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Voice Disorders Flashcards

1
Q

Aetiology of vocal nodules

A
  • Tissue reaction to frictional trauma between vocal folds
  • Excessive laryngeal tension
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2
Q

Pathophysiology of vocal nodules

A
  • Small, white, greyish protuberance on free margin of vocal folds
  • Junction of anterior 1/3 & posterior 2/3 of vocal folds (where the vocal folds bang together)
  • Usually bilateral & symmetrical
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3
Q

Early stages of vocal nodules

A
  • Localised capillary haemorrhage (bleeding)
  • Swelling
  • Redness
  • Soft
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4
Q

Later stages of vocal nodules

A
  • Fibrosis of epithelium (hard fibrotic lumps usually require an operation)
  • Rough
  • Semicircular
  • Nodule (increases mass and stiffness of vocal fold)
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5
Q

Speaker characteristics for vocal nodules

A
  • Incessant talker
  • Socially aggressive
  • Tense
  • Loud
  • Teachers
  • Lawyers
  • Auctioneers
  • Actors
  • Singers
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6
Q

Perceptual and physiological signs of vocal nodules

A
  • Perceptual:
    • Hoarseness
    • Breathiness (because cords aren’t closing properly)
    • Habitual cough & throat clearing
  • Physiological:
    • Airflow may be increased (because cords aren’t closing properly)
    • Early stages: Increased subglottal pressure (can achieve closure of vocal folds)
    • Later stages: Decreased subglottal pressure (can’t achieve closure of vocal folds)
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7
Q

Management of vocal nodules

A
  • If nodules are immature & nonfibrous: voice therapy
  • If nodules are fibrous: surgical removal & therapy
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8
Q

Voice therapy for vocal nodules

A
  • Reduction of voice usage (vocal rest)
  • Awareness of vocal hygiene
  • Elimination of vocal abusive behaviours (e.g. hard glottal attack)
  • Reduction of vocal intensity
  • Reduction of laryngeal tension
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9
Q
A

Vocal nodules

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10
Q

Aetiology of vocal polyps

A
  • Vocal fold trauma due to vocal abuse
  • Secondary reaction to:
    • Allergies
    • Upper respiratory tract infection (URTI)
    • Excessive smoking
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11
Q

Pathophysiology of vocal polyps

A
  • 2 types:
    • Sessile/broad based (blister-like/flap)
    • Pedunculated (attached to a stalk)
  • Usually unilateral
  • Junction of anterior 1/3 & posterior 2/3 of vocal folds
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12
Q

Perceptual & physiological signs of vocal polyps

A
  • Perceptual:
    • Diplophonia
    • Sudden voice breaks
    • Hoarseness
    • Roughness
    • Breathiness
  • Physiological:
    • Increased airflow
    • Increased sub glottal pressure (to overcome glottal incompetence/poor closure of vocal folds)
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13
Q

Medical management of vocal polyps

A
  • Pedunculated & large sessile: surgical removal
  • Small sessile: voice therapy
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14
Q

Voice therapy for vocal polyps

A
  • Similar to therapy for vocal nodules
  • 2-6 months before improvements in quality
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15
Q
A

Vocal polyp - sessile

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16
Q
A

Vocal polyp - pedunculated

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17
Q

Reinke’s oedema

A
  • Polypoid degeneration
  • Build-up fluid in first layer of lamina propria in Reinke’s space
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18
Q

Aetiology of Reinke’s oedema

A
  • Vocal fold trauma & misuse
  • Smoking (more frequent in females if long-term smokers)
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19
Q

Pathophysiology of Reinke’s oedema

A
  • Vocal fold full of fluid (boggy)
  • Oedema full length of vocal fold bilaterally
  • Oedema disturbs elasticity of vocal folds - reducing stiffness
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20
Q

Perceptual & physiological signs of Reinke’s oedema

A
  • Perceptual:
    • Low pitch
    • Hoarseness
    • Shortness of breath
  • Physiological:
    • Increased airflow
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21
Q
A

Reinke’s oedema

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22
Q

Chronic laryngitis

A

Long-standing inflammation of laryngeal mucosa secondary to phonotrauma

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23
Q

Aetiology of chronic laryngitis

A
  • Cigarette-smoking (most common)
  • Vocal abuse/misuse (coughing, throat-clearing)
  • Overuse of mouthwashes & gargles
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24
Q

Pathophysiology of chronic laryngitis

A
  • Vocal folds are:
    • Red
    • Irregular
    • Thick
    • Rounded (rather than sharp)
  • Small dilated blood vessels on surface
  • Oedema in supraglottic area
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25
Q

