text:
Speech-Language Pathology/Stuttering/Stuttering Modification

Stuttering modification therapy is primarily associated with Charles Van Riper.

The goal of stuttering modification therapy is not to eliminate stuttering. Instead, the goals are:

 Modify your moments of stuttering, so that your stuttering is less severe. Reduce your fear of stuttering, and eliminate avoidance behaviors associated with this fear.

Four Phases of Stuttering Modification Therapy
The therapy has four phases: identification, desensitization, modification, and stabilization.

Identification
You begin by identifying the core behaviors, secondary behaviors, and feelings and attitudes that characterize your stuttering.

Your speech-language pathologist points out your "easy or effortless stuttering." You learn to identify when you do these behaviors. The goal is to improve your awareness of what you do when you stutter.

Next, your speech pathologist trains you to identify and become aware of your avoidance behaviors, postponement behaviors, starting behaviors, word and sound fears, situation fears, core stuttering behaviors, and escape behaviors.

Finally, you identify feelings of frustration, shame, and hostility associated with your speech.

At first, identifying these behaviors is done in the speech clinic. Later, your speech pathologist takes you out of the clinic, to identify what you do in everyday conversations.

Desensitization
Van Riper called this "toughening the stutterer to his stuttering." You do this in three stages:

 Confrontation, or accepting that you stutter. You're expected to tell people that you stutter, and talk about what you are doing in therapy to change your stuttering. Freeze your core behaviors—repetitions, prolongations, and blocks. When you stutter, your speech pathologist raises a finger. You hold what you are doing, until she drops her finger. For example, if you were repeating a syllable, you have to continue to repeat that syllable. Your speech pathologist will make you freeze these core behaviors for longer and longer periods. The goal is for you to become less emotional or more tolerant of these behaviors.  Voluntary stuttering, or stuttering on purpose. This helps you remain calm when you stutter.

Modification
This is where you learn "easy stuttering" or "fluent stuttering," in 3 stages:

 Cancellations. When you stutter, you stop, pause for a few moments, and say the word again. You say the word slowly, with reduced articulatory pressure, and blending the sounds together.

Pull-outs. After you master freezing and cancellations, you use your "easy stuttering" while you are in a stutter, to pull yourself out of the stutter and say the word fluently.

Preparatory sets. After mastering pull-outs, you look ahead for words you're going to stutter on, and you use "easy stuttering" on those words.

Stabilization
The last stage of stuttering modification therapy seeks to stabilize or solidify your speech gains. This is accomplished through sub-goals:

The first is for you to become your own speech therapist. You take responsibility for making your own assignments and prescribed therapy activities.

Another sub-goal is "the automatization of preparatory sets and pull-outs."

The last subgoal is for you to change your self-concept from being a person who stutters to being a person who speaks fluently most of the time but who occasionally stutters mildly.

Efficacy Studies
A study indicated that naïve or nonprofessional listeners responded less well to stuttering combined with stuttering modification techniques than they did to stuttering (only). In other words, listeners may prefer to listen to untreated stuttering than to listen to a stutterer using stuttering modification therapy techniques.

Nineteen adult stutterers participated in the 3.5-week Successful Stuttering Management Program (SSMP, developed by Dorvan Breitenfeldt) program. Immediately post-treatment their speech had improved 10%. Six months later this modest gain had all but disappeared. Several measures of anxiety found a 10-15% psychological improvement. The researchers cautioned that six months isn't a long follow-up, and that this psychological improvement might not last, given the absence of improved speech. The researchers concluded, "…the SSMP appears to be ineffective in producing durable improvements in stuttering behaviors."

Approach-Avoidance Therapy (Joseph Sheehan)
In the 1940s, behavioral psychologist Neal Miller tied strings to rats, and sent them scampering down a runway towards food. He measured how hard the rats pulled on the strings to get to the food. He called this force the "gradient of force."

He then put an electric shock at the end of the runway, instead of food. The rats scampered away from the electric shock, and Miller called this the "gradient of avoidance."

He put the food and the electric shock together at the end of the runway. The rats wanted to scamper to the food, but away from the electric shock. They ended up running back and forth in a narrow space somewhere in the middle of the runway. This was called the "approach-avoidance conflict."

This reminded psychologist Joseph Sheehan of stutterers' repetitions and prolongations. In 1953, Sheehan developed the theory that stutterers want to say a word, but also want to avoid the word.

Why would stutterers wish to avoid saying words? Sheehan suggested that stutterers dislike the listener, or fear certain words, or fear certain situations, or feel guilt or anxiety about the emotional content of our message.

Sheehan believed that "stuttering is not a speech disorder, but a conflict revolving around self and role, an identity problem." He based this view on the fact that most stutterers have difficulty saying their names, and that many stutterers are fluent when acting (Sheehan, 1970).

Sheehan developed a stuttering modification therapy program based the reduction of avoidance.first, in the "self-acceptance" phase, you are trained to accept yourself as a stutterer. You are encouraged to maintain eye contact with listeners, and discuss your stuttering with friends and acquaintances.

In the "monitoring" phase, you improve your awareness of what you do when you stutter.

In the "initiation" phase, you seek out feared situations, and feared words, and stutter openly.

In the "modification" phase, you stutter openly and easily. You let the listener know that you are having trouble with a word. You do a prolongation on thefirst sound of the word. You do a "smooth release" onto the next sound.

Lastly, in the "safety margin" phase, you develop a tolerance for disfluency.

Sheehan did not believe that stutterers could or should speak fluently. In his therapy, "No practicing of special techniques for achieving fluency are involved—only openness and honesty and a changing role of self-acceptance as a stutterer will lead to overcoming the tyranny of stuttering."

Sheehan's stuttering therapy is practiced at the University of California—Los Angeles (UCLA).

Successful Stuttering Management Program (Breitenfeldt and Lorenz)
The "Successful Stuttering Management Program" (SSMP) is practiced by Dorvan Breitenfeldt and Dolores Rustad Lorenz at Eastern Washington University in Spokane, Washington. It's a three-week, intensive, residential group therapy program. The program is mainly stuttering modification therapy, emphasizing avoidance reduction.

The program begins with "confrontation of stuttering." The aim is to develop awareness of your stuttering, reduce use of avoidance techniques, and eliminate word and situation fears. The techniques are voluntary stuttering and stuttering surveys.

In a "stuttering survey," you go to a shopping mall, stop strangers, and ask them questions about their reactions to your stuttering. You stutter on purpose. You do 200-300 stuttering surveys in the program.

In the second phase, you learn the stuttering modification techniques: preparatory sets, cancellations, and pull-outs. This differs from other stuttering modification therapies, in which preparatory sets are learned after cancellations and pull-outs.

The second phase also includes changing your self-concept and lifestyle.

You also substitute continuents for plosives. You substitute /w/ for /b/, /s/ for /t/, and /z/ for /d/. For example, you say "wank" instead of "bank," and "zollar" instead of "dollar." You also add sounds with prolongations. For example, "water" becomes "oowater."

Other speech pathologists are skeptical of this technique:

This type of substitution behavior seems to go against the original philosophy of nonavoidance…the idea of teaching stutterers to substitute…strikes us as [an avoidance "trick"]…it may even strengthen clients' tendencies to scan ahead in anticipation of sounds that are feared and should be avoided.

In the third phase, you transfer your new skills to face-to-face and telephone conversations. You are also encouraged to do voluntary stuttering.

"Self-Therapy for the Stutterer" (Malcolm Fraser)
The book "Self-Therapy For The Stutterer," by Malcolm Fraser, shows how to do stuttering modification can be done as self-therapy, as opposed to going to a speech clinic. The book is published by the Stuttering Foundation of America.

Assumptions
Stuttering modification therapy assumes that stutterers will never be able to talk fluently, and so the best a stutterer can hope for is to be a better communicator while still stuttering. The effectiveness of other, more recently developed stuttering therapies for producing fluent speech makes this assumption questionable.

Identification Critiques
Improving self-awareness of stuttering behaviors, as well as psychological effects, is an excellent foundation for any speech therapy. The problem with this stage of stuttering modification therapy is that it was developed before the invention of video camcorders and biofeedback devices. Current technology can help you do this stage better and faster.

Desensitization Critiques
Telling people that you stutter is good. But freezing core behaviors and voluntary stuttering could strengthen the neural pathways for these behaviors, making these undesirable motor programs even harder to change.

Modification Critiques
"Cancellations" and "pull-outs" don't work if you have poor awareness of your stuttering. By the time you realize that you are stuttering your speech may be out of control. If stutterers' auditory processing underactivity results in poor awareness of one's speech, then stutterers who have a this neurological abnormality strongly can't be expected to modify their speech.

"Preparatory sets" teach stutterers to "scan ahead" for feared words, i.e., teach you another secondary behavior. In fact, the entire "modification" stage is arguably teaching you more secondary behaviors.

If modified stuttering sounds worse to listeners than untreated stuttering, increased listener discomfort may cause stress in the stutterer using stuttering modification techniques.

Stabilization Critiques
But "becoming your own speech pathologist" doesn't mean reading books about stuttering, taking a class, going to conventions, or learning about new research and therapies. "Becoming your own speech pathologist" means motivating yourself to do therapy activities indefinitely. You wouldn't do these therapy activities on your own, because you don't perceive resulting benefits. You need a speech pathologist to get you to do the activities.

Another goal is "the automatization of preparatory sets and pull-outs." But you're just told you to practice, and not taught techniques or practice schedules to maximize autonomous motor learning.

The last goal is for you to change your self-concept from being a person who stutters to being a person who speaks fluently most of the time but who occasionally stutters mildly. This would be a good goal if stuttering modification therapy trained you to be a person who stutters mildly. But if stuttering modification therapy "…appears to be ineffective in producing durable improvements in stuttering behaviors." then this self-concept may be difficult to maintain.

Personal Experiences with Stuttering Modification Therapy
Please read Speech-Language Pathology/Stuttering/How to Participate in this Wikibook before adding material.


text:
User:Babbage

Hi there!

I'm all over Wikimedia stuff, always as Babbage.

license: Creative Commons - Attribution Share-Alike - https://creativecommons.org/licenses/by-sa/4.0/

title: User:Babbage


text:
Super NES Programming/Homebrew SNES games

After the release of SNES there was great interest in reverse engineering the system to allow for homebrew and backup play. Nintendo fitted the machine with various security measures such as the lock-out chip to prevent unauthorized code running on the machine.

Eventually the homebrew community figured out how games ran on the SNES hardware and were able to bypass the security mechanisms. Companies such as BUNG releases hardware plugins such as Game Doctor SF series. These allow users to not only copy games but also run homebrew developed games to be run on the SNES hardware. Homebrew ROMS could be converted into the Game Doctor SF format and put onto a 3 1/2" floppy. Games as large as 12Mbits could be put fit on floppy disks formatted to 1.6Mbytes.

