must know basics for PG resident

1. Neurological affection of Pharynx and
Larynx
Dr. Raju Kafle
3rd year resident
ORL-HNS Dept, NMCTH
1

2. Introduction
• Upper aerodigestive tract: diverse purposes of breathing, eating and communicating.
• Ingested food and inspired air traversing the same space
• As in pharynx: patency should be maintained during respiration but should be
forcibly constricted during swallowing.
• As in larynx: most important function of the larynx is protective (aspiration)
• larynx should be open during breathing and tightly closed during swallowing
• Phonation is a more advanced evolutionary function.
2

3. • Glottic closure during forced exhalation: cough to clean the lungs and prevent
atelectasis.
• Also generate positive intrathoracic pressure for defecation, childbirth, and lifting
heavy objects.
• Sophisticated role in controlling airflow and pressure during breathing.
• Vocal folds open just before respiration and then close gradually during
exhalation: brake on expiratory airflow, controls rate of breathing.
3

4. • Functions: needs precise coordination
of motor activity and appropriate
response
Neurologic disorders
motor weakness
incoordination, and
impairment of sensation in upper
aerodigestive tract
4

5. PHASES OF SWALLOWING
 Oral (voluntary)
• Preparatory:
Mastication,
lubrication and bolus
formation
• Transit: To posterior
tongue
 Esophageal (involuntary)
• Primary peristalsis with swallow
reflex
• Secondary peristalsis: Thoracic
esophageal triggered by esophageal
distention
Non-peristaltic contraction: tertiary
peristalsis)
• Dysfunctional
• Isolated contractions
• prevalence increases with age
Pharyngeal (involuntary)
• Tongue movement posteriorly and
superiorly
• Thyropharyngeus: propulsion starts
• Velopharyngeal closure
• Hyoid, laryngeal elevation
• Laryngeal closure
• Epiglottis inverts to contact arytenoids
• False vocal folds close
• True vocal folds adduct
• Opening of UES
5

6. 6

7.  Cranial nerve IX and X and corticobulbar tract: key component
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8. 8

9. 9

10. 10

11. Aetiology
Supranuclear lesion : cortical
lesions --rare
• Requires bilateral symmetrical
lesion to cause paralysis of
pharynx and larynx
• Donot involves respiratory and
laryngeal movements.
11
Nuclear lesions:
Nucleus ambigus : PICA thrombosis, tumors
of medulla, bulbar palsy, syringobulbia, MND,
encephalitis, poliomyelitis, tabes dorsalis, lead
poisoning
• Combined paralysis of soft palate, pharynx
and larynx
• If only superior part involved : larynx
spared, involving only palatopharyngeal
palsy (syndrome of Avellis)

12. High vagal lesions
High vagal lesion : involves vagus
nerve at where it emerges from the
brainstem and leave the skull
• Along with it other nearby nerves IX,
XI and XII
• When involved with other nerves :
various syndromes of
laryngopharyngopalatal palsies are
named
12
Outside jugular
foramen

13. Low vagal lesions
• In the cervical course
• Causes: Penetrating injuries, tumors of hypopharynx, upper esophagus, thyroid ,
parapharyngeal space, enlargement / surgery of regional lymph nodes and surgery
of thyroid gland
• Left RLN : longer course—vulnerable to damage ( 60% vs 40% right RLN)
• Right RLN: shorter course, more vulnerable in thyroid surgery –as is more
anterior and lateral at inferior pole of thyroid rather than being protected in TE
groove.
13

14. NEURAL SYSTEM
Phase of Swallowing
 Oral: poor muscular control,
 Pharyngeal: Difficult to initiate,
cough during swallow, nasal
regurgitations, increased effort
for swallow, repeated swallows
 Esophageal: difficult to initiate
and maintain peristalsis,
constrictors spasm and
regurgitation
Neurologic: CN IX, X, XII
paralysis/ paresis, stroke
(Wallenberg: PICA, vertebral artery
)
Neuromuscular: Parkinson’s,
ALS, MS, myasthenia gravis,
oculo-pharyngeal muscular
dystrophy, inclusion body myositis,
inflammatory myopathy,
cricopharyngeal dysfunction
 Psychogenic
14

