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cd 660 final > Module 15 > Flashcards

Module 15 Flashcards

1
Q

Is obligatory errors passive or active?

A

passive

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2
Q

is optional errors passive or active?

A

active

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3
Q

What are obligatory errors?

A
  • Due to structural or neurogenic problems

* Require physical management

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4
Q

What are optional/learned errors?

A
  • Habituated errors that are the result of early mislearning
  • Exist despite adequate VP closure
  • Require speech remediation
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5
Q

What are the sources of early VP mislearning?

A
  • Deficient velopharyngeal valve
  • Absent of structurally aberrant bony partition
  • Hearing loss
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6
Q

Cleft palate speech includes deviations in the following

A

(RAAA)
• Resonance: leads to hypernasality.
• Airflow: leads to nasal air emission.
• Air pressure: leads to weak oral pressures/weak pressure consonants.
• Articulation: leads to maladaptive compensatory misarticulations.

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7
Q

What is hypernasality?

A

•The resonance deviation that is heard on vowels and vocalic consonants (glides and liquids)
- Cardinal feature of VPI
• Resonance distortion that results from abnormal coupling of oral and nasal cavities.

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8
Q

In hyper nasality, changes in resonance primarily affects:

A

vowels and vocalic consonants (glides and liquids/oral sonorants).

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9
Q

Causes of hypernasality

A

VP insufficiency and VP incompetency

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10
Q

What is hyponasality?

A

too little nasal resonance; cold-in-the-head sound; affects vowels, sonorants and nasal consonants; can perceptually mask a VPI.

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11
Q

What is mixed nasality?

A

elements of both hypernasality and hyponasality; there is increased nasal cavity resistance.

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12
Q

What is cul de sac resonance?

A

sound is trapped by anterior nasal cavity constriction; ex: deviated septum

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13
Q

what is nasal air emissions?

A

Airflow deviation characterized by speech airflow and emission through the nose.

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14
Q

causes of NAE

A

Inappropriate/abnormal coupling of oral and nasal cavities
o Coupling at the VP port due to true VPI or mislearning (poor VP closure)
o Coupling via the oral cavity due to a fistula (a hole)

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15
Q

What parts of speech does NAE primarily affect

A

It primarily affects high pressure consonants/obstruent consonants (stops, fricatives, affricates)

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16
Q

T/F NAE can be audible and inaudible

A

true

17
Q

T/F NAE is only obligatory

A

F, it can be obligatory or learned

18
Q

Is Inaudible NAE disruptive to speech?

A

No, but can be a sign of VP inadequacy

19
Q

How to tell inaudible NAE?

A

visibly detectible with mirror

20
Q

Audible NAE tends to co occur with what type of speech?

A

more with high pressure consonants

21
Q

Audible NAE can be turbulent or non turbulent..

A

turbulence is a snorting sound,

-implicated that VP port may be source of turbulence

22
Q

Learned NE (active) and 2 patterns commonly seen

A

able to do vp closure

  1. Phoneme-specific nasal emission (PSNE) – kids who never had any problems
  2. Persisting post-operative nasal emission – kids who have had repaired clefts
23
Q

What is Phoneme-specific nasal emission (PSNE) ?

A
  • pattern of learned NE
  • occurs in non-cleft population
  • Selective nasal emission: affects only certain pressure consonants; other pressure consonants use normal/oral airflow
24
Q

What is Persisting post-operative nasal emission?

A

-pattern of learned NE
• NE that persists in repaired CP speakers who have the physiologic ability to attain closure.
• Speaker continues the old pattern of directing air into the nasal cavity
• Not restricted to any certain sounds
• Sounds like a nasal fricative

25
Q

Causes of weak pressure consonants

A
  • losing air b/c you have a fistula (losing air through oral cavity) or poor VP closure
  • Results from reduced oral pressures
  • Due to the abnormal coupling of oral and nasal cavities
26
Q

What are compensatory misarticulations?(CMA)

A
  • They are errors of place
  • They tend to be “backed” below the defect causing VPI
  • Sounds are being done POSTERIOR to where the normal articulation occurs
  • They are backed sounds, backed away from the defect.
27
Q

How is this CMA produced? Glottal stop

A

must be made at the glottis (VFs); hard glottal attack; valving

28
Q

How is this CMA produced? Pharyngeal stop

A

made at the pharynx; base of tongue comes back and blocks air flow at the level of the pharyngeal wall. Tongue base and posterior pharyngeal wall.

29
Q

How is this CMA produced? Mid-dorsum palatal stop

A

middle of tongue hits top of roof of mouth; sounds like a cross between tk and dg. Cop and top will sound the same.

30
Q

How is this CMA produced? Pharyngeal fricative

A

the darth vadar sound (who-haaa);
base of tongue approximating the pharyngeal wall
-you tend to then push air through there and get narrowness and it sounds like hissing.

31
Q

How is the CMA produced? Pharyngeal affricate

A

something between a stop and a fricative in duration and force.
Just like a real affricate—a stop transitioning into a fricative; we are blocking temporarily and moving to a narrow space to get syllabant, frication sound.

32
Q

How is the CMA produced? Posterior nasal fricative

A
  • snorting sound made in posterior nasal cavity;
  • tongue attempts to help with the VP closure.
  • Very narrow space between soft palate and vp port gives turbulence which is the nasal fricative.
  • Frication created w/in posterior pharyngeal walls/nasal cavity.
33
Q

How is the CMA produced? Nasal fricative

A

audible airflow with NO turbulence; airy.

  • Simply directing air through the nasal passage.
  • The tongue is blocking the airflow, forces the airflow through the nasal passages
34
Q

What are Adaptive oral misarticulations?

A
  • Occur in response to oral structural deviations

* Are obligatory

35
Q

Adaptive oral misarticulations cause

A

o Dental deviations
o Occlusal deviations
o Lip incompetency (overbite, can not make lip contact)

36
Q

Impact of VPI on phonation

A
  • Causes hoarseness to vocal nodules in cleft palate individuals
  • Soft voice syndrome (as a person tries to disguise their abnormal speech)

cd 660 final (7 decks)

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