An alternative device was the Super Flash, by Tototek, allowed for multiple games to be burned into a flash memory chip of cartridge (allowing up to 48Mbits). This chip is the mask rom for the Super Flash development cartridge. The device is easy to use and has a nice user interface on the computer end. Simply plug in the Super Flash cartridge and upload the games you want. This was nice if you wanted to make a SNES game and play it in an actual cartridge rather than a floppy disk.

The legality of homebrew SNES game releases has not been tested in court, and it is debatable whether or not bypassing their security measures would fall foul of modern reverse engineering laws. However essentially homebrew games themselves can be produced legally for the SNES as long as no copyright material is included.

Previously in the 1990s, Nintendo sued Color Dreams for producing NES games without an official license. The outcome was an undisclosed settlement, but Color Dreams continued to produce unlicensed games. The strength of Color Dreams position lies with that they worked around the 10NES lockout chip code rather the illegally duplicating it.

List of homebrew SNES games

 * N-Warp Daisakusen, a recent game for eight players featuring impressive sound and visuals.


text:
Speech-Language Pathology/Stuttering/Improving Self-Awareness

Self-awareness of stuttering behaviors is the foundation of stuttering therapy. Have a friend or your speech-language pathologist videotape you speaking. Watch the video. For some stutterers, watching that video will be the hardest thing you’ve ever done. Some stutterers are unaware of their stuttering, or the severity of their stuttering. You can't couldn't change behaviors that you are unaware of.

Transcribe Your Speech
If your ego can handle more difficult homework, have someone videotape you in a stressful speaking situation. The tape should have you talking for at least three minutes.

Now play the tape back, and transcribe what you said. Count the syllables.

Watch the tape again, counting your dysfluencies. Calculate your stuttering rate. 2% or fewer dysfluent syllables is normal speech. 3-5% dysfluent syllables is mild stuttering. 6-10% is moderate stuttering. More than 10% dysfluent syllables is severe stuttering.

Watch the tape again, measuring your speaking time. Calculate your speaking rate in syllables per second. Non-stutterers can speak about five syllables per second, or three hundred syllables per minute.

Watch the tape again. Mark each dysfluent syllable in your written transcript.

Watch the tape again. Note each type of dysfluency:

 For repetitions, write down every repetition, e.g., "b-b-baseball." For prolongations, underline the prolonged sound. For silent blocks, write "<block>".

Watch the tape again. Pick out your three longest dysfluencies and time each. Write the times on your transcript.

Watch the tape again. Note your secondary symptoms. Write down every head jerk, facial grimace, eye blink, etc.

When you're finished, read aloud your transcription. Perform your stuttering exactly as did on the tape.

Give your script to your speech-language pathologist. Ask her to perform your script, modeling you.

Your Stuttering Autobiography
Write your stuttering autobiography. Add it to the chapter My Life in Stuttering.

Describe how stuttering affected your childhood, teenage years, and adult life. Describe your inner, emotional experience of stuttering. Describe each therapy program you've done, and the results.

Over- or Underaware of Stuttering?
Mild stutterers typically think their speech is worse than it is. A mild stutterer has one little block on baseball and panics. He thinks, "Did the listener notice? I should have been paying attention and seen that a b was coming up. Next time I'll say 'the great American pastime' instead. Or better yet, I'll keep his mouth shut for the rest of the day…"

Severe stutterers typically think that their speech is better than it is. Listeners impassively pretend not notice. During severe blocks, time stops for the stutterer. If you'd asked me how long a dysfluency had been, I would've said a second or two—even when it was actually five minutes or more.

Paradoxically, severe stutterers can be mentally healthier than mild stutterers. They can't hide severe stuttering. Severe stutterers can be willing to work hard at speech therapy. Fluent speech motor exercises, even at two-second stretch, get words out faster than severe stuttering. When severe stutterers learn to talk fluently, they often (not always) easily develop normal professional and personal relationships.

In contrast, mild stutterers, who can hide stuttering, often have more severe psychological disabilities. They're hesitant to do speech therapy. Using therapy skills (e.g., slow speech, or voluntary stuttering) alerts listeners that the individual stutters. Even if they successfully complete a speech therapy program and can talk fluently, they think their new fluent speech sounds "weird" and prefer their old speech (even after they hear themselves on tape and admit that their new speech sounds normal). Fluency shaping speech therapy can be a breeze for mild stutterers, because their brains don't need much rewiring. But their psychological disabilities can keep them from talking for years.


text:
Speech-Language Pathology/Stuttering/Anti-Stuttering Medications

Dopamine Antagonist Medications
Psychiatrist would like to use dopamine antagonists to reduce stuttering. However, these medications have side effects. Also, the long-term effects of the following medications are unknown. In some patients, even placebo can temporarily reduce stuttering. Rather than taking medication indefinitely, it may be better for a severe stutterer to take a medication at the start of a stuttering therapy program, and then reduce his dosage as his fluency improves, until he no longer needs the medication.

If you suspect that your child’s medication contributes to his or her stuttering—especially if your child is on several medications—I suggest that you consult a doctor. No drug has been more effective than placebo in clinical trials.

Haldol
Haloperidol (Haldol) is an old dopamine antagonist. It was the first medication to reduce stuttering in two clinical trials.

The side effects can be severe.

Risperdal
Newer medications more narrowly target certain dopamine receptors. The dopamine D2-receptor antagonist risperidone (Risperdal) reduces stuttering about 50%. Like other stuttering therapies, the drug is most effective in low-stress situations, and least effective in high-stress situations.

The drug is FDA-approved only for short-term (6-8 week) treatment of schizophrenia. Side effects include insomnia, agitation, anxiety, somnolence, extrapyramidal nervous system disorders, headaches, dizziness, constipation, rhinitis (a breathing disorder), rashes, tachycardia (a heart disorder), and breast growth in men and women (due to increased levels of the hormone prolactin), and neuroleptic malignant syndrome (potentially fatal).

Zyprexa
Olanzapine (Zyprexa) reduces stuttering on average 33%. Side effects may include permanent damage to the frontal lobe, weight gain, and drowsiness.

Other Dopamine Antagonists
Pimozide and Tiapride are other dopamine antagonists that have been reported to help stutterers. Pagoclone is currently being tested on stutterers.

Antidepressants Increase Stuttering
Some antidepressant medications boost dopamine. These medications include the selective serotonin reuptake inhibitor (SSRI) class, which includes Prozac and Zoloft. These medications have increased stuttering in stutterers. In a few cases, these drugs caused non-stutterers to stutter. However, there is no real evidence of this.

Another stutterer wrote:

I have tried 3 antidepressants: Prozac, Wellbutrin, and Zoloft. All increased my stuttering noticeably. The antidepressants that I have tried make me more able to get out of bed in the morning and restore my "get up and go"; however, they have caused me to go from being a person with a barely noticeable stutter to a more pronounced stutter. I had more occasions to talk.

I went into my psychiatrist yesterday and explained that the current antidepressant is making my stutter significantly worse. However, in the 10 minutes we talked I was practically perfectly fluent. He then concludes that obviously "it's not that unmanageable."

He prescribed 10mg Propanolol to take before I have to be in a difficult speaking presentation. It is supposed to "reduce performance anxiety." I don't feel like I have a tremendous amount of performance anxiety; stuttering just isn't very fun. I think he doesn't believe me about the severity of the stuttering.

Anti-Depressants and Stutter

I have tried one tri-cyclic anti-depressant called Trazodone, 150mg/day. After about a month of taking the pills I experienced mild to serious stuttering. I never remembered stuttering before or never had anyone comment on my stutter. The stutter brought on even worse anxiety while still on the pills. I then found myself having worse performance anxiety as well.

A month after stopping the regular taking of the pills my stutter was almost completely absent.

Ritalin
A speech pathologist asked on the Internet:

I'm treating an 8-year-old diagnosed ADHD and who suddenly began stuttering (advanced core and secondary behaviors) without any prior history of dysfluency, as a side effect of the medication Ritalin. He's had a whole neuro work-up which revealed nothing.

Another speech pathologist responded that many of the children he treated for stuttering were on Ritalin for ADHD.

Pharmacist Richard Harkness advises against Ritalin for children who stutter:

Ritalin increases dopaminergic neurotransmission and is contraindicated for use in those with Tourette's disorder. Ritalin has also, in rare cases, brought on symptoms of Tourette's disorder. Tourette's disorder has been likened to stuttering in that it involves a flaw in dopaminergic neurotransmission.

Botulinum Toxin
Botox, the toxin in botulism, has been injected into stutterers' vocal folds. The toxin partially paralyzes your vocal folds so you can't get into hard blocks. You also can't talk loudly or forcefully. The toxin reduces stuttering somewhat. It wears off in a few months, and you get a second shot. The second shot reduces stuttering less than the first. By the third shot, the toxin usually has no effect on stuttering.

Tranquilizers
Some doctors prescribe tranquilizers to stutterers on the erroneous belief that nervousness causes stuttering.

A psychiatrist had some pills he thought might help. Einer was to take one per day during the week remaining before the great day, and one extra big super pill on the morning of the wedding. The pills made him feel somewhat relaxed but had no noticeable effect on his speech. The wedding arrived, Einer took his super pill, and went off to London on the train to meet his relatives who had come for the ceremony.

An hour before the wedding Einer had still not returned. I kept the smiling calm that I had learned to assume in the face of all our difficulties and began dressing. Half an hour later I stood in white satin complete with veil and bouquet, looking out of the bedroom window towards the railway station, wondering what could have happened and preparing myself mentally for a last minute cancellation of the wedding. Had he thrown himself under a train, unable to continue life as a stutterer? Had he run back to Canada as a supreme act of avoidance? The minutes ticked by. Finally another train pulled in, and up the hill walked Einer, a lazy smile on his face, apparently unaware of the panic that he had caused. He had forgotten to take pencil and paper and so was unable to ask for guidance and had become hopelessly lost. However, the super pill had kept him smiling. I am glad to say that thanks to the kindly vicar in reading along with Einer, the wedding vows were the first and only fluent words my family heard Einer speak that summer.>

In general, tranquilizers have "more effect on the complexity or severity of the [stuttered] blocks than on their frequency."

Alcohol
No researchers have studied the effects of alcohol on stuttering. Anecdotally, alcohol reduces stutterers' fears and anxieties (e.g., about talking to persons of the opposite sex) and so reduces stuttering. But alcohol reduces one's ability to use therapy techniques, so increases stuttering.

