Lecture 2

Pregunta	Respuesta
vocal misuse	voice production behaviours that prevent the vocal mechanism form working smoothly and efficiently.
increased tension/strain	hard glottal attack (adduction of VF before phonation) high laryngeal position anterio-posterior laryngeal squeezing
inappropriate pitch level	puberphonia persistent glottal fry lack of pitch variability
excessive talking	vocal fatigue
Ventricular phonation	false VF move toward midline and cover true VF low pitch, hoarse, diplophonia
phonotrauma/vocal abuse	harsher than normal misuse behaviours
vocal nodules aetiology	tissue reaction to frictional trauma between VF - excessive laryngeal tension
vocal nodules pathophysiology	small, white, protuberance on free margin of VF. junction of anterior 1/3 and posterior 2/3 of VF usually bilateral and symmetrical
vocal nodules signs	hoarseness & breathiness habitual cough, throat clearing airflow may be increased increased subglottal pressure
vocal nodules management and therapy	immature & nonfibrous - voice therapy fibrous - surgical removal + therapy Therapy: decrease voice usage, vocal hygiene
vocal polyps aetiology	VF trauma due to vocal abuse secondary reaction to allergies, talking, smoking, URTI
vocal polyps pathophysiology	sessile/broad & pedunculated usually unilateral junction anterior 1/3 and posterior 2/3
vocal polyps signs	diplophonia, sudden voice breaks, hoarseness, breathiness, roughness increased airflow, increased subglottal pressure
vocal polyps management and therapy	pedunclulated & large sessile - surgical removal small sessile - therapy Therapy: similar to nodules, 2-6 months before quality improves
Reinke's oedema AKA polypoid degeneration	build up of fluid in superficial lamina propria
Reinke's oedema aetiology	effects women more than men VF trauma and misuse smoking gastroesophageal reflux hormonal changes
Reinke's oedema pathophysiology	VF full of fluid full length of VF bilaterally disturbs elasticity of VF
Reinke's oedema signs	low pitch, hoarseness, shortness of breath, increased airflow
Chronic laryngitis	long-standing inflammation of the laryngeal mucosa secondary to phonation
Chronic laryngitis aetiology	any long term irritation of the larynx (smoking, vocal abuse, reflux disease)
Chronic laryngitis pathophysiology	VF red, irregular, thick, rounded rather than sharp. small dilated blood vessels on surface oedema supraglottic area
Chronic laryngitis signs	hoarseness, high or low pitch, non-productive cough, sore throat. increased air flow and subglottal pressure
Chronic laryngitis management and therapy	surgical stripping - if therapy unsuccessful Therapy: program to reduce vocal abuse and misuse
Muscle tension dysphonia Aetiology	excessive muscularskeletal tension in head. and neck, intrinsic and extrinsic laryngeal muscles sensitive to emotional stress. hypercontraction of muscles
Muscle tension dysphonia symptoms	aphonia/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
Muscle tension dysphonia physiological bases	usually normal larynx may demonstrate abnormal function secondary mucoal changes may occur
Ventricular Dysphonia aetiology	excessive muscle tension may be substitute voice for severe deliberating disease
Ventricular Dysphonia pathophysiology	false VF approximate and begin to vibrate increase mass VF - unable to vibrate quickly -> low pitch.
