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Lecture 2
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- 1vocal misusevoice production behaviours that prevent the vocal mechanism form working smoothly and efficiently.
- 2increased tension/strainhard glottal attack (adduction of VF before phonation)
high laryngeal position
anterio-posterior laryngeal squeezing - 3inappropriate pitch levelpuberphonia
persistent glottal fry
lack of pitch variability - 4excessive talkingvocal fatigue
- 5Ventricular phonationfalse VF move toward midline and cover true VF
low pitch, hoarse, diplophonia - 6phonotrauma/vocal abuseharsher than normal misuse behaviours
- 7vocal nodules aetiologytissue reaction to frictional trauma between VF
- excessive laryngeal tension - 8vocal nodules pathophysiologysmall, white, protuberance on free margin of VF.
junction of anterior 1/3 and posterior 2/3 of VF
usually bilateral and symmetrical - 9vocal nodules signshoarseness & breathiness
habitual cough, throat clearing
airflow may be increased
increased subglottal pressure - 10vocal nodules management and therapyimmature & nonfibrous - voice therapy
fibrous - surgical removal + therapy
Therapy: decrease voice usage, vocal hygiene - 11vocal polyps aetiologyVF trauma due to vocal abuse
secondary reaction to allergies, talking, smoking, URTI - 12vocal polyps pathophysiologysessile/broad & pedunculated
usually unilateral
junction anterior 1/3 and posterior 2/3 - 13vocal polyps signsdiplophonia, sudden voice breaks, hoarseness, breathiness, roughness
increased airflow, increased subglottal pressure - 14vocal polyps management and therapypedunclulated & large sessile - surgical removal
small sessile - therapy
Therapy: similar to nodules, 2-6 months before quality improves - 15Reinke's oedema AKA polypoid degenerationbuild up of fluid in superficial lamina propria
- 16Reinke's oedema aetiologyeffects women more than men
VF trauma and misuse
smoking
gastroesophageal reflux
hormonal changes - 17Reinke's oedema pathophysiologyVF full of fluid
full length of VF bilaterally
disturbs elasticity of VF - 18Reinke's oedema signslow pitch, hoarseness, shortness of breath,
increased airflow - 19Chronic laryngitislong-standing inflammation of the laryngeal mucosa secondary to phonation
- 20Chronic laryngitis aetiologyany long term irritation of the larynx (smoking, vocal abuse, reflux disease)
- 21Chronic laryngitis pathophysiologyVF red, irregular, thick, rounded rather than sharp.
small dilated blood vessels on surface
oedema supraglottic area - 22Chronic laryngitis signshoarseness, high or low pitch, non-productive cough, sore throat.
increased air flow and subglottal pressure - 23Chronic laryngitis management and therapysurgical stripping - if therapy unsuccessful
Therapy: program to reduce vocal abuse and misuse - 24Muscle tension dysphonia Aetiologyexcessive muscularskeletal tension in head. and neck, intrinsic and extrinsic laryngeal muscles sensitive to emotional stress.
hypercontraction of muscles - 25Muscle tension dysphonia symptomsaphonia/dysphonia
breathiness, hoarseness, excessive high pitch, pain in larynx, pain in ears and chest, sensation of lump and tightness in throat, pain when pressure on larynx - 26Muscle tension dysphonia physiological basesusually normal larynx
may demonstrate abnormal function
secondary mucoal changes may occur - 27Ventricular Dysphonia aetiologyexcessive muscle tension
may be substitute voice for severe deliberating disease - 28Ventricular Dysphonia pathophysiologyfalse VF approximate and begin to vibrate
increase mass VF - unable to vibrate quickly -> low pitch. - 29Ventricular Dysphonia signslow pitch, diplophonia, very hoarse.
decreased range and airflow - 30Ventricular Dysphonia management and therapymedical management not used unless primary VF defect.
Therapy: retrain true VF if possible.
if not, compensation - improve false VF - 31Psychogenic VDConversion VD:
total or partial loss of phonation.
physical symptoms not linked to anatomical or physiological disease.
person convinced the problem is orgaic - 32Conversion mutenessmost extreme and incapacitating
cough present - normal VF function - 33Conversion Aphoniainvoluntary whispering
able to cough, laugh, cry - normal VF
larynx high in neck
80% female
onset sudden
hoarseness -> whisper
often triggered by colds
acute/chronic emotional stress - 34Conversion Dysphoniavarying degrees and types of hoarseness
with or without strained-harsh quality
falsetto breaks
breathiness
intermittent whispering
moments of normal voice - 35Psychogenic VD therapygoal: re-establish normal VF function by re-shaping vegetative vocal functions
- 36Puberphoniafailure to eliminate high pitched voice
structurally normal larynx
mainly males - 37puberphonia aetiologypsychological factors
strong feelings towards feminine attachment
rejects responsibilities of adulthood.
