Flashcards: Voice Exam #2

Behavioral Trauma (phonotrauma)◦ Vocal abuse◦ Vocal misuseMechanical Trauma◦ External sources◦ Automobile accidents◦ Assault from blunt objects◦ Penetrating injuries to larynx◦ Complications of tracheostomy◦ Internal sources◦ Improper endoscopic examination procedures◦ Endotracheal intubation◦ Indwelling nasogastric tubesTrauma due to burns◦ Thermal burns◦ Chemical burns

Vocal abuse◦ Yelling/screaming/cheering◦ Strained vocalizations (i.e., hyperadduction of the vocal folds because of attempts to make non-speech like sounds-plane/rocket sounds)◦ Excessive talking◦ Use of hard glottal attack◦ Throat clearing/coughing◦ Inhalation of cigarette smoke and environmental pollution◦ Poor singing technique ◦ Talking when the vocal folds are weakened◦ Cold◦ Menstrual cycle (hormone levels)◦ Allergies

Incorrect use of different aspects of voice production;◦Inappropriate loudness/intensity◦Inappropriate pitch/frequencyIncreased loudness/pitch may result from increased stress levels and/or habitual behaviors

**Often results in increased muscle tension in larynx**

The persistence of adolescent voice even after puberty in the absence of organic cause is known as puberphonia. This condition is commonly seen in males. The patient has an unusually high pitched voice persisting beyond puberty. This is uncommon in females because laryngeal growth spurt occurs commonly only in males.

Hyperfunctional dysphonia is one of the most common conditions associated with the voice. Also referred to as muscle tension dysphonia (MTD) or vocal hyper function, hyperfunctional dysphonia is the constriction and overexertion of the muscles around the larynx (voice box).

Contact Ulcer:◦ A benign lesion that develops on the vocal process of the arytenoid cartilages. May be unilateral or bilateral.◦ Etiology: results from vocal abuse such are regular hyperadduction of the vocal processes of the arytenoid cartilages. ◦ LPR/GERD may also be a significant factor in the formation of contact ulcers. In adults, more frequently seen in men.

Laryngeal Carcinoma Characteristics:Perceptual:• Hoarseness is the primary symptom. • May also see a lump in the neck, • Broadening of the larynx,• Tenderness in neck, • DysphagiaAcoustic:

• Frequency and amplitude perturbation will be increased.

• Changes dependent on severity of lesion.

Three major groups of symptoms:◦Respiratory difficulty due to airway obstruction◦Vocal changes:◦Hoarseness◦Weak or aphonic cry◦Dysphagia –swallowing problems

◦ Large dark reddish colored masses often found in the subglottic region; ◦ Rare;◦ Typically found in children, but may occur in adults;◦ Symptoms may appear 2-3 months after birth; most growth noted between 6-12 months and then spontaneously regress in size. Characteristics:◦ Perceptual –may be asymptomatic, or stridor, hoarseness, excessive coughing.◦ Acoustic - no known data

◦ Perceptual –◦ Asymptomatic if the web is not located on the level of the glottis◦ Very depending location and extent of lesion- may affect phonation and respiration (same as previous symptoms from medical trauma causing webs.◦ Acoustic –◦ No known data –if vibratory behavior is affected will affect habitual frequency

The general level of obstruction can be readily identified by fetal ultrasound and magnetic resonance imaging (MRI), but determining specific causes and severity of obstruction(e.g. long-segment laryngeal atresia vs a thin membrane) has been a challenge2. • Recent progress has shown the feasibility of using fetal laryngoscopy to evaluate the vocal cords of a fetus.

• A vertical opening between the larynx (cricoid cartilage) and the esophagus. • Cleft may be only in the region of the larynx or may form a complete laryngotracheoesophageal cleft.• Etiology: Results from a failure of the dorsal fusion of the cricoid lamina • Characteristics:• Symptoms usually occur shortly after birth; associate with other congenital anomalies• Respiration obstruction• Weak cry/aphonia• Repeated pneumonia

◦ Air or fluid filled dilation or herniation of the saccule (a small pouch located in the anterior portion of the ventricle) extending upward within the false vocal fold.