15. Neurological diseases
 Globus Pharyngeus
• Middle aged women, a/w anxiety and fears
• C/F: sensation of lump in throat(m/c), dryness and blockage of throat
• Though to be reflex vagal stimulation –alteration of tone of cricopharyngeal muscle ,
often a/w with hiatus hernia.
• Functional dysphonia
• Examination : no evidence of disease
• Investigations : blood count (anemia),barium swallow (cricopharyngea; spasm)
• Treatment : anxiolytics (diazepam) and speech therapy for functional dysphonia
15

16.  Glossopharyngeal Neuralgia
• Agonizing stabing pain in its distribution
• Usually starts in relation to tonsils and radiate downside of neck, in front of ear
and to back of mandible
• Precipiated by swallowing or protrusion of tongue ,external stimulation of ear,
cancers of tonsils and pharynx.
• Carbamazepines (400mg QID ) and sedatives
• If not improved , causes may be due to elongated styloid process, aberrant vessels
coursing over nerve ,neurofibroma-unsuspected and cholesteatoma
16

17. Herpes zoster
• Neurotrophic, involves CN IX and X cranial nerve
• mostly patients >50 years
• Vesicular eruptions in palate, pharynx, and laryngeal inlet at one side
• Isolated or if involved auricle and anterior faucial pillar (geniculate ganglion
herpes—Ramsay hunt syndrome)
Diptheria
• 2-10 years age, fatty degeneration of myelin sheaths of involved nerves and
consequent slowing of nerve conduction.
• Fauces : m/c site---ascent of toxin from faucial sites – medulla—palatal paralysis
• Cutaneous ascent : via nerves, if from Blood stream – paralysis of accomodation,
generalized polyneuropathy and myocardial infarction
17

18. • Palatal palsy : usually B/L, commonest after 2nd to 3rd weeks—nasal regurgitation
• Paralysis of accommodation : 3rd or 4th week
• Generalized polyneuropathy followed by paralysis of pharynx, intrinsic muscles of
larynx and the diaphragm.
• Risk of aspiration pneumonia and respiratory failure
Acute anterior poliomyelitis
• Destruction of anterior horn cells in the spinal cord and corresponding cells in the
nuclei of cranial nerves - wide spread muscular paralysis
• Bulbar type : paralysis of pharynx and larynx.
• 3 stages : paralytic stage(within 3 days)
• Brainstem damage : respiratory paralysis, fatal swallowing is impossible and
pharyngeal secretions are aspirated—fatal despite treatment
18

19.  Rabies :
• Virus enters via bites to infects many organs including salivary and lacrimal
glands.
• Degeneration of ganglion cells and perineural and perivascular round cell
infiltrates
• IP -10 days to years(usually 1-2 months)
• First general symptoms : depression, apprehension and insomnia
• Followed by hydrophobia (spasm of pharynx, larynx and respiratory muscles)
• All muscles of body producing Opisthotonous
19

20.  Myasthenia gravis
• Autoimmune disease, antibodies that blocks or
destroy nicotinic acetylcholine receptors (AChR) at the NMJ
in motor end plate.
• All ages and races, twice common in females
• Muscle fatiguability, EOM- most commonly affected, then
bulbar muscles causing dysarthia, dysphagia, regurgitation
through nose
 Palatal myoclonus
• Rythmical movt. of soft palate (60-180 times) per min -
palatal nystagmus
• Disorder of olivocerebellar modulatory projection on rostral
brain stem: multiple sclerosis and brain stem infarction
20

21.  Motor neuron disease
• Middle age
• affects motor neurons in anterior horn of spinal cord, certain somatic motor nuclei
of CN’s, and in the cerebral cortex
• Muscles of swallowing and respiration
• ALS, primary lateral sclerosis, progressive bulbarpalsy,
• Both UMN and LMN involved
• Most common presentation: wasting of upper limbs
• In ENT : features of progressive bulbar palsy –dysphagia and dysarthia
• Often combined with UMN signs and evidence of pseudobulbar palsy
• Bulbar presentation : degeneration of hypoglossal n. –tongue atrophy
• Dysphagia with aspiration is the most serious presentation
21

