The Larynx

Front 1

Laryngeal anatomy: position

Back 1

It is between C5 and C6 in the neck, it is not a fixed structure but it is mobile in extension and flexion of the head (it moves upwards and downwards respectively).

The position is different according to age and gender: usually, in women and children it’s higher. In the elderly it’s lower.

Front 2

Laryngeal anatomy: supraglottis

Back 2

5 subsites:

epiglottis, aryepiglottic folds, arytenoids, false vocal cords, fundus and roof of the Morgagni’s ventricle

Front 3

Laryngeal anatomy: glottis

Back 3

3 subsites:

true vocal cords, anterior and posterior commissures, floor of the ventricle

Front 4

Laryngeal anatomy: subglottis

Back 4

It goes from the inferior face of the vocal cords to the inferiormargin of the cricoid

Front 5

Laryngeal anatomy: cartilages

Back 5

3 large, unpaired cartilages (cricoid, thyroid, epiglottis)

3 pairs of smaller cartilages (arytenoids, corniculate, cuneiform)

Front 6

Extrinsic muscles of the larynx

Back 6

- Sternothyroid muscles depress the larynx.

- Omohyoid muscles depress the larynx.

- Sternohyoid muscles depress the larynx.

- Inferior constrictor muscles

- Thyrohyoid muscles elevates the larynx.

- Digastric elevates the larynx.

- Stylohyoid elevates the larynx.

- Mylohyoid elevates the larynx.

- Geniohyoid elevates the larynx.

- Hyoglossus elevates the larynx.

- Genioglossus elevates the larynx

Front 7

Laryngeal anatomy: intrinsic muscles

Back 7

Cricothyroid: stretches and tenses the vocal ligaments, and so is important for the creation of forceful speech. Attachments: Originates from the anterolateral aspect of the cricoid cartilage, and attaches to the inferior margin and inferior horn of the thyroid cartilage. Actions: Stretches and tenses the vocal ligament. Innervation: External laryngeal nerve.

Thyroarytenoid: acts to relax the vocal ligament, allowing for a softer voice. Attachments: Originates from the inferoposterior aspect of the angle of the thyroid cartilage, and attaches to the anterolateral part of the arytenoid cartilage. Actions: Relaxes the vocal ligament. Innervation: Inferior laryngeal nerve.

Posterior cricoarytenoids: sole abductors of the vocal folds, and thus the only muscle capable of widening the rima glottidis. Attachments: Originates from the posterior surface of the cricoid cartilage, and attaches to the muscular process of the arytenoid cartilage. Actions: Abducts vocal folds. Innervation: Inferior laryngeal nerve.

Lateral cricoarytenoid: the major adductors of the vocal folds. This narrows the rima glottidis, modulating the tone and volume of speech. Attachments: Originates from the arch of the cricoid cartilage, and attaches to the muscular process of the arytenoid cartilage. Actions: Adducts the vocal folds. Innervation: Inferior laryngeal nerve.

Transverse and Oblique Arytenoids: adduct the arytenoid cartilages, closing the posterior portion of rima glottidis. This narrows the laryngeal inlet. Attachments: Spans from one arytenoid cartilage to the opposite arytenoid. Actions: Adducts the arytenoid cartilages. Innervation: Inferior laryngeal nerve.

Front 8

Laryngeal anatomy: ligaments

Back 8

 Hyo-epiglottic ligament

 Thyro-epiglottic ligament

 Thyrohyoid membrane

 Crico-thyroid membrane

 Crico-tracheal membrane

 Quadrangular membrane

 Vestibular ligament

 Vocal ligament

 Conus elasticus

Front 9

Laryngeal anatomy: vessels

Back 9

The arterial supply to the larynx is via the superior and inferior laryngeal arteries.

Superior laryngeal artery: a branch of the superior thyroid artery (derived from the external carotid). It follows the internal branch of the superior laryngeal nerve into the larynx.

Inferior laryngeal artery: a branch of the inferior thyroid artery (derived from the thyrocervical trunk). It follows the recurrent laryngeal nerve into the larynx.

Venous drainage is by the superior and inferior laryngeal veins. The superior laryngeal vein drains to the internal jugular vein via the superior thyroid, whereas the inferior laryngeal vein drains to the left brachiocephalic vein via the inferior thyroid vein.

Front 10

Laryngeal anatomy: Recurrent laryngeal nerve

Back 10

The right RLN branches from the right vagus nerve in the neck at the left of T1-T2 or more inferiorly, anterior to the right subclavian artery. It travels inferior and posterior to the subclavian artery to ascend in the neck between the trachea and the esophagus, behind the right common carotid artery in the tracheoesophageal fascia. It enters the larynx at C6-C7 usually.

