DISORDERS OF VOICE UG CLASS

1. DISORDERS OF VOICE

2. • The intrinsic muscles of the larynx and their
actions. Heavy arrows indicate the direction of
muscle
• action; fine arrows indicate the motion of vocal
ligaments; and open arrows indicate the
motion of cricoid and thyroid cartilages.

4. DISORDERS OF VOICE
1.Dysphonia:
General change in voice quality.
 Dysphonia plica ventricularis.
2. Aphonia:
No sound is emanated from vocal folds when there is lack of vocal cord approximation or lack of
air passing through the glottis.
Functional (hysterical)
Organic
3. Diplophonia:
When vocal cords are affected differently they vibrate at two different frequencies.

5. DISORDERS OF VOICE
4.Puberphonia (mutational falsetto voice).
5.Phonasthenia
6.Disorders of resonance
7.Rhinolalia
Rhinolalia aperta (hypernasality)
Rhinolalia clausa (hyponasality).

6. HOARSENESS
• Hoarseness is defined as roughness of voice resulting
from variations of periodicity and/or intensity of
consecutive sound waves.
• For production of normal voice, vocal cords should:
1. Be able to approximate properly with each other.
2. Have a proper size and stiffness.
3. Have an ability to vibrate regularly in response to air
column.
• Any condition that interferes with the above functions
causes hoarseness.

7. • (a) Loss of approximation may be seen in vocal cord paralysis or fixation
or a tumour coming in between the vocal cords.
• (b) Size of the cord may increase in oedema of the cord or a tumour; there
is a decrease in partial surgical excision or fibrosis.
• (c) Stiffness may decrease in paralysis, increase in spastic dysphonia or
fibrosis.
• Cords may not be able to vibrate properly in the presence of congestion,
submucosal haemorrhages, nodule or a polyp.

8. AETIOLOGY
• Hoarseness is a symptom
and not a disease.

9. EVALUATION OF HOARSENESS
1. History. Mode of onset and duration of illness, patient’s occupation, habits and associated
complaints are important and would often help to elucidate the cause. Any hoarseness
persisting for more than 2 weeks deserves examination of larynx. Malignancy should be
excluded in patients above 40 years.
2. Indirect laryngoscopy. Many of the local laryngeal causes can be diagnosed.
3. Examination of neck, chest, cardiovascular and neurological system would help to find
cause for laryngeal paralysis.
4. Laboratory investigations and radiological examination should be done as per dictates of the
cause suspected on clinical examination.
5. Direct laryngoscopy and microlaryngoscopy help in detailed examination, biopsy of the
lesions and assessment of the mobility of cricoarytenoid joints.
6. Bronchoscopy and oesophagoscopy may be required in cases of paralytic lesions of the
cord to exclude malignancy.

10. DYSPHONIA PLICA VENTRICULARIS (VENTRICULAR DYSPHONIA)
DEFINITION:
Voice produced by apposition of false vocal cord
ETIOLOGY:
• Secondary
• Functional
SYMPTOMS:
• Voice-Harsh, low pitched with crackling rumbling sound.
• Disturbed phonation
• Good voice(ventricular band compensates)
• Diplophonia

11. SIGNS:
INVESTIGATIONS: Video-stroboscopy
TREATMENT:
• speech therapy
• Psychotherapy
• Laser excision

12. FUNCTIONAL APHONIA
(HYSTERICAL APHONIA)
DEFINITION:
Abrupt onset of loss of voice following emotional crisis giving rise to
functional paralysis of adductors during phonation.
ETIOLOGY:
• Psychological conditions-emotionally unstable individuals
SYMPTOMS:
• Aphonia
• Faint whisper
• Young female, psychological trauma.
• Laughing,crying,coughing-Normal

13. SIGNS:
Failure of vocal cords to oppose on phonation
VC oppose closely but without production of sound
Pharyngeal reflexes insensitive
Glottic closure-completely on attempted coughing
TREATMENT:
• Persuasion
Relapse common
• speech therapy
• Psychotherapy

14. PUBERPHONIA (MUTATIONAL FALSETTO VOICE)
Definition:
A functional voice disorder of pitch control where adolescent male
voice fails to descend to a normal pitch level at puberty.
Etiology:
Emotional stress
Personality disorder
Psychological changes during puberty
Pathology:
Hyperkinetic function and spasm of cricothyroid muscle.

