind.

Prof. Rafi Malach and his group members of the Institute’s Neurobiology Department research the phenomenon of spontaneous “resting-state” fluctuations in the brain. These mysterious slow fluctuations, which occur all over the brain, take place well below the threshold of consciousness. Despite a fair amount of research into these spontaneous fluctuations, their function is still largely unknown. The research group hypothesized that these fluctuations underlie spontaneous behaviors. However, it is typically difficult to investigate truly unprompted behaviors in a scientific manner for two reasons, since, for one, instructing people to behave spontaneously is usually a spontaneity-killer. Secondly, it is difficult to separate the brain’s spontaneous fluctuations from other, task-related brain activity. The question was: How could they isolate a case of a truly spontaneous, unprompted, behavior in which the role of spontaneous brain activity could be tested?

The same visual system is active when we see the world outside of us, when we imagine it, when we hallucinate, and probably also when we dream

Individuals experiencing Charles Bonnet visual hallucinations presented the group with a rare opportunity to investigate their hypothesis.  This is because in Charles Bonnet syndrome, the hallucinations appear at random, in a truly unprompted fashion, and the visual centers of the brain do not process outside stimuli (because these individuals are blind), and are thus activated spontaneously. In a study led by Dr. Avital Hahamy, a former research student in Malach’s lab who is now a postdoctoral research fellow at University College London, the relation between these hallucinations and the spontaneous brain activity has indeed been unveiled.

The researchers first invited to their lab five people who had lost their sight and reported occasionally experiencing clear visual hallucinations. These participants’ brain activity was measured using an fMRI scanner while they described their hallucinations as these occurred. The scientists then created movies based on the participants’ verbal descriptions, and they showed these movies to a sighted control group, also inside the fMRI scanner. A second control group consisted of blind people who had lost their sight but did not experience visual hallucinations. These were asked to imagine similar visual images while in the scanner.

The same visual areas in the brain were active in all three groups – those that hallucinated, those that watched the films and those creating imagery in their minds’ eye. But the researchers noted a difference in the timing of the neural activity between these groups. In both the sighted participants and those in the imagery group, the activity was seen to take place in response either to visual input or to the instructions set in the task. But in the group with Charles Bonnet syndrome, the scientists observed a gradually increasing wave of activity, reminiscent of the slow spontaneous fluctuations, that emerged just before the onset of the hallucinations. In other words, the hallucinations were not the result of external stimuli (eg., sensory images or instructions to imagine specific things), but were rather evoked internally by the slow, spontaneous, brain activity fluctuations.

The  visual centers in those seeing a film or imagining as instructed had similar timing in their brain activity, while those experiencing spontaneous hallucinations showed a gradual increase in slow fluctuations © Weizmann Institute of Science

“Our research clearly shows that the same visual system is active when we see the world outside of us, when we imagine it, when we hallucinate, and probably also when we dream,” says Malach. “It also exemplifies the creative power of vision and the contribution of spontaneous brain activity to unprompted and creative behaviors,” he adds.

In addition to the scientific value of the work, Hahamy hopes it may raise awareness of Charles Bonnet syndrome, which can be frightening to those who experience it. “These individuals may keep their visual hallucinations a secret – even from doctors and family – and we want them to understand that these visions are a natural product of a healthy brain, in which the visual centers remain intact, even if the eyes have ceased to send them sensory input,” she says.

Also participating in this research were Dr. Meytal Wilf, formerly in Malach’s lab, of Lausanne University Hospital, Switzerland; Dr. Boris Rosin, of the Ophthalmology Departments of Hadassah-Hebrew University Medical Center, Jerusalem, and University of of Pittsburgh Medical Center; and Prof. Marlene Behrmann of Carnegie Mellon University, Pittsburgh, Pennsylvania.

Provided by Weizmann Institute of Science

Hallucinations Induced in Lab Could be Key to Better Understanding And Treatment (Neuroscience)

Cognitive neuroscientists from UNSW Sydney say if we really want to understand and treat the pathological hallucinations that affect people with physical and mental illnesses, the best place to start is in the laboratory.