The left RLN branches from the left vagus nerve in the thorax. It travels inferior and then posterior to the arch of the aorta to ascend into the neck in between the trachea and esophagus. The terminal portion of both RLNs pass superiorly, deep to the inferior border of the inferior pharyngeal constrictor muscle, just posterior to the cricothyroid joint to supply the interarytenoid, posterior cricoarytenoid, and lateral cricoarytenoid muscles. It enters the larynx below C6-C7.

During anterior cervical diskectomy and fusion operations, the RLN can be exposed, causing traction or crush injuries, with postoperative dysphagia or hoarseness.

Front 11

Laryngeal anatomy: Superior laryngeal nerve

Back 11

The superior laryngeal nerve (SLN) branches from the main trunk of the vagus high in the neck. It descends in the neck adjacent to the pharynx, medial to the carotid sheath. The SLN divides into the internal and external branches approximately 2-3 cm superior to the superior pole of the thyroid.

Internal branch: General sensation, including pain, touch, and temperature for the tissue superior to the vocal folds, accompany the visceral sensory axons and run in the internal branch of the SLN. Secretomotor fibers are also in the internal laryngeal branch of the SLN. The internal branch of the SLN exits the larynx and pharynx through a foramen in the posteroinferior portion of the thyrohyoid membrane. The internal branch of the SLN is then united with the external branch of the SLN to ascend in the neck to join the rest of the vagus before it reaches the inferior vagal ganglion

External branch: The branchial motor axons in the external branch of the SLN supply the inferior constrictor muscles and the cricothyroid muscles. The external branch descends to the region of the superior pole of the thyroid and travels medially along the inferior constrictor muscle

Front 12

Laryngeal anatomy: Movements of the arytenoids

Back 12

When we have to produce our voice, we have to close the vocal cords.

The arytenoids move in three directions: - medial rotation,

rocking movement

slide towards the anterior part of the larynx “sliding movement”.

As a result, the voice is produced

Front 13

Laryngeal Histology

Back 13

Remember the histology, especially important when tackling benign and malignant neoplasias. You can find moving from superficial areas to deeper ones in the vocal cord:

- Mucosal epithelium,

- Basal membrane,

- Superficial layer of the lamina propria (Reinke’s space),

- Intermediate + Deep layer of the lamina propria (vocal ligament),

- Thyroarytenoid muscle (vocalis muscle).

Most of the epithelium is respiratory one, in some sites there is non-keratinised stratified squamous epithelium (epiglottis, the free margin of the vocal cords, the laryngeal side of the aryepiglottic folds and of the arytenoids) .

We have two kinds of tumors : adenocarcinoma and squamous cell carcinoma.

Front 14

Larynx: functions

Back 14

Respiratory,

Phonatory,

Deglutitory,

Sphincteric: when you lift a weight, you do this movement in apnoea;

Protective: close the airways when swallowing, also for the cough reflex,

Emotional: we laugh, we cry, we scream thanks to the larynx.

Front 15

Larynx: voice production

Back 15

Voice is “every sonority directly or indirectly produced by the human body with an informative or communicative valence”.

The larynx is present only in mammals. With the voice, we are able to show who we are, in terms of sex/age/health status. We express our feelings, we produce non-verbal and verbal messages; We produce the voice thanks to the interaction of

1- lungs and chest: make available the air

2- the vocal cords.

3- The sound has to be modified by the vocal tract, to gain the characteristic if timbre, resonance and articulation of speech.

4- They must be regulated by the CNS: a. the bulbar takes care of the respiratory mechanics, b. the mesencephalic part deals with the coordination c. the limbic areas are concerned of the emotional aspects and the d. cortex tackles the volitional, cultural and educational aspects.

5- We need also a feed-back control of the auditory system to regulate phonation intensity, frequency, intonation and timbre. When we speak, before we have to inspire and then during expiration we produce sounds. We change the intensity thanks to the expiratory pressure. We can reach very high pressure during singing. Important the pressure for the voice regulation. The movements are periodic vibrations, and are responsible for the production of sound.

Front 16

Dysphonia: definition

Back 16

Quantitative and/or qualitative alteration of the spoken voice secondary to a structural (organic dysphonia) and/or functional modification (functional dysphonia) of one or more organs involved in its production or to an inadequacy of the dynamic relationships between the different components of the pneumo-phonatory apparatus

Front 17

Dysphonia: when to think about a voice problem

Back 17

 Dysphonia lasting more than 15 days and not responsive to medical therapy

 Dysphonia after surgical interventions on neck, thorax and brain

 Dysphonia in a smoker

 Dysphonia in a voice-professionist

 Dysphonia, asthenic voice in a hyperkinetic/hypokinetic patient

 Dysphonia in a patient with psychologic problems

 Inappropriate voice respect of the patient’s physical characteristics

Front 18

Dysphonia: evaluation

Back 18

History:

- Characteristics of dysphonia,

- Familiarity: because there are congenital forms of dysphonia,

- Subjective sensations of the patient regarding phonation,

- Subjective sensations perceived on the larynx,

- Social use of voice

- Professional use of voice

- Life habits

- Patient’s character

- Concomitant pathologies potentially related with the voice problems complained by the patient (GERD, endocrinopathies, etc.)