◦ Three types of laryngoceles:◦ Internal laryngocele –when the inflated tissue does not penetrate the thyrohyoid membrane, but instead pushes against the false vocal folds

◦ External laryngocele –when the mass pushes up through the thyrohyoid membrane, forming a bulge or swelling on the side of the individual’s neck◦ Combination laryngocele –has features of both the internal and external types/the most common type of laryngocele.

◦ Etiology:◦ May occur in infants/children◦ May be acquired - excessive pressure within the larynx (i.e., when a person engages in an activity that requires a lot of laryngeal pressure such as playing an instrument, weight lifting, or habitual excessive coughing from asthma or smoking). ◦ Characteristics: ◦ Perceptual –often asymptomatic in infancy. ◦ Hoarse voice or cry◦ Inspiratory stridor◦ External bulge in neck◦ Acoustic –no known data

•A benign tumor that starts in the epithelium; may occur in various parts of the larynx (subglottal, at the level of the vocal folds and supraglottal)Etiology: •Caused by a virus (usually human papilloma virus types 6 and 11)Characteristics: •Perceptual –hoarseness, may also include low pitch, breathiness, and strained vocal quality in the adult patient. Children may present with a weak cry, chronic cough, swallowing difficulties and stridor.•Acoustic –no known data

◦ Excessive flaccidity of the supraglotticlarynx◦ Inspiratory stridor◦ Spontaneous recovery in 12-18 months is often noted◦ Etiology: ◦ Congenital; Delayed or insufficient calcium deposition in infants resulting in inadequate support for the cartilaginous epiglottis; causing the epiglottis to collapse/fold over the glottis during inspiration◦ Characteristics:◦ Perceptual –inspiratory stridor; dyspnea; cyanosis; cry is normal◦ Acoustic –no known data

◦ Identical appearance of laryngomalacia◦ Etiology: partial deletion of chromosome 5◦ Other symptoms include:◦ Mental/physical retardation, beak like profile, microcephaly, hypotonia, hyperterlorism, antimongoloid palpebral fissures, epicanthal folds, strabismus, medial oral clefts, visceral anomalies, speech and language delay. ◦ Characteristics: ◦ Perceptual –presence of a weak, wailing cry◦ Acoustic –no known data

◦ A narrowing of the airway between the glottis and the first tracheal ring◦Etiology:◦ Congenital: thickening of subglottic tissue and/or vocal folds◦ Cartilaginous narrowing of the cricoid cartilage (anterior to posterior) –small posterior opening◦ Acquired: often the result of prolonged intubation.

• Perceptual –stridor on inhalation and exhalation, less severe cases may be perceived as croup, reduced intensity of airway is limited.• Acoustic –no known data.

Any dysphonia which occurs as a result of an impairment in the innervation, function or motor planning aspects of the muscles involved in respiration, phonation, and resonation/articulation resulting in a change in voice production.◦Motor Speech Disorders ◦Disorders of speech resulting from neurologic impairment affecting the motor programming or neuromuscular execution of speech.◦Dysarthria◦Apraxia◦They are NOT language or cognitive-communication problems.