Experiences with Anti-Stuttering Medications
Please read Speech-Language Pathology/Stuttering/How to Participate in this Wikibook before adding material to this section.


text:
Speech-Language Pathology/Stuttering/Anti-Stuttering Devices

This chapter is divided into sections:

 * How Anti-Stuttering Devices Work

 * Delayed Auditory Feedback (DAF)

 * Frequency-Shifted Auditory Feedback (FAF)

 * Masking Auditory Feedback (MAF)

 * Sound Quality, Background Noise

 * Hearing Safety

 * Finding Help Paying for an Anti-Stuttering Device

 * FDA and Other Regulations

Specific Devices

 * Casa Futura Technologies

 * Defstut

 * DAF/FAF Assistant

 * Edinburgh Masker

 * Fluency Pal

 * Speech Monitor

 * Kay Elemetrics Facilitator

 * FluencyCoach DAF/FAF

 * Fluency Master

 * Fluency Enhancer

 * Ovation Speech Fluency System

 * SpeechEasy

 * VoiceAmp VA 601


text:
Speech-Language Pathology/Stuttering/How Anti-Stuttering Devices Work

Changing how stutterers hear their voices improves fluency. This can be done in many ways:

 Speaking in chorus with another person. Hearing your voice distorted. Hearing your vocal fold vibration (phonation) without hearing the articulation of your lips, jaw, and tongue. Hearing a synthesized sound mimicking your phonation (masking auditory feedback, or MAF). Hearing your voice delayed a fraction of a second (delayed auditory feedback, or DAF). Hearing your voice shifted higher or lower in pitch (frequency-shifted auditory feedback, or FAF).

Together these phenomena are called altered auditory feedback.

No brain scans have looked at stutterers' auditory processing while speaking with altered auditory feedback. However, one hypothesis is that introducing errors targeted at the area that integrates auditory and somatic processing increases blood ﬂow to that area. In other words, hearing what you're saying out of sync with what you feel your muscles doing raises a red flag. The red flag is raised in the area that's abnormally underactive in stutterers. Increased blood flows to this area. The activity level increases to normal, and stuttering diminishes.

The errors must not raise red flags in other brain areas, such as language processing. E.g., when you walk up to Fred and say, "Hi, Fred," a device that whispered in your ear, "Hi, Steve" likely wouldn't improve fluency.

Non-stutterers have difficulty speaking with altered auditory feedback. Most can't count to ten. They repeat or skip numbers, or giggle uncontrollably, then rip the headphones off. If altered auditory feedback increases blood flow to the auditory/somatic integration area, then in non-stutterers the devices raise activity to an abnormally high level. Too much activity is as bad as not enough activity. Interestingly, the effects of too much activity in this area are somewhat like stuttering—repeating words, or not being able to get words out.

Planum Temporale Abnormality and DAF
DAF effectiveness is has been associated with planum temporale (PT) abnormality. DMAF device uses vocal tone to improve fuency. The device is called StutterFree™ This effect is unlike DAF as it is not a temperary effect device but has proven perminate in some cases. Mostly works for children.

Immediate Effects of Anti-Stuttering Devices
The most effective types of altered auditory feedback are delayed auditory feedback (DAF) and frequency-shifted auditory feedback (FAF). Each reduce stuttering about 70%, immediately, without training, speech therapy, mental effort, or abnormal-sounding speech. Combined DAF/FAF reduces stuttering about 80%.

70-80% is the average improvement found in dozens of studies, with hundreds of stutterers. Rarely does DAF and/or FAF improve anyone's speech more than 90%, or less than 50%. If auditory processing underactivity were the only cause of stuttering, then DAF/FAF devices would make all stutterers 100% fluent. The 70-80% effectiveness shows that auditory processing underactivity is a factor in stuttering, but not the only factor. To get closer to 100% fluency an anti-stuttering device has to be combined with speech therapy.

Should Adults Use Anti-Stuttering Devices?
Hypothetically, the only treatment for stutterers' auditory processing abnormality is an altered auditory feedback device. No speech therapy is known to correct this abnormality.

Many people overcome stuttering by treating the other factors. But using an anti-stuttering device in conjunction with other therapies may make the other therapies easier, faster, and more effective. If so, you'll then need your anti-stuttering device less and less.

Even if you have success with speech therapy and can talk fluently in most situations, there will be a few situations in which you stutter. E.g., you may want an anti-stuttering device for public speaking.

Keep an anti-stuttering device plugged into your telephone can be an easy way to do speech therapy. If the device produces carryover fluency, after a few calls your speech may be improved for the rest of the day. Many states provide telephone-compatible anti-stuttering devices free.

Should Children Use Anti-Stuttering Devices?
For children under six, stuttering therapy is usually 100% effective, so anti-stuttering devices are unnecessary.

With seven- to thirteen-year-olds, DAF devices are usually used in school with a speech-language pathologist. Because such therapy is usually effective there's no need for a child to use an anti-stuttering device outside of therapy. However, if a child sees his speech-language pathologist for only ten or twenty minutes once or twice a week, the speech-language pathologist could train the parents to supervise their child practicing with a DAF device at home every day, to increase therapy time. A typical protocol for home therapy is ten minutes reading aloud, a ten-minute conversation with a family member, and a ten-minute telephone call (perhaps to a grandparent). Or the parent and child could play Say the Magic Word while driving to school.

We don't know whether children who stutter have the same neurological abnormalities as adult stutterers. Altering a child's brain activity might cause his brain to develop in a different way. Extensive use of an anti-stuttering device might cause the child's brain to develop normal auditory processing and the child would outgrow stuttering. But maybe extensive use of an anti-stuttering device would cause the child's brain to develop in another, unknown abnormal way.

Some anti-stuttering devices impair the user's hearing by occluding (blocking) the ear that the device is in. And some devices pick up, distort, and amplify background noise. If a child can't hear his teacher, he'll fall behind in school. He might get hit by a bus that he didn't hear coming. Users of some anti-stuttering devices have reported symptoms of permanent hearing damage, such as ringing in the ears or pain from loud noises.

References

 * 1) Watkins, K., S. Davis, P. Howell. Brain activity during altered auditory feedback: an fMRI study in persistent and recovered developmental stuttering, Oxford Dysfluency Conference (2005), found that for stutterers and non-stutterers DAF increased activity in the supplementary motor area, and DAF and FAF increased activity in the superior tem-poral cortex. The stutterers showed underactivity in the speech motor control area (opposite to what other studies found) and overactivity of the cerebellum.
 * 2) Foundas, A.L., Bollich, A.B., Corey, D.M., Hurley, M., Heilman, K.M. "Anomalous Anatomy in Adults with Persistant Developmental Stuttering: A Volumetric MRI Study of Cortical Speech-Language Areas," Neurology, 2001 57:207-215.
 * 3) A. L. Foundas, MD, A. M. Bollich, PhD, J. Feldman, MD, D. M. Corey, PhD, M. Hurley, PhD, L. C. Lemen, PhD and K. M. Heilman, MD. "Aberrant auditory processing and atypical planum temporale in developmental stuttering," Neurology, 2004;63:1640-1646.
 * 4) Kalinowski, J., Armson, J., Stuart, A., Graco, V., and Roland-Mieskowski, M. "Effects of alterations in auditory feedback and speech rate on stuttering frequency," Language and Speech, 1993, 36, 1-16; Sark, S., Kalinowski, J., Stuart, A., Armson, J. "Stuttering amelioration at various auditory feedback delays and speech rates," European Journal of Disorders of Communication, 31, 259-269, 1996; Brenaut, L., Morrison, S., Kainowski, J., Armson, J., Stuart, A. "Effect of Altered Auditory Feedback on Stuttering During Telephone Use," Dalhousie University, Halifax, Nova Scotia, Canada, 1995; Stager, S., Denman, D., Ludlow, C. "Modifications in Aerodynamic Variables by Persons Who Stutter Under Fluency-Evoking Conditions." Journal of Speech, Language, and Hearing Research, 40, 832-847, August 1997. Zimmerman, S., Kalinowski, J., Stuart, A., Rastatter, M. "Effect of Altered Auditory Feedback on People Who Stutter During Scripted Telephone Conversations." Journal of Speech, Language, and Hearing Research, 40, 1130-1134, October 1997.
 * 5) Ryan, Bruce and Barbara Van Kirk Ryan. "Programmed Stuttering Treatment for Children: Comparison of Two Establishment Programs Through Transfer, Maintenance, and Follow-Up," Journal of Speech and Hearing Research, 38:1, February 1995.
 * 6) Radford, N., Tanguma, J., Gonzalez, M., Nericcio, M.A., Newman, D. "A Case Study of Mediated Learning, Delayed Auditory Feedback, and Motor Repatterning to Reduce Stuttering," Perceptual and Motor Skills, 2005, 101, 63-71.


text:
Talk:Go/Contributors e.g. authors and editors

I'v added myself to the authers section as I have writen many things in this book but if anyone should have a problem with this move me into the editors section. Ulfrinn 04:10, 27 March 2006 (UTC)ulfrinn


text:
Speech-Language Pathology/Stuttering/Delayed Auditory Feedback

Delayed auditory feedback (DAF) can be used two, very different ways. The delay can be set between 50 and 70 milliseconds to reduce stuttering about 70% at a normal speaking rate, without training, mental effort, or abnormal-sounding speech.

DAF can also be used to support the fluency shaping target of slow speech with stretched vowels. For this purpose the delay is usually set at 200 milliseconds and then reduced to shorter delays (as short as 75 milliseconds) over the course of the therapy program.

For this latter purpose, a speech-language pathologist must train the stutterer. When the stutterer can complete a simple speaking task, such as counting to ten, using the slow speech target correctly, then he can use a DAF device. DAF therapy then has two goals:

 To increase the length and complexity of the utterance, and increase the stress of the speaking situation, while using the DAF device to support on-target fluent speech. To reduce the need for the DAF device, until the stutterer no longer needs the device.

For the first goal, after the stutterer can count to ten using the slow-speech target correctly (e.g., all syllables stretched equally, all syllables stretched to one or two seconds, no pauses between words, and no dysfluencies) without the DAF device, then use the device to have a conversation at the same slow speaking rate. When the stutterer can achieve the slow speech target with 100% fluency using the DAF device for utterances with the length and complexity of normal conversations, then the stutterer should take the device out of the speech clinic and use it in increasingly stressful conversations. The first goal is speech that is 100% fluent and on-target (i.e., slow) in any conversation. For a severe stutterer, this may mean using one- or two-seconds per syllables speech with the device set at 200 milliseconds.

When the stutterer achieves the first goal, then he gradually reduces his dependence on the device. He decreases the delay and increases his speaking rate. But if he has any dysfluencies he should go back to the longer delay and slower speaking rate. He can also decrease the volume, and use the device in one ear instead of both ears. He can use the device at the beginning of conversations, and then turn it off when he feels capable of speaking on target with the support of the device. He can discontinue using the device in low-stress conversations. Then he can discontinue using the device in medium-stress conversations, reserving the device only for stressful conversations such as public speaking. Eventually he should need the device only occasionally.

Mistakes in DAF Use
The common mistake with DAF is using a normal speaking rate with a long (slow) delay. If you want to talk at a normal speaking rate, set the DAF delay between 50 and 75 milliseconds. Don't use a delay longer than 75 milliseconds unless you're using closed-loop slow speech.