- Drug use that can be responsible for the modification of vocal cords.

It is important to carry out a physical examination: usually a patient with a normal voice is a gentleman, a breathy voice (hypokinetic) will reflect a depressed patient, a hyperkinetic voice will correspond to a dominant person

It is important to see how the patient breath: the movements of the thorax:

- diaphragmatic

- abdominal

- costo-diaphragmatic

- sternal-costal

- apical

Remember that the right breathing is the costo-diaphragmatic: expand both the thorax and the diaphragm without using the apex of the lungs. Make a deep breath now! Many of you breath incorrectly, you must use your abdomen, use the diaphragm so you introduce the correct amount of air in the lungs. You must see if the thorax is mobile or not.

Move the larynx:

- see the tone of the suprahyoid muscle

- see if the larynx is stiff or not

- thyroid-hyoid space

- Laryngeal vertical motility

- Lateral motility

Vocal attacks:

- Hard: vocal cords close and increase the subglottic pressure; then the vibratory cycles start, the first of which will have an explosive charactetistic

- Soft: the vocal cords close while the expiration starts

- Breathing attacks: the vocal cords are open and close incompletely only when expiration starts. Before the sound it’s possible to perceive a breathing

Soft attack is aaaa! The breath attack is like air in the abduction of vocal cords. AAAAaaa. Then A!A!A!AAAA this is a hard attack, a sort of explosion. You must listen how the patient attacks.

Front 19

Dysphonia: stroboscopy

Back 19

With stroboscopy, you see we are able to make visible a movement, that usually is too fast to be recorded by our eyes. This slow motion picture is an illusion, as the speed of actual vocal fold vibration is not changed by stroboscopy. This special viewing allows the voice care team to evaluate each vocal fold's vibration properties during the different phases of the vocal fold's vibration cycle.

I use this strategy, thanks to stroboscopic effect. Some spots of light will show, in every cycle, a different phase of the movement of the vocal cords and here they are a little bit decreased. So we reach a different phase and we reconstruct a different movement.

The parameters we take into consideration are:

- symmetry

- periodicity

- glottic closure

- amplitude and

- progression of the mucosal wave
I see an ondulatory movement. There are these modifications, in symmetric periodicity with glottic closure. Here you see a “lambda” movement (asymmetrical), typical of some pathologies.

Used to evaluate the degree of infiltration of malignant lesions, better define benign lesions, evaluate the results of surgery

Front 20

Dysphonia: narrow band imaging

Back 20

The light wave is the result of different radiations: with a filter, I can use only the blue and the green lights, that are strongly absorbed by the haemoglobin. In this way, I can make more visible the capillaries and post-capillary venules, with a brown or blue colour. If I have a suspicion about a tumour, then I can check.

Front 21

Dysphonia: autofluorescence

Back 21

The electrons get exposed to a source of energy, they will get excited. When the excitation stops, the electron will get back to the ground state, releasing energy, in the form of fluorescence. In our tissues, we have different fluorophores, located in different places. With different kinds of lights, we can make the fluorophores visible and see the fluorescence.

The tumoral tissues differ from the normal tissues for the following aspects:

- Minor quantities of NADH and FAD

- Lower intensity of fluorescence because of the thickness of the epithelium

- Variable quantities of bacteria containing porphyrins, that produce a red fluorescence

Front 22

Dysphonia: advantages of autofluorescence and NBI

Back 22

- Early diagnosis of cancers of the UADT

- Intra-operatory use for guided biopsies or excisions of the lesions

- Control of the surgical margins after laser surgery

- Better accuracy at follow-up.

Front 23

Dysphonia: Acoustic analysis

Back 23

It is important for the voice evaluation.

There is different software, good to evaluate the speech therapy efficacy according to different parameters: modification of the spectrum and others

Front 24

Functional dysphonias: definition

Back 24

Poor voice quality without any obvious anatomical, neurological or other organic difficulties affecting the larynx or voice box

Front 25

Functional dysphonias: causes

Back 25

Breathing is not correct. The costodiaphragmatic breathing allows the right control of the expiratory air flux and of the subglottic pressure. Breathing with the apex of lungs: just a limited quantity of air and a missed regulation of the expiratory air flux by the diaphragm and the abdominal muscles, thus the larynx and vocal cords will have the double role of vibration and energy source, which is not correct.

Problems with the posture of the body -> cannot introduce the right amount of air into lungs:

hyperkinetic habitus -> speak with a louder voice, which is not good.

Pathological laryngeal postures:

- Isometric hypercontraction

- Lateral hypercontraction/hyperadduction

- Supraglottic AP contraction

- Posterior glottic hyperadduction that will lead to incomplete adduction and hypotonic thyroarytenoid muscles.

