UC Davis Medical Center surgeons have demonstrated that artificial muscle can restore the eyeblinking ability in patients with facial paralysis.

The development that could benefit the thousands of people each year who no longer are able to close their eyelids due to stroke, nerve injury, facial surgery or combat-related injuries.

The technique, which uses a combination of electrode leads and silicon polymers, could be used to develop synthetic muscles to control other parts of the body.

The new procedure is described in an article in the January-February issue of the Archives of Facial Plastic Surgery.

“This is the first-wave use of artificial muscle in any biological system,” said Travis Tollefson, a facial plastic surgeon in the Department of Otolaryngology, Head and Neck Surgery. “But there are many ideas and concepts where this technology may play a role.”

In their study, Tollefson and his colleagues sought to develop the protocol and device design for human implantation of electroactive polymer artificial muscle, or EPAM, to create a long-lasting eyelid blink that would protect the eye and improve facial appearance.

EPAM is an emerging technology that has the potential for use in rehabilitating facial movement in patients with paralysis. Electroactive polymers act like human muscles by expanding and contracting, based on variable voltage input levels.

For people with other types of paralysis, the use of artificial muscles could someday mean regaining the ability to smile or control the bladder. Reanimating faces is a natural first step in developing synthetic muscles to control other parts of the body, said Craig Senders, a UC Davis otolaryngologist.

“Facial muscles require relatively low forces, much less than required to move the fingers or flex an arm,” Senders said.

Why blinking is essential

Blinking is an essential part of maintaining a healthy eye. The lid wipes the surface of the eye clean and spreads tears across the cornea. Without this lubrication, the eye is soon at risk of developing corneal ulcers that eventually can cause blindness.

Involuntary eye blinking is controlled by a cranial nerve. In most patients with permanent eyelid paralysis, this nerve has been injured due to an accident, stroke, or surgery to remove a facial tumor. Many patients have no other functioning nerves nearby that can be rerouted to close the eyelid. Other patients have been born with Mobius syndrome, characterized by underdeveloped facial nerves. These patients are expressionless and can neither blink nor smile.

Today, eyelid paralysis is treated by one of two approaches.

One is to transfer a muscle from the leg into face. However, this option requires six to10 hours of surgery, creates a second wound, and is not always suitable for elderly or medically fragile patients.

The other treatment involves suturing a small gold weight inside the eyelid. The weight closes the eye with the help of gravity. Though successful in more than 90 percent of patients, the resulting eye blink is slower than normal and cannot be synchronized with the opposite eye. In addition, some patients have difficulty keeping the weighted lid closed when lying down to sleep. In the United States, an estimated 3,000 to 5,000 patients undergo this surgery every year and therefore might benefit from an alternative treatment.

For their study, Senders and Tollefson inserted an eyelid sling mechanism (made from implantable fabric or muscle fascia) into a c, using titanium screws to secure it to the bones around the eye.

The doctors connected the mechanism to battery-operated artificial muscle, disguising the presence of the muscle device and battery by implanting them into a natural hollow, or fossa, at the temple.

When activated, the sling produces a blink — but only if the sling has sufficient force and stroke, as powered by the artificial muscle. Senders and Tollefson found the artificial muscle to be more then capable of doing the job. This capability may allow the creation of a realistic and functional eyelid blink that is symmetric and synchronous with the normal, functioning blink.

Artificial muscle and the power to blink

Engineers at SRI International in Palo Alto developed the three-layered artificial muscle in the 1990s. Inside is a piece of soft acrylic or silicon, layered with carbon grease. When a current is applied, electrostatic attraction causes the outer layers to pull together and squash the soft center. This motion expands the artificial muscle. Then, when the charge is removed, the muscle contracts — and, in the case of the sling mechanism for blinking — flattens the shape of the sling. As the sling flattens, the eye blinks. When the charge is reactivated, the muscle relaxes and the soft center reverts back to its original shape.

“The amount of force and movement the artificial muscle generates is very similar to natural muscle,” Tollefson said. An implanted battery source similar to those used in cochlear implants would power the artificial muscle.

For patients who have one functioning eyelid, a sensor wire threaded over the normal eyelid could detect the natural blink impulse and fire the artificial muscle at the same time. Among patients lacking control of either eyelid, an electronic pacemaker similar to those used to regulate heartbeats could blink the eye at a steady rate, and be deactivated by a magnetic switch.

The researchers are now refining the technique on cadavers and animal modes. They estimate the technology will be available for patients within the next five years.

A grant from the American Academy of Facial Plastic and Reconstructive Surgery funded the study.

David Ong is a senior public information representative for the UC Davis Health System