Hallucinations have been difficult to study and can be distressing for the person experiencing them, but hallucinations induced in the lab are much more benign. Credit: Shutterstock

Inducing hallucinations in the general population using visual stimulation procedures works similarly to illusions, and enables more objective and repeatable testing. It’s also much less distressing to the test subject than studying pathological hallucinations experienced by people with conditions like Parkinson’s disease or schizophrenia.

“By nature, [lab-induced hallucinations] can be induced in almost anyone at any time,” the neuroscientists write in an opinion piece published recently in Philosophical Transactions B journal.

“This can help to curb the current overreliance on studying pathological hallucinations, thereby reducing burdens placed on patients and simplifying recruitment and testing logistics.”

Seeing something that isn’t there

Most people naturally think of visual hallucinations as being realistic images or scenes, such as seeing humans or spiders (what we call ‘complex’ hallucinations). However, a hallucination in its broadest sense can be defined as the experience of seeing something that is not there. As such, visual hallucinations can also include seeing basic geometric shapes or colors (referred to as ‘simple’ hallucinations), and scientists can trigger both simple and complex hallucinations in the laboratory.

Professor Joel Pearson, the senior author of the opinion piece, says work the group did in 2016 showed that you could induce hallucinations in people reliably and safely using specific types of flickering lights.

“We showed that you could use flickering lights in an annulus—basically a flickering white ring like a doughnut on a black background—and you could induce hallucinations of little dark blobs which rotate around the ring,” he says.

“And you could use that to try and study the mechanisms behind visual hallucinations. But those flicker hallucinations are just the tip of the iceberg, and there are many other techniques for inducing hallucinations that are similar to pathological hallucinations in terms of the experience and underlying neural processes.”

Prof. Pearson says one of the trickier problems is working out which techniques can tell us something about pathological hallucinations.

“A lot of this work shows that it’s hard to separate hallucinations from illusions and veridical (reality-based) perception. Current hallucination definitions are too black and white, and aren’t up to the task of classifying many of these lab-induced experiences.”

Spectrum of experience

Professor Pearson and fellow authors Dr. Sebastian Rogers and Dr. Rebecca Keogh use a continuous spectrum of experience to distinguish hallucinations from other types of perception, based on the similarity between the physical stimulation of the senses (the light that enters the eye) and the actual conscious experience (the image we ‘see’ or experience).

Veridical perception (involving a strong relationship between what is ‘in reality’ and what one sees) is at one end of this spectrum and hallucinations (a weak relationship between what is present in reality and with what one sees) is at the other, with illusions falling somewhere in between.

According to lead author Dr. Rogers, “the thesis of the idea is that the further a lab-induced experience is toward the hallucination end of the spectrum, the more it can tell us about other types of hallucination.”

“If you really don’t want to call one of these lab-induced experiences a hallucination, that’s fine by us. We don’t really mind what the name is, we care most about whether we can study it to learn about pathological and other hallucinations. It’s a way to investigate hallucinatory processes any time we want in the lab, with anyone.”

Dr. Keogh says, “once we understand the underlying mechanisms, that is, what in the brain leads to seeing things that aren’t there, then we’ll be able to develop treatments. There are very few treatments for hallucinations at the moment, and most are medications that can lead to unwanted side effects.

“Using lab hallucination models can allow us to develop new avenues for more targeted treatments, such as electrical or magnetic brain stimulation.”

References: Sebastian Rogers et al. Hallucinations on demand: the utility of experimentally induced phenomena in hallucination research, Philosophical Transactions of the Royal Society B: Biological Sciences (2020). DOI: 10.1098/rstb.2020.0233

Provided by University of New South Wales

Schizophrenia May be Similar to Immune Disorders, Show Scientists (Psychiatry)

A study by clinical scientists at the University of Manchester has shown that schizophrenia may—in some part—be caused by disordered functioning of the immune system.

