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Resonance Disorders

There are a number of causes of resonance disorders, including velopharyngeal dysfunction, oronasal fistulas, obstruction in the nasal or pharyngeal cavity, and hearing loss. Specific causes are grouped below by type of resonance disorder. 


  • Velopharyngeal dysfunction (VPD) (See Classification of Velopharyngeal Dysfunction [PDF] for terminology and examples.)
    • Structural causes resulting in velopharyngeal insufficiency (e.g., overt, submucous, or occult submucous cleft palate; irregular adenoids, adenoid atrophy [usually in those just getting velo-adenoidal closure]; post-adenoidectomy, enlarged tonsils that intrude into the pharynx and prevent VP closure; post-tonsillectomy [rare but may occur due to scar tissue affecting lateral wall movement]; maxillary advancement; deep pharynx [palatopharyngeal disproportion]; velar hypoplasia or dysplasia; tissue deficit from tumor resection; shrinkage following radiation therapy).

    • Structural anomalies associated with genetic syndromes can also result in hypernasality. These syndromes include 22q11.2 deletion syndrome (also known as velo-cardio-facial, DiGeorge syndrome, Shprintzen syndrome, and Sedláčková syndrome), CHARGE syndrome, Treacher Collins syndrome, Nager syndrome, BOR syndrome, Turner syndrome, Beckwith-Wiedemann syndrome, Stickler syndrome, Kabuki syndrome, Opitz G/BBB syndrome, Jacobsen syndrome, and any syndromic form of Robin sequence (Kummer, 2014; Shprintzen, 1997, 2000; Ysunza, Jackson, & Lozon, 2013).

    • Neurogenic causes resulting in VP incompetency (e.g., traumatic brain injury, stroke, cerebral palsy, apraxia [congenital or acquired], velar paresis/paralysis [e.g., cranial nerve defects], neuromuscular disease [e.g., myasthenia gravis and muscular dystrophy], neurofibromatosis, and neurodevelopmental syndromes such as velo-cardio-facial syndrome, Prader-Willi syndrome, myotonic dystrophy, and nemeline myopathy [Shprintzen, 1997]). Neurogenic causes are often associated with dysarthria and hypotonia.

    • Velopharyngeal mislearning
      • Learned compensatory misarticulations (e.g., glottal stops and pharyngeal fricatives, nasal fricatives, tongue clicks) that develop due to the inability to generate adequate intraoral airflow for consonant production. These productions almost always persist after successful physical management of the VP mechanism. When these errors are present, the adjacent vowels may become nasalized due to coarticulatory effects, thus leading the listener to perceive hypernasality.
      • Lack of auditory feedback in individuals who are deaf or have significant hearing loss. Abnormal resonance is due to an inability to learn nasal and oral contrasts and later monitor resonance normally through auditory feedback.

  • Oronasal fistula (e.g., in individuals with a history of cleft palate; trauma to the oral cavity; or ablative surgery in the oral cavity)
    • May result in hypernasality only if the fistula size is large—small fistulas may cause nasal emission on anterior sounds but not necessarily hypernasality; some fistulas are asymptomatic.


  • Nasal cavity/nasopharynx obstruction (e.g., enlarged adenoids, restricted pharyngeal cavity space due to maxillary retrusion and other craniofacial anomalies).
  • Swelling (with or without nasal congestion) due to allergic rhinitis, common cold, adenoid hypertrophy, nasopharyngeal polyps, and hypertrophic tonsils.
  • Deviated septum (nasal septum is significantly “off-center”).
  • Choanal atresia (abnormal narrowing of the passageway from the nose to the pharynx). 
  • Stenotic nares (narrow nostrils, often seen in patients with cleft lip repair).
  • Unwanted complications of corrective surgery for VPD.
  • Problems with motor planning/execution (apraxia) that result in inconsistent, abnormal VP closure on nasal phonemes.
  • Lack of auditory feedback in individuals who are deaf or have significant hearing loss may result in perceived hyponasality due to atypical tongue position during speech.

Cul-de-Sac Resonance

  • Oral—microstomia (small mouth opening).
  • Nasal—blockage in the anterior part of the nose (e.g., stenotic nares, nasal polyps, or deviated septum).
  • Pharyngeal (most common)—large tonsils/enlarged adenoids; lack of auditory feedback in individuals who are deaf or have significant hearing loss may result in cul-de-sac resonance due to atypical tongue position during speech.

Mixed Resonance

  • Problems with motor planning/execution (apraxia) that result in inconsistent abnormal VP opening and closing.
  • Combination of VPD and any form of nasopharyngeal obstruction—hypernasality and hyponasality may co-occur; nasal resistance does not eliminate nasal resonance completely but prevents nasal consonants from maintaining their integrity (Peterson-Falzone et al., 2010).
  • Lack of auditory feedback in individuals who are deaf or have significant hearing loss may result in mixed resonance problems.    

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