Perceptual & physiological signs of chronic laryngitis

A
  • Perceptual:
    • Hoarseness
    • High/low pitch
    • Non-productive cough
    • Sore throat
  • Physiological:
    • Increased airflow
    • Increased subglottal pressure
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26
Q

Medical management of chronic laryngitis

A

Surgical stripping (if voice therapy is unsuccessful)

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27
Q

Voice therapy for chronic laryngitis

A

Reduction of vocal abuse & misuse

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28
Q
A

Chronic laryngitis

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29
Q

Muscle Tension Dysphonia

A
  • Second most common type of voice disorder (after vocal nodules)
  • Vocal muscle misuse
  • Can lead to vocal nodules
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30
Q

Aetiology of muscle tension dysphonia

A
  • Excessive musculoskeletal tension in the head and neck
  • Intrinsic & extrinsic laryngeal muscles are sensitive to emotional stress
  • Hypercontraction of muscles (common denominator in functional dysphonias)
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31
Q

Symptomatology of muscle tension dysphonia

A
  • Aphonia/dysphonia (more common)
  • Breathiness
  • Hoarseness
  • Excessive high pitch
  • Pain in laryngeal area
  • Referred pain to ears & chest
  • Sensation of a lump or tightness in larynx/pharynx
  • Pain in response to pressure on larynx
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32
Q

Physiological bases of muscle tension dysphonia

A
  • Usually normal larynx
  • May demonstrate abnormal function
  • Secondary mucosal changes may occur
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33
Q

Ventricular dysphonia

A
  • Voice is the result of the vibration of the false/ventricular vocal folds
  • Simultaneous vibration of true & false vocal folds lead to diplophonia
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34
Q

Aetiology of ventricular dysphonia

A
  • Excessive muscle tension
  • May be a substitute voice for a severe debilitating disease (e.g. paralysis)
35
Q

Pathophysiology of ventricular dysphonia

A
  • False vocal folds approximate & begin to vibrate
  • Increase mass in vocal folds, thus unable to vibrate quickly (leads to low pitch)
36
Q

Perceptual & physiological signs of ventricular dysphonia

A
  • Perceptual:
    • Low pitch
    • Diplophonia
    • Very hoarse
    • Reduced pitch range
  • Physiological:
    • Reduced airflow
37
Q

Medical management of ventricular dysphonia

A

Contraindicated (i.e. not recommended) (unless due to primary vocal fold defect)

38
Q

Voice therapy for ventricular dysphonia

A
  • If capable of true vocal fold phonation: retrain
  • If compensatory: improve characteristics of ventricular phonation (e.g. pitch & loudness)
39
Q
A

Ventricular dysphonia

40
Q

Psychogenic voice disorders

A
  • 2 subtypes:
    • Conversion voice disorders
    • Puberphonia
41
Q

Conversion voice disorders

A
  • A subtype of psychogenic voice disorders
  • Total (aphonia)/partial (dysphonia) loss of phonation due to conversion reaction
  • Physical symptoms not linked to anatomical or physiological disease
  • Person convinced problem is organic
  • Types:
    • Conversion Muteness
    • Conversion Aphonia
    • Conversion Dysphonia
42
Q

Conversion muteness

A
  • Most extreme & incapacitating
  • Neither whispers nor articulates
  • Involuntary & voluntary cough present (indicates normal vocal fold function)
  • Speaker may suffer from:
    • Chronic stress
    • Suppressed anger
  • Speaker may be neurotic
43
Q

Conversion aphonia

A
  • Involuntary whispering
  • Able to cough, laugh, cry involuntarily (indicates normal vocal folds)
  • Larynx high in neck & rigid
  • 80% female
  • Onset sudden or over a period of hours
  • Hoarseness leading to a whisper
  • Often triggered by colds (dysphonia remains)
  • Acute/chronic emotional stress
44
Q

Conversion dysphonia

A
  • Similar to conversion aphonia, but there is some voice
  • Varying degrees & types of hoarseness
  • With or without strained-harsh quality
  • High-pitched falsetto breaks
  • Breathiness
  • Intermittent whispering
  • Moments of normal voice (when not talking about the cause of dysphonia)
45
Q

Voice therapy for conversion voice disorders

A
  • Principal goal: Re-establish normal vocal fold function by reshaping vegetative vocal functions
  • Aim to achieve good voice first session
  • Adopt positive attitude with person
  • Focus on voice production NOT the cause
46
Q

Puberphonia

A
  • Failure to eliminate high pitched voice associated with puberty & substitute with lower pitch of adulthood
  • Structurally normal larynx
  • Mainly males (one octave change)
47
Q

