otolaryngology & ENT topic. etiology , anatomy and nerve supply of larynx. reccurent laryngeal nerve, superior laryngeal nerve .

1. Nerve Supply of Larynx & RLN
Paralysis
Dr Himanshu Mishra
1st yr PG

2. Introduction
• Vocal cord paralysis is a common problem found
in the practice of Otolaryngology. It is a sign of
disease and not a diagnosis.

3. Nerve supply
Vagus nerve
• The vagus nerve has three nuclei located within
the medulla:
1. The nucleus ambiguus
2. The dorsal nucleus
3. The nucleus of the tract of solitarius
4. Nucleus of spinal tract of trigeminal

4. • The nucleus ambiguus is the motor nucleus of the
vagus nerve.
• The efferent fibers of the dorsal (parasympathetic)
nucleus innervate the involuntary muscles of the
bronchi, esophagus, heart, stomach, small intestine,
and part of the large intestine.
• The afferent fibers of the nucleus of the tract of
solitarius carry sensory fibers from the pharynx,
larynx, and esophagus
• The spinal trigeminal nucleus receives sensory fibers
frpm outer ear ,dura & posterior cranial fossa.

5. The vagus nerve [X] carries GSA, GVA, SVA,
GVE,SVE fibers:
• The GSA fibers provide sensory input from the
larynx, laryngopharynx, deeper parts of the
auricle, part of the external acoustic meatus,
and the dura mater in the posterior cranial
fossa
• The GVA fibers provide sensory input from the
aortic body chemoreceptors and aortic arch
baroreceptors, and the esophagus, bronchi,
lungs, heart, and abdominal viscera in the
foregut and midgut;

6. • The GVE fibers are part of the parasympathetic
part of the autonomic division of the PNS and
stimulate smooth muscle and glands in the
pharynx, larynx, thoracic viscera, and abdominal
viscera of the foregut and midgut
• The SVA fibers are for taste from posterio most
part of tongue ,around the epiglottis and
pharynx;
• The SVE fibers aries from NA and supply
muscle of palate,pharynx and laryns.

7. Vagus nerve
Cranial part ;
vagus descends down
exits skull via jugular.f
sup. ganglion
inf.ganglion
descends down and enters carotid sheath
below inf.gang
gives SLN
At level of hyoid bone it divides into
external internal

8. Sensory and motor innervation of the larynx is by
two branches of the vagus nerves [X]-the
Superior laryngeal nerves and
Recurrent laryngeal nerves .

9. Superior laryngeal nerves
• The superior laryngeal nerves originate
from the inferior vagal ganglia .
• On each side, they descend medial to the
internal carotid artery and at the level of middle
constrictor it divide into internal and external
branches which is above the level of the
superior horn of the hyoid bone

10. • The internal branch
(internal laryngeal
nerve) passes
anteroinferiorly to
penetrate the
thyrohyoid
membrane-it is
mainly sensory and
supplies the laryngeal
cavity down to the
level of the vocal

11. • The external branch (external laryngeal nerve)
is thiner and it accompanies superior thyroid
artery .
• Descends along the lateral wall of the pharynx to
supply and penetrate the inferior constrictor of
the pharynx and ends by supplying the
cricothyroid muscle;
• It forms the pharyngeal plexus .

13. Recurrent laryngeal nerves
The recurrent laryngeal nerves are
• sensory to the laryngeal cavity below the level of
the vocal folds; and
• motor to all intrinsic muscles of the larynx
except for the cricothyroid.

14. • The left recurrent laryngeal
nerve originates in the
mediastinum at the level of
arch of aorta, whereas the
right recurrent laryngeal
nerve originates in the root
of the neck at the level of
subclavian artery.

15. • Both nerves generally ascend in the neck in the
groove between the esophagus and trachea and
enter the larynx deep to the margin of the
inferior constrictor. They may pass medial,
lateral, or through the lateral ligament of the
thyroid gland, which attaches the thyroid gland
to the trachea and lower part of the cricoid
cartilage on each side.

18. • The left RLN arises from inferior ganglia of
vagus . At the level of arch of aorta, loops around
it, ascends in tracheo-esophageal groove to
supply larynx.
• Due to longer course it is more prone to
paralysis.