22. Laryngeal Neurological Lesions
22

23. Hyperfunctional disorders
1. Dystonia
• sustained contractions of skeletal muscles
that frequently cause twisting and
repetitive movements or abnormal postures
• In ENT: Spasmodic dysphonia/ focal
laryngeal dystonia
• Hyperadduction or hyperabduction
• Due to faulty central neural integration
• Mixed pattern : in some patients =mixed
laryngeal dystonia
• Most common accepted current treatment
• Botulinum toxin : chemodenervations
23
Dystonia
Adductor
spasmodic
dysphonia (80%)
Abductor
spasmodic
dysphonia (20%)
During speech :
strained and strangled
voice
During speech
:intermittent or sustained
glottis opening, breathy
or whispering voice

24. Botulinum Toxin therapy (BoNT)
• Clostridium botulinum produces eight immunologically distinct
toxins : A1-8, B1-8, C1, Dc, E1-12, F1-8, G, and H.
• BoNT exerts its effect at the neuromuscular junction by inhibiting
the release of acetylcholine, causing a flaccid paralysis.
• Botulinum toxin type A onabotulinumtoxin A (Botox; Allergan),
abobotulinum Toxin A (Dysport), or incobotulinum toxin A
(Xeomin), is most commonly used.
• Dose in ADSD: 0.05-20 U (average dose: <1U per vocal fold)
• Starting dose: 1U in 0.1 ml of NS in b/l thyroarytenoid vocalis
complex (success : 60%-100% normal function)
• If non response on voice therapy : injection in supraglottis portion
of LCA
24

25. • Given by tuberculin syringe percutaneouly with 27 G
needles under EMG guidance
• Mean duration of effect : 3 and 4 months
• Adverse effect : mild breathy dysphonia for less than
2 weeks, mild choking on fluids (few days), dizziness,
hyperventilation, sore throat , hemoptysis and itching
For ABSD:
• Injection in PCA muscle, from behind the posterior
end of thyroid lamina. Or alternatively transcricoid
injection under EMG guidance while patient is asked
to sniff for maximal PCA activity.
25

26. PSEUDOBULBAR PALSY (UMN lesions of
V,IX,X,XII)
• results from bilateral lesions of the corticobulbar tracts.
• Patients have muscle spasticity and hyperreflexia of the pharynx, palate, lips,
tongue, and larynx.
• Voice: harsh, strained, and strangled
• Patients with PBP are easily distinguishable clinically
• associated signs of hypernasality; slow, labored articulation; emotional lability;
and subcortical cognitive impairments.
26

27. Myoclonus • Uncommon disorder
• rhythmic contractions of the soft palate, pharynx, and
larynx at a rate of 1-2 contractions /second.
• patient complaint of clicking in the ear (involvement of
the eustachian tube and tensor veli palatini muscles)
• Cause : lesion in the central tegmental tract
• Voice: choppy, broken voice with intermittent
hypernasality.
• Rx: drug therapy :serotonin, carbamazepine, clonazepam,
and trihexyphenidyl
• Usually unresponsive to drug therapy
• So, local injection of BoNT into palate and
thyroarytenoid muscles
27

28. ESSENTIAL TREMOR
• Tremor : involuntary, purposeless rhythmic movement of a part of the body.
• 6- to 8-Hz :Shaking of the hands, head titubation, and tremulous/wavy/quavering
voice (s/o vocal tremor).
• Cause: Dysfunction in the central networks of the basal ganglia and the cerebello-
thalamocortical system.
• Typically absent at rest, maximal during maintenance of a posture, movement, and
accentuated at termination of movement.
• 60% have a family history.
• Voice: Pitch breaks and phonation arrests with visible vertical oscillations of the
larynx.
28

29. • Medical Rx: Propranolol and primidone.
Others :
• Deep brain stimulation (DBS) and thalamotomy: effective.
• Local injection of BoNT into the most tremulous muscles .
• Although the toxin does not eliminate the tremor, it decreases the amplitude
reducing the severity of the symptom.
29