Aetiology of puberphonia

A
  • Psychosocial factors
  • Strong feelings of feminine attachment
  • Rejects responsibilities & rules of adulthood
  • Organic:
    • Endocrine disorders
    • Severe hearing loss
    • Disease affecting respiration (e.g. motor neurone disease/amyotrophic lateral sclerosis)
48
Q

Pathophysiology of puberphonia

A
  • Larynx is high in neck & tilted downwards
  • Vocal folds are lax (slack)
  • Phonation: Arytenoids adduct tightly (posterior portion of vocal folds are prevented from vibrating)
  • Thyroarytenoid muscle fails to contract leading to a decrease in vocal fold mass (only thin edge of vocal folds vibrate)
49
Q

Voice therapy for puberphonia

A
  • Principal goal: shape vegetative vocal production to end up with a normal voice
  • Excellent prognosis
50
Q

Vocal process granuloma (contact ulcer)

A
  • Small ulceration on the medial surface of the vocal processes of arytenoid cartilages
  • Continued irritation in presence of bacteria (leads to ulcer & granulation tissue)
51
Q

Aetiology of vocal process granuloma (contact ulcer)

A
  • Repeated, forceful hyperadduction of vocal processes
  • Hard glottal attack
  • Low pitch
  • Glottal fry
  • Intubation trauma
  • Stress-related gastrointestinal difficulties
52
Q

Pathophysiology of vocal process granuloma (contact ulcer)

A
  • “Cup & saucer” appearance (protuberance on one process & crater on the other)
  • Early stages: strand of mucous seen between the 2 processes (contact ulcer diathesis)
53
Q

Perceptual & physiological signs of vocal process granuloma (contact ulcer)

A
  • Perceptual:
    • Constant throat-clearing
    • Vocal fatigue
    • Breathy
    • Hoarse
    • Discomfort: Unilateral in area of thyroid cartilage
  • Physiological:
    • Increased subglottal pressure
    • Increased airflow
    • Increased intensity
54
Q

Medical management of vocal process granuloma (contact ulcer)

A

Surgery (only if intensive voice therapy has failed to reduce/eliminate the contact ulcer)

55
Q

Voice therapy for vocal process granuloma (contact ulcer)

A
  • Eliminate vocal abusive behaviours
  • Alter voice production methods
56
Q
A

Vocal process granuloma (contact ulcer)

57
Q

Laryngeal nerve paralyses

A

2 types:

  • Superior laryngeal nerve paralysis
  • Recurrent laryngeal nerve paralysis
58
Q

Perceptual signs of superior laryngeal nerve paralysis

A
  • Vocal fatigue
  • Hoarseness
  • Loss of vocal range
59
Q

Recurrent laryngeal nerve paralysis

A
  • Left recurrent laryngeal nerve (RLN) lesions are 10x more frequent that right RLN
  • Lesion may be unilateral or bilateral
  • 2 types:
    • Adductor
    • Abductor
60
Q

Unilateral adductor paralysis

A

Vocal fold will not move to midline

61
Q

Bilateral adductor paralysis

A

Neither vocal folds are able to move to the midline (phonation impossible)

62
Q

Unilateral abductor paralysis

A

Vocal fold remains in fixed adducted position

63
Q

Bilateral abductor paralysis

A

Both vocal folds remain in the adducted position (difficulty with respiration)

64
Q

Aetiology of unilateral recurrent laryngeal nerve paralysis

A
  • Intrathoracic neoplasms
  • Aneurysms
  • Mitral valve stenosis (left auricle enlarges & stretches RLN)
  • Neck trauma
  • Idiopathic
65
Q

Aetiology for bilateral recurrent laryngeal nerve paralysis

A
  • Thyroidectomy
  • Neck trauma
  • Tumours
  • Infection
66
Q

Perceptual & physiological signs of unilateral recurrent laryngeal nerve paralysis

A
  • Perceptual:
    • Mild breathiness
    • Hoarseness
    • Reduced loudness
    • Shortness of breath
  • Physiological:
    • Increased airflow
    • Decreased subglottal pressure
67
Q

Perceptual & physiological signs of bilateral recurrent laryngeal nerve paralysis

A
  • Perceptual:
    • Inhalatory stridor
    • Voice is quite good (because both vocal folds are weakly adducted)
  • Physiological:
    • Increased airflow
    • Decreased subglottal pressure
68
Q