20. Laryngeal paralysis
• Laryngeal paralysis may be unilateral or
bilateral, and may involve
1. Recurrent laryngeal nerve.
2. Superior laryngeal nerve.
3. Both recurrent and superior laryngeal nerves
(combined or complete paralysis).

21. Classification of laryngeal paralysis
Topographical manner :
• Supra nuclear.
• Nuclear. There is involvement of nucleus ambigus
in the medulla. The causes are vascular, neoplastic,
motorneurone disease, polio and syringobulbia. In
nuclear lesions, there would be associated paralysis
of other cranial nerves and neural pathways.

22. • High vagal lesions. Vagus nerve may be
involved in the skull, at the exit from jugular
foramen or in parapharyngeal space .
• Low vagal or recurrent laryngeal nerve
• Systemic causes. Diabetes, syphilis,
diphtheria, typhoid, streptococcal or viral
infections, lead poisoning.
• Idiopathic. In about 30% of cases, cause
remains obscure.

23. Recurrent laryngeal nerve
paralysis
Unilateral
• Unilateral injury to recurrent laryngeal nerve
results in ipsilateral paralysis of all the intrinsic
muscles except the cricothyroid. The vocal cord
thus assumes a median or paramedian position.
• This position of vc is explained by Semon’s law
and Wagner and Grossman hypothesis

24. • Semon’s law which states that, in all
progressive organic lesions, abductor fibres of
the nerve, which are phylogenetically newer, are
more susceptible and thus the first to be
paralyzed compared to adductor fibres.
• Wagner and Grossman hypothesis which
states that cricothyroid muscle which receives
innervation from superior laryngeal nerve keeps
the cord in paramedian position due to its
adductor function.

25. Position of the vocal cord
Position of the
cord
Location of
the cord from
midline
Health Disease
Median Midline Phonation RLN paralysis
Paramedian 1.5 mm Strong whisper RLN paralysis
Intermediate 3.5 mm --- Combined
paralysis
Gentle abduction 7.0 mm Quiet respiration Paralysis of
adducters
Full abduction 9.5 mm Deep inspiration Paralysis of
adducters

27. Causes of recurrent laryngeal nerve
paralysis.
• RIGHT :
- neck trauma
- thyroid disease
- malignancy
- iatrogenic
- cervical
lymphadenopathy
- aneurysm of SCA
- CA.apex rt.lung
- TB of cer.pleura
- idiopathic

28. Left
1. In the NECK
-accidental trauma
- thy. disease
- iatrogenic
- malignancy
- cervical lymphadenopathy
2.In the mediastinum
-Bronchogenic.CA
- CA.esophagus
- aortic aneurysm
- Mediastinal. lymphadenopathy
- ortner syn.
- intrathoracic surgry

29. • Both side
-thy.surgry
-CA.thyroid
-CAcer. oeso
-cer. lymphadenopathy

30. CLINICAL FEATURES
• Unilateral recurrent laryngeal paralysis may
pass undetected
• Some patients have change in voice but no
problems of aspiration or airways obstruction.
• The voice in unilateral paralysis gradually
improves due to compensation by the healthy
cord which crosses the midline to meet the
paralyzed one.

31. Clinical examination (vocal)
 Glottic fry
 Hard glottal attacks
 Breathy voice
 Diplophonia
 Pitch breaks
 Phonation breaks
 Tense phonation

32. Glottic fry
 Creaky voice
 Cords vibrate slowly
 Pt feels as if breath has run out while speaking

33. Hard glottal attack
 Excessive air pressure is built up under the
closed vocal cords
 Sudden release of this causes the speaker to
speak in explosive voice
 Voice tires easily

34. Breathy voice
 Murmered voice
 Vocal cord vibrates normally but are held
further apart then normal
 Excessive air escape occurs between the cords

35. Diplophonia
 Simultaneous production of sound of different
pitches
 Common in UVCP
 Common in mass lesions of vocal folds

36. Pitch breaks
 Speaking in inappropriately high pitch
 Voice seems to be out of control
 Pt does not know what sound will come out next

37. Phonation break
 Complete cessation of phonation
 Temporary
 Commonly follows excessive use of voice

38. Tense phonation
 Appears like speech while lifing something
heavy
 Laryngeal muscle tensed
 Supralaryngeal muscle tensed
 Loud, high pitched and harsh voice

