The devastation of dementia hallucinations: ‘Grandpa saw soldiers parachuting from the ceiling’

Hippos in flight, doors drifting downstream and a fraught audition for Strictly Come Dancing are just some of the hallucinations which Grandpa had that I remember. All my life I had known him to be a practical and intelligent person with a dry, often sanguine sense of humour. As a teen he lost an eye in a slingshot accident. The eyepatch he wore, combined with his name, Roger, used to raise suspicions of a pirate’s past. But he was a man of the land. He spent his childhood fishing for trout in the headwaters of Buckinghamshire’s river Wye and read agriculture at Oxford University before going into farm management.

His life was punctuated by death. He saw active service as a paratrooper and endured the death of his elder and only brother, Barry, during the Second World War. Then, in 2013 he lost the love of his life to cancer. This stoic, stiff-upper-lipped man was without his other half; it was as though the ground beneath him suddenly dissolved. For the first time, Grandpa seemed lost.

Mum and Grandpa were sitting in the snug one day when he gazed out of the window overlooking his garden and mused, “Magnificent birds, aren’t they?” After inspecting the barren sky, silent pear trees and still hedgerows, Mum responded: “Birds?”

“Yes, the cassowaries,” Grandpa impatiently gestured. He was witnessing a shock of cassowaries prowling about the old barn. Prehistoric casques atop a vivid cobalt blue, shaggy bodies and thick legs. There was nothing incongruous about them in his mind, and to his eye they were truly real.

We had known something was wrong with Grandpa, but we had no clue what it could be, or if his condition even had a name. After the loss of his wife, he lived by himself, and when my family visited he would earnestly recount other absurdities. Mum would later come to gain a sixth sense for predicting his hallucinatory episodes. There would be no discernible change in Grandpa’s demeanour or physicality; she described it as a separate entity awakening.

From then on, Grandpa had many more visitations. We would stumble across washcloths strewn about the hallways and the patio outside his bedroom window, which Grandpa had interpreted as mischievous cats wreaking havoc in the night. A recurring hallucination manifested as a black dog – a comforting familiar that followed the long lineage of black Labradors and retrievers that Grandpa had raised in his real life. Despite being an illusion, this one was a grounding presence, stationed peacefully at his bedside.

Rapidly, however, his condition worsened. In 2014 Grandpa was admitted to the hospital, where his hallucinations mutated like bacteria. Every interaction was laced with scrutiny or panic. His diagnosis: dementia with Lewy bodies (DLB). My family and I knew nothing about it, but we understood the disease had weight. It had many manifestations and, like knotweed, its roots pierced through the foundations of reality.

DLB is the third-most common form of dementia. It can often be misdiagnosed initially as Alzheimer’s or Parkinson’s disease, and all three fall under the umbrella of neurodegenerative diseases. It is born from alpha-synuclein protein aggregates, known as Lewy bodies, misfolding within the brain’s nerve cells. The presence of these Lewy bodies damages the cells, negatively impacting mobility, memory and how the affected person thinks. DLB is notionally different to Lewy body dementia, which is a wider term used to encompass both DLB and Parkinson’s disease dementia (PDD).

So, what causes these virulent protein clusters? Current research suggests a link between exposure to air pollution and Lewy body dementia.

DLB bears many similarities to PDD, such as altered perception and judgment, sleep disturbance, impaired balance and resting tremors. Rimona Weil, a professor of neurology at UCL’s Dementia Research Centre, explains how both Lewy body dementia diseases “particularly affect thinking processes involved in organising things like booking holidays or going shopping, as well as visual processing and knowing where different parts of the body are in space”. She also runs a clinical service supporting patients with both PDD and DLB, observing their commonalities and differences. “Patients that I see in my clinic often have difficulty using an iPhone, or folding clothes,” she says.

Patients with DLB and PDD can also have symptoms of fluctuating cognitive ability, hallucinations and REM sleep disorder. In Lewy body dementia, Weil describes the primary difference between the two diseases as the timing of symptoms: “Parkinson’s dementia starts with the movement symptoms of Parkinson’s disease and the dementia follows at least a year after the Parkinson’s starts. DLB is where the thinking and memory problems happen first or around the same time as the movement symptoms.”