Front 26

Functional dysphonias: primary vs secondary

Back 26

Primary:

- Vocal abuse/misuse

- Difficulty in pitch discrimination

- Imitation of vocal models

Secondary:

- Organic

-- compensatory

-- audiogenic

- Psychogenic

-- Conversion diseases

-- VCD

-- Disturbances of the vocal molt

-- Depression

Front 27

Functional dysphonias: treatment

Back 27

- vocal hygiene

- speech therapy

- physiotherapy

- relaxation techniques (yoga, autogenic training)

- psychotherapy (psychogenic dysphonia)

Front 28

Organic dysphonias: causes

Back 28

RESPIRATORY DISORDERS:

Restrictive respiratory insufficiency

Obstructive respiratory insufficiency

Mixed respiratory insufficiency

LARYNGITIS

ANATOMIC ALTERATIONS OF THE VOCAL CORDS

Congenital

Acquired

OTHERS:

- drugs

- hormonal diseases (hyper/hypogonadism, hyper/hypothyroidism)

- thesaurismosis: remember the problem of amyloidosis (in case of amyloidosis one targets is the vocal cords, mucopolysaccharidosis, etc.

- Inappropriate pitch in transsexual.

- Alterations of the vocal tract.

Front 29

Vocal cords disease: congenital -> vergeture (french pronunciation)

Back 29

Aka sulcus vocalis. On the free margin, there is a depression on both vocal cords. This is due to an atrophy of the mucosa, and the mucosa is attached to the vocal ligament, so you don’t have mucosal wave where the mucosa is attached. The result would be a breathy/diplophonic voice.

Front 30

Vocal cords disease: treatment of vergeture

Back 30

The treatment is speech therapy to correct the dysfunctional compensatory mechanism. Surgery: you can try to detach the scar but of course the results are usually frustrating. What do we do? First of all we perform coagulation of the vessels of the vocal cords, then incision of the mucosa of the vocal cords, then dissection of the attachment of mucosa and vocal ligament and then we reposition the mucosa. But usually the mucosa attaches again on the vocal ligament: very frustrating!

Front 31

Vocal cords disease: cyst

Back 31

Congenital: open or closed epidermoid cyst

Acquired: mucosal or retention cyst.

On the vocal cords, we have salivary glands, and if the ducts of these salivary glands close you can have a retention cyst.

The treatment: always speech therapy, hygiene, surgery. What do we do? Superior cordotomy, dissection of the cyst, removal of the cyst and repositioning of the mucosa.

Front 32

Vocal cords disease: acquired -> nodules and polyps

Back 32

Polyp or nodule. These are typical in case of vocal abuse or misuse. Remember that usually the polyp is monolateral and the nodules are always bilateral (they are called also kissing nodules).

Treatment: Speech therapy is the first treatment. Plus, of course vocal hygiene and smoking cessation.

In case of residual pathology, we can remove them. In case of nodules, the surgery is reserved only for keratoric nodules that are not responsive to speech therapy (usually, the nodules heal with speech therapy)

Front 33

Vocal cords disease: acquired -> Reinke's edema

Back 33

Reinke's edema, also known as polypoid degeneration, is the swelling of the vocal folds due to fluid collection (edema) in superficial lamina propria of vocal folds (Reinke's space)

Due to smoking, Gerd, hormonal changes.

• Rough voice -> due to the use of false vocal cords

• Lower pitch

• Increased voice effort

• Higher voice intensity

• Type I oedema visible on stroboscopy only

• Type II bilateral fusiform oedema monolateral localised oedema (serosal pseudocysts)

• Type III severe bilateral oedema

• Type IV severe polypoid oedema

(for type III and IV -> surgery)

Treatment:

Stop smoking, vocal hygiene, hormonal therapy.

Surgery: Superior cordotomy; aspiration of the edema; of course lifting of mucosa, because if you have an excess of mucosa you have to adapt the mucosa, so you cut the excess of mucosa, and then you have to reposition the mucosa onto the vocal cords.

Front 34

Vocal cords disease: acquired -> Posterior granuloma

Back 34

Typical of gastroesophageal reflux disease (GERD). You see this kind of ulcer, granuloma, on the vocal process.

The treatment: first of all there is the treatment of GERD, so prokinetics, food hygiene, proton pump inhibitors (PPI) and so on.

Our treatment is speech therapy: in this case, you don’t have to use surgery to treat the patient because you will have a recurrence after some weeks. You have to try and remove the granuloma in an automatic way, and you use speech therapy

Front 35

Vocal cords disease: acquired -> laryngeal papilloma

Back 35

Laryngeal papilloma: the papillomatosis of the larynx, caused by HPV, could be of the adult type (usually there is only one lesion) but we can have also the juvenile papillomatosis that is interesting not only the vocal cords but also the tracheobronchial tree.

The treatment: in the case of the larynx, the treatment is to perform laser resection or vaporization of the lesion and to inject into the vocal cord some antiviral drugs (usually we can use interferon or cidofovir), that are important to control the replication of the virus.