©WebMD

The first ever trial in schizophrenia of the powerful immune suppressant drug, Methotrexate, produced what the team described as ‘promising’ effects on what are known as positive symptoms, such as hearing voices.

Though the team stress the sample size was too small to show if Methotrexate could work as an add-on treatment for schizophrenia, they found a ‘puzzling’ therapeutic effect on symptoms of early schizophrenia.

And that, they argue, warrants further investigation.

The findings published in the Journal of Translational Psychiatry shed new light on the devastating and difficult to treat condition, which causes distress and disability worldwide.

Schizophrenia is categorized by so called ‘positive symptoms’ such as hearing voices (hallucinations) and ‘negative symptoms’ (disordered thinking, poor motivation, poor social function).

Negative symptoms, which contribute significantly to the disability associated with schizophrenia are hard to treat with currently available medication.

The study was funded by the Stanley Medical Research Institute in the United States in collaboration with the Pakistan Institute of Living and Learning.

The trial took place in Pakistan, led by Professor Imran Chaudhry from The University of Manchester who after years of service to the NHS relocated to Pakistan to continue to practice psychiatry.

The lack of available treatments for these symptoms encouraged Professor Chaudhry’s team to investigate new treatment options for schizophrenia.

Methotrexate is often used to treat inflammatory diseases such as rheumatoid arthritis and Crohn’s disease.

Inflammatory and autoimmune conditions are more common in patients with schizophrenia, possibly indicating that there is a shared underlying cause to these diseases.

“Methotrexate is thought to help treat autoimmune disorders by resetting the way T cells—an important part of the immune system—work,” said Professor Chaudhry.

“This action on the central nervous system may account for the improvement in symptoms we found in our study,” he added.

They used a low 10mg dose of the drug, which was given alongside the patients’ routine psychiatric medication.

No significant side-effects were reported by the patients taking Methotrexate, suggesting it was relatively well tolerated.

Nusrat Husain, Professor of Psychiatry and Director of Research in Global Mental Health at The University of Manchester added: “We used the lowest clinically effective dose in autoimmune disorders which often needs to be increased so higher doses could produce a more powerful effect in schizophrenia.

“However, the health risks of methotrexate are substantial and require careful monitoring which is why we would rule out large unfocussed trials.”

Psychiatrist Dr. Omair Husain, who is an honorary researcher at The University of Manchester and an Assistant Professor based at The University of Toronto said: “Immune systems could be involved in schizophrenia and that raises fascinating questions.

“Perhaps one day we might be able to identify subsets of people with schizophrenia who may respond to treatments that act on the immune system.

“The small, unexpected effect we found in our study warrants further investigation which we now believe is feasible.

“Future work needs to focus on identifying these subgroups possibly through studies that use advanced brain imaging techniques and state of the art immune profiling techniques.”

Reference: I. B. Chaudhry et al. A randomized clinical trial of methotrexate points to possible efficacy and adaptive immune dysfunction in psychosis, Translational Psychiatry (2020). DOI: 10.1038/s41398-020-01095-8 https://www.nature.com/articles/s41398-020-01095-8

Provided by University of Manchester

Potential Means of Improving Learning and Memory in People With Mental Illnesses (Psychiatry)

More than a dozen drugs are known to treat symptoms such as hallucinations, erratic behaviors, disordered thinking and emotional extremes associated with schizophrenia, bipolar disorder and other severe mental illnesses. But, drug treatments specifically able to target the learning, memory and concentration problems that may accompany such disorders remain elusive.

Average brain activity during a working memory task in a group of healthy subjects as measured by fMRI. The colors represent higher brain activity in the carriers of the G version of the GCPII enzyme, where brains are less efficient at performing the task, compared with those carriers with the A version of the enzyme. ©Bigos laboratory

In an effort to find such treatments, Johns Hopkins Medicine researchers report they have identified a genetic variation in the brain tissue of a subset of deceased people — some with typical mental health and some with schizophrenia or other psychoses — that may influence cognition and IQ. In the process, they unearthed biochemical details about how the gene operates.