• A group of motor speech disorders resulting from disturbances in muscular control over the speech mechanism• Due to damage of the central or peripheral nervous system• Results from paralysis, paresis, or incoordination of the speech musculature

◦ Definition: ◦ When one or both vocal folds are unable to move either towards or away from midline.◦ Etiology:◦ Damage to cranial nerve X (vagus nerve) anywhere along its path from the medulla to the larynx can result in voice difficulties as a result of vocal fold paralysis◦ Approx 90% of all vf paralyses are due to peripheral causes (i.e., lower motor neuron lesions)◦ Characteristics:◦ Vf paralyses result in flaccid dysphonias due to a reduction in muscle tone resulting from a loss in of motor supply to the muscle

◦ Usually the result of lesions high in the trunk of the vagus nerve or at the nuclei of origin in the medulla ◦ Etiology: ◦ tumors, carcinoma, or trauma; most cases are associate with intracranial pathology (hydrocephalus, etc)◦ Type: abductor or adductor; both are life threatening◦ Voice concerns are secondary to respiratory and feeding status ◦ Adductor vf paralysis: neither vocal fold is capable of moving towards the midline; making phonation impossible and placing the individual at risk for aspiration◦ Abductor vf paralysis: vocal folds remain at midline, causing serious respiratory problems; patients will often need a tracheostomy

◦ Most common cause of unilateral vf paralysis is disruption of the recurrent laryngeal nerve (RLN) on one side. ◦ Etiology: disease or trauma to the RLN. ◦ RLN is compromised on one side, ◦ laryngeal adductor muscles (LCA, IA) cannot adduct the vf;◦ paralyzed vf remains fixed in position during both inspiration and exhalation (including during phonation)

◦ Perceptual –markedly dysphonic or aphonic; ◦ Vocal quality –breathy, hoarse◦ Phonation time –reduced◦ Loudness –reduced or monoloud◦ Other –diplophonia, pitch breaks

◦ Myasthenia gravis is a chronic condition that causes muscles to tire and weaken easily.◦ an autoimmune disease in which the neuromuscular junction becomes impaired as the patient uses that particular muscle or muscle group resulting in extreme muscle fatigue◦ Muscles innervated by cranial nerves in the head and neck muscles are very vulnerable to this disease;◦ Possible difficulty swallowing◦ Results in flaccid dysarthria/dysphonia◦ Most often dx in women between ages 20 and 40 or men between ages 50 and 70.

◦ Etiology –◦ Damage to the receptors at the neuromuscular junction, prevent the normal transfer of impulse from the nerve in the particular muscleCharacteristics: ◦ Perceptual –◦ Typically normal voice changes to weak, breathy, barely audible voice; a few minute of voice rest, voice is restored but cannot be sustained after a brief period of usage.

Before the neostigmine test,• the glottic openness during normal breathing was incomplete due to weakness of the abductor muscle (Picture 1) and;• glottic closure when pronouncing the “e” sound was incomplete due to weakness of the adductor muscle (Picture 2);Right after the neostigmine test, • the glottis openness during normal breathing (Picture 3) and;• closure when “pronouncing the “e” sound (Picture 4) were more complete due to enhanced performance of the abductor and adductor muscles, respectively.

◦ Focal demyelination of spinal and cranial nerves◦ Flaccid dysarthria/dysphonia◦ Possible dysphagia◦ Etiology –◦ Unknown cause but frequently preceded by a viral infection◦ Affects extremities as well as facial, oral-pharyngeal and ocular muscles

◦ Lesions related to the Central Nervous System involving the pyramidal and extrapyramidal tracts◦ Spastic –◦ Muscular hypertonia: significantly increased muscle tone wherein the limb cannot be moved passively or volitionally with ease. ◦ Ataxic –◦ lesion in the cerebellum, loss of regulatory movements

◦ An upper motor neuron dysphonia primarily characterized by spasticity of the laryngeal muscles.◦ Etiology: ◦ Small bilateral lesions that occur just above the nucleus of the vagus nerve◦ Degenerative disease, vascular causes, TBI, unknownCharacteristics –◦ Perceptual –◦ Vocal parameters –strained, strangled, harsh vocal quality, low pitch, monopitch/pitch breaks, monoloud/reduced/variable loudness, possible hypernasality.◦ Speech: slow, effortful, imprecise artic.