Front 36

Organic dysphonias: neuromuscular pathologies

Back 36

MOTION DISTURBANCES:

- Anchylosis of the arytenoid

- Lesions of the peripheral nerves

NEUROLOGICAL DISTURBANCES:

- Bulbar or pontine lesions

- CNS lesions (chorea, parkinson, cerebellar...)

MUSCULAR PATHOLOGIES:

- Dystrophy

- Myastenia

Front 37

Laryngeal palsies: Central vs Peripheral

Back 37

Central:

- bilateral

- incomplete

Peripheral:

- unilateral

- complete

Front 38

Central laryngeal palsies: causes

Back 38

Infectious:

- meningitis

- meningoencephalitis

- poliomyelitis

Demyelinating:

- multiple sclerosis

Degenerative:

- syringomyelia

Stroke

Front 39

Peripheral laryngeal palsies: causes

Back 39

Traumatic / Infiltrative / Compressive lesions of:

- Vagus nerve (superior and inferior laryngeal)

- Recurrent laryngeal nerve

Front 40

Peripheral laryngeal palsies: unilateral vs bilateral

Back 40

If the paralysis is involving only one vocal cord, the vocal cord can be paralysed in adduction or in abduction: in both cases you will have dysphonia, but the treatment can be different.

You can have also bilateral palsies and the situation is different according to the position of the vocal cords: the most common is the fixation in adduction, so in this case you will have dyspnea, because of course if you have the vocal cords that are closed you are not able to breathe.

If fixed in abduction (rare): aphonia

You can have also the paralysis of the interarytenoid muscles, that is called Gerhardt's syndrome: usually this situation is visible in cases of tertiary syphilis, when you have lesions of the brainstem.

Front 41

Peripheral laryngeal palsies: treatment

Back 41

If we have a monolateral paralysis first of all we start with the speech therapy; if the compensation is not good we can increase the volume of the mobile vocal cord with the vocal injection of some different substances (the best one is the autologous fat injection, but you can use also other materials) or we can try to adduct the paralysed vocal cord with a thyroplasty, so creating a medialization of the vocal cord by the thyroid cartilage, so we create a small window on the skeleton of the larynx and we medialize the vocal cord.

On the other side, if I have bilateral adduction palsy, I have to create a hole to guarantee breathing of the patient, and in this case I have to damage the vocal cords, I have to remove these vocal cords to acquire space for breathing and to avoid tracheotomy, otherwise the patient has a permanent tracheotomy.

Front 42

Swallowing: oral cavity

Back 42

- Lips

- Teeth

- Hard and soft palate

- Cheeks

- Floor of the mouth

- Mandible

- Tongue

- Palatal pillars

- Several sensors (tactile, gustatory – taste buds-, kinaesthetic, etc.)

- Several muscles

Front 43

Swallowing: pharynx

Back 43

The pharynx is a muscular tube connecting the nose, oral cavity and throat to the esophagus (concerning the oral cavity) and the trachea (concerning the throat).

- Pharyngeal quadrivium, made of 4 valves: velopharyngeal sphincter, glosso-velopharyngeal sphincter, glottic sphincter, upper esophageal sphincter

- Muscular cavity (pharyngeal constrictors): superior, middle and inferior

- Cricopharyngeal muscle, which behaves as the upper oesophageal sphincter and has to relax during swallowing.

Front 44

Swallowing: structures involved

Back 44

- Oral Cavity

- Pharynx (rhinopharynx, oropharynx, hypopharynx)

- Larynx

- Esophagus

Front 45

Neurology of swallowing

Back 45

The swallowing process has a complex neurologic control, in which both central (motor-sensory cortex, limbic system, brainstem, hypothalamus) and peripheral (ascending and descending pathways provided by several cranial nerves) play a fundamental role.

- Hemispheric control (cortical and subcortical): control of the ORAL phase: initial, voluntary stage of swallowing.

*Motor-sensory: controls motor acts in a coordinated way thanks to the afferent information coming from the oropharyngeal mucosa and muscles.

*Limbic system: conserves an archaic memory of innate actions and is connected to emotions (e.g. fear to swallow some bitter foods because they are perceived as poisonous)

*Hypothalamus: hunger centre.

- Brainstem control: the voluntary starting of swallowing is not necessary, swallowing can be involuntarily evoked by a reflex centre of deglutition situated in the caudal part of pons and bulb, where the motor nuclei of CN V, VII, IX, X, XI, XII are located. It corresponds to the PHARYNGEAL AND OESOPHAGEAL PHASE of swallowing.

- Peripheral: ascending and descending pathways, with cranial nerves and spinal roots.

Front 46

Phases of swallowing: Extraoral

Back 46

Vision of food -> stimulation of taste buds and other receptors (e.g. mechanoreceptors in oropharyngeal mucosa) -> salivation

Front 47

Phases of swallowing: Oral preparatory

Back 47

Food is in contact with the tongue and the different tastes are appreciated. Its duration depends on the food consistency, taste, alimentary circumstances, ambient, hunger, motivation.