Results of their work, described in the Dec. 1 issue of the American Journal of Psychiatry, could advance the development of drugs that target the enzyme made by this gene, and thus improve cognition in some people with serious mental illnesses or other conditions that cause reduced capacity in learning and memory.

Typical antipsychotic medications that treat schizophrenia symptoms regulate the brain chemical dopamine, a transmitter of nerve impulses associated with the ability to feel pleasure, think and plan, which malfunctions in patients with the disorder. However, previous genetic studies have also shown that another brain chemical signal transmitter, glutamate, a so-called “excitatory” chemical associated with learning and memory, plays a role as well. Another so-called neurotransmitter in this process, N-acetyl-aspartyl-glutamate (NAAG), specifically binds to a protein receptor found on brain cells that has been linked to schizophrenia, but how it impacts this disorder is unknown.

The research of clinical pharmacologist Kristin Bigos, Ph.D., assistant professor of medicine at the Johns Hopkins University School of Medicine, sought to explore more deeply the role of NAAG in cognitive impairment with the goal of eventually developing therapies for treating these learning, memory or concentration problems.

Using tissues gathered from a repository of brains from deceased donors belonging to the Lieber Institute for Brain Development, Bigos and her team measured and compared levels of certain genetic products in the brains of 175 people who had schizophrenia and the brains of 237 typical controls.

Bigos and her colleagues specifically looked at the gene that makes an enzyme known as glutamate carboxypeptidase II (GCPII), which breaks down NAAG into its component parts ? NAA and glutamate. In the brains of people with schizophrenia and in the typical controls, they found that carriers of this genetic variant (having one or two copies of the gene variation) had higher levels of the genetic product that makes the GCPII enzyme.

In the gene for the enzyme, the only difference in the versions was a single letter of the genetic code, either G or A (for the nucleotide bases guanine and adenine). If people had the version of the gene with one copy of G, then the tissue at the front of their brain ? the seat of cognition ? had 10.8% higher levels of the enzyme than those who had the version of the gene with A, and if people had two copies, they had 21% higher levels of the enzyme.

To see if this genetic variation in GCPII controlled the levels of NAAG in the brains of living people, the researchers measured levels of NAAG in the brain using magnetic resonance spectroscopy, which uses a combination of strong magnetic field and radio waves to measure the quantity of a chemical in a tissue or organ.

In this experiment, they focused on 65 people without psychosis and 57 patients diagnosed with recent onset of psychosis, meaning many of them were likely to eventually be diagnosed with schizophrenia, at the Johns Hopkins Schizophrenia Center. Participants averaged 24 years of age, and 59% were men. About 64% of participants identified as African American, and the remaining 36% were white.

The researchers found 20% lower levels of NAAG in the left centrum semiovale — a region of the brain found deep inside the upper left side of the head — in the white participants both with and without psychosis who had two copies of the G version of the enzyme compared with other white people who had the A version.

To see if having the G or A version of the gene plays a role in cognition, the researchers tested IQ and visual memory in the healthy participants and those with psychosis, both white and African American. They found that people with the most NAAG in their brain (in the top 25%) scored 10% higher on the visual memory test than those in the bottom 25%. They also found that people with two copies of the G version of the GCPII sequence scored 10 points lower on their IQ test on average than the people with the A version of the gene, which the researchers say is a meaningful difference in IQ.

Finally, they showed that healthy carriers of the G version of the GCPII sequence had less efficient brain activity during a working memory task, as measured by functional MRI, by at least 20% compared with those people with the A version of the gene.

“Our results suggest that higher levels of the NAAG are associated with better visual and working memory, and that may eventually lead us to develop therapies that specifically raise these levels in people with mental illness and other disorders related to poor memory to see if that can improve cognition,” says Bigos.

Additional authors on the study include Caroline Zink, Peter Barker, Akira Sawa, Min Wang, Andrew Jaffe, Joel Kleinman, Thomas Hyde, Kayla Carta and Marcus van Ginkel of Johns Hopkins Medicine, and Daniel Weinberger, Henry Quillian, William Ulrich, Qiang Chen, Greer Prettyman and Mellissa Giegerich of the Lieber Institute for Brain Development.