◦ Cerebellar dysfunction resulting in a breakdown of the rhythmic, coordinated muscle patterns of speech (incoordination of voluntary muscle movement).◦ Related Dysphonia: changes in vocal parameters as a result of poor regulation of muscle tone and coordination of muscle activityCharacteristics –◦ Perceptual -◦ Vocal parameters: vocal quality may be normal or hoarse/harsh quality, low pitch or monopitch, monoloudness, inappropriate/imprecise prosody, excessive loudness, vocal tremor

◦ Disorders associated with a depletion of, or functional reduction in, the effect of the neurotransmitter dopamine on the activities of the basal ganglia. Acetylcholine is another type of neurotransmitter functioning within the basal ganglia.◦ An imbalance within the two neurotransmitters causes movement disorders with related dysarthrias/ dysphonias.

an extrapyramidal movement disorder due to a depletion of dopamine in the striatum, secondary to a slow degeneration of the substantia nigra of the basal ganglia (Parkinson’s Disease).◦ Characteristics: ◦ Perceptual –◦ Vocal parameters: breathy, harsh vocal quality, reduced loudness, monoloudness, monopitch, reduced stress◦ Imprecise articulation, intermittent rushes of speech

movement disorders in which the speech muscles are “quick, jerky, and irregular”.◦ 3 Types◦ Quick –Chorea/ Huntington’s disease, Myoclonus, Tourette’s syndrome◦ Slow –Athetosis, drug-induced dyskinesia, dystonia◦ Tremor – organic voice tremor

◦ Chorea –a disease of the basal ganglia◦ Purposeless, irregular, fleeting, involuntary movements of the limbs and facial muscles◦ Etiology: lesions that damage the striate nucleus of the basal ganglion◦ Characteristics: ◦ Perceptual –◦ Vocal parameters (may vary depending on type) :◦ Harsh, strangled/strained , intermittent breathiness vocal quality, ◦ Limited pitch range◦ Limited loudness range, intermittent variability ◦ Inappropriate and imprecise stress patterns –disruption of prosody

◦ a movement disorder that results in a hyperkinetic dysarthria characterized by episodic moments of abnormal speech production due to short rhythmic movements of the laryngeal and supraglottic musculature.◦ Etiology-◦ Lesions in the pathways connecting the red nucleus, the olivary bodies of the medulla and the dentate nucleus of the cerebellum.Characteristics:◦ Perceptual: Vocal parameters: voice arrest during vowel prolongation /singing◦ Myoclonus movements usually go unnoticed during connected speech.◦ Short, rhythmic contractions throughout the speech systems◦ Acoustic: Voiced/voiceless segments may be altered when compared to normal

episodic periods of “uncontrolled, abnormal, speech production due to rapid, tic-like movements and involuntary vocalizations◦ Etiology –unknown◦ Characteristics –◦ Perceptual: tics, dysfluency, throat clearing, coprolalia (use of obscene language), and echolalia◦ Typically, limited, if any change to voice parameters◦ Acoustic: N/A

a rare movement disorder “ characterized by involuntary, unpatterned, arhythmic wriggling and writhing movements of the head, neck, torso, and extremities.”◦ May interfere with all voluntary body movements.◦ Etiology: congenital (cerebral palsy) or acquired (neuronal degenerative disease, encephalitis, cerebral arteriosclerosis-hardening or blockage of arteries in the brain, hyperthyroidism◦ Characteristics: ◦ Perceptual :◦ Vocal parameters –hoarse, breathy vocal quality, monopitch, monoloudness or dramatic variations in loudness levels, inappropriate and imprecise stress patterns◦ Irregular movements of the face, cheeks, lips, mandible and tongue

