2. 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.
3. – (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.
HOARSENESS
4. – AETIOLOGY
– Hoarseness is a symptom and not a disease .
– 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.
– 3. Examination of neck, chest, cardiovascular and neurological system
– 4. Laboratory investigations and radiological 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.
5. DYSPHONIA PLICA VENTRICULARIS
(VENTRICULAR DYSPHONIA)
– Here voice is produced by ventricular folds (false cords) which have
taken over the function of true cords.
– Voice is rough, low-pitched and unpleasant.
– Ventricular voice may be secondary to impaired function of the true cord
such as paralysis, fixation, surgical excision or tumours.
– Functional type of ventricular dysphonia occurs in normal larynx. Here
cause is psychogenic. In this type, voice begins normally but soon
becomes rough when false cords usurp the function of true cords.
6. DYSPHONIA PLICA VENTRICULARIS
(VENTRICULAR DYSPHONIA)
– Diagnosis is made on indirect laryngoscopy; the false cords are
seen to approximate partially or completely and obscure the view
of true cords on phonation.
– Ventricular dysphonia secondary to laryngeal disorders is difficult
to treat but the functional type can be helped through voice
therapy and psychological counselling.
7. FUNCTIONAL APHONIA
(HYSTERICAL APHONIA)
– It is a functional disorder mostly seen in emotionally labile females in the age
group of 15–30 years. Aphonia is usually sudden and unaccompanied by other
laryngeal symptoms. Patient communicates with whisper.
– On examination, vocal cords are seen in abducted position and fail to adduct on
phonation; however, adduction of vocal cords can be seen on coughing,
indicating normal adductor function.
– Even though patient is aphonic, sound of cough is good.
– Treatment given is to reassure the patient of normal laryngeal function and
psychotherapy.
8. PUBERPHONIA (MUTATIONAL
FALSETTO VOICE)
– Normally, childhood voice has a higher pitch.
– When the larynx matures at puberty, vocal cords lengthen and the
voice changes to one of lower pitch. This is a feature exclusive to
males.
– Failure of this change leads to persistence of childhood high-
pitched voice and is called puberphonia.
– It is seen in boys who are emotionally immature, feel insecure and
show excessive fixation to their mother.
9. PUBERPHONIA (MUTATIONAL
FALSETTO VOICE)
– Psychologically, they shun to assume male responsibilities though
their physical and sexual development is normal.
– Treatment is training the body to produce low pitched voice.
– Pressing the thyroid prominence in a backward and downward
direction relaxes the overstretched cords and low tone voice can
be produced (Gutzmann’s pressure test).
– The patient pressing on his larynx learns to produce low tone voice
and then trains himself to produce syllables, words and numbers.
Prognosis is good.
11. ADDUCTOR DYSPHONIA
– The adductor muscles of larynx go into spasm causing vocal cords
to go into adduction.
– Voice becomes strained or strangled, and phonation is
interrupted in between leading to voice breaks. Larynx is however
morphologically normal.
– Severity of the condition differs from mild and intermittent
symptoms to those with moderate or severe dysphonia.
– Flexible fibreoptic laryngoscopy is useful during which patient’s
speech, sustained phonation and respiratory activities are studied.
Patient may have tremors of larynx, palate and pharynx.
12. – Aetiology of the condition is uncertain but one should exclude neurological
conditions such as Parkinsonism, myoclonus, pseudobulbar palsy, multiple
sclerosis, cerebellar disorders, tardive dyskinesia and amyotrophic lateral
sclerosis. CT scan and MRI are not useful but help to rule out neurological
conditions.
– Treatment consists of botulinum toxin injections in the thyroarytenoid muscle
on one or both sides to relieve spasm.
– Percutaneous electromyography (EMG) guided route through cricothyroid space
is preferred. Dose of botulinum toxin depends on severity of the condition.
ADDUCTOR DYSPHONIA
13. – Toxin injections relieve voice breaks due to spasms and improve airflow but the
benefit lasts only up to 16 weeks or so when repeat injection may be needed.
– Sometimes, if dose of toxin is not regulated it may cause breathiness of voice
and discomfort to swallow.
– Voice therapy is useful to improve voice and the duration of benefit.
– Voice therapy alone without injection does not help much.
– Section of recurrent laryngeal to paralyze the cord/cords has been used in the
past but it interferes with glottic closure leading to breathy and weak voice and
swallowing discomfort.
– This treatment is still used when injection treatment fails and the spasms are
severe.
ADDUCTOR DYSPHONIA
14. ABDUCTOR DYSPHONIA
– It is due to spasms of posterior cricoarytenoid muscle (the only
abductor) and thus keeping the glottis open. Patient gets a breathy
voice or breathy breaks in voice.
– The condition is gradually progressive and the symptoms get
aggravated during periods of stress or when patient uses
telephone.
– Like adductor spasm dysphonia, cause of abductor spasmodic
dysphonia is not known.
15. ABDUCTOR DYSPHONIA
– Treatment is injection of botulinum toxin in posterior
cricoarytenoid muscles. It can be done by percutaneous or
endoscopic route. Results of injection are not as good as in
adductor spasmodic dysphonia. Only about 50% of patients
improve and the duration of improvement is also less.
– Disadvantages of injection treatment are that it may compromise
vocal cord movements with respiration leading to airway
obstruction.
16. – Patients who do not respond to toxin injection can be treated by thyroplasty
type I or fat injection. A prior gelfoam injection can be used to judge the
effectiveness of the above procedure.
– Speech therapy should be combined with injection treatment as speech therapy
alone may not be effective.
– MIXED DYSPHONIA
– It is more complex, both the adductor and abductor function may be affected.
18. HYPONASALITY (RHINOLALIA
CLAUSA)
– It is lack of nasal resonance for
words which are resonated in the
nasal cavity, e.g. m, n, ng. It is due
to blockage of the nose or
nasopharynx.
HYPERNASALITY (RHINOLALIA
APERTA)
– It is seen when certain words
which have little nasal resonance
are resonated through nose. The
defect is in failure of the
nasopharynx to cut off from
oropharynx or abnormal
communication between the oral
and nasal cavities.
19. STUTTERING
– It is a disorder of fluency of speech and consists of hesitation to start, repetitions,
prolongations or blocks in the flow of speech.
– When well-established, a stutterer may develop secondary mannerisms such as
facial grimacing, eye blink and abnormal head movements.
– Normally, most of the children have dysfluency of speech between 2 and 4 years.
– If too much attention is given or child eprimanded by parents and peers, this
behaviour pattern may become fixed and child may develop into an adult stutterer.
– Stuttering can be prevented by proper education of the parents, not to overreact to
child’s dysfluency in early stages of speech development.
– Treatment of an established stutterer is speech therapy and psychotherapy to
improve his image as a speaker and reduce his fear of dysfluency.