This work was supported by the Lieber Institute for Brain Development, the National Institutes of Mental Health (MH092443, MH094268, MH105660 and MH107730) and the National Institute on Drug Abuse (DA040127).

Some patient or volunteer recruitment costs were supported by the Mitsubishi Tanabe Pharma Corporation.

Provided by Johns Hopkins Medicine

Study Finds Evidence Of Neurobiological Mechanism For Hallucinations And Delusions (Neuroscience)

A new study from researchers at Columbia University Vagelos College of Physicians and Surgeons has found evidence of a potential neurobiological mechanism for hallucinations and delusions that fits within the hierarchical model of psychosis and can explain their clinical presentation.

The study was published in eLife.

Columbia researchers Kenneth Wengler, PhD, a Postdoctoral Research Fellow and Guillermo Horga, MD, PhD, Florence Irving Associate Professor of Psychiatry, investigated the neurobiological mechanisms of two symptoms of schizophrenia: hallucinations and delusions. These two symptoms form the syndrome of psychosis, an immensely disabling psychiatric condition where patients lose their ability for reality testing.

“Typically, patients with more severe hallucinations also have more severe delusions, and these two symptoms respond similarly to antipsychotic medications. But this is not always the case; some patients have very prominent hallucinations but less severe delusions and vice versa,” says Wengler. “This suggests that these symptoms may share a common neurobiological mechanism while simultaneously depending on symptom-specific pathways.”

Some experts in the field believe that a hierarchical perceptual-inference model can explain the mechanisms behind psychosis. Wengler explains, “In its simplest form, the hierarchical model has two levels to the hierarchy: low and high. The low level makes inferences about basic features of stimuli and the high level makes inferences about their causes. An intuitive example of this is inferring the weather. In this scenario, you must decide if you are going to take an umbrella with you when you leave the house. The stimulus in this scenario is what you see when you look out the window; let’s say it’s cloudy. The context in this scenario is what you expect the weather to be like on a given day in the city you are in; let’s say you are in Seattle. Although it is not currently raining, because it’s cloudy and you are in a city where it often rains, you may decide to take an umbrella with you. The hierarchical model of psychosis frames hallucinations as resulting from dysfunction at the lower levels of the hierarchy and delusions as resulting from dysfunction at the higher levels of the hierarchy. Critically, these levels of inference are distinct but interconnected, so a dysfunction at one level would likely propagate upwards or downwards to other levels, therefore explaining why these symptoms tend to co-occur.”

To investigate the neurobiological mechanisms of hallucinations and delusions within the framework of the hierarchical model, the researchers used functional magnetic resonance imaging to measure intrinsic neural timescales throughout the brain. These neural timescales reflect how long information is integrated in a given brain region. Most importantly, these neural timescales are organized hierarchically, making it a fitting measure to test the hierarchical model of psychosis.

The researchers collected data from 127 patients with schizophrenia from various online databases and determined how an individual’s neural timescales related to their hallucination and delusion severities together. They found that neural timescales in the lower levels of the hierarchy tended to be longer in patients with more severe hallucinations, while neural timescales in the higher levels tended to be longer in patients with more severe delusions. These results provide the first direct evidence of a potential neurobiological mechanism for hallucinations and delusions that fits within the hierarchical model of psychosis and can explain their clinical presentation. The common neurobiological mechanism for both symptoms could result in increased neural timescales, but the symptom-specific pathways are the level of the hierarchy at which the neural timescales are increased. “Our findings open the door for the development of treatments to target specific symptoms of psychosis depending on an individual subject’s symptom profile, in line with the current push for individualized medicine,” says Horga.

References: Kenneth Wengler , Andrew T Goldberg, George Chahine, Guillermo Horga, “Distinct hierarchical alterations of intrinsic neural timescales account for different manifestations of psychosis”, Neuroscience, 2020. DOI: 10.7554/eLife.56151 link: https://elifesciences.org/articles/56151

Provided by Columbia University Irving Medical Center

You Have a Beautiful, Powerful Mind (Psychology)

Our thoughts are so powerful that they actually do shape our reality.

