A substance found in chilli peppers has been used to create a painkiller which prevents suffering without the usual side-effects of conventional anaesthetics, such as unconsciousness and paralysis. The new drug can be targeted against only those nerves involved in sending pain signals to the brain, making pain relief far more effective and safer than existing anaesthetics, researchers believe.

They also think the new analgesic could benefit people suffering from so-called pathological pain – long-term discomfort which is not caused by any obvious injury – as well as chronic itching which can seriously affect quality of life.

A painkiller that blocks only pain neurons – the nerve cells leading to the central nervous system – could allow women to give birth painlessly using an epidural which does not paralyse the lower body, or allow a patient to have open-heart surgery while remaining conscious.

"Current nerve-blocks cause paralysis and total numbness. We're offering a targeted approach to pain management that avoids these problems. This new strategy could profoundly change pain treatment," said Clifford Woolf, of the Massachusetts General Hospital in Boston, who led the study with Bruce Bean, of Harvard Medical School.

"Eventually, this method could completely transform surgical and post-surgical analgesia, allowing patients to remain fully alert without experiencing pain or paralysis. In fact, the possibilities seem endless," Dr Woolf added.

"I could even imagine using this method to treat itch, as itch-sensitive neurons fall into the same group as pain-sensing ones."

The new painkiller is based on combining two molecules. One is normally an inactive ingredient of the local anaesthetic lidocaine, called QX-314, and the other is capsaicin, the chemical in chilli peppers that makes them taste spicy or feel hot when rubbed on the skin.

When combined, the two molecules create an analgesic that works only on pain-sensitive nerves and leaves other types of nerves unaffected, the scientists found. Their study, published in the journal Nature, found it to be effective in laboratory tests on rats. When injected into the animals' paws, the drug anaesthetised the rodents against heat and pain but their movements and other normal bodily functions were unaffected. The effects lasted for up to two hours.

Further work is needed before tests can begin on humans but Dr Woolf believes the drug will work. He said: "We are optimistic that this method will eventually be applied to humans and change our experience during procedures ranging from knee surgery to tooth extractions."

The secret of how the two molecules combine to kill pain lies in how they target a molecule "pore" which exists only in the membrane of nerve cells involved in pain detection. By blocking the opening of the pore, the scientists, in effect, disconnected pain-sensitive nerve cells.

"We introduced a local anaesthetic selectively into specific populations of neurons," said Professor Bean. "Now we can block the activity of pain-sensing neurons without disrupting other kinds of neurons that control movements or non-painful sensations."

Story Landis, of the US National Institute of Neurological Disorders and Stroke, which funded the research, said it could be a landmark in the development of new painkillers.

"The holy grail in pain science is to eliminate pathologic pain without impairing thinking, alertness, co-ordination, or other vital functions of the nervous system," Dr Landis said.

"This finding holds the promise of major future breakthroughs for millions of people who suffer with disabling pain."

How it works

Conventional painkillers work by blocking the tiny channels in nerve cell membranes, which are essential for a cell to function properly. However, as well as blocking pain, anaesthetics also block anything to do with movement or non-pain sensations, causing paralysis, numbness or unconsciousness. The new drug works specifically against a type of channel called TRPV1, which exists only in the membrane of pain cells. The drug has two active ingredients which work together in unison. The capsaicin molecule from chilli peppers opens the TRPV1 channel and allows it to act as a gate through which the second molecule, derived from the anaesthetic lidocaine, enters pain-sensitive cells.

(Por  Steve Connor, The Independent, 04/10/2007)