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SPCH 277 > quiz 2 > Flashcards

quiz 2 Flashcards

1
Q

describe airflow

A
  • generated via lungs
  • pressure sensitive consonants
  • greatest on voiceless consonants via lack of impedance from vf vibration
  • increased in press via articulators
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2
Q

describe voice

A
  • generated via vf vibration
  • modified as travels via vt
  • voiced consonants and vowels
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3
Q

describe the resonance & airflow chart

A
  • vf vibrations -> sound -> resonance -> vowels & cons
  • open glottis -> airflow -> increased air press -> press cons
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4
Q

describe normal resonance pt 1

A
  • amplifies & dampens signals
  • vowels -> resonance
  • conso -> no res
  • sonorants -> have resonance & anti-resonants
  • can sing it? resonance
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5
Q

describe the source filter theory

A

vocal cords -> source
vt = filter
enhancement of formant frequencies change sound qual = resonance

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6
Q

describe regular resonance vs resonance for speech

A
  • resonance -> system vibration, varying amplitude
  • resonance 4 speech -> modified phoned sound, varying frequencies, articulators & cavities
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7
Q

describe the container to formant ratio

A
  • container 2 (oral cav) -> formant 2
    container 1 (pharynx) -> formant 1
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8
Q

what determines resonance for speech?

A

-velopharyngeal valve
- size n shape of resonating cavs (pharyn, oral, nasal)

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9
Q

describe the Bernoulli principle

A
  • increase of fluid velocity = decrease in pressure
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10
Q

describe the size & shape of cavities

A

shorter/ smaller cavities -> higher formants

longer/larger cavities -> lower formants

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11
Q

describe vowel production

A
  • produce by oral cavity changes
  • high vowels = more nasal
  • high tongue position = increase in transpalatal transmiss & decrease in oral transmiss
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12
Q

describe resonance disorders

A
  • abnormal transmiss of sound energy
  • via resonatory cavities
  • 4 types
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13
Q

describe hypernasality

A
  • 2 much sound in nose during oral sounds
  • abnormal coupling
  • vowel heavy
  • low volume via absorption in pharyn/nose
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14
Q

describe severe hypernasality

A

voiced plosive -> nasalized -> become nasal cognates (m/b, n/d, ing/g)

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15
Q

describe obligatory errors

A
  • artic placement = normal
  • distortion -> abnormal structure
  • Tx -> correct surgery, no speech

i.e - hypernasal/VP insuffic
i.e - nasalized cons

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16
Q

describe compensatory errors

A
  • artic placement = abnormal
  • TX -> correct structure + speech

i.e - substitution of /n/ for oral sound|leak in VP valve | inadequate airflow

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17
Q

what causes hyper nasality ?

A
  • VP opening
  • thin velum via sub mucous cleft
  • large oronasal (palatal) fistula
  • Nasal artic on specific oral sounds via mislearning
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18
Q

describe hyponasality & denasality

A
  • reduction in nasal res on nasal sounds
  • sounds “stuffed up”
  • no nasal res during speech at all

i.e - nasal cons sound like oral cogs (m/b, n/d, ing/g OR stops)

19
Q

what causes hypo & denasality

A
  • blockage in nose &/or pharynx
  • allergic rhinitis, common cold, adenoid hypertrophy, shallow pharynx, hypertrophic tonsils
20
Q

what does hypo & denasality commonly occur with?

A
  • cleft lip/palate
  • deviated septum (unilateral cleft)
  • Choanal stenosis or atresia
  • stenotic naris
  • maxillary retrusion
  • overcorrection of VPI surgery
21
Q

describe cul-de-sac resonance

A
  • sound blocked from exiting, cannot escape
  • absorbed by soft tissues
  • muffled, low vol
  • “muppet voice”
22
Q

whats oral CDS Resonance ?

A

causes -> mumbling, microsomia = small mouth opening

23
Q

whats nasal CDS resonance ?

A
  • VPI & anterior nasal blockage -> most noticeable

-common with cleft lip/palate + VPI + nares stenosis block

24
Q

whats pharyngeal CDS resonance ?

A
  • sound in oropharynx
  • palatal tonsils enlarged
25
Q

What’s mixed resonance ?

A
  • hyper + hypo + cul-de-sac reson
  • caused vis VPI + obstruction & apraxia
26
Q

what causes resonance disorders ?

A

VP dysfunction -> hyper nasality &/or nasal air emission

obstruction -> hypon or CDS res

27
Q

describe referrals for resonance disorders

A

hyper? cleft/craniofacial team, vp function specialist

hypo? ENT 4 upper airway

28
Q

describe vp function during nasal breathing & speech production

A

velum comes down -> nasal

goes up -> oral

LPWs moves medially

29
Q

describe the 4 types of vp dysfunction

A

dysfunction = general abnormal VP function

VPInsuff = structural defect

VPIncom = Neurophysiology defect

VPM = learning behavior

30
Q

hyper nasality vs nasal emission?