movement disorder characterized by “slow involuntary movements and severe postural deformities resulting from fixed muscle contractions”◦ May be focal or generalized throughout the bodyEtiology: damage to the extrapyramidal system due to encephalitis, degenerative basal ganglia disease, trauma, intoxication, unknown causes.◦ Characteristics: ◦ Perceptual : vocal parameters intermittent, harsh, strained-strangled, breathy vocal quality, limited pitch and loudness ranges, inappropriate variations in loudness, inappropriate and imprecise stress, forced inspirations and exhalation◦ Irregular movements of the lips, mandible, tongue◦ Other associated symptoms include neuromuscular and dysarthric symptoms

a “finely oscillating tremor” that can be found in individuals without any other conditions.◦ Etiology –idiopathic or an involuntary, benign hereditary laryngeal tremor◦ Characteristics: ◦ Perceptual: ◦ quivering intonation, voice arrests◦ Lip, mandibular, soft palate, or tongue tremor may be present◦ Acoustic:◦ Increased variation in intensity and frequency

dysphonias comprised of characteristics from flaccid, spastics, ataxic, hypokinetic, hyperkinetic dysarthria◦ Amyotrophic Lateral Sclerosis –a “progressive degenerative debilitating disease of the anterior horns, cranial nerve motor nuclei, and the corticobulbar and corticospinal tracts results in mixed flaccid-spastic dysarthria”◦ Onset of disease –usually middle –late age ◦ Etiology –no known etiology

ALS Perceptual Characteristics◦ Harsh, breathy vocal quality, monopitch, monoloudness◦ Hypernasality◦ Strained, strangled voice◦ See Table for additional speech/voice changes• ALS Acoustic Characteristics◦ Increase noted in stop gaps in stop consonants and vowel durations ◦ Changes in fundamental frequency, jitter, shimmer, intensity and HNR seem to be most affected

a demyelinating disease characterized by deposits of plaque anywhere in the central nervous system. ◦ Symptoms may be mild initially with long period of remission or latency in between episodes. Severity of symptoms increase as disease progresses. ◦ Results in a mixed dysarthria (impacts multiple motor systems)◦ Occurs around age 30◦ Etiology: unknown, assumed to be an autoimmune disorder

◦ Perceptual:◦ vocal parameters include harsh vocal quality, reduced pitch and impaired loudness control, hypernasality◦ Poor respiration, poor sustained phonation◦ Associated symptoms: ◦ Articulation errors◦ Decreased neuromuscular coordination for respiration; decreased vital capacity◦ Nystagmus (A rapid, involuntary, oscillatory motion of the eyeball)

progressive lenticular degeneration which results in a mixed ataxic-hypokinetic-spastic dysarthria◦ Etiology –inadequate processing of dietary copper due to a rare, inherited autosomal recessive disorder◦ Characteristics –◦ Perceptual : ◦ Vocal parameters –harsh vocal quality, low pitch, reduced range of pitch and loudness◦ Acoustic: ◦ No definitive parameters ◦ Motor speech symptoms: difficulty noted in the face, lips, mandible, velopharyngeal movement◦ Neuromuscular symptoms

◦ Cause: increasing evidence that most cases of spasmodic dysphonia are neurogenic or having to do with the nervous system (brain and nerves-probably supranuclear although once thought psychogenic). „ • AD type• VF's spasm shut◦ Vocal strain, voice blocks • AB type ◦ VF's spasm open ◦ Breathy voice, aphonic moments ◦ Worse during unvoiced consonants „ • Mixed type• TASK SPECIFIC! Symptoms only occur during connected speech

◦ Etiology –a lesion that separates Broca’s area from the motor association area that deals with motor planning; most often secondary to a CVA.◦ Characteristics: ◦ Perceptual: ◦ Vocal parameters –may have intermittent aphonia, voicing errors◦ Acoustic:◦ No definitive parameters ◦ May have an absence of voluntary or imitative respirationAssociated symptoms –◦ changes in motor programming for articulation◦ pauses or hesitations in conversation speech

• A recently described neurodegenerative disorder in which patients present with an isolated apraxia of speech.• Focal degeneration of superior premotor and supplementary areas implicated.• Due to the novel nature of PPAOS, there is limited understanding of the progression of this disease.