15. Symptoms:
Adolescent male-High pitch voice
Vocal fatigue easily
Normal adult larynx
Signs:
Stretched vocal cords in falsetto phonation
Mutational Triangle
Omega shaped epiglottis
Nonspecific congestion of vocal cords
Gutzman’s pressure test-Positive

16. Investigations:
• Stroboscopy
• Radiology of neck-narrowing of cricothyroid space.
Treatment:
• Vocal Rehabilitation & re-education
• Botox Injection into Cricothyroid Muscle
• Isshiki Thyroplasty type 3

17. PHONASTHENIA
DEFINITION:
Characterized by functional weakness of voice-Thyroarytenoid and interarytenoids or
both may be affected.
ETIOLOGY:
Faulty use of voice
Following laryngitis.
Emotionally labile individuals
SYMPTOMS:
• Unpleasant sensation around neck,throat,larynx
• Doctors, teachers are more prone
• Voice weak

18. SIGNS:
IDL-
• Reddening of vocal cord margins
• Tenderness around strap muscles+

19. TREATMENT:
• Speech therapy
• Removal of causative factor
• Psychological counselling
• Voice rest & Vocal Hygiene

20. SPASMODIC DYSPHONIA
DEFINITION:
• SD is a voice disorder arising from a focal dystonia involving certain
laryngeal muscles but reflecting central motor processing
issues/abnormalities.
• Background of normal speech overlain by vocal spasms that are not
under voluntary control (strained & strangled speech pattern).
ETIOLOGY:
• Unknown /idiopathic
• patient may relate onset to a specific event (eg: flulike syndrome or an
emotionally traumatic event).
• combination of genetic predisposition interacting with acquired factors
later in life.

21. SYMPTOMS:
• SOCIAL IMPLICATONS-impacts on the patient’s quality of life.
• phonation breaks and strangled quality of the voice.
• task-specific dystonia
SIGNS:
ENDOSCOPIC EXAMINATION: At rest—normal
At attempted phonation-Spasm of laryngeal muscles seen & heard.
Worsened by anxiety, telephone conversation
Symptoms ameliorated by Alcohol.
AIRWAY NOT COMPROMISED

22. Types
Based on Symptoms
• Adductor
• Abductor
• Mixed

23. ADDUCTOR SD
• 90% of patients with SD
• The characteristic adductor spasm results in a strangled and
staccato voice.
• Mistaken for muscle tension dysphonia.
• characterized by phonation breaks associated with vowels, in
particular words ending with a vowel and being followed on by a
word starting with a vowel (we – eat’) and words with two vowels
in tandem (for example, eighty-year – eels). The vowels /i/ (‘ee’)
and /a/ (‘ah’) are particularly problematic.
• Relatively normal phonation on a continuous vowel sound.
• Hyper-functional voice and psychogenic voice disorder may be
confused with SD. Spastic UMN conditions may also be
misdiagnosed as SD.

24. Abductor SD
• 10% of individuals presenting with voice dystonias.
• SD have particular difficulty with voice onset after voiceless consonants at
the beginnings of words or phrases (words starting with /w/, /b/,/s/, /t/, /p/,
/f/, etc.), often leading to problems with vocal fold closure for the following
sound.
• examples -‘who has hidden Harry’s hat?’.
• Attempts to pronounce such sounds lead to voiceless voice breaks.
• Abductor SD should be differentiated from psychogenic voice disorders
such as whisper dysphonia and neurologic disorders.

25. DIAGNOSIS
• The diagnosis of SD is made on clinical grounds, and usually solely
by the listening skills of an experienced clinician.
• Electromyography (EMG) will demonstrate bursts of involuntary
spasms of electrical activity overlaid on normal interference pattern.
In adductor SD, increased thyroarytenoid activity is observed during
these bursts.
• Assessment of SD requires evaluation by a multidisciplinary team.
• Nasendoscopic inspection and recording with playback to the patient
is the gold standard.
• The voice assessment includes repetition of sentences loaded with
voiced segments and vowels, as this will provoke (worsen)
symptoms (i.e. more strain, voice breaks)

26. TREATMENT OF SPASMODIC
DYSPHONIA
• Speech therapy: little role
• Medical therapy:
Isolated SD, no role.
SD associated with other dystonias (facial dystonia, for
example), low-dose benzodiazepines useful.
• Botulinum toxin:
• The mainstay of treatment of SD is repeated botulinum toxin
injections.
• In clinical practice in the UK, most clinicians use botulinum
toxin type A.