A
  • hyper = phoned sound in nose
    • vowels, cons
  • nasal emiss = leak in airflow into nasal cav
    • pressure cons (voiceless)

both have incomplete vp valve closure

31
Q

describe nasal emission

A
  • airflow leak
    via vp valve or fistula
  • audible on plosives, fricatives, affricates
  • most audible on voiceless sounds
  • w/ or w/ out hypernas
  • large opening = low velocity/pressure
    *small opening = high v/p
32
Q

describe inaudible nasal emission (large)

A

weak/omitted consonants

short utterance length

compensatory artic produc

nasal grimacing
- done 2 close vp valve
- mm contractions

33
Q

describe audible nasal emission (medium)

A

greater resistance = audible friction

less hypernasality

inadequate airflow

34
Q

describe nasal rustle/small opening/nasal turbulence

A
  • bubbling sound
    -airflow -> small opening -> high air pressure
  • Nasal rustle (NR) -> inconsistent,
    • increases w increase in rate of speech, utterance length, phonemic complexity, and fatigue.
      - more audible w nasal congestion
35
Q

describe phoneme-specific nasal emission (PSNE)

A
  • AKA compensation
  • placement -> altered, manner -> maintained.
  • produced in pharynx
  • pharyngeal fric or posterior nasal fricative is subed 4 an oral fricative (often /s/)

VPI comp errors
Glottal stops -> added /d/
Pharyngeal plosives -> /kha/
Glottal fricative -> (/h/)
Pharyngeal fricatives
Posterior nasal fricatives -> s = ck

Oronasal fistula error
- back of mouth
Palatal-dorsal production
“top” example
velar fricative

36
Q

describe dysphonia

A
  • breathiness, hoarseness, low intensity, and/or glottal fry during phonation
  • clefts, craniofacial anomalies, or VPI = high risk
  • Vocal nodules 2nd to hyperfunction in vt 2 achieve VP closure
  • Congenital laryngeal anomalies
  • Complications from long-term tracheostomy
  • Breathiness as a compensatory strategy
37
Q

what causes VPI ?

A
  • History of cleft palate
  • Submucous cleft palate (overt or occult)
  • Deep pharynx
  • Adenoid atrophy
  • Irregular adenoids
  • Hypertrophic in the nasopharynx

*20-30% affected w cleft after palatoplasty

38
Q

sub mucous cleft may cause ?

A

Anterior orientation of the levator veli palatini muscles

Zona pellucida

Hypoplastic musculus uvulae muscles

Defect in the posterior border of the velum

39
Q

what’s deep pharynx?

A

Ppw lays on top of cervical spine

Cervical spine &/or cranial base anomalies = cause

Velum may be normal, but unable to reach the ppw bc of its depth

40
Q

what’s adenoid atrophy?

A

small gap /nasal emission

Adenoid atrophy begins around age 6, and escalates during puberty

Can increase the depth of the pharynx, causing gradual onset of VPI

Risk is mostly with a history of cleft or submucous cleft palate

41
Q

what can interfere w complete closure of the velum?

A

tonsils

42
Q

describe the surgeries that can cause VPInsuff

A

Adenoidectomy

  • sudden increase in the nasopharyngeal dimension
  • temporary, resolves w/in 6 weeks
  • Permanent VPI is a risk w/ history of cleft or submucous cleft
  • VPI post adenoidectomy cannot be corrected with speech therapy. Surgical intervention is required.

Le Fort I Maxillary Advancement

  • Often done 4 patients w history of CLP 2 correct maxillary retrusion with midface deficiency
  • Done surgically or through distraction

Nasopharyngeal Tumors

  • Treatment of nasopharyngeal tumors
  • Resection (surgical removal) of tumor
  • Radiation therapy 2 shrink tumor
  • Can cause increase in nasopharyngeal space & cause VPI
43
Q

describe VPincomp causes

A

Cranial Nerve Damage

  • Cranial nerve damage -> velopharyngeal paralysis or paresis (muscular weakness)
  • Often unilateral, causing a unilateral VP opening
  • Common w hemifacial microsomia
  • Cortical damage can cause:

Hypotonia
- low muscle tonicity & reduced muscle strength
- velocardiofacial syndrome
Dysarthria
- Slow rate, Hypernasality, Weak or omitted cons, Poor breath support, Short utt length, Decre volume
Apraxia
- Inconsistent errors, Artic errors, Nasal/oral subs, Voiced/voiceless substi, Increase in errors (including hypernasality) + increase in utterance length & phonemic complexity

44
Q

describe VPM causes

A
  • articulation disorder via sub of a nasal or pharyngeal sound 4 an oral sound.
  • Results in an open vp valve during prod of the sound, causing “phoneme-specific” hypernasality or nasal emission.

phoneme specific hyper nasality

  • nasal sound = substituted 4 oral sound (e.g., ŋ/l or ŋ/r); or there’s an opening only on the high vowel /i/.

SPCH 277 (3 decks)

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