Age and genetics have long been noted as internal causes for the onset of DLB. But now there is reason to look outwards to our environment. New and ongoing studies have found substantial evidence that prolonged exposure to particulate matter 2.5 air pollution (PM2.5) can spark the formation of Lewy bodies, thereby increasing the risk of Lewy body dementia.

With a single particle measuring just 2.5 micrometres (roughly 30 times smaller than the width of a human hair), PM2.5 comprises minuscule solid particles or droplets, both man-made and naturally occurring. Wildfires, industrial plants, vehicle exhausts, fireplaces, even plant spores and incense are all known sources of PM2.5 pollution. This particulate matter can stay airborne for long durations until inhaled and absorbed into the bloodstream, potentially permeating organs.

As may be expected, urbanised areas yield higher concentrations of PM2.5 and, consequently, those living in cities are generally more susceptible to health complications related to air pollution.

It is on this premise that research conducted by Johns Hopkins University exploring the link between air pollution and Lewy body dementia began, more than 20 years ago.

Between 2000 and 2014, researchers analysed hospital data from 56.6 million US patients with neurodegenerative diseases, focusing on first-time patients admitted with symptoms typical of Lewy body dementia. They collated data from patients’ postcodes to approximate their long-term exposure to PM2.5, and found that exposure to these particulates increased the risk of DLB by 12 per cent. A connection was made, but how air pollution increases risk was, at this point, unclear.

Back to the present, and we are closer to understanding. On September 4, the university published findings from a recent study in which mice were exposed to PM2.5 every other day for a 10-month period. They exposed a control group and a group of genetically modified mice in which the alpha-synuclein protein was absent. Within the control group they observed brain deterioration and diminished cognition, while in the brains of the genetically modified mice they noted no major changes.

The research team then monitored genetically modified mice possessing hA53T, a human gene mutation associated with early-onset Parkinson’s. After five months, the mice had developed ubiquitous alpha-synuclein clusters strongly resembling Lewy bodies found in humans. Although obtained from rodents, the findings are considered credible evidence of PM2.5 being an external trigger for Lewy body dementia in humans.

As visions of mice and Lewy bodies float about my mind, I cannot help but recall the time when Grandpa told us of a mouse who scurried about his slippers as he watched TV. We’d humoured it as another hallucination until Mum noticed some nibbled plums and Dad, who was sitting reading with Grandpa, spotted two beady eyes peering out from the fruit bowl.

After Grandpa’s diagnosis, my family and I lived in his farmhouse while renovations were made to our semi-detached home to accommodate him permanently. For five years until his death, aged 93, my parents, two sisters and I lived with Grandpa, trying to navigate the vastness and unpredictability of the illness.

Some days he seemed to tread water and keep his head above the surface, completing mundane tasks such as shaving and getting dressed with relative ease. These “easy” days were often inspired by the anticipation of a visiting nurse or one of his children. His sense of duty and respect towards authority was a stubborn core that remained impenetrable to the dementia. On days when visitors were expected, Mum would come downstairs to begin the long, usually challenging morning routine and be surprised to find her father-in-law at the kitchen table with a clean-shaven face, jumper worn correctly, shoes neatly tied, patiently awaiting breakfast.

In retrospect, my teenage years were heavily moulded by DLB and my family’s decision to care for Grandpa. This period of our life was defined by isolation as we withdrew from one another and the world around us.

I never really expressed to my friends the anxiety and confusion I felt living with him. Witnessing the dread on his face as he pointed to soldiers parachuting from his ceiling. The fear I felt as he rang his bell in the dead of night to tell me that his room was awash with my sister’s blood. As I pleaded with him to believe me and not the hallucination, his accusatory glare was that of a cornered animal – and in that moment, he wasn’t Grandpa.

The hallucinations were, sometimes literally, the elephant in the room. It was difficult for Grandpa to accept that he had dementia when he could recall details from his past or remembered to ask me about the results from a history test I had taken at school the week before, something that even my parents had forgotten about. The present moment was the issue. How often in our daily lives do we question whether the shopkeeper we talk to or the stray cat we stop to stroke are real? His hallucinations were so tangible that any logic dictating that the boiler cupboard couldn’t actually be the engine room of a navy ship dissipated. On one occasion Dad had attempted to discuss the nature of his hallucinations, only to have an exasperated Grandpa retort: “The sound of your voice explaining reality is annoying me.”

