IMPLICATIONS FOR THE FUTURE
What does the future hold? Much promise, I think. The creation of a National
Institute of Communication Disorders in Washington, D.C. has insured substantial
and continued Federal funding for research into stuttering.
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
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.
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