Autumn rain: being damp is inferred rather than truly felt. Photo: Getty
Show Hide image

On our nerves: what makes us itch or feel wet?

Michael Brooks’s science column. 

We’re all going to feel some unwanted damp on the skin over the next few weeks – welcome to autumn. But for those who feel wet due to a medical condition rather than the weather, researchers at Loughborough University have made what might just prove to be a welcome breakthrough.

It starts with a seemingly innocuous question: what makes wet stuff feel wet? By the end of this exploration, we will have encountered Joni Mitchell, patients with multiple sclerosis (MS) and a host of people suffering in ways that evoke Dante’s Inferno.

To some animal species, wetness is so critical to survival that evolution has equipped them to determine their state of external hydration: insects have humidity sensors. Human beings, however, don’t have wetness sensors on their skin, so understanding how we differentiate the sense of wetness from other sensations is a puzzle.

We have found clues in some of the tricks one can play on our species. The Loughborough researchers have shown that if you reduce the skin’s temperature using a dry cooling method, people feel as though their skin is wet. If you put something wet in contact with the skin, but at a temperature warmer than it, people don’t perceive it as wet.

So, clearly, we don’t feel wetness, we infer it. Our skin has an array of sensors for temperature and pressure, and it is a combination of these senses which tells us that something we are touching is wet. To find out what that combination might be, the Loughborough team experimented on 13 students, blocking and releasing their nerve sensitivities.

It turns out that crucial to wetness perception are nerves known as A-nerve fibres. Block the blood supply to these – using something like a blood-pressure cuff – and you become far worse at sensing wetness. Unsurprisingly, it is easier to sense cold wetness than warm wetness. The interplay of these different sensitivities enabled the researchers to create a model for the brain’s interpretation of wetness; in essence, it applies a weighting to each set of inputs in order to come to a probability-based conclusion on the body’s state.

This is more than an academic discovery because skin sensitivity is a serious medical issue. People suffering with MS frequently report an unpleasant feeling of cold wetness on their skin. It is a couple of short steps from feeling cold wetness to pain. One side effect of diabetes, for instance, can be dysaesthesia, when diabetics experience a burning or stabbing sensation on their skin, or feel the slightest touch from clothing or bedlinen as excruciating pain. In other cases, some diabetics can’t feel heat or touch sensitively enough to avoid injuring themselves.

It’s not just about the side effects of recognised diseases, though. There are various medical conditions associated with nerves sending pain signals in response to (apparently) nothing. Sufferers of central pain syndrome can report sensations such as being torn apart with hot knives, or being burned alive. No wonder it gets referred to as a Dante-type condition. Another oddity is Morgellons Disease. Joni Mitchell is perhaps the best-known sufferer of this unstoppable itching, which feels as if something is crawling under the skin. The medical orthodoxy is that the condition is indicative of a psychiatric disorder. However, if we knew more precisely what our skin’s nerve endings transmit to the brain, we might be able to help sufferers, delusional or not. 

Michael Brooks holds a PhD in quantum physics. He writes a weekly science column for the New Statesman, and his most recent book is At the Edge of Uncertainty: 11 Discoveries Taking Science by Surprise.

This article first appeared in the 08 October 2014 issue of the New Statesman, Grayson Perry guest edit

Getty
Show Hide image

An antibiotic-resistant superbug is silently spreading through UK hospitals

There have already been outbreaks in Manchester, London, Edinburgh, and Birmingham, but deaths are not centrally recorded. 

Lying in a hospital bed, four months pregnant, Emily Morris felt only terror. She had caught a urinary tract infection and it was resistant to common antibiotics. Doctors needed to treat it as it could harm the baby, but the only drugs that could work hadn’t been tested on pregnant women before; the risks were unknown. Overwhelmed, Emily and her husband were asked to make a decision. A few hours later, gripping each other’s arms, they decided she should be given the drugs.

In Emily’s case, the medicine worked and her son Emerson (pictured below with Emily) was born healthy. But rising antibiotic resistance means people are now suffering infections for which there is no cure. Doctors have long warned that decades of reliance on these drugs will lead to a "post-antibiotic era"– a return to time where a scratch could kill and common operations are too risky.

It sounds like hyperbole – but this is already a reality in the UK. In the last four years 25 patients have suffered infections immune to all the antibiotics Public Health England tests for in its central lab, the Bureau of Investigative Journalism has discovered.

While these cases are rare, reports of a highly resistant superbug are rising, and infection control doctors are worried. Carbapenem resistant enterobacteriaceae (CRE) are not only difficult to pronounce, but deadly. These are bugs that live in the human gut but can cause an infection if they get into the wrong place, like the urinary tract or a wound. They have evolved to become immune to most classes of antibiotics – so if someone does become infected, there are only a few drugs that will still work. If CRE bacteria get into the bloodstream, studies show between 40 per cent and 50 per cent of people die.

These bugs are causing huge problems in India, certain parts of Asia, the Middle East and some countries in southern Europe. Until recently, most infections were seen in people who had travelled abroad, had family members who had, or had been in a foreign hospital. The boom in cheap cosmetic surgery in India was blamed for a spate of infections in Britain.

Now, doctors are finding people who have never boarded a plane are carrying the bug. There have already been outbreaks in Manchester, London, Liverpool, Leeds, Edinburgh, Birmingham, Nottingham, Belfast, Dublin and Limerick among other areas. Patients found with CRE have to be treated in side rooms in hospital so the bacteria does not spread and harm other vulnerable patients. But in many of Britain’s Victorian-built hospitals, single rooms are in sparse supply. Deaths from CRE aren’t centrally recorded by the government - but it is thought hundreds have already died. 

Across the country, doctors are being forced to reach for older, more toxic drugs to treat these infections. The amount of colistin – called the "last hope" antibiotic as it is one of few options still effective against CRE infections - rose dramatically in English hospitals between 2014 and 2015, the Bureau has revealed. Colistin was taken off the shelves soon after it was introduced, as it can harm the kidneys and nervous system in high doses, but was reintroduced when infections became immune to standard treatment. The more we use colistin the more bacteria develop resistance to it. It’s only a matter of time before it stops working too, leaving doctors’ arsenal near-empty when it comes to the most dangerous superbug infections.

Due to a kidney problem, Emily Morris suffers repeat urinary tract infections and has to be hospitalised most months. Her son Emerson comes to visit her, understanding his mummy is ill. If she catches a superbug infection, she can still be given intravenous antibiotics to stem it. But she worries about her son. By the time he is an adult, if he gets ill, there may be no drugs left that work.

Madlen Davies is a health and science reporter for the Bureau of Investigative Journalism