For the year we lived at Grandpa’s, I often escaped to a bundle of hodgepodge fields to climb on top of a hay bale and wait for stars to appear. A soothing quietness would wash over me. On the outskirts of the field, there was a small tree and I would study its blue silhouette and search for answers until the branches bled into the night.

In that dark atmosphere, there swarmed a plethora of invisible triggers. The sweet plume of bonfires, the thrum of a tractor’s engine. In light of recent research, I can’t help but wonder when, and how, Grandpa’s DLB was activated.

The majority of his life was spent in the countryside, eluding urban air pollution. From 1956, however, he worked for a major company in crop protection and was, naturally, exposed to a variety of pesticides and farming chemicals. Could these have been the trigger? Curious, I approached Sonia Gandhi, a professor of neurology at University College London (UCL) and an assistant research director at the biomedicine charity the Francis Crick Institute.

It is understood that pesticides are included in the environmental factors linked to Parkinson’s disease, but it is not yet apparent whether they affect DLB. Gandhi states, however, that environmental toxins may play a role.

“Pesticides affect the mitochondria of cells, causing a decline in the energy production – this is believed then to cause a bioenergetic deficit that puts the brain cells in a ‘stressed’ state in which proteins such as alpha-synuclein may misfold,” she says.

We cannot be certain that pesticides are the culprit for Grandpa’s DLB, or whether it is even possible for them to have been a catalyst decades before his diagnosis, but current work seeks to decipher the how and why of our environment’s role in neurodegenerative diseases. We may never know in Grandpa’s case, but there is hope for future patients.

In 2024, researchers from the Francis Crick Institute and UCL launched an ongoing project named Role of Air Pollution in Dementia (Rapid), which aims to uncover the specific process(es) of and conditions for PM2.5 to incite neurodegeneration.

Gandhi says: “Our work in Rapid is designed to examine a range of different hypotheses about how PM2.5 may affect brain health. What is clearly needed, though, is research that can understand the route of exposure, the timing and duration of exposures, the effect of combinations of exposures – as this is what happens in the ‘real world’ – and the actual mechanisms by which either pesticides or air pollution, or both, may affect the brain.

“For air pollution, we do not yet know the exact mechanisms – it may affect states of inflammation within the brain, or it may interact directly with the protein alpha-synuclein to change its propensity to aggregate or cause neurodegeneration.”

How PM2.5 triggers neurodegenerative diseases is not yet determined, but what is clear is that air quality, which is already linked to numerous chronic conditions, must be improved. Some pollution is unavoidable. We can’t put lids on volcanoes or snuff out every spore-spurting plant. But we do have the capacity to manage PM2.5 produced by human activity.

In the UK, the Air Quality Standards Regulations 2010 sets legal limits for particulate matter concentrations to regulate our exposure to PM2.5, while the National Emission Ceilings Regulations 2018 places legal caps on air-pollutant emissions. Environmental policies must now consider the implications of this new research in neuroscience and make amendments.

“The idea that we may be able to prevent or delay the onset of a condition by changing our environment – this opens a new door in conditions that currently lack cure/disease-modifying therapies,” says Gandhi.

Weil comments: “This is an important and exciting research finding. It is important to find a potential cause for Lewy body dementia, and finding this link could provide a potential new avenue for treatments, which is what all the patients in my clinic are eager to see.”

Even if Grandpa had known that DLB was an inevitability, I don’t think he would have chosen to live his life any other way.

Despite the difficulties and emotional toll of caring for Grandpa as a family, there were always moments of relief and humour. He became mostly unfazed by his hallucinations – as we learnt when he informed us about the night he discovered a huge horse (a creature of which he was always wary) lying in bed with him and he responded by simply turning over to go back to sleep.

After a goodnight kiss and “See you in the morning”, he would often respond with something along the lines of, “We’ll see about that” or “If you’re lucky”. The humour Grandpa found in his own mortality reflected an acceptance of death he had developed from an early age to cope with the grief in his life. However, I would like to imagine that, during these final years spent with us, this acceptance instead stemmed from the knowledge that he was loved and cared for dearly. That despite the hallucinations, there was absolute clarity in the care he felt from my family.

We were all deeply affected by DLB, and some of this pain lingers still, yet the truth is we knew that Grandpa needed us and our daily commotions to ground him. Surrounded by life and the patterns of our home, the dementia would be quelled for a while and I would watch him in his sun-soaked armchair, at peace.

[Source: Daily Telegraph]