VPI

VPI

Velopharyngeal Insufficiency (VPI) and Apraxia

By

Karen Golding-Kushner, Ph.D., CCC-SLP

By definition, apraxia is difficulty coordinating speech movements in the absence of muscle weakness or paralysis. Therefore, the presence of a structural problem is likely to preclude a diagnosis of apraxia. Unfortunately, children with velopharyngeal insufficiency (VPI) and structurally-based speech problems are frequently misdiagnosed as having apraxia.

What is VPI? Velopharyngeal closure (VPC) occurs when the soft palate (velum) and sides and back of the throat (pharynx) move toward each other and seal the air passages behind the nose during speech. This prevents air escape through the nose and allows the build-up of air pressure in the mouth for good articulation. VPI occurs when the velum and pharynx do not seal off during speech; this results in hypernasality. VPI may be due to structural problems, such as a cleft palate (not enough tissue to close off even with good movement) or certain types of dysarthria (a neurological problem resulting in muscle weakness or paralysis – not enough movement to close off). Some structural problems cannot be diagnosed by simply looking in the mouth. For example, an occult submucous cleft palate is a type of cleft in which oral examination is normal and palate even feels intact, but the muscle structure on the nasal surface of the palate is abnormal. This can only be diagnosed using nasendoscopy. Although anything is possible in medical and behavioral science, VPI does not usually occur in individuals with acquired apraxia associated with brain damage or with developmental apraxia of speech.

Why are children with VPI often misdiagnosed with apraxia? Some children with VPI compensate for the loss of air through the nose by articulating sounds lower in the vocal tract, so that the sounds can be produced before the air pressure escapes through the nose. The most common of these compensatory articulation errors, a glottal stop, is produced by sharp contact of the vocal folds to stop the air instead of contact of the lips (for /b,p), tongue-tip (for /t, d/), or back of the tongue (for /k,g/). To an untrained ear, the speaker sounds like he or she is omitting consonants: kitty cat sounds like ih-ee-a and big boy sounds like ih-oy. This error is called a glottal stop because the opening between the vocal folds is the glottis. Because the child has already produced the sound (although at the vocal folds instead of in the mouth), he or she does not use the lips or tongue. In other words, the child does not move the articulators. Speech pathologists inexperienced with VPI and compensatory articulation misinterpret this lack of movement as an inability to control the lips and tongue, and conclude that the child has apraxia. In reality, this is simply an error in the place of articulation. The lips and tongue are not weak and do not need strengthening or stimulation; they are simply not being used because the child has articulated the sounds using the vocal folds instead. Therefore, oral exercises and stimulation are inappropriate. Speech therapy is needed.

A history or suspicion of cleft palate, velocardiofacial syndrome, hypernasality, or a combination should raise a red flag. They are more likely to be associated with compensatory articulation errors (glottal speech) than with apraxia.


(Dr. Golding-Kushner is the executive director of the Velo-Cardio-Facial Syndrome Educational Foundation. She is internationally recognized for her work with cranio-facial disorders and serves as a Fellow of the American Speech Language and Hearing Association. She has specialized in craniofacial disorders, cleft palate, and velopharyngeal function for over 25 years. She is author of the bestseller Therapy Techniques for Cleft Palate Speech and Related Disorders (Singular Publishing Group, 2001) and has also published over 20 articles and chapters. She has made over 100 presentations at national and international conferences, primarily on the diagnosis and treatment of speech disorders associated with VPI and velocardiofacial syndrome.)

VPI

Velopharyngeal Insufficiency (VPI) and Apraxia

By

Karen Golding-Kushner, Ph.D., CCC-SLP

By definition, apraxia is difficulty coordinating speech movements in the absence of muscle weakness or paralysis. Therefore, the presence of a structural problem is likely to preclude a diagnosis of apraxia. Unfortunately, children with velopharyngeal insufficiency (VPI) and structurally-based speech problems are frequently misdiagnosed as having apraxia.

What is VPI? Velopharyngeal closure (VPC) occurs when the soft palate (velum) and sides and back of the throat (pharynx) move toward each other and seal the air passages behind the nose during speech. This prevents air escape through the nose and allows the build-up of air pressure in the mouth for good articulation. VPI occurs when the velum and pharynx do not seal off during speech; this results in hypernasality. VPI may be due to structural problems, such as a cleft palate (not enough tissue to close off even with good movement) or certain types of dysarthria (a neurological problem resulting in muscle weakness or paralysis – not enough movement to close off). Some structural problems cannot be diagnosed by simply looking in the mouth. For example, an occult submucous cleft palate is a type of cleft in which oral examination is normal and palate even feels intact, but the muscle structure on the nasal surface of the palate is abnormal. This can only be diagnosed using nasendoscopy. Although anything is possible in medical and behavioral science, VPI does not usually occur in individuals with acquired apraxia associated with brain damage or with developmental apraxia of speech.

Why are children with VPI often misdiagnosed with apraxia? Some children with VPI compensate for the loss of air through the nose by articulating sounds lower in the vocal tract, so that the sounds can be produced before the air pressure escapes through the nose. The most common of these compensatory articulation errors, a glottal stop, is produced by sharp contact of the vocal folds to stop the air instead of contact of the lips (for /b,p), tongue-tip (for /t, d/), or back of the tongue (for /k,g/). To an untrained ear, the speaker sounds like he or she is omitting consonants: kitty cat sounds like ih-ee-a and big boy sounds like ih-oy. This error is called a glottal stop because the opening between the vocal folds is the glottis. Because the child has already produced the sound (although at the vocal folds instead of in the mouth), he or she does not use the lips or tongue. In other words, the child does not move the articulators. Speech pathologists inexperienced with VPI and compensatory articulation misinterpret this lack of movement as an inability to control the lips and tongue, and conclude that the child has apraxia. In reality, this is simply an error in the place of articulation. The lips and tongue are not weak and do not need strengthening or stimulation; they are simply not being used because the child has articulated the sounds using the vocal folds instead. Therefore, oral exercises and stimulation are inappropriate. Speech therapy is needed.

A history or suspicion of cleft palate, velocardiofacial syndrome, hypernasality, or a combination should raise a red flag. They are more likely to be associated with compensatory articulation errors (glottal speech) than with apraxia.


(Dr. Golding-Kushner is the executive director of the Velo-Cardio-Facial Syndrome Educational Foundation. She is internationally recognized for her work with cranio-facial disorders and serves as a Fellow of the American Speech Language and Hearing Association. She has specialized in craniofacial disorders, cleft palate, and velopharyngeal function for over 25 years. She is author of the bestseller Therapy Techniques for Cleft Palate Speech and Related Disorders (Singular Publishing Group, 2001) and has also published over 20 articles and chapters. She has made over 100 presentations at national and international conferences, primarily on the diagnosis and treatment of speech disorders associated with VPI and velocardiofacial syndrome.)



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