Did you happen to see the movie A Beautiful Mind? It was released in 2001 to great critical success, and it won four Academy Awards, including best picture.

The main character of the film, played by Russell Crowe, is John Nash, a real-life mathematician who actually won the Nobel prize, as the movie depicts, and also suffered from schizophrenia, as Crowe masterfully interprets.

Source: Sasha Lebedeva/ Unsplash

Schizophrenia is a terrible mental illness that involves hearing and seeing things that aren’t actually there. People with schizophrenia believe that what they are seeing and hearing is real. Typically, these hallucinations are extremely negative ones that center on the person with the illness. Nash, for example, heard voices in his head that told him constantly that he was a failure. Even though the world saw him as a great success, Nash could not believe that this was true because of his schizophrenia. Not even distinguished positions at some of the world’s greatest universities or accolades as high as the Nobel Prize could convince him otherwise. Part of Nash’s hallucination was that he was a failure, even as he was admired throughout the world.

I once read a study about models. Some of the most beautiful people in the world are models, yet when asked if they consider themselves beautiful, this research revealed the surprising fact that most did not. Most models felt they were average, and most reported being dissatisfied with some noticeable flaw to their appearance. Gracing the covers of magazines and walking the world’s most elite runways didn’t shake these models’ views that they were ordinary, or even less than ordinary.

It’s possible that you’re reading these examples, and you’re wondering what these words have to do with you. You may be thinking, “I’m not a supermodel or a brilliant mathematician. I’m just an average Joe.” I won’t try to convince you otherwise, because the bottom line is that you’re absolutely right. We are always right, and whatever we think about ourselves is true and correct.

Whatever we are feeding our minds, that’s what we are. Our thoughts are so powerful that they actually do shape our reality. Never mind the fact that they may have nothing to do with what’s true or apparent to others. What we feed our minds is what we believe, and what we believe is our truth.

If we feel we do not have enough, we suffer. This is true, even if in the world’s eyes we have everything we could possibly need. The root cause of our suffering is not what we have or don’t have, or what we’ve accomplished or not accomplished. At the base of our suffering is our thoughts about our lives.

What we are feeding our minds throughout the day will be our reality. This is true even if our reality is madness. What we are feeding our minds matters.

The first thing we have to do is discover what it is that we are thinking about all day long. This involves a straightforward assessment without judgment. We must take a walk past the metaphorical mirror and take a look. Maybe we are saying, “I’m bad, “I’m ugly,” or “I’m stupid.” Do we like these feelings? Probably not. So let’s focus on something else.

John Nash could still see his hallucinations, but he made the remarkable choice to focus on what was real. If our thoughts are hurting us, we should focus on other things. If our thoughts about ourselves are negative, they will only lead to suffering. If we are to live happy lives—and obviously that is our goal, since we are meeting here in the space—we need to take control of the thoughts that hurt us.

The thoughts we experience have to do with all parts of our lives. Maybe we focus our attention on our looks, our success, our health, or even where we live. All of these things have the ability to cause us to suffer if we allow them to, or if we go on wishing our lives were different.

I live and work in Southern California. Public transportation here is not the best, and most of us get around by car. When we get a car, usually we love the feeling. We can get ourselves around from place to place and be productive while doing what we enjoy. But then we get on the road, and we can’t help but notice that others have nicer cars than we do. We might think, “My car is ugly” or “I hate it.” These are the sorts of thoughts we create all day long. But we have a choice in the thoughts we express or believe.

One final step we can take is a hard one, but so worthwhile. I talk about it often, so it may sound familiar, but it is this: Stop paying attention to your thoughts. Instead, just be. Instead of shifting your attention to positive things, just live in the now, and really savor each moment and each breath. We don’t need to label everything as good or bad. Rather, we can choose to experience each new breath with wonder as if we are experiencing it for the first time. If we think about the car analogy, perhaps we can stop thinking about whether our car is pretty or nice or fast, and instead we can experience it as if it is brand new and we are driving for the very first time. We can say, “Wow! I have a car!” And we can exhilarate in the feeling of the wind whipping through the windows and the speed with which we get from here to there.

