ANNA can be walking happily one moment, and the next her legs freeze and she
cannot take another step. Suddenly she feels disconnected from her body, as if
she were looking at herself from a distance. It’s a sensation that can bring on
a panic attack.
This frightening, frozen state is one of the most common and debilitating
symptoms of Parkinson’s disease. Anna’s only option to release herself is to
take off her belt, lay it on the ground in front of her and step over it. Once
she’s going again she can carry on—until the next time.
Another Parkinson’s patient carries a walking stick with a folding extension
at the bottom. When he freezes, he flicks a switch which releases the extension,
James Bond style, so that it lies horizontally across his path. He can step over
it and carry on walking. Others use the patterns on carpets or checks on
lino.
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All these people are using the same curious process to release themselves
from their disease. That process is now at the heart of an experimental
technique which promises to let people with Parkinson’s walk or even run without
fear of freezing. It needs no drugs and has no apparent side effects. It’s all a
matter of fooling the brain.
Parkinson’s disease is suffered by about 1.5 million Americans and some 120
000 Britons, most of them over the age of 55. It’s a progressive neurological
disorder stemming from the death deep in the brain of cells that produce the
neurotransmitter dopamine. What triggers the destruction of these cells is not
known, and as yet the disease is incurable. People with Parkinson’s find that
their muscles become rigid, and they walk with a tottering, running gait. Many
people also develop a constant tremor. But the worst symptom is akinesia, where
a person’s stride length gets gradually shorter until they become frozen to the
spot.
Since the late 1960s, doctors have treated severe Parkinson’s with L-dopa,
the chemical precursor of dopamine. This added boost of dopamine can have a
dramatic effect, freeing people trapped by akinesia. But the drug has its
drawbacks. For a start, a patient’s response can vary widely over the course of
a dose, so a woman like Anna can suddenly freeze as the L-dopa level falls below
the therapeutic threshold. The second disadvantage is that after a while
patients on L-dopa begin to develop symptoms at the opposite extreme—they
suffer from dyskinesia, or too much movement. They begin to move uncontrollably,
with head rocking and shoulders and arms continually jerking.
It is these movement problems that the new technique is designed to deal
with. Made possible by advances in virtual reality technology, it relies on a
paradox at the heart of Parkinson’s akinesia, known as “kinesia paradoxa”. That
is, patients who find themselves frozen can often climb the stairs or step over
obstacles. This is how Anna frees herself when she steps over her belt.
The technique is the brainchild of Tom Riess of San Anselmo, California, who
has suffered from Parkinson’s for 16 years. Riess, who was a foot surgeon, was
diagnosed at the age of 33 and began to notice his own sensitivity to visual
cues. “Even though I was totally incapable of walking I could move normally up
and down stairs,” he says. “This led me to explore what was unique to stairs
that enabled gait.”
Riess found out for himself that by placing small objects, even pennies, on
the floor at intervals in front of him he could walk when otherwise he would be
frozen to the spot. What he needed, he reasoned, was a way to carry these visual
cues around with him. There followed a series of “bizarre contraptions”
including a device made of sticks and sprockets from a toy construction set and
another with camera lenses that repeatedly “zoomed in”, giving the wearer the
impression of moving forward faster than they actually were; he even tried
sticking things to his shoes.
Then, in 1993, Riess heard about Virtual Vision, a company that had produced
a prototype head-mounted display called the Sport. He contacted the company, a
spin-off from the Human Interface Technology Laboratory at the University of
Washington, Seattle, and so began his collaboration with Suzanne Weghorst, a
psychologist and HITL’s director of interface design.
Although the Sport can be used to immerse the wearer in virtual reality, it
can also generate augmented reality. “The idea is to stick something on top of
the real world without obliterating it,” says Riess. The Sport consists of a
visor with a liquid crystal display mounted above one eye. The image on the
display is projected back into the eye by a reflecting lens stuck to the tinted
visor below the line of vision. As with immersive virtual reality, the image is
distorted so that it appears to come from a couple of metres in front of the
eye.
Last year Riess and Weghorst published their first results (Interactive
Technology and the New Paradigm for Healthcare, K. Morgan and others, IOS
Press). Preliminary trials on about 20 Parkinson’s patients, including Riess
himself, showed that the virtual cues allowed akinetic patients to walk normally
and even run. But the spacing of the cues was vital. To initiate the first step,
a cue needed to appear directly in front of the toes, and thereafter successive
cues needed to scroll towards the feet at stride-length intervals—so they
appear stationary on the floor.
Looking good
Images of simple horizontal lines usually did the trick, but people with
severe akinesia needed bolder lines, projected closer to the centre of the
visual field. To their surprise, Riess and Weg-horst found that the visual cues
also helped to alleviate dyskinesia. To Riess, this suggests that akinesia and
dyskinesia “are very likely manifestations of the same underlying
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The Sport weighs only 150 grams and can be worn like sunglasses, so it has
the mobility that Riess had searched for. In addition, it costs about
$600, which is a snip compared to the price of an immersive head-mounted
display—last April, the British Journal of Therapy and
Rehabilitation put the price of a good quality immersive display at
£65 000. And because, in this application, the Sport’s reality is only
augmented, it produces none of the motion sickness seen with immersive VR.
