Why FC proponents constantly invoke apraxia and how they’ve got it all wrong
Perhaps no condition is as poorly understood by proponents of facilitated communication, and yet as frequently cited by them in defense of FC, as apraxia. Indeed, one of the most common criticisms leveled by FC proponents against us critics is that we’re ignoring apraxia and haven’t kept up with the latest research on it.
FC proponents invoke apraxia, particularly apraxia of speech, for three reasons: as a non-cognitive explanation for the minimal speech of many individuals with autism; as the justification for why these people purportedly communicate best through FCed typing; and as a reason why their speech often conflicts with that typing.
A broader notion of apraxia—also called “dyspraxia,” or problems with “praxis”—is invoked by FC proponents as well: it’s supposed to explain why the behaviors of FCed individuals are often inconsistent both with what they type and with the level of linguistic mastery displayed in their typed messages. For example, it’s supposed to explain why an FCed person types “pancakes” in answer to what they want for breakfast but then grabs a cereal box instead. And it’s supposed to explain why an FCed person is able to type, via FC, words like “nightmare” and “oblivious” but, during a standard FC-free vocabulary assessment, when prompted to “put your finger on the picture that shows a cup,” points instead to the picture of the duck or the flower.
And yet apraxia as clinically defined, diagnosed, and treated does not explain these things.
In an earlier post, I discussed what apraxia actually is in terms of its diagnostic and commonly observed symptoms, as compared to what FC proponents claim it is. Here’s a quick recap. For speech apraxia, the ASHA Leader (the main publication of the American Speech-Language-Hearing Association), lists these criteria:
A limited consonant and vowel repertoire.
Minimal variation between different vowel sounds.
Vowel errors and distortions.
Inconsistent errors and idiosyncratic error patterns.
Reduced rate or accuracy with diadochokinetic tasks [how quickly one can accurately repeat a series of rapid, alternating sounds like “puh-tuh” and “puh-tuh-kuh”]
Oral groping behaviors [resorting to trial and error tactics for making speech sounds]
Prosodic differences (reduced rate, excess or equal stress, “choppy” words and syllables, monotone speech).
Increased errors with increased length or complexity of utterances.
More difficulty with volitional utterances compared to modeled or automatic utterances.
But for FC proponents, speech apraxia is only about difficulty with volitional speech. That is, per FC proponents, speech apraxia is supposed to explain why someone says “popcorn” while they’re typing out sentences about the nature of language and communication—even when “popcorn” is pronounced without any of the above errors.
Here, in short, is the contrast between the standard clinical/scientific and the FC-world accounts of speech apraxia:
The standard clinical/scientific account: pronouncing intended words with speech errors
The FC-world account: pronouncing unintended words, often without speech errors
Then there’s apraxia more generally (see my earlier post for details), which:
As per the standard clinical/scientific account: involves difficulty using tools or pantomiming the use of a tool, perhaps because of loss of the semantic memory associated with the tool, and is the result, most likely, of a stroke or neurodegenerative disorder.
As per the FC-world account: is a generalized mind-body disconnect that impedes the ability to point to the items one intends to point to, and is a manifestation of autism that’s present in early childhood.
Another way to grasp the difference between what apraxia is and what FC supporters say it is—and what I’ll be doing below—is to compare the actual evidence-based interventions for apraxia with the interventions that FC proponents propose instead.
The standard evidence-based interventions, as reported on the website of the American Speech-Language-Hearing Association (ASHA), involve practice with the speech movements associated with particular sounds; practice with the different intonation patterns (melody, rhythm, and stress) for different functional uses of language; and instruction in the linguistic rules for when different sound combinations are used. Speech movement practice, the most important of these components, involves verbal directions (“spread your lips wide”) combined with auditory, visual, proprioceptive, and tactile cues as feedback to shape the child’s speech productions. Visual cues about the shape, placement, or movement of the speech articulators (tongue, lips, jaw, uvula, larynx) can include both hand signals and high-tech tools (e.g., an artificial electrode-studded palate inserted along the roof of the mouth and computerized, visually-displayed feedback about what the person’s speech articulation looks or sounds like). Tactile cues include pressure on the child's face, neck, and head.