The typical mistake is for a stutterer to experience a 50% fluency improvement at 50 milliseconds and then a 75% improvement at 75 milliseconds. He sees that the dial goes up to 200 milliseconds. He thinks, "I'll crank up this baby! I'll redline it! I'll turn it up all the way to 200 milliseconds and I'll be 200% ﬂuent!"

DAF doesn't work like that. 200 milliseconds is for speech ﬁve to ten times slower than normal. Non-stutterers can't talk normally with a 200-millisecond delay (with rare exceptions due to a linguistic abnormality) but most stutterers are capable of forcing themselves to "tune out" the delay. This appears to be due to stutterers' auditory processing underactivity. In other words, if you use DAF incorrectly you may be able to make your auditory processing underactivity worse. This may explain why some stutterers have reported that a DAF device lost effectiveness or "wore off" over time.

Another mistake is to use a DAF device in low-stress situations (such as reading aloud) and expect carryover to high-stress situations. Carryover works the other way. For example, a child could use a DAF device only when called on to speak in class. Or an adult could a DAF device when speaking on the radio at work, but not for conversations with his wife at home. As a rule, use an anti-stuttering device in situations in which you stutter, and don't use it in situations where you speak fluently.

Long-Term Effects of DAF
Nine adult stutterers used DAF devices thirty minutes per day, for three months. The thirty minutes consisted of ten minutes reading aloud, a ten-minute conversation with a family member, and a ten-minute telephone call. The subjects received no speech therapy.

The devices were used with binaural (two ears) headsets. The subjects were allowed to set the delay where they wanted. Most selected delays around 100 milliseconds.

Long-Term Effects of DAF

Before three months of DAF use, the subjects stuttered on 37% of words, on average. When they put on the DAF device their stuttering dropped to 10%. I.e., the device improved their speech about 70%.

Three months later the subjects stuttered on 17% of words, when not using the DAF device. When wearing the DAF device they stuttered on 13% of words.

This shows that, when not wearing the devices, the subjects' stuttering diminished from 37% of words to 17% of words, or a 55% improvement. This is "carryover fluency." Put another way, the devices trained the users to need the devices less.

The increase (from 10% to 13%) in stuttering when wearing the devices wasn't statistically significant. Examining this more closely, stuttering when wearing the device increased only for "automatic speech," such as reciting days of the week, and for repeating words and sentences after the examiner. No change in effectiveness was found in conversations or in a "picture description" task. This suggests that any "wearing off" effects occurred in less-important speaking situations.

The "carryover fluency" effect was the same across all speaking tasks.

In another study, an eleven-year-old boy received fourteen hours of structured therapy with mediated learning and a School DAF. His stuttering diminished from 9% dysfluencies to 4.8% dysfluencies (when speaking without the device, a 47% improvement). One year later he still had 4.8% dysfluencies. Another fourteen hours of treatment reduced his stuttering to 4.1% dysfluencies.

Two other studies combined speech therapy with a DAF device. One study was of adults, the other of children. Both studies found that combining DAF and stuttering therapy trained the subjects to speak fluently (less than 2% stuttering) and no longer need the devices.

References

 * 1) Sark, S., Kalinowski, J., Stuart, A., Armson, J. "Stuttering amelioration at various auditory feedback delays and speech rates," European Journal of Disorders of Communication, 31, 259-269, 1996.
 * 2) Van Borsel, J., Reunes, G., Van den Bergh, N. "Delayed auditory feedback in the treatment of stuttering: clients as consumers," International Journal of Language and Communication Disorders, 2003, 38:2, 119-129.
 * 3) Radford, N., Tanguma, J., Gonzalez, M., Nericcio, M.A., Newman, D. "A Case Study of Mediated Learning, Delayed Auditory Feedback, and Motor Repatterning to Reduce Stuttering," Perceptual and Motor Skills, 2005, 101, 63-71.
 * 4) Ryan, B.P., Van Kirk, B. "The Establishment, Transfer and Maintenance of Fluent Speech in 50 Stutterers Using Delayed Auditory Feedback and Operant Procedures." Journal of Speech and Hearing Disorders, 39:1, February, 1974.
 * 5) Ryan, Bruce and Barbara Van Kirk Ryan. "Programmed Stuttering Treatment for Children: Comparison of Two Establishment Programs Through Transfer, Maintenance, and Follow-Up," Journal of Speech and Hearing Research, 38:1, February 1995.


text:
Muggles' Guide to Harry Potter/Characters/Petunia Dursley

Overview
Petunia Dursley, née Evans, is Harry Potter's aunt (she is his mother's sister). She and her husband Vernon Dursley reluctantly and bitterly took Harry in as a baby, while they had their own son, Dudley. Petunia hates Harry's magical abilities and wishes to "stamp it out of him," and partly as a result of this, relations between her and Harry have never been good.

Philosopher's Stone
Vernon Dursley kisses his wife, Petunia, goodbye as he leaves for work. Several unnerving things happen during the day, but while he is tempted to call Petunia, he does not, instead waiting until he is back home before asking casually about her sister's family, the Potters, and what they had named their son. Petunia says the son was named Harry Potter, an "awfully common name."

Discussing the Dursley family, Minerva McGonagall questions Albus Dumbledore's decision to place the infant Harry with the Dursleys, saying that they are "the worst kind of Muggles." She reports that she had seen their child hitting Petunia, demanding candy. Dumbledore says he is aware that Harry would have a home in any Wizarding household, but that he has his reasons for putting Harry there.

We are told that it is Petunia Dursley who finds the infant Harry on the Dursley doorstep. Apparently, it is also Petunia who handles most of the "odd things" happening around Harry: when his hair will not remain cut the way she wants it, she cuts it short, only to have it grow back overnight; she is trying to force a hideous sweater over Harry's head when it mysteriously shrinks to the point that it will not even fit over his hand; and she receives the school reports about odd things happening there, such as Harry climbing on the roof.

In the events surrounding Dudley's eleventh birthday and the subsequent appearance of Harry's first Hogwarts letter, Vernon is the center of the action, while Petunia largely backs Vernon up. While Petunia does receive the phone call from Mrs. Figg saying that she won't be able to look after Harry, and then comforts Dudley in his dismay at having to have Harry along, she thereafter remains largely in the background as Vernon drives them to the zoo, buys treats for Dudley, retrieves Dudley from the snake enclosure, and punishes Harry for this odd event by locking him back in his cupboard under the stairs. And when Harry's Hogwarts letter arrives, it is Vernon who takes it from him and opens it. While Vernon and Petunia do discuss what to do about this letter, it is Vernon who decides that they will simply not answer it. When more letters arrive, Vernon intercepts and destroys them. It is Vernon who, in the end, decides that they must leave the house to escape the letters. Dudley asks Petunia at this point if "Daddy has gone mad"; Petunia does not seem to be able to answer him.

When the family finally settles in the hut on the island, Petunia still has not had much role in things. When Hagrid arrives, he tells Harry that his mother, Lily, Petunia's sister, was an extremely good witch. Petunia, apparently pushed beyond her endurance, bursts out that Lily was a freak, coming home with pockets full of frog spawn, and that she was doted on by her parents. Only Petunia saw what she really was. Petunia's malevolence is only stopped when she mentions that Harry's parents had gotten themselves blown up. Harry interjects that Petunia had told him that his parents had been killed in a car crash, which prompts Hagrid to respond angrily that no car crash could have done anything to James and Lily Potter. The conversation then is carried by Vernon and Hagrid until Vernon insults Dumbledore. Enraged, Hagrid gives Dudley a pig's tail, and the Dursleys retreat in confusion, leaving Harry and Hagrid the front room.

When Vernon takes Harry to Kings Cross Station to board the train a month later, Dudley and Petunia are in the car; Vernon has only consented to take Harry to London because they need to go to a specialist to get Dudley's tail removed before school starts. During the trip, she says nothing; but we see her laughing at Harry as the car drives away, leaving Harry to hunt for Platform Nine and Three Quarters.

Petunia is at King's Cross Station when Harry returns from school, but says nothing, simply watching as Vernon verbally collects Harry and directs him towards the exit.

Chamber of Secrets
Harry is not surprised when nobody in the house remembers that it is his birthday. Vernon has important visitors arriving that night, and Petunia and Dudley are called upon to rehearse their lines. Harry is hard-put to avoid laughing at the excesses that they are planning, but Petunia is overcome instead by what she sees as Dudley's brilliance.

Later, when Harry is in the garden, Dudley taunts him about having received no mail from his "weird friends at that school". Harry, angered, says he was thinking about how to set the hedge on fire, and starts mumbling nonsense words. Panicking, Dudley calls for his mother; Petunia swings at Harry's head with a soapy frying pan, but misses. As punishment for daring to use magic, Petunia gives Harry a long sequence of tasks to help her cleaning up the house for Vernon's visitors, then sends him up to his room after a very sketchy dinner.

When Harry is locked into his room, Petunia does periodically bring him meals which she pushes through a cat-flap in his door. Neither Harry nor Hedwig finds cold vegetable soup particularly appealing, but that being all they have, they make do.

Petunia again is present when Harry returns from school, but says nothing, leaving the conversation to Vernon.

Prisoner of Azkaban
Petunia and Vernon are listening to the new kitchen TV when the newscaster talks about a murderer who has escaped from prison, Sirius Black. Apparently at the mention of a reward for information, Petunia looks out the kitchen window, as if expecting Black to be hiding in their backyard.

For the rest of Harry's time there, however, she is quite overshadowed by Vernon's sister, Marge, who visits for a week starting on Harry's birthday.

Goblet of Fire
Dudley's school nurse has seen what Petunia, so quick to see a fingerprint on her walls or what the neighbors are doing, could not see: that Dudley is not just fat, but massively obese. Petunia has, under prompting, put him on a diet, and so he would not feel alone, has put the rest of the family on a diet as well.

Mr. Weasley has managed to get tickets to the Quidditch World Cup and agrees to pick Harry up and take him to The Burrow. While they are waiting for the Weasley family to arrive, Petunia is compulsively straightening cushions in the sitting room. Mr. Weasley arrives through the boarded up fireplace, rather explosively, with Ron, Fred and George, and Petunia tries to hide behind Vernon. When Dudley eats one of the Twins' accidentally-on-purpose dropped Ton-Tongue Toffees, it makes his tongue become several feet long; we see Petunia struggling with it, trying to get it out of his mouth. During the ensuing mayhem, Harry departs at Mr. Weasley's orders; it seems that Petunia is largely having hysterics at this point.

Petunia is not present at Kings' Cross Station when Harry returns from school.