But it also has drawbacks. Riess feels that because the visor looks odd its
appearance is “not socially acceptable”. Also the wearer needs to carry a video
player and other equipment. “A full video signal, and its accompanying playback
hardware and cables, was really overkill for this application—and
difficult for an average Parkinson’s patient to use,” says Weghorst. “But it
proved the concept.”
Although Weghorst maintains an interest in the area, HITL has bowed out of
the project. Riess, however, has not given up. “He’s the ultimate in tenacity,”
says Weghorst. “It’s his life.” He has set up a company, called HMD
Therapeutics, with a view to designing more practical and socially acceptable
systems, and getting the Food and Drug Administration to approve them.
One of his models has a battery, electronics, speed control, a vertical array
of light-emitting diodes and a cylindrical lens all crafted into the side bars
of a pair of wrap-around sunglasses. The lens changes each point of light from
the diodes into a horizontal bar and projects it onto a transparent, curved
screen in front of one eye. When the diodes light up in sequence, the wearer
sees the bars moving downwards in front of the eye (see
Diagram).
This model, which is now being tested by researchers at the National
Institutes of Health, needs no video display. Riess admits that it is still not
perfect: wearers need to tilt their heads downwards slightly so the lines appear
to move along the floor. But he thinks he’s already solved that problem—by
projecting a pattern like telegraph poles whizzing past the periphery of both
eyes. “All you seem to need is a sense of motion through the environment,” he
says.
According to Peter Fletcher, a physician at the Delancey Hospital in
Cheltenham, Gloucestershire, who treats people in the later stages of
Parkinson’s, the idea is “a brilliant piece of lateral thinking”. He stresses
that the idea of people unfreezing themselves with visual cues is nothing new:
he teaches the technique in his therapy groups.
Precisely how visual cues jar the brain into action is still a matter of
debate. Parkinson’s disease is caused by the death of cells in the substantia
nigra, one of a group of nerve centres deep in the cerebral hemispheres known as
the basal ganglia. A few years ago, these organs were found to regulate signals
sent to the muscles by the motor cortex, where instructions to make complex
movements are planned and generated. The basal ganglia appears to fine-tune, or
smooth, these signals. (“The intricate wiring that lets us move”, New
Scientist, 10 March 1990, p 60).
Fletcher believes kinesia paradoxa works because visual cues stimulate a
separate, intact motor circuit in the brain. “There are two ways into the motor
cortex,” says Fletcher—via the premotor cortex or the basal ganglia. If
the basal ganglia is damaged then people have movement difficulties. “So you
initiate it via a different route. And vision is the route we use.” This
explanation, he says, is conceptual and not anatomically proven.
Contrasting problems
Parkinson’s disease used to be thought of as a disease that just affected the
circuitry in the brain devoted to motor functions, but this view is too
simplistic, says Weghorst. “While that is undoubtedly the primary site of the
disease, our results suggest that some of these symptoms may actually be due to
an interplay between the visual processing and motor control parts of the
brain,” she says. Cognitive problems in Parkinson’s patients are now well
documented, including visual deficits such as reduced sensitivity to contrasts
of light.
Riess has his own ideas about what is happening in the brain. He believes
that the importance of visual cues suggests that the basal ganglia normally feed
back sensory data to the cortex about how a person is moving in relation to the
outside world. This feedback takes place below the threshold of consciousness
and allows a person to perform automatic actions such as walking. The abnormal
gait of Parkinson’s patients, he says, arises when the basal ganglia’s ability
to perform this task is impaired. “What we believe we’re doing is supplying some
missing optical flow information that tells the brain how the person is moving,”
says Weghorst.
Riess and Weghorst see virtual-reality technology as a prosthesis for
Parkinson’s patients rather than a treatment—more akin to a pair of
glasses for the visually impaired. “The fact that VR works as a therapeutic aid
in Parkinson’s disease will not lead to the discovery of the underlying causes,”
says Riess. “However, studying this phenomenon should be very useful in
understanding better how the brain works and interacts with the external
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There could also be long-term benefits for someone with Parkinson’s. L-dopa
is only effective for a limited time, says Fletcher. This “window of
opportunity” ends when side effects such as dyskinesia set in, and the drug
becomes less effective. Particularly in younger people, doctors try to use other
drugs to keep Parkinson’s at bay for as long as possible, holding back the trump
card, L-dopa, for the more advanced stages. Weghorst speculates that Riess’s
glasses may replace drug treatment to some extent, allowing doctors to withhold
L-dopa for longer.
In the distant future, she says, the visual cues could be provided by some
kind of retinal or brain implant. Until then, lightweight glasses are the most
feasible approach for alleviating the symptoms of an insidious disease. Riess
has a powerful motive for perfecting the approach: when he takes his glasses
off, he freezes. “They’re like an on-off switch,” he says. “Once I had a tool
which could impact the disease, I could not put it down.”
