Nerve supply of larynx & laryngeal paralysis

8,448 views 59 slides Sep 26, 2018
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About This Presentation

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


Slide Content

Nerve Supply of Larynx & RLN P aralysis Dr Himanshu M ishra 1 st yr PG

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

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

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.

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 T he 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 ;

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 .

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

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

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

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

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 .

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 .

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.

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.

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.

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).

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

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.

R ecurrent 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

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.

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

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

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

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

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.

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

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

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

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

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

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

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

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

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

Manual Compression Test

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

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

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 .

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.

Treatment algorithm

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 )

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

Type 1 T hyroplasty

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

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.

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 ).

L ess 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 .

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.

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