In clinical trials, an improved interface for this type of prosthetic arm allowed volunteers to use their limbs to perform a variety of tasks up to seven times faster than before, after only minimal training. Previous systems only allowed people to make a few movements, one after the other, but the new one can be used to direct 16 distinct arm, hand and finger movements.

The approach, called targeted muscle reinnervation (TMR), was first proposed by Gerald Loeb, a professor of biomedical engineering at the , in Los Angeles, US. He suggested in 1980 that it might be possible to detect and use signals from the motor and sensory nerves that once served a severed limb to control a prosthetic, by reconnecting them to nearby muscle and skin.

The idea was taken up by , then a medical student and now a pioneering rehabilitation researcher at the (RIC), and , also in Chicago, US.

Surviving motor and sensory nerves are first surgically separated from the stump of a patient’s arm. Nerves serving chest muscles that once helped support and move the missing limb, but that are no longer useful, are also cut. The motor nerves once used to control the patient’s arm are then grafted to those connected to the chest muscles, while the sensory nerves from the missing arm are redirected to tissue under the skin of the chest.

“All the information is still contained in the nerves,” because the brain continues to send movement signals to the amputated limb, says , a biomedical engineer working with Kuiken at the RIC.

Once the reattached nerves become functional again, within four to six months, patients can feel their chest muscles contract when they think of moving their arm or hand. They can also feel pressure, heat, or vibration in their chest as if it were coming from their missing arm or hand.

The chest muscles act as a “biological amplifier” of the patient’s natural nerve impulses, says Kuiken, while the overlying skin can receive tactile feedback from the prosthetic arm, hand, or fingers.

In a forthcoming article in the Kuiken’s group describes how it has now refined the interface that detects and interprets electrical signals from reinnervated chest muscles.

This lets the system determine what movement the patient wants to make and command the artificial limb to make the desired movement more effectively.

Previous versions of Kuiken’s system were only able detect and use two movements, opening or closing the hand and bending or extending the elbow. The team expects that patients will be able to do far more with this method, with 16 coordinated movements being possible.

Bernard Hudgins, Director of Biomedical Engineering at the University of New Brunkswick, at Fredericton, New Brunswick, Canada, applauds Kuiken’s work. “Even given current limitations, TMR has proven its worth as a new approach in treating individuals with high-level amputations,” he says.

The key is a player’s level of testosterone, the hormone related to both sex
and aggression. Testosterone levels are known to be higher in men who are
sexually active. Researchers have often assumed that a low sex drive is a
consequence of low levels of testosterone, but studies by Emmanuele Jannini of
the University of L’Aquila in Italy show that testosterone levels rise after an
increase in sexual activity.

Jannini measured testosterone in the blood of more than 80 patients with
long-term impotence. He found that while the impotent men’s testosterone levels
were about two-thirds those of sexually active men their age, they were not low
enough to cause impotence.

After three months of psychological, mechanical or medical therapy, which did
not include hormone treatment, Jannini and his colleagues found a dramatic rise
in testosterone levels in the men who were treated successfully. Those who made
a partial recovery had a smaller rise in testosterone. But men whose treatment
wasn’t successful continued to produce low amounts of testosterone.

Because the testosterone level rose with the amount of sexual activity, and
was not related to the source of the impotence or the type of treatment, Jannini
believes he can sort cause from effect. “It didn’t matter which type of therapy
we used, as long as the therapy worked,” he says. “It’s the restoration of
sexual activity that raises testosterone to normal levels.”

Jannini thinks that in men the body adjusts testosterone levels to match
sexual drive to the level of sexual activity, and the same may be true for
women. “It’s an adaptive mechanism,” he says. “If a man has sexual intercourse,
testosterone causes him to desire the next sexual intercourse.”

The lesson that sportsmen can draw from the research is that the decision
whether to abstain from sex before a game depends partly on whether the sport
requires aggression and partly on the player’s character. “We discuss this each
Sunday before the games,” says Jannini. “Some athletes think it’s important not
to have it. It’s a matter of the character of the athlete. If he needs to be
more aggressive it’s better to have sex,” he says.

David Handelsman, a doctor who studies reproductive medicine at the
University of Sydney, says the research is thought-provoking and sheds new light
on what testosterone does. “This is the first clear evidence in the vexed
relationship between male sexuality and testosterone,” he says. “There’ve only
been three good, large-scale, placebo-controlled treatment studies.” He says
none of these studies provided data about testosterone levels before and after
treatment.