30. STUTTERING
• Movement disorder, characteristically includes abnormal, involuntary, and
inappropriate use of the muscles of speech production that results in dysfluency.
• The abnormal movements are task specific and may be repetitive and stereotyped.
• Stuttering occurs in three subsystems of speech—respiratory, phonatory, and
articulatory—and it is a result of increased muscle tension in these subsystems,
which causes the muscles to move too quickly and too far.
• In addition, other cranial musculature may inappropriately contract, including the
eyelids and other muscles of facial expression.
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31. HYPOFUNCTIONAL DISORDERS
• Neuromuscular Junction Disorders: myasthenia gravis and Eaton-Lambert disease
• Infective: Poliomyelitis, rabies
• Myopathies: Inclusion body myositis, dermatomyositis, muscular dystrophy, and
metabolic myopathies
• Medullary Disorders affecting motor neurons: ALS, primary lateral sclerosis,
postpolio syndrome, Arnold-Chiari malformations, and medullary strokes.
• Parkinsonism
• multiple sclerosis
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33. 33

34. Vocal cord position
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35. Superior laryngeal nerve palsy
• often clinically unrecognized
If U/L involvement ; voice not affected severely and
compensation by another cord.
Findings:
• Askew position : anterior commissure is rotated to healthy
side
• Shortening of cord with loss of tension (wavy/ bowed and
flabby, affected side : being longer in absence of its
tensor)
• Flapping of paralysed cord, sags down during inspiration
and vice versa
• Arytenoid movements are unimpaired
• EMG of cricothyroid muscle: for diagnosis
35

36. Bilateral SLN palsy
• Uncommon condition, both cricothyroid paralyzed + anesthesia of upper larynx
• Inhalation of pharyngeal secretions and food: cough and choking fits
• Symmetry of larynx at rest and during phonation : makes diagnosis difficult
• Folds are bowed: air leakage during phonation –voice becomes lower, weaker (husky),
breathy and lacks inflection
36

37. Unilateral RLN Paralyis
• Ipsilateral paralysis of all intrinsic muscles (except cricothyroid) + ipsilateral
anesthesia in lower portion of larynx
Findings
• VC : median or paramedian position
Explained by
• Semons law : motor fiber innervating the adductors and abductor muscles lay in
separate bundles in RLN and they had different susceptibilities to advancing lesions
–giving rise to paralysis of abductors first (phylogenetically newer) –median/PM
position
37

38. Wagner and Grossman hypothesis
• Wagner (1890) and Grossman(1897) proposed this theory
• In the absence of cricoarytenoid fixation, immobile vocal fold in paramedian
position has a total pure U/L RLN palsy
• And immobile VF in lateral - cadaveric position has a combined paralysis of SLN
and RLN (since the adductive action of cricothyroid is lost)
38

39. Bilateral RLN/ Abductor paralysis
Findings
• Position of cords:
• Median or paramedian position ( unopposed action of cricothyroid muscles :
adduction)
Clinical features
• As cords are in median or PM position : airway is inadequate causing dypnea and
stridor , but voice is good
• Dyspnoea and stridor becomes worsens on exertion or during an attack of acute
laryngitis
39

40. Combined paralysis (RLN + SLN)
 Unilateral combined paralysis
• All muscles are paralyzed on one side except interarytenoid : which receives
innervation from other side
• Thyroid surgery : m/c
• High vagal lesions
Findings
• Position of vocal cord: cadaveric position
• The healthy cord is unable to approximate the paralyzed cord : glottic incompetence
• Results : hoarseness of voice and aspiration of liquids , cough is ineffective due to
air leak
40

41.  Bilateral SLN + RLN palsy
• Rare conditions
• All laryngeal muscles are paralysed and complete anesthesia throughout the larynx
Position of vocal cord
• cadaveric position
Clinical features
• Aphonia
• Aspiration
• Dyspnoea
• Bronchopneumonia : cough --, retention of secretions in lower airway, repeated aspirations and
retention of secetions
41