It’s a voluntary phase, whose aim is to transform the food in an appropriate bolus for swallowing, mixing it with saliva. The tongue collects the food particles and keeps them in contact with the middle of the palate.

Front 48

Phases of swallowing: Oral

Back 48

Transport of the bolus towards the pharyngeal isthmus. The tongue moves up and backwards, keeping its contact with the palate and squeezing the bolus towards the pharynx.

This phase ends when the bolus goes through the palatal pillar. It lasts 1 sec.

Lips closure (orbicularis)

Hyperbuccal tone (buccinators)

Tongue motility

Mastication (masseter, temporalis, internal and external pterygoid)

Retraction of the base of the tongue (hyoglossus, styloglossus, palatoglossus)

Velum-pharyngeal closure (elevator of the palate, superior constrictor of the pharynx)

Front 49

Phases of swallowing: Pharyngeal (in general)

Back 49

Iit’s involuntary, it’s evoked by the contact of the bolus with the sensitive receptors of the pharyngeal pillars, the lateral and posterior oropharyngeal walls and by the tongue base. The bolus moves through the pharyngeal quadrivium, which grants its proper direction.

Front 50

Phases of swallowing: Pharyngeal - velopharyngeal closure

Back 50

Pharyngeal narrowing (superior constrictors and palatal-pharyngeal muscles); Raising of the pharyngeal and intraoral pressure necessary for bolus progression; Start of the pharyngeal peristalsisis an important part of speech.

Importance in speech production: all phonemes in the English language with the exception of 3 (/m/, /n/, /ng/) are produced with oral airflow, meaning that the velopharynx should be closed.

The nasal phonemes (/m/, /n/, /ng/) are produced with nasal resonance, requiring that the velopharynx be open during their production. In describing the problem of hypernasal speech, differentiation between velopharyngeal mislearning, velopharyngeal incompetency, and velopharyngeal insufficiency (VPI) is important. Velopharyngeal mislearning is best described as incorrect closure of the velopharyngeal port in the nasopharynx as a result of articulation difficulties. Velopharyngeal incompetency is inadequate VPC secondary to a functional problem due to oral motor difficulties (eg, paresis, apraxia, dysarthria). VPI, in contrast, is inadequate closure of the velopharyngeal port resulting from a structural problem with the velum (eg, submucous cleft palate, shorted velum relative to the depth of the posterior pharyngeal wall, overt cleft palate). The effect of velopharyngeal incompetency or VPI on the patient's speech is usually the same; therefore, these 2 terms typically are used interchangeably or best referred to in general as velopharyngeal dysfunction (VPD)

Front 51

Phases of swallowing: Laryngeal closure

Back 51

Laryngeal elevation; Pharyngeal dilatation;

The bolus goes down to the hypopharynx and at the same time the crico-pharyngeal muscle relaxes.

Exclusion of the upper airways: the vocal cords are adducted (central inhibition of respiration); the larynx rises; the tongue base is over the larynx; the epiglottis is pushed backwards.

During swallowing there is apnoea. Interruption of the expiratory phase during the respiratory cycle (never in inspiration!)

90% or the swallowing act is made during expiration.

After swallowing, the respiratory cycle restarts with an expiration

Front 52

Phases of swallowing: Bolus propulsion

Back 52

• The tongue moves through the pillars and reaches the posterior pharyngeal wall

• The maximal laryngeal closure is obtained immediately before the detachment of the tongue base from the posterior pharyngeal wall

• The pharyngeal peristalsis begins with the synergic action of the pharyngeal constrictors

• Narrowing of the pharyngeal caliber

• Bolus progression toward the hypopharynx

Front 53

Phases of swallowing: Esophageal

Back 53

Begins when the bolus moves through the UES and ends when it passes the LES; it lasts 8-20 sec.

The peristaltic waves are generated by the involuntary contraction of the esophageal musculature.

Front 54

Dysphagia

Back 54

Swallowing is a complex motor sequence, and can result as a consequence of:

- Functional problems: neurological, muscular, metabolic pathologies or can be psychogenic

- Mechanical problems: benign, malignant oropharyngolaryngeal pathologies and surgical outcomes.

Front 55

Oropharyngeal dysphagia

Back 55

Oropharyngeal dysphagia arises from abnormalities of muscles, nerves or structures of the oral cavity, pharynx, and upper esophageal sphincter.

It can be moderate to very severe (as severe as to give a complete inability to swallow). It can even be life-threatening.

COMPLICATIONS can be:

- Decreased effectiveness of swallowing, malnutrition and dehydration

- Decreased safety of swallowing, choking, aspiration, aspiration bronchopneumonia

It is present in 30% of stroke patients; 52-82% of parkinsonian patients; 40% of myasthenic patients, 84% of Alzheimer’s patients, 60% of institutionalised patients.