Sometimes the world seems to think highly of us. Other times, it does not. But I’m making the choice just to suck the marrow out of life. When we need to shift our thoughts to something else, we can—or we can just enjoy the presence and stillness of living life one moment at a time.

This article is republished here from psychology today. Author of this article is Robert Puff.

Cancer Anti-sickness Drug Offers Hope For Hallucinations in Parkinson’s (Medicine)

A world-first double-blind clinical trial, will investigate if a powerful drug used to treat nausea in chemotherapy patients, could alleviate hallucinations in people with Parkinson’s.

Parkinson’s UK, the largest charitable funder of Parkinson’s research in Europe, is partnering with UCL, and investing £1 million in a pioneering phase II clinical trial to explore if the drug ondansetron is safe and effective against hallucinations. There are currently 145,000 people living with Parkinson’s in the UK and 75 per cent of them will experience visual hallucinations at some point.

The trial comes at a crucial time as a survey carried out by the charity worryingly found that 1 in 10 people with Parkinson’s reported an increase in hallucinations during lockdown, which led to an increase in calls to their helpline.¹

The funding for this four-year project comes via the charity’s drug development arm, the Parkinson’s Virtual Biotech. Launched in 2017, the innovative programme is plugging the funding gap to fast-track the projects with the greatest scientific potential to transform the lives of people with Parkinson’s. This is the second clinical trial to be added to the Virtual Biotech’s pipeline of projects in a drive to develop better drug treatments for people with Parkinson’s.

Dr Arthur Roach, Director of Research at Parkinson’s UK said:

“It’s vital we find better treatments for people with Parkinson’s who have seen their hallucinations worsen at home and ondansetron offers much hope for them and their families. If successful, positive results from the trial could see this drug, which is already used in the NHS, quickly repurposed to become an available treatment in Parkinson’s.

“With the support of Parkinson’s UK, UCL has been rapidly adapting the research during the pandemic, to enable us to drive forward and launch this promising trial, which marks another milestone in our thriving Parkinson’s Virtual Biotech programme.”

Treating hallucinations is one of the most challenging aspects in people with Parkinson’s and it can have a big effect on their quality of life. It can be extremely distressing for carers as well as people with Parkinson’s, putting stress on relationships. The only medications available to treat it today are anti-psychotic drugs which can worsen Parkinson’s symptoms and potentially cause serious side effects. This urgent need for new treatments is why hallucinations are a top priority for the Parkinson’s Virtual Biotech.

The 12-week, double-blind, placebo-controlled trial is set to recruit 216 people over 2 years in 20-25 NHS clinics across the UK. Patients will be randomised to receive either drug or placebo tablets, to take at home for 12 weeks. To accommodate social distancing, researchers will conduct the majority of the study via video or telephone consultations, with face-to-face assessments limited to only three for essential blood tests or ECGs. Visual and other types of hallucinations, as well as delusions (false beliefs), will be assessed after 6 and 12 weeks of treatment, along with Parkinson’s related motor and non-motor symptoms.

Lead Researcher, Suzanne Reeves, Professor of Old Age Psychiatry and Psychopharmacology at UCL said:

“Visual hallucinations pose a particular challenge in Parkinson’s as the very treatments for motor symptoms in Parkinson’s can also trigger and worsen this distressing symptom. Finding treatments for hallucinations that are both effective and safe is an area of great unmet need.

“Ondansetron influences visual processing in the brain and its potential for treating visual hallucinations in Parkinson’s was first identified in small studies in the early 1990s.

“This trial will enable us to find out if ondansetron is effective and safe as a treatment and if it is, we could see clinicians prescribing an inexpensive drug with fewer side effects to people with Parkinson’s throughout the UK.”

Provided by Parkinson’s UK