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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
Perceptual & physiological signs of chronic laryngitis
* Perceptual: * Hoarseness * High/low pitch * Non-productive cough * Sore throat * Physiological: * Increased airflow * Increased subglottal pressure
26
Medical management of chronic laryngitis
Surgical stripping (if voice therapy is unsuccessful)
27
Voice therapy for chronic laryngitis
Reduction of vocal abuse & misuse
28
Chronic laryngitis
29
Muscle Tension Dysphonia
* Second most common type of voice disorder (after vocal nodules) * Vocal muscle misuse * Can lead to vocal nodules
30
Aetiology of muscle tension dysphonia
* 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)
31
Symptomatology of muscle tension dysphonia
* 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
32
Physiological bases of muscle tension dysphonia
* Usually normal larynx * May demonstrate abnormal function * Secondary mucosal changes may occur
33
Ventricular dysphonia
* Voice is the result of the vibration of the false/ventricular vocal folds * Simultaneous vibration of true & false vocal folds lead to diplophonia
34
Aetiology of ventricular dysphonia
* Excessive muscle tension * May be a substitute voice for a severe debilitating disease (e.g. paralysis)
35
Pathophysiology of ventricular dysphonia
* False vocal folds approximate & begin to vibrate * Increase mass in vocal folds, thus unable to vibrate quickly (leads to low pitch)
36
Perceptual & physiological signs of ventricular dysphonia
* Perceptual: * Low pitch * Diplophonia * Very hoarse * Reduced pitch range * Physiological: * Reduced airflow
37
Medical management of ventricular dysphonia
Contraindicated (i.e. not recommended) (unless due to primary vocal fold defect)
38
Voice therapy for ventricular dysphonia
* If capable of true vocal fold phonation: retrain * If compensatory: improve characteristics of ventricular phonation (e.g. pitch & loudness)
39
Ventricular dysphonia
40
Psychogenic voice disorders
* 2 subtypes: * Conversion voice disorders * Puberphonia
41
Conversion voice disorders
* 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
Conversion muteness
* 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
Conversion aphonia
* 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
Conversion dysphonia
* 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
Voice therapy for conversion voice disorders
* 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
Puberphonia
* Failure to eliminate high pitched voice associated with puberty & substitute with lower pitch of adulthood * Structurally normal larynx * Mainly males (one octave change)
47
Aetiology of puberphonia
* 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
Pathophysiology of puberphonia
* 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
Voice therapy for puberphonia
* Principal goal: shape vegetative vocal production to end up with a normal voice * Excellent prognosis
50
Vocal process granuloma (contact ulcer)
* 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
Aetiology of vocal process granuloma (contact ulcer)
* Repeated, forceful hyperadduction of vocal processes * Hard glottal attack * Low pitch * Glottal fry * Intubation trauma * Stress-related gastrointestinal difficulties
52
Pathophysiology of vocal process granuloma (contact ulcer)
* "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
Perceptual & physiological signs of vocal process granuloma (contact ulcer)
* Perceptual: * Constant throat-clearing * Vocal fatigue * Breathy * Hoarse * Discomfort: Unilateral in area of thyroid cartilage * Physiological: * Increased subglottal pressure * Increased airflow * Increased intensity
54
Medical management of vocal process granuloma (contact ulcer)
Surgery (only if intensive voice therapy has failed to reduce/eliminate the contact ulcer)
55
Voice therapy for vocal process granuloma (contact ulcer)
* Eliminate vocal abusive behaviours * Alter voice production methods
56
Vocal process granuloma (contact ulcer)
57
Laryngeal nerve paralyses
2 types: * Superior laryngeal nerve paralysis * Recurrent laryngeal nerve paralysis
58
Perceptual signs of superior laryngeal nerve paralysis
* Vocal fatigue * Hoarseness * Loss of vocal range
59
Recurrent laryngeal nerve paralysis
* Left recurrent laryngeal nerve (RLN) lesions are 10x more frequent that right RLN * Lesion may be unilateral or bilateral * 2 types: * Adductor * Abductor
60
Unilateral adductor paralysis
Vocal fold will not move to midline
61
Bilateral adductor paralysis
Neither vocal folds are able to move to the midline (phonation impossible)
62
Unilateral abductor paralysis
Vocal fold remains in fixed adducted position
63
Bilateral abductor paralysis
Both vocal folds remain in the adducted position (difficulty with respiration)
64
Aetiology of unilateral recurrent laryngeal nerve paralysis
* Intrathoracic neoplasms * Aneurysms * Mitral valve stenosis (left auricle enlarges & stretches RLN) * Neck trauma * Idiopathic
65
Aetiology for bilateral recurrent laryngeal nerve paralysis
* Thyroidectomy * Neck trauma * Tumours * Infection
66
Perceptual & physiological signs of unilateral recurrent laryngeal nerve paralysis
* Perceptual: * Mild breathiness * Hoarseness * Reduced loudness * Shortness of breath * Physiological: * Increased airflow * Decreased subglottal pressure
67
Perceptual & physiological signs of bilateral recurrent laryngeal nerve paralysis
* Perceptual: * Inhalatory stridor * Voice is quite good (because both vocal folds are weakly adducted) * Physiological: * Increased airflow * Decreased subglottal pressure
68
Surgical management of unilateral recurrent laryngeal nerve paralysis
* 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
Surgical management of bilateral recurrent laryngeal nerve paralysis
* Tracheostomy * Arytenoidectomy
70
Voice therapy for recurrent laryngeal nerve paralysis
Facilitative techniques to reduce glottal incompetence (e.g. push-pull technique)
71
Spasmodic dysphonia
* 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
Aetiology of spasmodic dysphonia
* 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
Adductor spasmodic dysphonia
* 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
Abductor spasmodic dysphonia
* 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
Mixed abductor-adductor spasmodic dysphonia
* Both adductor & abductor laryngospasms * Aphonic, breathy periods, voice arrests
76
Medical management of spasmodic dysphonia
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
Voice therapy for spasmodic dysphonia
* Breathy voicing * Elevation of pitch (reduces spasms) * Easy voice onsets & articulatory contacts * Relaxation therapy * Co-ordination of exhalation & voice onset
78
Aetiology of hypokinetic dysphonia
Parkinson's disease
79
Pathophysiology of hypokinetic dysphonia
* Vocal folds normal in structure * Phonation: closure incomplete (bowing of vocal folds) * Unable to tense vocal folds
80
Perceptual & physiological signs of hypokinetic dysphonia
* Perceptual: * Monopitch * Monoloudness * Reduced loudness * Reduced stress * Harsh vocal quality * Breathiness * Physiological: * Increased airflow * Decreased subglottal pressure
81
Medical management of hypokinetic dysphonia
Drug therapy: Parkinson's disease medication (levodopa)
82
Voice therapy for hypokinetic dysphonia
* Very effective * Increased vocal fold adduction * Increased loudness & intonation * Lee Silverman Voice Treatment (LSVT)
83
Hypokinetic dysphonia

Voice (5 decks)

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