It is the first symptom in 60% of ALS patients.

Front 56

Oropharyngeal dysphagia: signs and symptoms

Back 56

- Difficulty in beginning swallowing

- Cough and choking during swallowing

- Food “standing in the throat”

- Hyper-salivation

- “wet voice”

- Velar incompetence

- Weight loss

- Dysphonia

- Dysarthria

Front 57

Oropharyngeal dysphagia: evaluation

Back 57

Clinical:

- History, physical and neurological evaluation

- Evaluation of language and cognitive functions

- Bedside: Water test: measure of the time employed to swallow 150 ml of water in the sitting position. It is a simple and repeatable test. Positive: speed of swallowing < 10 ml/s. (normally > 10 ml/s)

Instrumental:

- FEES: Functional endoscopic evaluation of swallowing.

It has 5 phases:

- Observation of the anatomy of the UADT -> Integrity and trophism

- Observation of the motility and sensitivity of the pharyngolaryngeal tract -> motility of the tongue base, pharyngeal walls, arytenoids + sensitivity of he tongue base, aryepiglottic folds, vocal cords, epiglottis

- Observation of the secretions and their management -> site, nature, quantity, efficacy of the clearing manoeuvres

- Evaluation of swallowing of foods ->solid, semisolid, liquid; upper or lower position of the fiberscope

- Observation of the effects of the facilitating manoeuvres or postures

Advantages: easy, almost 3D vision, possibility of bed-side examination, not obliged pt position, repeatable as many times as necessary, possibility to prolong examination (to evaluate fatigability), immediate evaluation of the efficacy of the dietary modifications and /or of the facilitating postures, guarantees a visual feedback (thanks to the recordings), low cost.

Disadvantages: only partial evaluation of the oral phase and incomplete study of the sole pharyngeal phase (deglutitory white-out)

- Electrophysiologic evaluation: Carried out by positioning two surface electrodes at the level of the suprahyoid muscles and a transducer at the level of the inter-cricothyroid membrane. A needle is then positioned at the level of the UES to evaluate its relaxation.

- Videofluoroscopy: Videorecording of the fluoroscopic image obtained after swallowing of a contrast medium in different volumes and viscosities, with a sequence of lateral and antero-posterior positions.

Advantages: - Real time study of the whole act of swallowing - Optimal evaluation of aspiration

Disadvantages: - Radiation exposure - Expensive procedure - Bidimensional evaluation (underestimation of the stasis of saliva) - Limited number of observations (unable to evaluate fatigability) - Not feasible in bed-patients

Physical examination:

- Symmetry of the oro-facial musculature

- Adequate closure of the lips and mandible

- Motility and force of the tongue

- Inspection of the oral cavity and oropharynx

- Evaluation of the reaction to stimulation of the pillars

- Symmetry and position of the soft palate at rest during phonation

- Pharyngo-laryngeal elevation

- Efficacy of the cough reflex

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Neurogenic dysphagia: Parkinson's

Back 58

• Chewing: incoordination of the tongue movements. “Rocking and rolling“ festinating-type motion

• Incomplete laryngeal closure: typical immobility of the epiglottis (intra-swallowing aspiration)

• Reduced pharyngeal peristalsis: with the presence of pharyngeal residue (post-swallowing aspiration)

• Delay of the swallowing reflex: dysfunction of the crico-pharyngeal m.

• Decrease of the frequency of the automatic acts of swallowing of saliva: salivation

• “Start hesitation” in pts. with L-Dopa

Front 59

Neurogenic dysphagia: Stroke

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- Severe delay of the swallow trigger: pre/intra-swallowing penetration/aspiration

- Pharyngeal residue: post-swallowing penetration/aspiration

- Frequent aspiration of liquids: aspiration bronchopneumonia.

Minimal and repeated activations of the submental/suprahyoid musculature (insufficient amplitude and duration of the EMG signal).

Very low amplitude and scattered appearance of the elevation and backward flexion of the pharyngo-laryngeal structures.

Absence of the inhibitory pause of the cricopharyngheal muscle.

Scarce activation of the submental/suprahyoid musculature; prolonged activation of the pharyngolaryngeal structures with prolongation of the time interval between the propulsive oral phase and pharyngeal phase.

Incomplete relaxation of the cricopharyigeal muscle during the hypopharyngeal phase of swallowing.

Improvement of the pharyngeal phase of swallowing (reappearance of the inhibitory phase of the UES).

Wallenberg: brainstem -> vagus damage: recurrent laryngeal palsy + no cricopharyngeal relaxation -> food gets into the pharynx but not into the oesophagus -> post-swallowing aspiration -> food into the pharynx.

Front 60

Neurogenic dysphagia: ALS

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- Progressive degeneration of the first 3 phases of swallowing.

- Prolongation of the activation of the pharyngeal phase in the voluntary swallowing, but the pharyngeal phase is activated only as an involuntary reflex.