28. ADDUCTOR SD – BOTULINUM TOXIN
INJECTIONS
• The injections of the thyroarytenoid muscle with botulinum toxin may be performed permucosally
(under local or general anaesthetic) or, more commonly, transcutaneously.
• The transcutaneous injection technique approaches the thyroarytenoid muscle through the
cricothyroid membrane.
• The needle is advanced in the midline through the cricothyroid membrane.
• Having entered the skin and passed through the cricothyroid membrane, the needle is angled 15
degrees cranially and 30 degrees laterally and then advanced into the body of the thyroarytenoid
muscle.
• electromyographic (EMG) monitoring to ensure that the tip of the injection needle is appropriately
placed in the thyroarytenoid muscle.
• When the needle tip is thought to be in the muscle, the patient is asked to phonate (/i/) – this causes
a characteristic burst of activity on the EMG monitor, and the botulinum toxin can be rapidly delivered
in to the muscle.
• In general, patients will receive a low dose of botulinum toxin (between 3 and 10 units of dysport
(equal approximately to between 1 and 3 units of botox)) into one or both thyroarytenoid muscles. In
practice, a newly diagnosed patient will usually receive a small dose of botulinum toxin into one or
other vocal fold.
• The frequency of dosing is variable.

29. ABDUCTOR SD – BOTULINUM TOXIN
INJECTIONS
• More technically challenging.
• It may be approached transcutaneously by manually rotating the larynx into a position
where the posterior cricoid ring can be accessed.
• If the PCA is injected transcutaneously, EMG guidance is essential; the muscle can be
difficult to locate, and EMG confirmation (by asking the patient to abduct the vocal folds with
a forced sniff) is required to confirm needle placement.
• prefer to perform PCA injections under general anesthetic.
• Care must be taken to direct the injection laterally; erroneous injection of both PCA muscles
might result in complete failure of the patient to be able to abduct both vocal folds.
• Less effective than for adductor SD. A larger dose is usually required to achieve adequate
results.

30. SURGERY
Recurrent laryngeal nerve section/crush:
• Unilateral RLN section for Adductor SD Long term results not maintained.
Recurrent laryngeal nerve selective denervation and reinnervation:
• first, the muscle may be prone to atrophy; and second, there is a likelihood of
reinnervation by the cut end of the RLN.
• Selectively denervating the thyroarytenoid and lateral cricoarytenoid muscles,
followed by providing tone to the muscles with an ansa cervicalis anastomosis,
might preserve muscle tone
Thyroarytenoid myotomy:
• Thyroarytenoid inactivity has been proposed by coagulating the muscle with a
laser.
Type 2 thyroplasty:
• Isshiki has proposed a type 2 thyroplasty as treatment for adductor SD

31. HYPONASALITY (RHINOLALIA
CLAUSA)
• Blockage of the nose or nasopharynx results in lack of nasal resonance for “m”,
“n” and “ing” sounds.
• Articulation substitutions of “b”, “d” and “g” are common
Etiology
• Rhinosinusitis
• Allergic and nonallergic rhinitis
• Nasal masses such as polyps and tumors
• Nasopharyngeal mass and adenoids
• Familial or habitual speech pattern
• Other causes: Deviated nasal septum (DNS), choanal atresia and turbinate
hypertrophy.
Treatment
• After treating the cause, the patient is sent for voice therapy.

32. HYPERNASALITY (RHINOLALIA
APERTA)
• The failure of the nasopharynx to cut off from oropharynx or undue
passage between the oral and nasal cavities results in nasal
resonance of all the words.
Etiology:
• Velopharyngeal insufficiency)/velopharyngeal dysfunction
• Oronasal fistula
• Familial or habitual speech pattern.
Treatment:
• Treatment of the cause is important. Voice therapy helps in
functional causes.

33. STUTTERING
• Stuttering is a neurologic, movement disorder in which abnormal,
involuntary and inappropriate use of the speech muscles results in
dysfluency.
• Result of increased muscle tension in the three subsystems of
speech.
Risk Factors
• Too much attention or reprimands to childhood dysfluency between 2
years and 4 years.
Clinical Features
• characterized by hesitation to initiate, repetitions, prolongations or
blocks in speech flow.
• The patient later on may develop secondary mannerisms.

34. Factors Relieving Stuttering
• Factors, which may increase fluency for a period of time, are:
 Emotional arousal or sensory stimuli
 Motor actions such as walking
 Use of rhythmic patterns such as a metronome or monotone.
 Singing or speaking in a sing-song voice
 Shouting
 Foreign accent or slurred articulation.
Factors Aggravating Stuttering
• The factors, which may increase stuttering include communicative
pressures.