Ventricular Dysphonia signs	low pitch, diplophonia, very hoarse. decreased range and airflow
Ventricular Dysphonia management and therapy	medical management not used unless primary VF defect. Therapy: retrain true VF if possible. if not, compensation - improve false VF
Psychogenic VD	Conversion VD: total or partial loss of phonation. physical symptoms not linked to anatomical or physiological disease. person convinced the problem is orgaic
Conversion muteness	most extreme and incapacitating cough present - normal VF function
Conversion Aphonia	involuntary 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
Conversion Dysphonia	varying degrees and types of hoarseness with or without strained-harsh quality falsetto breaks breathiness intermittent whispering moments of normal voice
Psychogenic VD therapy	goal: re-establish normal VF function by re-shaping vegetative vocal functions
Puberphonia	failure to eliminate high pitched voice structurally normal larynx mainly males
puberphonia aetiology	psychological factors strong feelings towards feminine attachment rejects responsibilities of adulthood. Organic: endocrine disorder, severe hearing loss, URTI
puberphonia pathophysiology	larynx 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)
puberphonia management and therapy	Therapy: goal - shape vegetative vocal production to normal voice. if therapy fails, VF augmentation is possible
Organic VD	due to trauma associated with organic mass lesions (cancer) disorders related to endocrine disorders/changes
Vocal process granuloma (contact ulcer)	small ulceration medial surface of vocal processes of arytenoid cartilages continued irritation in presence of bacteria
Granuloma aetiology	repeated, forceful hyperadduction hard glottal attack, low pitch, glottal fry intubation trauma stress-related gastro-intestinal difficulties
granuloma pathophysiology	"cup&saucer" appearance early stages - stand of mucus seen between processes
granuloma signs	constant throat clearing, vocal fatigue breathy, hoarse discomfort, unilateral in area of thyroid cartilage increased subglottal pressure, increased airflow, increased intensity
Granuloma management and therapy	Therapy: eliminate vocal abuse, alter voice production methods. if intensive VT fails, surgery
Neurological VD	- laryngeal nerve paralysis SLN or RLN - spasmodic dysphonia - hypokinetic dysphonia
SLN	innervates cricothyroid muscle tenses VF to increase pitch contributes to VF adduction vocal fatigue, hoarseness, loss of vocal range
RLN	left 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
RLN paralysis	unilateral 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)
RLN paralysis aetiology	u-RLN: intrathoracic neoplasms, aneurysms, mitral valve sternosis, neck trauma. b-RLN: thyroidectomy, neck trauma, tumours, infection
RLN paralysis signs	u-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
RLN 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.
RLN paralysis management (result) & therapy	voice excellent post op deteriorates as oedema resolves improvement in one week. Therapy: techniques to reduce glottal incompetence
Spasmodic dysphonia	strained, choked, effortful voice similar to stuttering relatively rare resistant to traditional VT
Spasmodic dysphonia aetiology	psychology based - conversion reaction, muscularskeletal tension. neurologically based - organic/essential tremor idiopathic - unknown origin often associated with URTI, emotional stress
Spasmodic dysphonia types	adductor abductor mixed
Spasmodic dysphonia (ad)	true and false VF hyperadduct in intermittent and irregular spasms abrupt, vocal explosions, strained-strangled, voice breaks, harsh larynx normal at rest
Spasmodic dysphonia (ab)	sever breathy aphonia - intermittent breaks VF episodically abduct not as common as (ad) difficult transition from voiceless consonant to vowels
Spasmodic dysphonia (mixed)	both ad and ab laryngospasms aphonic, breathy periods and voice arrests
Spasmodic dysphonia management	botox injections ad - thyroarytenoid/vocalis ab - psoterior cricoarytenoid causes muscle paralysis (botox is neurotoxin - blocks transmission of nerve impulse to muscle)
Spasmodic dysphonia mx results	significant improvement (ad - 90% & ab - 70%) airflow increased and normalised reduced hyperfunction require re-injection (3-5 months)
Spasmodic dysphonia therapy	breathy voicing elevation of pitch, easy voice onsets and artic contacts relaxation therapy co-ordination exhalation and voice onset
Hypokinetic dysphonia aetiology	parkinson's
Hypokinetic dysphonia pathophysiology	VF normal in structure phonation - closure incomplete unable to tense VF
Hypokinetic dysphonia signs	monopitch, monoloudness reduced loudness reduces stress harsh, breathy increase airflow, decreased subglottal pressure
Hypokinetic dysphonia management and therapy	drug therapy increase VF adduction increase loudness and intonation Lee Silverman Voice Treatment

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