42. Congenital vocal cord paralysis
• Unilateral or bilateral
• Unilateral is more common
• Causes : birth trauma, congenital anomalies of great vessels or heart
• B/L paralysis : hydrocephalus, Arnold chiari malformation, intracerebral
hemorrhage during birth, meningocele, cerebral or nucleus ambigus agenesis
42

43. Approaches(ref : cummings 7th edi)
Approach
Examination
Flexible
laryngoscopy
and stroboscopy
Ancillary testing
Performance
measures and
investigations
43

44. Examination
Oral cavity Oropharynx—soft palate
44
Assess motion , strength and
symmetry
• Athetoid motion : tardive
dyskinesia
• Fasciculations of tongue : ALS
• Jaw and tongue thrusting :
oromandibular dystonia
Assess motion, strength and
symmetry
• Slow and repeatitive jerking:
palatal myoclonus

45. Flexible Laryngoscopy and Stroboscopy
Soft palate Pharynx Larynx
45
“Kitty cat” or /ka/ tests
• Assesses velopharyngeal closure
Pooling of secretions
• Suggests poor
swallowing function
Tremor at rest
• Suggests essential tremor
Repeat sniff and /ee/
• May unmark paresis
Pitch glide
• Assesses cricothyroid function
“We eat eggs every Easter” or count from 80
to 90
• Adductor spasmodic dysphonia
“Harry’s happy hat” or count from 60 to 70
• Abductor spasmodic dysphonia

46. 46
Ancillary testing
GRBAS/ Voice handicapped index Acoustic analysis
• GRBAS: Grade, Roughness,
Breathiness, asthenia and Strain) each
0-3 and total of 15
• VHI –10 (each 0-4 and total of 40)
• To investigate the value of
standard deviation of fundamental
frequency, jitter (pitch) and
shimmer (amplitude) for
evaluation of voice quality
• To assess severity of voice problem
• To assess outcomes post treatment

47. 47
Performance measures and
investigations

48. 1. VIDEOFLUOROSCOPY
• Modified barium swallow (MBS)
• Different from standard barium swallow :
• varying ingested consistencies
• primarily oropharyngeal fluoroscopy
• Evaluation of transit time, residues in pharyngeal recesses,
penetration, presence and timing of aspirations, structural
lesions, peristalsis, improvement with postural adjustments or
swallowing maneuvers.
48

49. 2. Barium swallow :
• Large barium bolus distends esophagus and reveals
structural abnormalities, dysmotility, and GERD under
videoradiography
3. Flexible endoscopic evaluation of swallowing
(FEES)
• Visualization of laryngopharynx before and after
pharyngeal phase of swallowing with dyed boluses of
varying consistencies
• Optimal for evaluation of glottic competence, tolerance of
secretions, vallecular stasis
49

50. 4. Flexible endoscopic evaluation of swallowing with sensory testing (FEEST) :
• FEES + sensory testing of laryngopharynx with pulsed air to prognosticate
penetration and aspiration
• Unilateral or bilateral sensory deficits classified from mild to severe based on
pressure of air required for laryngeal adductor reflex.
• ≤3 mm Hg : normal laryngeal sensation
• ≥6 and 9 mm Hg : severe impairment
• 9 mm Hg: moderate sensory impairment
• >9 mm Hg: severe sensory impairment
5. Transnasal esophagoscopy
50

51. 6. High-resolution manometry
• Esophageal intraluminal pressure graph vs. time, using circumferential pressure
transducers
• Gold standard for diagnosis of esophageal motility disorder
7. Aerodynamic assessment
• acoustic analysis, phonatory and respiratory air flow and subglottic phonatory
air flow
8. Glottography
• Photoglottography
• Electroglottography
51

52. 10. Electromyography
• If cricothyroid function absent suggests vagus
nerve injury
• If cricothyroid function intact suggests
recurrent laryngeal nerve injury
• Presence of giant waves and fibrillation
potentials suggest nerve denervation
• Fatiguing muscle recruitment suggests
myasthenia gravis
• Regular 4–8 Hz signal suggests essential
tremor
11. Panendoscopy, plain radiographs of chest,
CT and MRI of Head, base of skull to thorax
52