Order of the Phoenix
Petunia opens the door to a clearly ill Dudley (he vomits all over the mat) being supported by Harry. Both Dudley and Harry have been attacked by dementors. Once inside, Dudley accuses Harry of using magic on him. Harry replies that while he had his wand out and had threatened Dudley with it, he had not used it against Dudley. After much arguing back and forth, complete with arrivals of owls threatening Harry with imprisonment and expulsion from Hogwarts, Uncle Vernon demands to know what these Dementors are that Harry was supposedly protecting Dudley from. Petunia tells him that they are the guards from the Wizard prison, Azkaban. Suddenly realizing what she has said, she claps her hand over her mouth, then explains that she had heard "that awful boy" (Snape) talking about them with her sister, Lily. This proves too much for Vernon, who now demands that Harry leave the house. Another owl arrives, this one with a Howler addressed to Petunia. Harry, knowing what Howlers will do if left alone, recommends that she open it. Once she does, a menacing voice says, "REMEMBER MY LAST, PETUNIA!!!" before the letter dissolves into flames.

Still in shock, Petunia now says that Harry will have to stay with them. Over Vernon's protests, and with her voice strengthening as her self-assurance returns, she says that evicting Harry from the house will attract awkward questions from the neighbours. Vernon reluctantly agrees and sends Harry to his room instantly.

Harry remains in his room until Vernon receives notification that he may be the winner of the Best-Kept Suburban Lawn Competition. The Dursleys go off to the competition venue, and Harry departs Privet Drive for Number Twelve, Grimmauld Place with the Advance Guard.

In Harry's conversation with Dumbledore after the battle at the Ministry, we learn that the Howler which had changed Petunia's mind so that she overruled Vernon about throwing Harry out was, in fact, sent by Dumbledore. We also learn the reason Harry has been forced to stay with the Dursleys: Lily dying to save Harry from Voldemort had created a powerful protective charm, but it could only be maintained while Harry had a place that he could call home that was shielded by Lily's blood – in this case, Petunia, Lily's sister.

When Harry returns to London on the Hogwarts Express, the Dursleys are there waiting for him. A group of wizards, led by Alastor Moody, confronts them, saying that they expect to hear regularly from Harry, and that if they find out that Harry is mistreated at any point, the Dursleys will have to answer to them. While most of the conversation is directed at Vernon, Harry does notice that Petunia seems most distressed, not by the appearance of this flock of wizards, but rather by Nymphadora Tonks' hair, which is its usual shocking pink color.

Half-Blood Prince
Dumbledore tells Harry that he will be arriving to take Harry to The Burrow only a fortnight after school ends. Harry only half believes him, and has not told the Dursleys, so Dumbledore's arrival at 11PM comes as a shock to them. At his arrival, Petunia comes out of the kitchen where she has been giving all the surfaces their nightly wipedown, wearing a house-dress and rubber gloves. Dumbledore propels a couch into the three Dursleys, forcing them to sit down, then suggesting drinks, summons several glasses of mead, which he sends across the room to the Dursleys. Vernon, Petunia, and Dudley ignore the glasses of mead, which become more insistent as the conversation goes on. Harry notes that one of the glasses is bouncing repeatedly off Vernon's head, spilling its contents in its insistence to be noticed; another must be acting similarly with Petunia. Dumbledore tells Vernon and Petunia that he had expected that they would treat Harry as one of their own children, and was very disappointed that they had not; however, he was pleased that Harry had not been as badly treated as the child sitting between them. Both Petunia and Vernon look around, appearing to think that Dumbledore was referring to someone other than Dudley. Dumbledore also says that, while Harry will be visiting again briefly, he will not stay long over the next summer break, as the charm that protects him will end when he reaches his majority, at seventeen.

When Dumbledore summons Kreacher in an attempt to determine whether the house at Grimmauld Place has passed to Harry, as Sirius had intended, Harry sees Petunia's look of revulsion, and thinks that nothing as dirty as Kreacher had likely ever been in her house.

Petunia says very little during this visit of Dumbledore's, and Harry does not return to Privet Drive in this book.

Deathly Hallows
We see Petunia only briefly at the beginning of this book; as she and Vernon are preparing to leave for a place of safety, Dudley says that he does not believe that Harry is a waste of space. Petunia seems aware that this is effusive compliments from Dudley, but her only response is a nod of the head to Harry as she leaves the house.

In Severus Snape's memories, we see the young Petunia and her sister Lily, before Lily goes to Hogwarts. We see Petunia's fear when Lily demonstrates that she can make a flower open and close, and we see Petunia's distrust of the young Snape. We also see that Petunia eavesdrops on Lily and Severus talking about the Wizarding world, particularly about the Dementors and Azkaban Prison. On the platform where Lily is about to board the Hogwarts Express, we also learn that Petunia had sent a letter to Hogwarts asking to be accepted into the school, and had received a refusal.

Strengths
It's shown that Petunia is a very neat person and likes everything else neat and tidy, also.

Although she is not fully aware of it, Petunia projects Lily's protection of Harry due to their blood relation.

Weaknesses
Petunia's desire that things be neat and clean borders on obsession. It appears that before she goes to bed at night she has to scrub down the kitchen completely; in Harry Potter and the Half-Blood Prince we see her with her nightdress and housecoat, wearing rubber gloves and clearly in the middle of her bedtime wipe-down of all the kitchen surfaces. In Harry Potter and the Chamber of Secrets, we learn also that she expects to take all day cleaning up the house for the Masons, dinner guests and potential clients of Vernon Dursley.

Relationships with Other Characters
She is Lily Potter's older sister, and thinks that her sister is a "freak". She has the same opinion of her nephew, Harry Potter. She married Vernon Dursley, and had a son, Dudley Dursley.

We are told that she spends large parts of each day snooping on the neighbours, and of course we see that she models her behaviour based on what the neighbours would think. Any relationships with other characters, including "batty old Mrs. Figg", are going to be coloured by a need to keep up appearances. Relationships with Wizards, such as Albus Dumbledore, will be primarily tinged with fear; she fears and distrusts the magic that, by her lights, took her sister away from her.

Petunia's relationships with her family are somewhat varied, though apparently uniformly shallow. Toward Harry, we see that Petunia makes no accommodation to Harry's needs, rather seeing him as unpaid domestic help; in the first three books, we see her setting him tasks like making breakfast, weeding the gardens, scrubbing pans, and similar work. We have seen that Vernon often restricts Harry to his room for days at a time; Petunia assists in this by preparing food, barely enough to sustain Harry's life, and pushing it through a cat-flap installed in Harry's bedroom door, at intervals. Petunia never shows Harry the slightest bit of affection. As Harry matures and becomes more powerful as a wizard, Petunia's feelings towards him shift, becoming less aloof and more fearful.

Petunia acts completely differently towards her son, Dudley, showering him with gifts and making nearly infinite allowances for his desires. It is hard to know how much of this is from affection, and how much is from fear; it seems Dudley is quite capable of hitting Petunia and does so when provoked.

It is hard to determine Petunia's actual feelings, if any, towards her husband, Vernon. It does seem that she discourages intimacy. One gets the feeling almost that Petunia has gotten married because that is what people do, rather than out of any particular affection for the man she is married to.

Analysis
Petunia seems to be inordinately interested in what other people are doing, and thus, is extremely concerned with what other people think of her. Having accepted Harry into her house, reluctantly, we see that her rationale for keeping him there as he grows is that people would wonder what had gone wrong were he suddenly to disappear. Nearly everything that Petunia does is done to look good in the eyes of the neighbours, with the possible exceptions of her private treatment of Harry and her treatment of Dudley. We see this in particular at the start of Harry Potter and the Order of the Phoenix, where Harry is almost thrown out of the house before Petunia rationalizes the instructions she has received in terms of what the neighbours would think, and again at the end of that same book where she seems dismayed in particular by the unconventionality of Tonks' hair colour.

Petunia's stated reason for the Dursleys' treatment of Harry is to "stamp that (magic) stuff out of him", to make him normal so that he can take his place in "normal" society. However, her parsimonious treatment of Harry, giving him Dudley's cast-off and horribly oversized clothes, and her attempts to cut his hair, rather undercut his chances at ever being accepted into normal society. Petunia obviously feels that providing a roof for Harry should be enough, and that he should be grateful for that, and for any scraps the family deigns to send his way.

One thing which should be mentioned is the Howler delivered to Petunia at the beginning of Harry Potter and the Order of the Phoenix. While we do eventually learn that this came from Dumbledore, we never hear any more about the circumstances. The fact that Dumbledore says "Remember my last [letter], Petunia," has been seen as proof that there has been ongoing correspondence between them, as if there had only been the one letter that had been left with Harry, the Howler would instead have said something like "Remember my letter". It is confirmed that Dumbledore had written to Petunia earlier — we find out in Harry Potter and the Deathly Hallows that Dumbledore had rejected her application to attend Hogwarts — but we are uncertain whether that and the letter left with Harry are the only two times Dumbledore has written to her, or whether there has been a trickle of correspondence over the years. Given the shock with which the Dursleys received Harry's first Hogwarts letter, one must suspect that there was little, if any, correspondence over the years, so the "last" to which Dumbledore referred in the Howler was most likely the letter that he had left with the infant Harry some fourteen years earlier. It is a safe assumption that Dumbledore had, in that letter, informed Petunia of the threat facing Harry should Voldemort return, and why Petunia was Harry's best hope of survival. Presumably, Petunia did not inform Vernon of the full details; if he knew them, Petunia would likely have mentioned them rather than talking about what the neighbours would think.

Questions

 * 1) How much does Petunia actually know about the wizarding world?
 * 2) How does Petunia rationalize her treatment of Harry?
 * 3) Why is Petunia so concerned with her appearance to her neighbours?

Greater Picture
One of the things that most clearly defines Petunia, as we see in Harry Potter and the Philosopher's Stone, is her fear and distrust of things magical, which has been a large part of the reason Harry has been kept ignorant of his ancestry. While she is joined in this distrust by her husband Vernon, one must wonder, having completed the series, how much of this on Petunia's part is jealousy. Yes, Lily's magical ability had frightened her, and she had serious doubts about young Severus, who was evidently of a lower social class. Yet she had, as it turns out, written to Dumbledore pleading for admission to Hogwarts and been refused. It is likely that a large part of her jealousy was sour grapes: "the magical world has refused me, so I will refuse it." Harry, as part of the magical world, was similarly refused any part of Petunia's concern; it was likely only by telling herself that she could stamp the magic out of Harry, that she could countenance having him in her house at all.


text:
Radiation Oncology/Staging

The purpose of this page is to provide a quick comparison of the stages that are used for various malignancies. It is not meant to go into detail of what constitutes each stage. For that information, see the article on each specific malignancy.

This page uses the latest AJCC 6th edition from 2002.

Note: should move this information into table form

Notes: M-stage not listed unless it is different than the commonly used M0 or M1. For simplicity, N(1-3) means N-stage can be N0 or N1-3. However, N(0-1) means N-stage is N0 or N1. These schemes are different but easier to remember. All sites also contain T0 (no tumor) but this isn't listed below. Many sites contain Tis and Stage 0 but these aren't listed below.

The headings below are per the AJCC Cancer Staging Handbook and do not necessarily follow the Table of Contents organization of this wikibook.

