An X-ray vision
23rd April 08
LIKE so many victims, he was a young man. The lesion was high up in the spinal cord at the level of the fifth and sixth vertebrae.
He was near death when he came in, but they saved him: his mind intact, his body paralysed from the neck down.
It was years ago, yet even now the patient’s words to the medical team still haunt Marios Papadopoulos: ‘I hate you all. You resuscitated me — and I can’t even kill myself.’
Back then Marios was a second-year registrar at the old
‘Spinal cord injury is bad because it happens to young people. Any way you look at it, the outcome is pretty devastating,’ says Marios, 41.
‘You are looking at someone who is going to have near-normal life expectancy, but is going to be disabled for the rest of their life. There is no treatment to improve outcome.
‘These people are so desperate. If you are paralysed from the neck down, what is there to do?’
New research by Marios and colleagues, to be published in the journal Brain, may go some way towards answering that question. It follows several years of work on aquaporins — water-channel proteins — in the central nervous system.
In the brain, AQP4 (aquaporin-4) is important in water balance and in scar formation in the glial cells that support neurones. Both are major factors that affect the outcome of an injury.
The team’s new work focuses on the way in which AQP4 allows excess water to enter damaged spinal cord, leading to swelling and pressure — and, often, loss of function. Studies show that inhibiting AQP4 may protect the spinal cord and prevent what can otherwise be catastrophic injury.
For a patient with a spinal lesion, even limited damage prevention could make a significant difference, says Marios: ‘Unlike in the brain, in the spinal cord any neurones you save are useful. For example, it could be enough for you to stand and walk.’
Even if a patient were confined to a wheelchair, they could still retain, say, bowel and bladder function. Patients like the American actor Christopher Reeve, who was dependent on a ventilator for most of his life after spinal injury, might retain the ability to breathe unaided.
As yet no method of inhibiting AQP4 has been identified. This is the next task for Marios and his colleagues. One possibility is siRNA (small inhibitory RNA) technology, which involves using short molecular fragments to ‘switch off’ genes. Widely used in the lab, the process of using it on patients is more challenging.
Inevitably, such research is expensive. Funding so far has come from the Neurosciences Research Foundation, and the team is seeking grants to take their work further.
Marios and his
It’s a long-term partnership that demonstrates the high international profile of
It was at the
The unit is one of the busiest in the country — and, apart from the
Marios divides his time between patients and research. He believes surgical training pays dividends in academic terms. ‘In surgery, when you’re there at 3am and things are going wrong, you become good at seeing a shorter way from point A to point B.’
He thrives on the inherent uncertainty of neurosurgery: ‘It’s like a fighter pilot. They send you to achieve a mission, but there are so many unknowns in the way.
‘You can only find out by doing it. You can’t learn as a junior doctor on the wards. You have to be there, holding the knife.
‘But there’s confidence, and there’s arrogance. Anything can go wrong at any time. Humility is the best quality you can have, because at the end of the day in neurosurgery you are operating on an organ that you can’t even begin to understand.’
To make a donation to Neurofund, the fundraising arm of the Neurosciences Research Foundation, contact neurosurgery@sgul.ac.uk or write to St George’s, University of London Academic Neurosurgery Unit, Cranmer Terrace, London SW17 0RE
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