We are beginning to see the results of this research. In 1989 several investigators reported discovering the area in the brain responsible for the locking of the vocal cords in stutterers. This finding means that researchers may now begin to attempt to develop medications targeted to work in that area. It is conceivable that in the future stuttering might be treated by the simple expedient of taking a pill.

Researchers at the National Institutes of Health are attempting to deal with the problem of stuttering by injecting a chemical substance into the muscles which move the vocal cords. The action of this substance is to temporarily weaken or paralyze the cords, thus preventing them from locking. Preliminary findings have been have shown some reduction of stuttering and further research is underway with larger numbers of patients. It seems likely that one future approach to the treatment of stuttering may involve injections to the the vocal cords once or twice a year. Most individuals who stutter would probably be willing to undergo this procedure if they knew it to be effective.

Perhaps the most exciting line of research currently under way is based on a study recently conducted by the National Center for Stuttering in conjunction with a major New York hospital. In this study, we anesthetized the vocal cords in a group of four stutterers to determine if we could eliminate the neurological trigger for stuttering - the nerve impulses that report vocal cord tension to the brain. If the brain never realized there was tension on the vocal cords, stuttering could be avoided.

The nerves in the vocal cords are intricate mechanisms that actually serve two functions. On the one hand, they are sensory nerves, detecting tension within the vocal cord muscles and sending this information to the brain. On the other hand, they are also motor nerves, receiving impulses from the brain which instruct the vocal cords to contract or relax. Any procedure designed to numb the nerves must be able to isolate the sensory portion of the nerve, for numbing the motor portion as well would result in paralysis of the cords and then, of course, speech would be impossible.

Fortunately, the fibers within the nerve are arranged in such a way that we can selectively target the sensory function. The motor fibers carrying nerve impulses to the muscles are clustered together in the center, while the sensory fibers carrying nerve impulses from the muscles are arranged on the outer surface. When a nerve is injected with anesthetic, it is initially blocked in both directions, but after a period of time, usually about twenty minutes, the inner core (motor portion) recovers, followed by the outer surface. If our thinking was correct, injection to the nerves on both sides would result in immediate total paralysis of the cords followed by initial return of the motor ability to tense the cords followed by a return of sensation from the cords.

In all, four adult stutters received the injections. The first, a man of about forty-five, possessed a severe stutter of life-long duration. Ten minutes after receiving the bilateral injections he became aphonic - that is, he was unable to make any sound whatsoever; his paralyzed cords were too weak to approximate one another. He was able to mouth the words but they were rendered in silence.

Thirty-seventh minutes following the injection a weak breathy voice started to be heard. And over the course of the next twenty-six minutes the voice became progressively stronger as the anesthetic in the inner core of both nerves wore off.

The remarkable aspect of this patient's speech was that during the twenty-six minute period he was totally fluent - not only on words spoken in isolation, but also in sentences, ongoing conversations, and even telephone calls. After this period of fluency, he gradually began to stutter as the sensory portion of his nerve recovered from the effects of the anesthetic. During the next twelve minutes he completely relapsed into his former stuttering pattern.

The other three patients in the study demonstrated similar responses: first total loss of voice, followed by a weak but fluent voice which regained strength progressively, and then lastly an initial mild stutter which over a relatively short period of time attained its preanesthetic level of severity.

This finding confirmed our hypothesis that if we could selectively block the outer (sensory) surface of the nerve fibers going to the vocal cords we could probably eliminate stuttering.

One of my colleagues at New York University is now working on just such an approach. The work is at the test tube stage, though. Small portions of mixed nerves taken from animals are being kept alive in supportive media while a variety of enzymes are being applied to the nerves. Some of these enzymes have an affinity for sensory nerves - in a sense, they eat them. Studies are underway to find the best approach that most cleanly eliminates the sensory nerves while leaving the motor portions intact.

The implication of this line of inquiry is obvious: if we can prevent the brain from receiving sensory information from the cords we will have removed the trigger for stuttering and there will be no stuttering. Furthermore, all that would likely be required would be a single injection on either side of the larynx administered once. The patient would be rendered fluent on a permanent basis.

In another area of research, it has been shown that if a stutterer speaks against a very loud background noise, the stuttering tends to be totally eliminated. Indeed, in the ancient literature of stuttering there is occasional mention of individuals whose stutter was totally absent when they spoke near the base of a waterfall.

Many explanations have been developed to account for this waterfall phenomenon. Some feel that the loud noise serves as a distraction, while others say that the presence of the noise somehow leads the stutterer to conclude that his words will not be heard and this in turn reduces stress and produces fluency.

This historical experience of a loud noise tending to eliminate stuttering formed the basis for the development by a team of researchers at the University of Edinburgh of an electronic device known, appropriately, as the Edinburgh Masker. The principle of its operation is quite simple. A microphone is attached to the patient's neck by an elastic band. When the vocal cords start to vibrate, the vibration is detected by the microphone and the impulses are sent to a small device known as a white noise generator. White noise sounds very much like hissing steam. As soon as the white noise generator receives the impulses from the throat microphone it becomes activated and the sound is amplified and sent through earphones worn by the patient.

This creates the following situation: when the patient is silent the noise is off and he can hear the speech of others around him but as soon as he starts to speak the noise comes on and it is of sufficient loudness that he is unable to hear himself. This tends to stop stuttering, but the price the patient must pay is obvious. First is the paraphernalia that must be worn at all times - a throat microphone, an amplifier, noise generator, earphones and the associated wiring to connect them. The patient is also obviously dependent on batteries and the hope that they do not run out in the middle of a conversation. Second, there is some evidence to suggest a possibility of nerve damage to the hearing nerves when there is prolonged exposure to loud noise. And third, there is the difficulty associated with phone conversations, since the earphones do not permit the convenient placement of the telephone against the ear.

There is one other serious problem associated with the device. The noise generator comes on initially after the first sound is produced, but as we have discovered, the locking of the vocal cords occurs before speech begins. And so the Masker is inoperative during the critical prespeech period. The result is that the cords are still free to lock. In order to deal with that problem, one is often forced to use a starter, such as a brief humming sound to get the Masker going to deal with this deficiency.

The principle behind the Masker is an admirable one. The waterfall effect is real. The reason it works, however, did not come to light until recently. The hearing nerve, as it courses to the brain, attaches to the nerves coming up from the vocal cords. There is a co-mingling of fibers and impulses. When a loud noise is presented to the ears a very strong signal comes up the hearing nerve, and this signal, when it co-mingles with the vocal-cords nerve signals alters them. This altered signal is no longer the correct stimulus for triggering stuttering - and no stutter occurs.

In the future small implantable devices will be placed in the middle ear to accomplish the same end. They will make use of the hearing nerve to intercept the impulses coming up from the vocal cord nerves so that the impulses no longer have cue value to elicit stuttering.

It is clear from the foregoing that what every stutterer in the world is looking for is an expeditious cure. A cure that requires no effort. The prospects for the future are thus particularly appealing because they are passive. Apart from the act of presenting himself for treatment, the patient is not called upon to participate in any way in his recovery. In addition, the treatment usually requires a single intervention and the recovery period is short.

It is my belief that by the year 2006 some of these approaches will begin to be manifest. Research is well under way and knowledge is accumulating at a rapid rate. The next chapter in the treatment of stuttering will probably read, Stuttering: Its Speedy, Total, and Permanent Cure.