 * See also: TNM by organ categories - excellent web-based staging guide

AJCC Staging Editions
Return to Top

Current edition: 7th edition, 2009

 * Listing of editions: First date is the date of release; date range in parentheses is the date of use. Usually the edition is referred to by the year of release rather than the first year of use—e.g. 5th edition (1997)
 * 1st edition: 1977 (1978–83), Cancer Staging Manual by the AJC
 * 2nd edition: 1983 (1984–88), Manual for Staging of Cancer
 * 3rd edition: 1988 (1989–1992) - PDF of AJCC 3rd ed
 * 4th edition: 1992 (1993–1997)
 * 5th edition: 1997 (1998–2002)
 * 6th edition: 2002 (2003–2009) - PDF of AJCC 6th ed (staging forms only)
 * 7th edition: 2009 (2010–2017)
 * N.B. See, including 7th Edition Staging Manual ERRATA
 * 8th edition: 2017 (2018-)
 * See for errata

Full text (PDF) of past editions (1st-5th)

See also:
 * 5th/6th Edition Comparison Guide (PDF) - by the AJCC
 * Comparison of 5th and 6th ed. (HTML)

The AJCC was organized in 1959 as the American Joint Committee for Cancer Staging and End-Results Reporting (AJC). Its name was changed to American Joint Committee on Cancer (AJCC) in 1980.

Head and Neck
Return to Top

Note: Overall staging the same for all except nasopharynx and thyroid. N-stage is the same for all (except the above 2). T-stage is similar for all subsites, with only minor differences.
 * Overall staging: I (T1 N0) - II (T2 N0) - III (T3 N0, T1-3 N1) - IVA (T4a, N2) IVB (T4b, N3) IVC (M1)
 * Lip and Oral Cavity - I - II - III - IVA IVB IVC
 * T(T1-4 and T4a, T4b), N(N1, N2a N2b N2c, N3)
 * Oropharynx - I - II - III - IVA IVB IVC
 * T(T1-4 and T4a, T4b), N(N1, N2a N2b N2c, N3)
 * Hypopharynx - I - II - III - IVA IVB IVC
 * T(T1-4 and T4a, T4b), N(N1, N2a N2b N2c, N3)
 * Nasopharynx - I - II - III - IVA IVB IVC
 * T(T1, T2a T2b, T3, T4), N(N1, N2, N3a N3b)
 * Larynx - I - II - III - IVA IVB IVC
 * supraglottis and subglottis: T(T1, T2, T3, T4a T4b)
 * glottis: T(T1a T1b, T2, T3, T4a T4b)
 * for all: N(N1, N2a N2b N2c, N3)
 * Nasal cavity and paranasal sinuses - I - II - III - IVA IVB IVC
 * T(T1-4 and T4a, T4b), N(N1, N2a N2b N2c, N3)
 * Salivary glands - I - II - III - IVA IVB IVC
 * T(T1-4 and T4a, T4b), N(N1, N2a N2b N2c, N3)
 * I (T1 N0) - IIA (T2a N0) IIB (T1-2 N1, T2b N0) - III (T3 N0-2, T1-3 N2) - IVA (T4 N0-2) IVB (N3) IVC (M1)
 * Thyroid
 * Overall stage: papillary or follicular: (Under 45 years) I - II. (45 yrs+) I - II - III - IVA IVB IVC
 * Overall stage: medullary: I - II - III - IVA IVB IVC
 * Overall stage: anaplastic: IVA IVB IVC
 * T(T1-4 and T4a, T4b), N(N1a and N1b). Anaplastic is T4a or T4b only.

Gastrointestinal
Return to Top

 * Note: These sites (the next 6) are all different with no pattern.
 * Esophagus - I - IIA IIB - III - IVA IVB
 * T(1-4), N(0-1), M(0, 1a 1b) - M1a not applicable for midthoracic primary tumors
 * I (T1 N0) - IIA (T2-3 N0) IIB (T1-2 N1) - III (T3N1 or T4) - IVA (M1a) IVB (M1b)
 * Stomach - IA IB - II - IIIA IIIB - IV
 * T(T1, T2a T2b, T3, T4), N(1-3)
 * IA (T1N0) IB (T1N1, T2N0) - II (T1N2, T2N1, T3N0) - IIIA (T2N2, T3N1, T4N0) IIIB (T3N2) - IV (T4N1-3, N3, M1)
 * Mnemonic - IA add to 1, IB add to 2, II - 3, IIIA - 4, IIIB - 5
 * Small intestine - I - II - III - IV
 * T(1-4), N(0-1)
 * I (T1-2 N0) - II (T3-4 N0) - III (N1) - IV (M1)
 * Appendix (carcinoma) - I - IIA IIB IIC - IIIA IIIB IIIC - IVA IVB IVC
 * T(1-4,4ab), N(0-2), M(0,1a/b)
 * I (T1-2 N0) - IIA (T3 N0) IIB (T4a N0) IIC (T4b N0) - IIIA (T1-2 N1) IIIB (T3-4 N1) IIIC (N2) - IVA (N0 M1a G1) IVB (N0 M1a G2-3,N+ M1a) IVC (M1b)
 * Appendix carcinoid - I - II - III - IV
 * T(1-4,1ab), N(0-1)
 * I (T1 N0) - II (T2-3 N0) - III (T4 or N1) - IV (M1)
 * Carcinoid (non-appendiceal) - I - IIA IIB - IIIA IIIB - IV
 * T(1-4),N(0-1)
 * I (T1 N0) - IIA (T2 N0) IIB (T3 N0) - IIIA (T4 N0) IIIB (N1) - IV (M1)
 * Colon and rectum - I - IIA IIB - IIIA IIIB IIIC - IV
 * T(1-4), N(1-2)
 * I (T1-2 N0) - IIA (T3 N0) IIB (T4 N0) - IIIA (T1-2 N1) IIIB (T3-4 N1) IIIC (N2) - IV (M1)
 * Anal canal - I - II - IIIA IIIB - IV
 * T(1-4), N(1-3)
 * I (T1 N0) - II (T2-3 N0) - IIIA (T1-3 N1, T4 N0) IIIB (T4 N1, N2-3) - IV (M1)
 * Gastrointestinal Stromal Tumor (GIST)
 * T(1-4), N(0-1). Mitotic rate: Low or High
 * Gastric GIST: IA IB - II - IIIA IIIB - IV
 * Gastric GIST: IA (T1-2 N0, low mit.) IB (T3 N0, low mit.) - II (T1-2 N0, high mit.; T4 N0, low mit.) - IIIA (T3 N0, high mit.) IIIB (T4 N0, high mit.) - IV (N1 or M1)
 * Small Intestinal GIST: I - II - IIIA IIIB - IV
 * Small Intestinal GIST: I (T1-2 N0, low mit.) - II (T3 N0, low mit.) - IIIA (T1 N0, high mit; T4 N0, low mit) IIIB (T2-T4 N0, high mit.) - IV (N1 or M1)
 * Liver - I - II - IIIA IIIB IIIC - IVA IVB
 * T(1-4), N(0-1)
 * I (T1 N0) - II (T2 N0) - IIIA (T3a N0) IIIB (T3b N0) IIIC (T4 N0) - IVA (N1) IVB (M1)
 * Barcelona Clinic Liver Cancer (BCLC) Staging System
 * Cancer of the Liver Italian Program (CLIP) Score
 * Okuda Staging System
 * Gallbladder - I - III - IIIA IIIB - IVA IVB
 * T(1a 1b, 2, 3, 4), N(0-2)
 * I (T1 N0) - II (T2 N0) - IIIA (T3 N0) IIIB (T1-3 N1) - IVA (T4 N0-1) IVB (N2 or M1)
 * Extrahepatic bile ducts
 * Perihilar bile ducts - I - II - IIIA IIIB - IVA IVB
 * T(1,2a/b,3,4), N(0-2)
 * I (T1 N0) - II (T2a-b N0) - IIIA (T3 N0) IIIB (T1-3 N1) - IVA (T4 N0-1) IVB (N2 or M1)
 * Distal bile duct - IA IB - IIA IIB - III - IV
 * T(1-4), N(0-1)
 * IA (T1 N0) IB (T2 N0) - IIA (T3 N0) IIB (T1-3 N1) - III (T4) - IV (M1)
 * Intrahepatic bile ducts - I - II - III - IVA IVB
 * I (T1 N0) - II (T2 N0) - III (T3 N0) - IVA (T4 N0, Any N1) IVB (M1)
 * Ampulla of Vater - IA IB - IIA IIB - III - IV
 * T(1-4), N(0-1)
 * IA (T1 N0) IB (T2 N0) - IIA (T3 N0) IIB (T1-3 N1) - III (T4) - IV (M1)
 * Pancreas - IA IB - IIA IIB - III - IV
 * T(1-4), N(0-1)
 * IA (T1 N0) IB (T2 N0) - IIA (T3 N0) IIB (T1-3 N1) - III (T4) - IV (M1)

Lung
Return to Top

 * Lung - IA IB - IIA IIB - IIIA IIIB - IV
 * T(1a,1b,2a,2b,3-4), N(1-3)
 * IA (T1 N0) IB (T2 N0) - IIA (T1 N1) IIB (T2 N1, T3 N0) - IIIA (T3 N1-2, T1-3 N2) IIIB (T4, N3) - IV (M1)
 * Pleural mesothelioma - IA IB - II - III - IV
 * T(T1a T1b, T2, T3, T4), N(1-3)
 * IA (T1a N0) IB (T1b N0) - II (T2 N0) - III (T1-2 N1-2, T3 N0-2) - IV (T4, N3, M1)

Musculoskeletal
Return to Top

 * Bone - IA IB - IIA IIB - III - IVA IVB
 * T(1-3), N(0-1), M(1a, 1b). Grade is also used to determine stage.
 * IA (T1 N0, Low grade) IB (T2 N0, Low grade) - IIA (T1 N0, High grade) IIB (T2 N0, High grade) - III (T3 N0) - IVA (M1a) IVB (N1, M1b)
 * Soft tissue sarcoma - I - II - III - IV
 * T(1a 1b, 2a 2b), N(0-1). Grade is also used to determine stage.
 * I (Low grade N0) - II (High grade T1a/b-T2a N0) - III (High grade T2b N0) - IV (N1, M1)

Skin
Return to Top

 * Carcinoma of the skin - I - II - III - IV
 * T(1-4), N(1,2a/b/c,3)
 * I (T1 N0) - II (T2 N0) - III (T3 N0, T1-3 N1) - IV (N2-N3 or T4 or M1)
 * Merkel cell carcinoma - IA IB - IIA IIB IIC - IIIA IIIB - IV
 * T(1-4), N(0,1a/b,2)
 * IA (T1 pN0) IB (T1 cN0) - IIA (T2-3 pN0) IIB (T2-3 cN0) IIC (T4 N0) - IIIA (N1a) IIIB (N1b/N2) - IV (M1)
 * Melanoma - Clinical node staging: IA IB - IIA IIB - III - IV - Pathologic node staging: IIIA IIIB IIIC
 * T(1a 1b, 2a 2b, 3a 3b, 4a 4b), N(1a 1b, 2a 2b 2c, 3), M(1a 1b 1c). Note: all M1 are the same overall stage.
 * Clinical - IA (T1a N0) IB (T2a, T1b N0) - IIA (T3a, T2b N0) IIB (T4a, T3b N0) IIC (T4b N0) - III (N+) - IV (M1)
 * Pathologic - IIIA (N1a or N2a with no ulceration T1-4a) IIIB (N1b or N2b or N2c with no ulceration T1-4a, or N1a or N2a with ulceration T1-4b) IIIC (N1b or N2b or N2c with ulceration T1-4b,or any N3)
 * Hint: ulceration always upstages by one