39. Evaluation – Physical Examination
• Complete Head and Neck Examination,IDL
• Flexible Fiberoptic Laryngoscopy
• Rigid laryngeal endoscopy
• 90 degree Hopkins Rod-lens Telescope
• Adequacy of Airway, Gross Aspiration
• Assess Position of Cords
▫ Median, Paramedian, Lateral
▫ Posterior Glottic Gap on Phonation

40. Manual Compression Test

41. Quantitative evaluation
 Sustaining a single tone at the fundamental
frequency F0 (reduced in patients with vocal
abuse, cord paralysis)
 Variations in amplitude (Shimmer) – variations
due to decreased stability of vocal folds
 Variations in pitch (jitter) – correlates with
degree of hoarseness

42. Stroboscopy
 Helps in dynamic assessment of vocal folds
 If frequency of strobe light is the same as
fundamental voice frequency then vocal folds
will not be seen in movement at all
Here we look for:
 Symmetry of movement
 Aperiodicity
 Glottic closure configuration
 Horizontal excursion

43. TREATMENT
• Generally no treatment is required as
compensation occurs due to opposite healthy
cord.
• Temporary paralysis recovers in 6–12 months
and it is advisable to wait.
• Injection of gelfoam or fat can be used to
improve the voice in the waiting period.

44. • Laryngoplasty type I can be used if
compensation does not take place.
• Laryngoplasty type I with arytenoid adduction is
done if posterior glottis is also incompetent.
• Teflon injection has been used in the past to
medialize the cord permanently but is not
favoured these days.

45. Treatment algorithm

48. Vocal Cord Injection - Materials
Teflon
Fat
Collagen
Autologous Collagen
Homologous Micronized
Alloderm (Cymetra)
Heterologous Bovine Collagen
(Zyderm
Hyaluronic Acid
Calcium Hydroxyapatite gel
(Radiance FN)
Polydimethylsiloxane gel
(Bioplastique )

49.  Under LA
 Horizontal incision over midportion of thyroid
cartilage
 Window in thyroid ala created 8 mm posterior to
ant. Commissure and 3 mm superior to its inferior
border
 Inner perichondrial flaps created by inferior and
posterior incisions
 Under laryngoscopic guidance measurement for
medialization is taken
 Silastic block of appropriate size fashioned and
inserted
 Voice checked on the table
 Cartilage from the window is ideally removed
 Inner perichondrium if preserved it is better

50. Type 1 Thyroplasty

51. Bilateral RLN palsy
• As all the intrinsic muscles of larynx are
paralyzed, the vocal cords lie in median or
paramedian position due to unopposed action of
cricothyroid muscles
ETIOLOGY :
neuritis
thyroid surgery

52. CLINICAL FEATURES
• As both the cords lie in median or paramedian
position, the airway is inadequate causing
dyspnoea and stridor but the voice is good.
Dyspnoea and stridor become worse on exertion
or during an attack of acute laryngitis.

53. MANAGEMENT :
• Tracheostomy
• Widening the respiratory airway without a
permanent tracheostomy (endoscopic or
through external cervical approach).
• This can be achieved by
• (i) arytenoidectomy with suture,
• (ii) arytenoidopexy (fixing the arytenoid in
lateral position),
• (iii) lateralization of vocal cord
• (iv) laser cordectomy (removal of one cord).

57. • Less invasive techniques such as:
• 1. Transverse cordotomy (Kashima operation).
Soft tissue at the junction of membranous cord
and vocal process of arytenoid is excised
laterally with laser.
This provides
good airway. In case airway is still insufficient
more tissue can be removed at subsequent
operation.
• 2. Partial arytenoidectomy. Medial part of
arytenoid is excised with laser. Sometimes only
the vocal process of arytenoid is ablated.

58. • 3. Reinnervation procedures. These have been used
to innervate paralyzed posterior cricoarytenoid
muscle by implanting a nerve–muscle pedicle of
sternohyoid or omohyoid muscle with its nerve
supply from ansa hypoglossi.
• These procedures have not been very successful.
• 4. Thyroplasty type II. It creates lateral expansion
of larynx and is similar to vocal cord lateralization.