Organic: endocrine disorder, severe hearing loss, URTI - 38puberphonia pathophysiologylarynx high in neck and tilted down
VF lax
VF prevented from vibrating (arytenoids adduct tightly)
thryroarytenoid muscle fails to contract (decrease VF mass, only thin edge of VF vibrate) - 39puberphonia management and therapyTherapy: goal - shape vegetative vocal production to normal voice.
if therapy fails, VF augmentation is possible - 40Organic VDdue to trauma
associated with organic mass lesions (cancer)
disorders related to endocrine disorders/changes - 41Vocal process granuloma (contact ulcer)small ulceration medial surface of vocal processes of arytenoid cartilages
continued irritation in presence of bacteria - 42Granuloma aetiologyrepeated, forceful hyperadduction
hard glottal attack, low pitch, glottal fry
intubation trauma
stress-related gastro-intestinal difficulties - 43granuloma pathophysiology"cup&saucer" appearance
early stages - stand of mucus seen between processes - 44granuloma signsconstant throat clearing, vocal fatigue
breathy, hoarse
discomfort, unilateral in area of thyroid cartilage
increased subglottal pressure, increased airflow, increased intensity - 45Granuloma management and therapyTherapy: eliminate vocal abuse, alter voice production methods.
if intensive VT fails, surgery - 46Neurological VD- laryngeal nerve paralysis
SLN or RLN
- spasmodic dysphonia
- hypokinetic dysphonia - 47SLNinnervates cricothyroid muscle
tenses VF to increase pitch
contributes to VF adduction
vocal fatigue, hoarseness, loss of vocal range - 48RLNleft lesions more common than right
innervates all intrinsic muscles of larynx (not cricothyroid)
lesion may be uni or bi lateral
2 types:
Adductor or Abductor - 49RLN paralysisunilateral ad - VF not move to midline
unilateral ab - VF remain fixed adducted
bilateral ad - neither VF move to midline (phonation impossible)
bilateral ab - both VF remain adducted (respiratory difficulty) - 50RLN paralysis aetiologyu-RLN: intrathoracic neoplasms, aneurysms, mitral valve sternosis, neck trauma.
b-RLN: thyroidectomy, neck trauma, tumours, infection - 51RLN paralysis signsu-RLN: mild breathiness, hoarseness, reduced loudness, shortness of breath.
b-RLN: inhalatory stridor, voice good but both VF weakly adducted.
- increased airflow, decreased subglottal pressure - 52RLN paralysis management VF Medialisation (types)injection - into/lateral to thyroarytenoid muscle, lamina propria.
implantation - medial to thyroid cartilage at level of VF.
arytenoid adduction - rotation of arytenoid cartilage so that tip of VP moves to midline. - 53RLN paralysis management (result) & therapyvoice excellent post op
deteriorates as oedema resolves
improvement in one week.
Therapy: techniques to reduce glottal incompetence - 54Spasmodic dysphoniastrained, choked, effortful voice
similar to stuttering
relatively rare
resistant to traditional VT - 55Spasmodic dysphonia aetiologypsychology based - conversion reaction, muscularskeletal tension.
neurologically based - organic/essential tremor
idiopathic - unknown origin
often associated with URTI, emotional stress - 56Spasmodic dysphonia typesadductor
abductor
mixed - 57Spasmodic dysphonia (ad)true and false VF hyperadduct in intermittent and irregular spasms
abrupt, vocal explosions, strained-strangled, voice breaks, harsh
larynx normal at rest - 58Spasmodic dysphonia (ab)sever breathy aphonia - intermittent breaks
VF episodically abduct
not as common as (ad)
difficult transition from voiceless consonant to vowels - 59Spasmodic dysphonia (mixed)both ad and ab laryngospasms
aphonic, breathy periods and voice arrests - 60Spasmodic dysphonia managementbotox injections
ad - thyroarytenoid/vocalis
ab - psoterior cricoarytenoid
causes muscle paralysis (botox is neurotoxin - blocks transmission of nerve impulse to muscle) - 61Spasmodic dysphonia mx resultssignificant improvement (ad - 90% & ab - 70%)
airflow increased and normalised
reduced hyperfunction
require re-injection (3-5 months) - 62Spasmodic dysphonia therapybreathy voicing
elevation of pitch, easy voice onsets and artic contacts
relaxation therapy
co-ordination exhalation and voice onset - 63Hypokinetic dysphonia aetiologyparkinson's
- 64Hypokinetic dysphonia pathophysiologyVF normal in structure
phonation - closure incomplete
unable to tense VF - 65Hypokinetic dysphonia signsmonopitch, monoloudness
reduced loudness
reduces stress
harsh, breathy
increase airflow, decreased subglottal pressure - 66Hypokinetic dysphonia management and therapydrug therapy
increase VF adduction
increase loudness and intonation
Lee Silverman Voice Treatment
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