35. Treatment
• Speech therapy and training.
• Antidepressants
• injection botulinum toxin (1 unit or less, bilaterally) produce
improvement in 50% cases.
• “SpeechEasy”:Using both delayed and frequency-altered
auditory feedback in the ear devices (a frequency shift of +500
Hz with delayed auditory feedback of 60 m/sec) has shown
significant improvement in fluency and normalcy of speech in
both youth and adult subjects. It is marketed under the
trademark “SpeechEasy”.

36. MUSCLE TENSION DYSPHONIA
• Functional voice disorder.
• Excessive tension in the extrinsic laryngeal muscles affects intrinsic
laryngeal muscles and vocal cord mucosa and leads to abnormality
in phonatory process.
• The supraglottic larynx becomes hyperfunctional for attempting to
compensate for the GI. MTD has two types: primary and secondary.
• Primary MTD: It is common in females. Vocal cords show atypical or
abnormal movement during phonation but there is no organic vocal
cord pathology. It is associated with excessive supraglottic
hyperfunction.
• Secondary MTD: It is the result of compensation for underlying GI.

37. Endoscopic supraglottic findings
classification:
• MTD type 1: Posterior open chink due to hypertonic state of
posterior cricoarytenoid muscle; laryngeal isometric
contractions.
• MTD type 2: Adducted vestibular folds.
• MTD type 3: Anteroposterior contractions bringing epiglottis
closer to arytenoids; posterior shift of base of tongue.
• MTD type 4: Extreme anteroposterior contractions squeeze the
supraglottis and larynx cannot be viewed.
• Differential diagnosis: For spasmodic dysphonia

38. SULCUS VOCALIS
• common in Indian subcontinent.
• Irreversible loss of viscoelasticity of SLP (Reinke’s space).
• Etiology: Not certain
• Clinical features:
• Patient has breathy voice. The characteristic finding is a furrow
or sulcus at the free edge of vocal cord leading to abnormal
vocal cord vibrations and GI.
• History of voice abuse is common. Significant loss of tissue can
cause GI.

39. • Types: On the basis of depth and shape of the sulcus, it is
grouped into three types:
• Type I: Superficial sulcus with no symptoms
• Type IIa: With moderate dysphonia
• Type IIb: With severe dysphonia.
• Treatment: Injection augmentation or permanent implant
provides vocal projection and volume and may correct GI.

40. MYOCLONUS
• Myoclonus is a disease of central nervous system. It consists of sudden,
brief, shock-like involuntary movements, which are caused by either
muscular contractions (positive myoclonus) or inhibitions (negative
myoclonus, asterixis).
• Laryngeal Features
• Broken speech pattern and respiratory dysrhythmia (ventilatory
dysfunction).
• Vocal cords often show slow rhythmic adduction and abduction at the
same timing and frequency as the palatal, pharyngeal and occasionally
diaphragmatic contractions.
• Treatment
• Pharmacotherapy: Though given serotonin, carbamazepine, clonazepam,
tetrabenazine and trihexyphenidyl are generally unresponsive.
• Local injection of botulinum toxin into the thyroarytenoid muscles has been
tried successfully.

41. TOURETTE’S SYNDROME
• This tic disorder is characterized by involuntary vocalizations of
articulate words or inarticulate sounds. It may be associated with
multiple tics of several body parts. Lingual tics present as hisses and
nasal tics as sniffs and snorts.
• Clinical Features
• Onset may be in childhood or adolescence.
• Obsessive-compulsive behavior.
• Laryngeal tics: Inappropriate coughing, barking, throat clearing,
hooting and grunting.
• The chronic voice abuse may make the voice harsh and results in
polypoid changes of the vocal mucosa.

42. • Treatment
• Phenothiazines such as haloperidol.
• Alpha-2-adrenergic agonist such as clonidine.
• Benzodiazepine such as clonazepam.
• Local injections of botulinum toxin to manage rapid facial tics
and dystonic tics such as refractory loud barking sounds.

43. PARKINSON’S DISEASE
• Clinical features: Voice becomes monopitch, weak or breathy.
Speech intelligibility decreases.
Treatment:
• Lee Silverman Voice Therapy improves vocal quality, intensity and
speech intelligibility. Therapy focuses
• on following five concepts:
1. Think loud
2. High effort across the speech system
3. Intensive therapy
4. Recalibrate sensory deficits
5. Quantify improvement.