In a refreshing break from the endless parade of S2C miracle stories in local news reports around the country, a 2019 Detroit-area local news segment recounted how a young autistic boy with severe apraxia learned how to speak through some of the above interventions. We hear him sing “Happy Birthday” and clearly pronounce the word “hamster.” There is no question that he is the one directing the oral movements that pronounce these words.
A systematic review by Murray et al. (2014) finds three specific interventions to be particularly effective: Integral Stimulation/DTTC, ReST, and Integrated Phonological Awareness Intervention. Each of these “demonstrated preponderant evidence… with positive treatment and generalization effects across several children.” DTCC, Marray et al. find, is particularly effective for children with more severe apraxia. In DTCC, as described by ASHA:
Movement gestures are shaped, beginning with direct imitation, moving to simultaneous production with tactile or gestural cues if direct imitation was unsuccessful, and then fading the simultaneous cue and again moving to direct imitation. The key element of this approach is that the clinician is constantly adding or fading auditory, visual, and tactile cues as needed after each practice trial.
Meanwhile, Integrated Phonological Awareness Intervention, most effective for 4-7-year-olds with mild to severe speech apraxia, uses picture cards and word games to teach letter-sound awareness and to target specific problems like the deletions of consonants at the ends of words, common consonant substitution errors (e.g., substituting /d/ or /t/ for /s/; or /b/ or /p/ for /f/; or /k/ or /g/ for /d/ or /t/), and difficulty with consonant clusters (e.g., deleting the s-sound in words with initial st, sl and sp clusters).
Finally, ReST, most effective for 7-10-year-olds with mild-to-moderate speech apraxia, according to ASHA, involves
repetition of varied sequences of real or nonsense syllables to train motor planning flexibility… [and] intensive practice in producing multisyllabic, phonotactically permissible pseudo-words [nonsense words] to improve accuracy of speech sound production, rapid and fluent transitioning from one sound or syllable to the next, and control of syllable stress within words.
Thus, the standard, evidence-based approaches for apraxia involve various forms of practice making speech sounds, combined with extra cues about one’s speech productions that are faded over time.
For FC proponents, in contrast, the intervention for apraxia is… FC. That is, holding the person’s hand/arm (in classic FC) or holding up the letterboard and verbally prompting (in RPM/S2C), are supposed to bypass the purported oral apraxia and the purported inability to point, and to redirect the person’s “language pathways” through their arm/hand. Or, put another way, instead of working with these individuals to improve their speech, FC proponents dismiss that speech. And instead of using cues temporarily as tools for language instruction, they use cues permanently (however unwittingly, and however subtle and invisible to naïve eyes these cues can become over time) as tools for language control.
On top of this, there’s little evidence that those subjected to FC even have speech apraxia.
First, it remains unclear whether apraxia is particularly prevalent in autism: different studies draw different conclusions. FC proponents have cited one study (Tierny et al., 2015) as showing that 64% of autistic children have apraxia of speech. However, this study only included children with communication delays. Other studies (Shriberg et al., 2011 and Cabral & Fernandez, 2021) find little-to-no correlation between autism and speech apraxia.
What’s most relevant for FC proponents, or so one would think, is apraxia that’s so severe that it’s arguably more fruitful to bypass it than to remediate it. But here, too, the correlations with autism are questionable. A recent article, Chenausky et al. (2023), reviewed case reports of 375 children with speech apraxia (abbreviated here as CAS) and examined which factors (comorbidities) correlated with apraxia (CAS) severity:
Over 95% of children had comorbid expressive language impairment. Children with comorbid intellectual disability (78.1%), receptive language impairment (72.5%), and nonspeech apraxia (37.3%; including limb, nonspeech oromotor, and oculomotor apraxia) were significantly more likely to have severe CAS than children without these comorbidities. However, children with comorbid autism spectrum disorder (33.6%) were no more likely to have severe CAS than children without autism. [Boldface added].