53. Management of chronic aspiration
Medical Management :
• Swallow posture adjustment: chin tuck, head rotation and head tilt posture
• Swallowing maneuvers
• Supraglottic swallow maneuver: Breath hold during swallow, allowing earlier CP
opening and prolonged airway closure
• Super-supraglottic swallow maneuver: Breath hold and Valsalva maneuver during
swallow
• Effortful swallow maneuver: Maximally contract all muscles of swallowing
• Mendelsohn maneuver: Manually elevate larynx for 2 s at mid-swallow
• Bolus size and diet modification : Thickened liquids, smaller bolus.
• Nasogastric feeding tubes, percutaneous endoscopic gastrostomy 53

54. Surgical Management
• Tracheostomy : does not prevent aspiration, but improves pulmonary toilet
• Vocal fold medialization : In cases of glottic insufficiency secondary to unilateral
vocal fold paralysis, especially with laryngeal sensory deficit
• Placement of endolaryngeal stent Reversible glottis obturation with silicon stent
(with or without slit for phonation)
• Narrow field laryngectomy
• Removal of laryngeal skeleton with sparing of hyoid bone and strap muscles,
high tracheotomy and maximal preservation of pharyngeal mucosa, including
aryepiglottic folds and vallecula
54

55. • Vertical laryngoplasty or tubed laryngoplasty : reversible
• Epiglottopexy : reversible
• Epiglottic flap used to close laryngeal inlet. Speech is allowed via small
posterior laryngeal inlet
• Glottic closure
• Via trans-thyrotomy, true and false vocal folds are closed after stripping
their mucosa.
• Irreversible
• Requires tracheostomy and eliminates phonation
55

56. • Lindeman procedure: Tracheoesophageal
diversion
• Separation of upper respiratory and digestive tract
• Proximal trachea anastomosis with esophagus thus
diverting aspirated secretions into esophagus
• Distal trachea sutured to skin to create a
tracheostoma
• Laryngotracheal separation is similar, except
proximal tracheal stump is over-sewn as blind
pouch
• Reversible. Eliminates phonation
• Total laryngectomy
• Remains procedure of choice for definitive
treatment of life-threatening aspirations.
56

57. For treatment purpose
57
Vocal fold
paralysis
glottic insufficency : breathy
dysphonia (m/c)
Breathlessness while speaking and
breathlessness during physical
exertion
Bilateral
Unilateral
glottic obstruction : stridor and
dyspnea

58. UNILATERAL VOCAL FOLD PARALYSIS
• Patients with unilateral laryngeal paralysis : hoarseness and hypophonia.
• Dysphagia with possible frank aspiration: less often than voice complaints.
• Dysphagia-related complaints : more frequent in ‘high’ vagal injury.
58

59. OBSERVATION
• Patients with hemilaryngeal paralysis, especially of short duration, may simply be
observed ( as a rule, laryngeal auto innervation is possible)
• Factors favouring observation include:
1. no evidence of aspiration
2. injured laryngeal nerve(s) : structurally intact and potential for recovery
remains
3. minimal vocal disability and/or minimal vocal demand
4. comorbidities that discourage or prevent intervention
• Voice and swallowing therapy may be used as needed during the observation
period
59

60. INJECTION LARYNGOPLASTY
• In those who needs temporary relief of
symptoms even when eventual recovery is
expected.
• Accomplished by injection of an absorbable
bulking substance into the paralyzed fold in
lamina propria in the plane of thyroarytenoid
muscles : to improve the glottic insufficiency.
• May be performed via direct laryngoscopy, or
perorally or transcutaneously under topical
anaesthesia.
60
Factors favouring injection
augmentation include:
1. dysphagia
2. high degree of vocal disability
or high vocal demand
3. Good/indeterminate functional
prognosis
4. small glottic gap (2- 3 mm)
5. no posterior glottic gap
6. short life expectancy

61. • Injection augmentation is regarded as temporary
since the abandonment of polytetrafluoroethylene
polymer -Teflon™- which was permanent because
of well-known adverse tissue response.
• Calcium hydroxylapatite particle paste: durable
(1 year)
• Disadvantages: Injectation into an unintended site –
typically the superficial layers of the vocal fold,
impairs mucosal phonatory vibration.
• In those corrective intervention is challenging and
patients may have to await natural resolution over
weeks to months.
61
Agents
1. Hyaluronic acid preparations
2. Calcium hydroxyapatite paste
3. Micronized human dermis
4. Autologous fat and
5. Carboxymethylcellulose
glycerine gel.