Surgical management of unilateral recurrent laryngeal nerve paralysis

A
  • Vocal fold medialisation:
    • Injection of material into the vocal fold itself
    • Materials (fat, collagen, Teflon, hydroxyapatite (Radiance)) used to “plump up” paralysed vocal folds
    • Injection into/lateral to thyroarytenoid muscle, lamina propria
  • Implantation of material into the larynx (pushes vocal fold medially)
    • Insert material medial to thyroid cartilage at the level of the vocal fold
    • Serves as a wedge to move paralysed vocal fold to midline
    • Type 1 thyroplasty
  • Arytenoid adduction
    • Rotation of arytenoid cartilage so that the tip of the vocal process moves to the midline

If surgery is a success:

  • Voice usually excellent immediately post-op
  • Deteriorates a little as the oedema resolves
  • Improvement in one week
  • Permanent level in 2 weeks
69
Q

Surgical management of bilateral recurrent laryngeal nerve paralysis

A
  • Tracheostomy
  • Arytenoidectomy
70
Q

Voice therapy for recurrent laryngeal nerve paralysis

A

Facilitative techniques to reduce glottal incompetence (e.g. push-pull technique)

71
Q

Spasmodic dysphonia

A
  • Also called spastic dysphonia or laryngeal dystonia
  • Strained, choked, effortful voice patter
  • Similar to stuttering of the voice
  • Relatively rare disorder
  • Resistant to traditional voice therapy
  • 3 types:
    • Adductor spasmodic dysphonia
    • Abductor spasmodic dysphonia
    • Mixed abductor-adductor spasmodic dysphonia
72
Q

Aetiology of spasmodic dysphonia

A
  • Can be:
    • Psychologically-based (conversion reaction, musculoskeletal tension), or
    • Neurologically-based (organic/essential tremor, dystonia), or
    • Idiopathic
  • Onset: 4th-5th decade
  • Often associated with an upper respiratory tract infection (URTI), emotional stress, may be insidious
73
Q

Adductor spasmodic dysphonia

A
  • Phonation: true & false vocal folds hyper adduct in intermittent & irregular spasms
  • Attribute to organic pathology (psychological factors co-exist)
  • Abrupt, staccato, vocal explosions, strained-strangled, intermittent voice breaks, harsh
  • Larynx normal at rest
  • Most common type
74
Q

Abductor spasmodic dysphonia

A
  • Severe breathy aphonia (intermittent breaks)
  • Vocal folds episodically abduct to lateral position
  • Not as common as adductor spasmodic dysphonia
  • MAY be related to conversion reaction
  • Difficult to transition from voiceless consonant to vowel
75
Q

Mixed abductor-adductor spasmodic dysphonia

A
  • Both adductor & abductor laryngospasms
  • Aphonic, breathy periods, voice arrests
76
Q

Medical management of spasmodic dysphonia

A

Botox (botulinum toxin) injections:

  • Thyroarytenoid/vocalis (adductor spasmodic dysphonia (ADSD))
  • Posterior cricoarytenoid (abductor spasmodic dysphonia (ABSD))
  • Results in muscle paralysis through chemical denervation
  • Botox is a neurotoxin (blocks transmission nerve impulses to muscle)
  • Injected bilaterally via the mouth or percutaneously in the neck
  • Provides significant voice improvement:
    • 90% of normal function (ADSD)
    • 70% of normal function (ABSD)
  • Airflow rates are increased and normalised
  • Reduction in intrinsic laryngeal muscle hyperfunction
  • Require re-injection every 3-5 months
77
Q

Voice therapy for spasmodic dysphonia

A
  • Breathy voicing
  • Elevation of pitch (reduces spasms)
  • Easy voice onsets & articulatory contacts
  • Relaxation therapy
  • Co-ordination of exhalation & voice onset
78
Q

Aetiology of hypokinetic dysphonia

A

Parkinson’s disease

79
Q

Pathophysiology of hypokinetic dysphonia

A
  • Vocal folds normal in structure
  • Phonation: closure incomplete (bowing of vocal folds)
  • Unable to tense vocal folds
80
Q

Perceptual & physiological signs of hypokinetic dysphonia

A
  • Perceptual:
    • Monopitch
    • Monoloudness
    • Reduced loudness
    • Reduced stress
    • Harsh vocal quality
    • Breathiness
  • Physiological:
    • Increased airflow
    • Decreased subglottal pressure
81
Q

Medical management of hypokinetic dysphonia

A

Drug therapy: Parkinson’s disease medication (levodopa)

82
Q

Voice therapy for hypokinetic dysphonia

A
  • Very effective
  • Increased vocal fold adduction
  • Increased loudness & intonation
  • Lee Silverman Voice Treatment (LSVT)
83
Q
A

Hypokinetic dysphonia

Voice (5 decks)

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