Breast
Return to Top

 * Breast - IA IB - IIA IIB - IIIA IIIB IIIC - IV
 * T(1mic 1a 1b 1c, 2, 3, 4a 4b 4c 4d), N(1 mi 1a 1b 1c, 2a 2b, 3a 3b 3c), M(0,cM0(i+),1). Note: all subtypes of a stage are the same overall stage.
 * IA (T1 N0) IB (T0-1 N1mi) - IIA (T1 N1, T2 N0) IIB (T2 N1, T3 N0) - IIIA (N2, T3 N1) IIIB (T4) IIIC (N3) - IV (M1)

Gynecologic
Return to Top

In all, T-stage parallels the FIGO stage, except there is no T4b (Stage IVB is M1), and in cases where the FIGO stage includes node-positive disease as a distinct stage (e.g. uterine corpus Stage IIIC). Except for vulvar, N+ makes the overall stage the highest Stage III stage. There is no T4 (and thus no IVA) for ovary and fallopian tube. N-stage changes the FIGO stage in most, but only in vulvar cancer is there N1 vs N2.
 * Vulva - IA IB - II - IIIA IIIB IIIC - IVA IVB (FIGO staging)
 * T(1a 1b, 2, 3), N(1a 1b, 2a 2b 2c, 3)
 * IA (T1a N0) IB (T1b N0) - II (T2 N0) - IIIA (T1-2 N1) IIIB (T1-2 N2a-b) IIIC (T1-2 N2c) - IVA (T3 or N3) IVB (M1)
 * Vagina - I - II - III - IVA IVB (FIGO staging)
 * T(1-4), N(0-1). N+ is Stage III.
 * Cervix - IA1 IA2 IB1 IB2 - IIA1 IIA2 IIB - IIIA IIIB - IVA IVB (FIGO staging)
 * T(1a1 1a2 1b1 1b2, 2a1 2a2 2b, 3a 3b, 4), N(0-1). N+ is Stage IIIB in AJCC only, not used in FIGO stage.
 * Endometrial carcinoma - IA IB - II - IIIA IIIB IIIC1 IIIC2 - IVA IVB (FIGO staging)
 * T(1a 1b, 2, 3a 3b, 4), N(0-2)
 * IA (T1a N0) IB (T1b N0) - II (T2 N0) - IIIA (T3a N0) IIIB (T3b N0) IIIC1 (T1-3 N1) IIIC2 (T1-3 N2) - IVA (T4) IVB (M1)
 * Uterine sarcoma - IA IB IC - II - IIIA IIIB IIIC - IVA IVB
 * T(1a 1b 1c, 2, 3a 3b, 4), N(0-1)
 * IA (T1a N0) IB (T1b N0) IC (T1c N0) - II (T2 N0) - IIIA (T3a N0) IIIB (T3b N0) IIIC (T1-3 N1) - IVA (T4) IVB (M1)
 * Ovary - IA IB IC - IIA IIB IIC - IIIA IIIB IIIC - IV (FIGO staging)
 * T(1a 1b 1c, 2a 2b 2c, 3a 3b 3c), N(0-1). N+ is IIIC.
 * Fallopian tube - IA IB IC - IIA IIB IIC - IIIA IIIB IIIC - IV (FIGO staging)
 * T(1a 1b 1c, 2a 2b 2c, 3a 3b 3c), N(0-1). N+ is IIIC.
 * Gestational trophoblastic tumors - IA IB - IIA IIB - IIIA IIIB - IVA IVB (FIGO staging)
 * T(1-2), N stage is not used, M(1a 1b). Risk group (high or low or unknown) is also used in staging.

FIGO Staging
Return to Top

Links about FIGO staging.

Latest revision: 2009
 * See also: individual GYN chapters for FIGO staging references

 * 2009 PMID 19367689 -- "Revised FIGO staging for carcinoma of the vulva, cervix, and endometrium." (Pecorelli S, Int J Gynaecol Obstet. 2009 May;105(2):103-4.)

Guidelines: Guidelines for Gynaecological Cancers"
 * 2000 PDF "Staging Classifications and Clinical Practice

Genitourinary
Return to Top

 * Penis - I - II - IIIA IIIB - IV
 * T(Ta, 1a 1b, 2-4), N(1-3)
 * I (T1a N0) - II (T1b-T3 N0) - IIIA (T1-3 N1) IIIB (T1-3 N2) - IV (T4, N3, M1)
 * Prostate - I - IIA IIB - III - IV
 * T(1a 1b 1c, 2a 2b 2c, 3a 3b, 4), N(0-1), M1(1a 1b 1c). Now incorporates PSA + Gleason score.
 * I (T1-T2a N0 M0 PSA<10 G≤6) - IIA (T1-2 up to PSA<20 and G7) IIB (T1-2 PSA≥20 or G≥8 or T2c) - III (T3 N0) - IV (T4, N1, M1)
 * Testis - IA IB IS - IIA IIB IIC - IIIA IIIB IIIC (there is no Stage IV)
 * T(1-4), N(1-3), M(1a 1b—affects stage), S(1-3)
 * IA (T1 N0 M0 S0) IB (T2-4 N0 M0 S0) IS (Any T N0 M0 S1-3) - IIA (Any T N1 M0 S0-1) IIB (Any T N2 M0 S0-1) IIC (Any T N3 M0 S0-1) - IIIA (Any T Any N M1a S0-1) IIIB (S2 and N1-3 or M1a) IIIC (S3 and N1-3 or M1a, or M1b)
 * Kidney - I - II - III - IV
 * T(1a 1b, 2, 3a 3b 3c, 4), N(1-2). Substage does not change overall stage.
 * I (T1 N0) - II (T2 N0) - III (T3, N1) - IV (T4, N2, M1)
 * Renal pelvis and ureter - I - II - III - IV
 * T(1-4), N(1-3). Note: all N+ are the same overall stage.
 * I (T1 N0) - II (T2 N0) - III (T3 N0) - IV (T4, N+, M1)
 * Bladder - 0a 0is - I - II - III - IV
 * T(Ta Tis T1, 2a 2b, 3a 3b, 4a 4b), N(1-3). Substages 4a and 4b change overall stage but T2 and T3 substages do not. All N+ (N1-3) is the same overall stage.
 * I (T1 N0) - II (T2 N0) - III (T3 N0, T4a N0) - IV (T4b, N+, M1)
 * Urethra - 0a 0is - I - II - III - IV
 * T(Ta Tis, 1-4), N(1-2)
 * I (T1 N0) - II (T2 N0) - III (T1-3 N1, T3 N0) - IV (T4, N2, M1)

Ophthalmic sites
Return to Top

Note: Rarely used

 * Retinoblastoma - No AJCC stage grouping
 * Clinical: T(1a 1b, 2a 2b 2c, 3, 4), N(1-2), M(1a 1b)
 * Pathologic: T(1, 2a 2b 2c, 3a 3b 3c, 4), N(0-1)

Central nervous system
Return to Top

No AJCC staging system

For more information on CNS tumors, see the CNS page

Lymphoid malignancies
Return to Top

TNM does not apply.
 * Lymphoma - Ann Arbor Stage: I - II - III - IV with modifiers.
 * Multiple myeloma - Durie-Salmon staging: IA IB - IIA IIB - IIIA IIIB.

title: Radiation Oncology/Staging


text:
Speech-Language Pathology/Stuttering/Finding Help Paying for an Anti-Stuttering Device

Many states, including Texas, California, Massachusetts, Georgia, Wisconsin, North Carolina, and Arizona have special telephone equipment distribution programs that provide telephone-compatible anti-stuttering devices free to qualified residents. (See below.)

If you're unemployed and stutter, your state's vocational rehabilitation program will help get you a job, including paying for speech therapy and/or an anti-stuttering device. See the section Vocational Rehabilitation.

If you're employed, ask your employer to help pay for an anti-stuttering device.

If your employer were to say no, you could say that the Americans with Disabilities Act requires employers to pay for "reasonable accommodations" requested by employees with disabilities.

Some speech clinics will handle your insurance billing for anti-stuttering devices. The CPT/HCPCS procedure code for electronic anti-stuttering devices is E1399-NU. The diagnosis code for stuttering is 307.0.

Special Telephone Equipment Distribution Programs
Most states have programs to help individuals with disabilities use telephones. States that DO NOT provide anti-stuttering telephone devices include:

 Alabama (no program) Colorado (hearing impaired only) Idaho (hearing impaired only) New Hampshire (independent living only) New York (no program) Ohio (no program)

Other states may provide anti-stuttering devices on a case-by-case basis. Find other state programs on the TEDPA website. In general, if a program's mandate includes speech-impaired individuals then the program might help stutterers. If a program's mandate is only for hearing-impaired individuals then the program doesn't help stutterers.

The following information may be inaccurate or out of date. Please check with your state's program.

Arizona
 Arizona Telecommunications Equipment Distribution Program (AzTEDP)

No income limit

Website: http://www.aztedp.org/

Telephone: (866) 223-3412 or (602) 264-6876

California

California Telephone Access Program (CTAP)

No income limit

Website: http://www.ddtp.org/CTAP/

Telephone: (800) 806-1191

Georgia

Georgia Telecommunications Equipment Distribution Program (GATEDP)

Income cannot exceed $36,208 for family of four

Website: http://www.gachi.org/gatedp/intro.htm

Telephone: (888) 297-9461 or (404) 297-9461

Maryland

Maryland Accessible Telecommunications (MAT)

Individual must be on welfare (SSI, SSDI, TDAP or TCA) or a "hardship case"

Website: http://www.mdrelay.org/equipment.html

Telephone: (800) 552-7724

Massachusetts

Massachusetts Specialized Telephone Equipment Program

No income limit

Website: http://www22.verizon.com/foryourhome/SAS/Massachusetts_Availability.asp

Telephone: (800) 974-6006

Missouri

Telecommunications Access Program for Telephone (TAP for Telephone)

Missouri resident; Income cannot exceed $60,000

Website: http://at.mo.gov/tap.html

Call local Independent Living Centers (see website for telephone numbers)

North Carolina

North Carolina Telecommunications Equipment Distribution Program (NCTEDP)

Income cannot exceed 250% of the current federal poverty level

Website: http://www.relaync.com/get_equipment/get_equipment.html

Telephone: (800) 999-5737

Pennsylvania

Telecommunication Device Distribution Program

No website

Telephone: (866) 227-6810 (ext. 8728)

Address: Hiram G. Andrews Center Attention: R.D. Robinson, Program Manager 727 Goucher Street Johnstown, PA 15905

Texas

Specialized Telecommunications Assistance Program (STAP)

No income limit

Website: http://www.dars.state.tx.us/dhhs/stap.shtml

Telephone: (512) 407-3250

Texas STAP provides a voucher worth up to $995. Only devices that plug into telephones are covered.