- Since there is no voluntary swallowing, the patient needs gastrostomy

Front 61

Neurogenic dysphagia: Alzheimer

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- Progressive loss of the motor scheme of swallowing -> inability to trigger the oral phase; activation occurs only in the pharynx

- Persistence of the archaic movements only, e.g. suction, bite-reflex, etc.

Front 62

Neurogenic dysphagias: treatment

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Speech therapy: It aims at preserving residual activity.

Compensatory strategies: - Facilitating postures - Modification of food consistency (no mixing of consistencies)

Rehabilitation strategies: - Exercise to reinforce the oro-facial and suprahyoid musculature - Exercises to reinforce and improve the elevation and closure of the larynx during swallowing - Stimulation of the swallowing reflex

Enteral feeding

- NG tube: if aspiration > 10% of bolus, if bolus transit is delayed on VFS (> than 10 sec), if easy fatigability.

- Gastrostomy: preferable when a brief resolution of dysphagia is not possible, to propose in advance in pts with motorneuron diseases (in order to guarantee an adequate caloric intake and to preserve muscle mass), better tolerated than the NG tube, guarantees a better food intake.

- Jejunostomy: in patients with GORD, aspiration bronchopneumonia with NG-tube feeding; less physiologic (especially for insulin-secretion), continuous feeding, worse quality of life.

Botulinum toxin: it is used when there is a hypertone as an alternative to myotomy, results are visible after some days/weeks and are transient. It is carried out under EMG-monitoring.

Front 63

Post-surgical dysphagia

Back 63

Different resections give different damages.

- Impairment of bolus preparation: lips, tongue

- Impairment of the propulsive forces: tongue base, pharyngeal muscles

- Impairment of the bolus transit: pyriform sinuses, UES

- Impairment of the pharyngolaryngeal sensitivity: section of the superior laryngeal nerves

- Impairment of the protective mechanisms: epiglottis, tongue base, vocal cord motility, larynx elevation

Another factor to consider is radiotherapy, which can cause:

- Mucositis

- Xerostomia

- Tissue fibrosis, with reduction of motility of the oral and pharyngeal muscles -> limited larynx elevation.

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Anterior Resections

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Impairment of the oral phase:

- Lips: labia incompetence -> loss of food from the mouth

- Floor of the mouth: impairment of the oral preparatory phase, prolongation of the oral transit

- Mandible (anterior resection -> resection of the genioglossus and of the suprahyoid muscles): infero-posterior position of the tongue + reduced elevation of the larynx

- Mobile tongue: reduction of the lingual movements (problems with speech) + loss of sensitivity of bolus position

- Hard palate: loss of contact between the tongue and the palate

Front 65

Posterior resections

Back 65

Impairment of the pharyngeal phase:

- Tongue base: loss of bolus progression into the pharynx

- Retromolar trigone-anterior palatine pillars: reduction of pharyngeal propulsion, possible passive bolus progression into the pharynx before the pharyngeal swallow trigger -> pre-swallowing aspiration

- Soft palate: rhinopharyngeal reflux and insufficient oral pressure to guide bolus propulsion into the pharynx

- Pharyngeal wall, especially posterior: pyriform sinus residue + risk of post-swallowing aspiration (the pharyngeal residue enters the larynx when it opens at the end of the pharyngeal phase of swallowing).

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Reconstruction

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We have to perform reconstruction in order to guarantee function.

For the inferior lip we can use a free flap or a pedicled flap.

For the floor of the mouth, we can use a thin flap: fasciocutaneous flap from the forearm, or the platysma or a FAMM (fascial artery musculomucosal???) flap.

To reconstruct the mandible, we can take the iliac crest of the fibula and model to bone in order to get the shape that we need. As an alternative to bone, we can use a titanium plate, covered with the pectoralis major muscle. If the anterior part of the mandible has been resected, reconstruction is necessary, while in case the posterior part of the mandible is involved, stabilisation may be enough. As for the mobile tongue and floor of the mouth, we can use a free flap from the forearm of the thigh.

A RFFF (radial forearm free flap) can be used for the reconstruction of the hard palate, the lateral and posterior wall of the oropharynx and the soft palate.

As for the larynx, there are two kinds of possible resection:

- Partial laryngectomy, in which you have to preserve one mobile crico-arytenoid unit for speech and swallowing

- Circumferential laryngectomy, in which you have to reconstruct the continuity. If you resect the hypopharynx, reconstruction can be carried out using an RFFF, a pectoralis major flap, a lateral thigh flap or a jejuna flap.

The jejunum is tubular and has intrinsic peristalsis, factors which make it optimal for pharynx reconstruction, it needs few suture lines (< intraoperatory risk), its diameter is similar to the oesophageal diameter, it can be considered sterile and relatively devoid of intrinsic pathologies and the mesentery can be used to cover the big vessels. Furthermore, a segment of the jejunum can be exposed through the incision in order to check for post-operative problems.