Second, as I discuss in an earlier post:
Reduced attention to speech is characteristic of children with autism and begins in early infancy.
Early reduced attention to speech both delays and derails speech acquisition.
Autism severity is correlated with reduced attention to social stimuli, including speech.
Those most likely to be subjected to FC tend to be at the more profound end of the autism spectrum.
What these four factors entail is that the lack of speech in many individuals with profound autism may be the result, not of severe apraxia, but of their minimal attention to people’s speech and their resulting minimal opportunities to acquire speech, as typical children do, from the social environment that surrounds them.
Third, apraxia is diagnosed based on speech errors and therefore, practically speaking, cannot be diagnosed in children with no speech at all. As for the many FCed individuals who do speak, however minimally, few of the many I’ve observed exhibit the pronunciation errors that (see above) characterize speech apraxia—e.g., a limited consonant and vowel repertoire, vowel errors and distortions, and oral groping behavior. Indeed, the non-automatic speech of many of these FC victims (non-automatic speech being the kind of speech most susceptible to apraxia) is typically quite accurate. Some of them clearly enunciate the letters they type while FCed, and/or clearly pronounce the words they type out after the fact. Others clearly pronounce messages, some of them while being FCed, that appear (at least to those outside the FC world) to be not reflexive but fully volitional: “No more!”; “Go home!”.
In short, for all the many occasions in which FC proponents invoke apraxia to explain why FC is valid and to show how critics are ignoring the research, FC proponents, in fact, neither seem to know what apraxia actually is, nor are able to back up their claims that most FCed individuals are afflicted with it.
Presume competence. As that constant exhortation of FC proponents and disability rights advocates suggests, we should (in the absence of evidence to the contrary) presume that most FCed individuals are, in fact, apraxia-free. We should, furthermore, presume that the most disabling affliction that besets these individuals is something that comes not from within themselves but from outside forces embedded in the most ableist corners of society: namely, the communication-hijacking effects of FC, RPM, and S2C.
REFERENCES:
American Speech Language Hearing Association (ASHA). ASHA.org. https://leader.pubs.asha.org/do/10.1044/2021-0514-childhood-apraxia-of-speech; https://www.asha.org/practice-portal/clinical-topics/childhood-apraxia-of-speech#collapse_6
Cabral, C., & Fernandes, F. (2021). Correlations between autism spectrum disorders and childhood apraxia of speech. European Psychiatry, 64(Suppl 1), S209. https://doi.org/10.1192/j.eurpsy.2021.557
Chenausky, K. V., Baas, B., Stoeckel, R., Brown, T., Green, J. R., Runke, C., Schimmenti, L., & Clark, H. (2023). Comorbidity and Severity in Childhood Apraxia of Speech: A Retrospective Chart Review. Journal of speech, language, and hearing research : JSLHR, 66(3), 791–803. https://doi.org/10.1044/2022_JSLHR-22-00436
Murray, Elizabeth, et al. (2014). A systematic review of treatment outcomes for children with childhood apraxia of speech. American Journal of Speech-Language Pathology, vol. 23, no. 3.
Shriberg, L. D., Paul, R., Black, L. M., & van Santen, J. P. (2011). The hypothesis of apraxia of speech in children with autism spectrum disorder. Journal of autism and developmental disorders, 41(4), 405–426. https://doi.org/10.1007/s10803-010-1117-5
Tierney, C., Mayes, S., Lohs, S. R., Black, A., Gisin, E., & Veglia, M. (2015). How Valid Is the Checklist for Autism Spectrum Disorder When a Child Has Apraxia of Speech?. Journal of developmental and behavioral pediatrics : JDBP, 36(8), 569–574. https://doi.org/10.1097/DBP.0000000000000189