•excessive nasal resonance during non nasal sounds (i.e., vowels and vocalic consonants)•Etiology: velopharyngeal incompetence or failure of the velopharyngeal port to attain and/or maintain sufficient closure; • Organic and nonorganic etiologies where velopharyngeal closure is negatively affected.◦ Structural deficits: (i.e., cleft palate)◦ Neurologic deficits:(i.e., spastic dysarthria)• Vocal parameters –increased nasal resonance◦ Non organic: no associate symptoms◦ Hypernasal non-organic voice sample◦ Organic: faulty articulation, nasal emissions, facial grimacing, laryngeal abnormalities, reduced intensity/loudness

◦ Speech productions that are deficient or lacking in nasal resonance.Etiology:◦ Organic origin: more typical- resulting from an obstruction in the nasopharyngeal area◦ Enlarged adenoids, nasal polyps, allergies resulting in edema of the nasal membranes, nasal papilloma, trauma in the nasal area, tumors, mucosal congestion, high palatal arch, overcorrection for hypernasality◦ Non organic origin: uncommon◦ May be residual after organic origin is resolved; desired resonance• Vocal parameters - Voice has a “muted” sound, sounds like patient has a “head cold”.

Evidence for both hypernasality due to velopharyngeal dysfunction and hyponasality• May be due to nasal obstruction• Often reduced nasal air emission from one naris on mirror exam

◦ a “muffled and hollow” vocal quality, lacking full resonance.Etiology: tongue deeply retracted and posteriorly placed in the pharynx◦ Usually a nonorganic basis◦ May occur due to organic origin such as deafness, flaccid and spastic dysarthria, athetoid cerebral palsy, and oral apraxia.

• Airway obstruction due to vocal fold closure• Occurs during speech and inhalation• Etiology: no definitive etiology, frequently mistaken for asthma◦ Possible causes:1. psychological causes2. airway hyperactivity3. potential neurogenic causes4. pharmacological5. unspecified

Excess or dysregulated/imbalanced activity of the intrinsicand extrinsic laryngeal muscles is the primary cause of thevoice disturbance.• A voice disorder in the absence of visible structural orneurological laryngeal pathology (or where the vocal foldpathology is insufficient to explain the degree of thedysphonia).

• Psychological &/or personality factors induce laryngeal tension. • Technical misuses of the vocal mechanism. • Learned adaptations following upper respiratory infection. • Extreme compensation for underlying vocal fold pathology. Increased laryngeal tone secondary to LPR.

• Key feature is laryngeal and paralaryngeal hypertonicity • No particular voice quality or glottic configuration is uniquely identified with MTD. • Extrinsic and intrinsic laryngeal muscle dysregulation contributes to the abnormal voice. • Muscle tension pulls larynx out of “natural” position. • Larynx is suspended high in the neck & the entire hyoid-laryngeal sling is stiff

• Laryngeal tenderness, soreness, pain, tightness which intensifies with extended voice use (especially with palpation) • Unilateral symptoms are more common• Pain radiates to one or both ears/fullness of the ears • Vocal fatigue, increased effort, “swellings” in the tongue base/neck regions • Dynamic range restricted (decreased loudness/pitch) • May be seen/witnessed in voice and or dysphagic patients

• Etiology: Aging of the vocal mechanism• Perceptual characteristics: ◦ Altered pitch (male –rising;female –lowering)◦ Hoarseness; roughness, breathiness, strain, slowed rate of speech• Visual characteristics: ◦ Bowing of the vocal fold edge, vocal fold atrophy, a spindle shaped gap during phonation.

◦ Increased F0 in males◦ Decreased F0 in females ◦ Decreased intensity ◦ Increased noise-to-harmonics ratioNOTE: ◦ Presbyphonic changes are not atypical in otherwise healthy elderly individuals.◦ Presbyphonia can significantly impact quality of life.