62. LARYNGEAL FRAMEWORK SURGERY
• Framework surgery is generally reserved for treatment of glottic
insufficiency from unilateral paralysis that is not expected to improve.
Favorable factors are:
• Dysphagia
• High degree of vocal disability or vocal demand
• poor functional prognosis
• Large glottic gap (2 mm to 3 mm)
• Posterior glottic gap
• Shortened life expectancy.
62

63. 63
In medialization laryngoplasty, a medialization shim of biologically inert material is inserted into the
paraglottic space through a thyroid cartilage window to displace the vocal fold towards the midline

64. • Typically, this operation is performed under a local anaesthetic, with or without
additional intravenous sedation.
• The surgeon, guided by patient phonation and endoscopic visualization
• Medialization via thyroplasty, in contrast to injection, is precise, predictable and
durable.
• safer and better suited to high-risk patients than injection under general
anaesthesia.
• Serious complications: include airway obstruction and perforation into the
laryngeal lumen.
64

65. Arytenoid repositioning surgery
• Is added to medialization thyroplasty when there is a
poorly supported arytenoid or posterior gap
• Is designed to internally rotate and/or suspend the
arytenoid in physiologic phonatory position
• Either approached from inf. constrictor muscle and
around back of thyroid lamina and suturing with non
adsorbale suture or,
• Directly opening of cricoarytenoid joint capsule and
suturing the arytenoid in optimal position in crest of
the cricoid (Adduction arytenoidopexy)
65

66. RE-INNERVATION
• Re-innervation using nearby nerves – both the ansa cervicalis and the hypoglossal
nerves.
• Because of complex innervation of vocal fold muscles, re-innervation generally
stands to improve the bulk and tone of vocal fold muscle but will not restore
physiologic motion.
• Ideally suited when the vocal fold is known to be completely denervated (e.g. if
the recurrent nerve or vagus has been sectioned during surgery
66

67. BILATERAL VOCAL FOLD PARALYSIS
• A clinician encountering bilateral vocal fold immobility should consider the
possibility of joint fixation or posterior glottic scar, particularly when the condition
follows intubation.
• Patients with bilateral vocal fold paralysis typically complain of dyspnea, noisy
breathing and exercise intolerance.
• The severity of these respiratory symptoms is inversely proportional to the size of
the glottic aperture between the two immobile vocal folds.
• Respiratory noise is worse on inspiration, as negative pressure pulls the denervated
vocal folds into closer approximation.
67

68. • In acute bilateral vocal fold paralysis : life-threatening requiring tracheostomy.
• Typical scenario is unexpected respiratory distress after extubation from thyroid
surgery
• In progressive cases, as found in certain neurologic diseases, patients may
compensate as the paralysis becomes denser, and may tolerate unexpectedly small
glottic airways.
• Lateralization of the vocal fold or removal of arytenoid and or vocal fold tissuesto
enlarge the glottic aperture
68

69. VOCAL FOLD PARESIS
• Vocal fold paralysis is not an all-or-none phenomenon.
• Paresis, or incomplete paralysis in which some gross vocal fold mobility is
preserved
• Predominant symptoms: Glottic insufficiency, even with bilateral involvement,
Impairment of abduction (glottic obstruction)- rare in paresis
• Phonatory glottic function affected even in mild asymmetries in neural input, thus
may affect pitch, vocal stamina and high or low intensity phonation.
• Stroboscopy and EMG: confirms subtle decrease in muscular tone.
69

70. Thankyou
70
References
1. Grays anatomy student version, 4th edition
2. Scott brown 6th edition
3. Scott brown 8th edition
4. Cummings head and neck surgery 7th edition
5. Thiemes clinical ENT 4th edition
6. Laryngology by Marvin P , 3rd edition