Wisconsin

Telecommunications Equipment Purchase Program (TEPP)

No income limit.

Website: http://psc.wi.gov/consumerinfo/assistancePgms/tepp/tepp-ind.htm.

Telephone: (608) 231-3305

Wisconsin TEPP provides a voucher worth up to $1600. The consumer must send a $100 co-payment to the vendor. Only devices that plug into telephones are covered.


text:
Orthopaedic Surgery/Tendons

Sometimes linear cord like, sometimes broad and sheet like, tendons in the body vary in structure, macroscopically, at the microscopic level and at the level of the intracellular aparatus depending upon the particular setting in which they act. Tendons impart the force of contraction of a muscle to bone either to stabilize its position in space against an external force or to accelerate the bone through space. From the standpoint of the joint in the first case the motion of the joint is prevented by the neutralization of an external force the length of the muscle tendon unit remains relatively fixed or in the second case the motion of the joint is produced by shortening of the muscle-tendon unit with relaxation and relative lengthening of the antagonist muscles.

While the classic conception of a concentric contraction affecting flexion or extension of a joint provides a basic statement of the manner in which a muscle tendon unit functions, in the body the function is often more complex. It is the role of the muscle tendon unit to dampen impact forces to the skeleton and to modulate the motion by the allowance for eccentric contraction leading to smooth decelerations and the imparting of forces through a transfer of potential energy in the form of spring like elastic forces contained by the stretched muscle tendon units. The muscle contraction serves to maintain tension in the muscle tendon unit so that the transfer of kinetic and potential energy can occur. This biomechanically more complex arrangement is especially evident in the highly coordinated activities of running and throwing. Aging results in a less elastic structure within tendon leading to deteriorating performance in these activities after age 40. Tendinosis within the supraspinatus tendon is present in somewhat less than 1/3 or individuals under the age of forty with increasing frequency with age but still absent in 10% of 80 year olds thus the changes conflate with aging but may not be justifiably characterized as due to aging. Tendinosis is noted in a higher percentage of torn tendon samples than in intact tendons suggesting that this process does contribute to a vulnerability to injury. Inflammation as defined by the presence of neutrophils occurs at the sight of tendon rupture however they may be there in response to necrotic tenocytes and disrupted collagen. While submaximal strains may result in collagen disruption which stimulates an inflammatory response, the cytokine activity stimulated by the inflammatory response may further weaken the tendon leading to failure upon repeated strains prior to structurally competent remodeling.

Gait analysis reveals the perfect, or in the pathologic state the imperfect, balancing of floor reaction force vectors, as derived from force plate data, in relation to joint axis and just sufficient opposing torque, as derived from dynamic EMG data, imparted by the contracting muscle tendon unit such that the center of gravity can be advanced in an energy efficient manner. Feedback via stretch receptors (golgi organs) at the terminal ends of sensory neurons terminating mostly on the surface of tendons and especially at the musculotendinous junction provide the feedback to mediate these reflex contractions.

In the case of the elaborate programmed and learned activities such as these the proprioceptive function of the tendons provide for anticipatory reflexive contractions to occur whereby the joints are spared excessive forces. In this way the coordinated function of the muscle tendon unit protect the skeleton and the cartilage from damage. Joint architecture in conjunction with periarticular ligamentous structures are likewise evolved to enable motion while avoiding deleterious shear forces upon the cartilage which is durable in compression but prone to structural damage when exposed to shear. Joints act in series to permit a greater arc of overall motion while maintaining joint contact forces perpendicular to the opposing joint surfaces, thus allowing for the range of motion while remaining a mechanically sound environment compatible with the working material parameters of cartilage. The segmental structure of the spine and the serial structure of the wrist and ankle are examples.

Human movement evolves in patterns by which combinations of posture and gesture communicate intent and social relation augmenting or undermining verbal communication. The effect crosses cultural and even species barriers. Movement Histology of tendons reveal columns of tenocytes elongated with oval nuclei in aligned with the linear pattern of collagen the concentric production of collagen extruded from the tenocyte and arrayed in the extracellular matrix resulting in the fascicle pattern observed. There are associated blood vessels and nerves a peritenon and epitenon with a slight fluid layer between in larger tendons. Bursae are frequently associated as in the shoulder and about the achilles tendon and hamstring insertion at the knee.

The smallest functional unit that we acknowledge is a fascicle consisting of collagen aligned end to end a quarter staggered array. Fibril diameters vary from 10 to 500 nm depending upon species and age. Fibrils are bundled to form fascicles which are surrounded by loose connective tissue endotenon through which course blood vessels lymphatics and nerves.

Tendon structure has variation in the size of fascicles and variations in the degree of crimp of the collagen within the matrix, a feature that serves ot dampen sudden strains and responsible for the toe region of the stress strain curve. The crimping straightens after which the stress strain curve becomes linear from about 2% strain to 4% strain after which bond slippage and finally failure begins to occur with gross failure at 8% strain on average. High strain rates and obliquity of strain increase the likelihood of failure. Tendons which typically handle higher sudden loading generally exhibit greater crimp angles. Some tendons notably the rotator cuff may be subject to compressive and shear forces which the structure must contend with. These tendons have more complex ultrastucture with some transverse and spiral patterned collagen fiber orientation. Muscle tendon units that cross more than one joint may be uniquely vulnerable by virtue of more complex patterns of mechanical stresses, the achilles tendon the hamstrings and the extensor carpi radialis brevis tendon are noteworthy in this regard.

While the majority of forces are in line tension the structures of muscle tendon units vary with resultant differences in excursion which appear to match the role the muscle tendon unit plays with multipennate and unipennate pattern which favor a priority upon power or excursion. Tendons transmit tension forces through a matrix composed predominantly of type I collagen (95%, very small amounts of elastin which is capable of 200% strain to failure as opposed to collagen in with a 8% strain typically results in failure. Type III collagen is seen in healed tendons, its presence in normal tendon represents a minor contribution under normal conditions. Proteoglycan is present and is felt to play a larger role in compressive forces where present. The subtleties of the composition vary through the body in a manner commensurate with the varying function of tendons. Lower extremity tendons involved in running and shoulder tendons involved in throwing have compositions with more elastin.  Tendons involved in grasp and fine motor function are stiffer with more extensive cross linking of type I collagen. Distinctions in ultastructure are also noted with smaller fascicles in flexor tendons and larger fascicles in weight bearing tendons

The potential strength of a muscle contraction is proportional to the cross sectional area of the muscle. This strength of contraction can be made to vary with training and disuse and the atrophy or the hypertrophy of the muscle may be readily observed over a matter of days or weeks. The tendon, too, will respond to physiologic stress and lack of use thus as a living structure it thrives on regular mechanical strains to order itself. Adaptive change and functional reserve are facilitated by gradual transitions whereas sudden changes especially unanticipated high strain rate loading or sudden changes in the frequency of loading, like a new weekend project taken on by a white collar worker, can lead to injury. Indeed daily injury and mechanical stresses trigger adaptive remodeling by tendon modulating rates of cell proliferation and apoptosis in keeping with changing mechanical demands resulting in periodic renewal of tendon cellular structure and material composition. The mechanism and degree of adaptive changes occurring in tendons in response to conditioning remain ill defined. Likewise the presumed mechanism of chronic tendinosis leading to attritional failure as a consequence of a remodeling process out of step with demand remains a matter of speculation.

Tendon can withstand up to 1000 Kilograms per square centimeter, and at times appears to be subject of forces as within the achilles tendon during running which at 12 times body weight exceed the ultimate tensile strength of the tendon. The muscle tendon unit is protected by reflex relaxation of the muscle at higher strains.

Tendon displays viscoelastic properties consistent with the organic polymeric structure of its constituent type I collagen. Viscoelasticity is defined by such behaviors as increasing strain with sustained stress (creep) and decreasing stress at constant strain (stress relaxation), properties which one can appreciate in the process of conducting a stretching regimen. Another viscoelastic property is an increase in apparent stiffness at higher strain rates, which will also tend to mean a lower ultimate tensile strength and failure at a lower % strain at higher strain rate. These material properties also play a role under cyclic loading whereby phase lag (hysteresis) will contribute to the dissipation of mechanical energy. Atomic force microscopy of collagen structure suggests that its inherent mechanical strength is partly explained by the cross linking and hydrogen bonding between the triple helical strands of collagen which function as sacrificial bonds which break thus absorbing load and then rapidly reform.

It is hypothesized that repeated submaximal strains can result in an altered balance of proliferation and programmed cell death (apoptosis). Nuclear fragmentation characteristic of apoptosis is observed in tendinosis of the rotator cuff. Tendon remodeling which pushes the limit of its capacity to keep up results in a tendon structure that may be weaker and thus more readily prone to failure at a lower percent strain or at a lower strain rate than would otherwise be required. Lipoid and mucinous degeneration are both noted in tendon.

While many systemic factors come in to play one common thread may be a common influence upon the local blood flow to portions of certain tendons. Hypoxia with overuse may result in anoxic injury, reperfusion injury due to reactive oxygen species is suggested by the finding of enzymes in tenocytes that function to neutralize the toxic effect of reactive oxygen species. Watershed areas are implicated in the suprapinatus and achilles tendons. It is in keeping with the pruning effect of smoking on small blood vessels that the lack of colleral supply in these watershed areas may come into play.

It is debated whether the findings of fibroangioblastic change associated with tendinosis is in keeping with this hypothesis or not. The seemingly contradictory proliferation of blood vessels may reflect an attempt to overcome a previous phase of dysvascularity. It is also unknown whether apoptosis represents a primary pathologic process such as occurs in some forms of musculodystrophy or alzheimers or whether this process is secondary to some other pathology representing a normal remodeling process in response to that injury.

Ultimately it is the resident cell population of tenocytes that maintain the functional integrity of the matrix which provides the mechanical properties of the tendon although in cases of tendon laceration, both an intrinsic and extrinsic repair potential comes into play.

title: Orthopaedic Surgery/Tendons


text:
User talk:Je suis

You have been temporarily blocked from editing Wikibooks. Please use the "edit this page" feature to improve a page, not destroy it. We do not allow vandalism at Wikibooks. --Kernigh 06:38, 27 March 2006 (UTC)

RE: Blocked, you have been blocked for vandalizm, please stop, I won't give up. Whopper 21:34, 20 April 2006 (UTC)

title: User talk:Je suis