Unilateral Vocal Fold Paralysis

TITLE: Unilateral= Vocal Fold Paralysis
SOURCE: Grand Rounds Presentation, University o= f Texas Me= dical Branch,
Departmentof Otolaryngology<= br> DATE: February 25, 2011
RESIDENT PHYSICIAN: Naren Venkatesan M.D
FACULTY PHYSICIAN: Michael Underbrink MD
DISCUSSANT: Michael Underbrink MD
SERIES EDITOR: Francis B. Quinn, Jr., MD
ARCHIVIST: Melinda Stoner Quinn, MSICS

&q= uot;This material was prepared by resident physicians in partial fulfillment of educational requirements established for the Postgraduate Training Program = of the UTMB Department of Otolaryngology/Head and Neck Surgery and was not intended for clinical use in its present form. It was prepared for the purp= ose of stimulating group discussion in a conference setting. No warranties, eit= her express or implied, are made with respect to its accuracy, completeness, or timeliness. The material does not necessarily reflect the current or past opinions of members of the UTMB faculty and should not be used for purposes= of diagnosis or treatment without consulting appropriate literature sources and informed professional opinion."

Introduction

Unilateral Vocal Fold Paralysis is a disease oft= en encountered by Otolaryngologist. Its causes are multifold so an understandi= ng of these causes is necessary for both diagnosis and treatment. While patien= ts may be referred following a surgical complication, other cases of vocal fold paralysis present to the clinic as voice changes.

Brief Outline

In this discussion, we will begin with a brief r= eview of anatomy and physiology of the laryngeal structures and involved neurolog= ical structures. Then,

Anatomy

Neurologically, the true vocal folds are enervat= ed by the Recurrent Laryngeal Nerve and the Superior Laryngeal Nerve. Nerve fibers begin at Cerebral Cortex and descend through the Internal Capsule. From her= e, these fibers synapse at the Nucleus Ambiguus in the Medulla. The Nucleus Ambiguus manifests its actions thorugh the cranial nerve X, the Vagus Nerve. The Vagus Nerve descends bilaterally along with the Common Carotid Artery a= nd Internal Jugular Vein.

The Vagus Nerve gives off both the Superior Lary= ngeal Nerve and the Recurrent Laryngeal Nerve. Of these, the SLN branches into a internal and external branch. The Internal Branch provides sensation to the larynx above the level of the TVF while the Recurrent Laryngeal Nerve provi= des sensation below. The Extrenal branch of the SLN provides enervation to the Cricothyroid muscle alone. The Recurrent Laryngeal Nerve provides enervatio= n to the Posterior Cricoarytenoids, Lateral Cricoarytenoids, Thyroarytenoids, and the Interarytenoid. It is important to note a couple reminders regarding the muscles. The Posterior Cricoarytenoids is the only abductor of the TVFs. Al= so, while most muscles are paired, the Interarytenoid is not paired and shares enervation from both Left and Right RLN.

With regards to anatomy, it is important to also remember the different paths of the RLN on the left and right side. On the left, the RLN travels into the mediastinum where it loops around the Arch o= f the Aorta prior to penetrating the larynx thus making the left RLN more vertica= l at its point of penetration. The Right RLN loops around the Subclavian, and du= e to this shorter path, it returns and penetrates more horizontally. This differ= ence due to embryological changes following the Right 6^th arch vessel becoming the Subclavian artery while the Left 6^th arch vessel becomes the Arch of the Aorta.

An anatomical anomaly may occur with regards to = the recurrent laryngeal nerve. Approximately 5 out of 1000 people have a nonrecurrent laryngeal nerve on the right. A nonrecurrent laryngeal nerve occurs only on the right, except in the rare case of situs inversus. It branches from the vagus nerve at the level of the cricoid cartilage and ent= ers the larynx directly, without looping around the subclavian artery. This ano= maly occurs in conjunction with a retroesophageal right subclavian artery.

At this point, please refer to the PowerPoint presentation, as the next several slides demonstrate the muscular anatomy of the larynx. It is important to remember the penetration sites of the SLN and RLN to aid in both surgical procedures and for understanding regarding poss= ible injuries. The internal division of the SLN penetrates the thyrohyoid membra= ne with the laryngeal artery and supplies sensory innervation to the larynx. T= he external division of the SLN provides motor innervation to the cricothyroid (CT) muscle.

At this point, our basic anatomy has been review= ed but a quick note a few terms and processes. First, defining the terms paraly= sis and paresis is important. Paralysis refers to complete immobi= lity of a muscle although muscle tone may be noted secondary to re-innervation. = Paresis means hypofunction or hypomobility secondary to neurologic injury.

Having mentioned re-innervation, a further expla= nation here is needed. The concept of re-innervation is also referred to as= Synkinesis.

Paralysis first begins with axonal injury. Follo= wing this injury, there is Wallerian Degeneration, which we recall as step by st= ep breakdown of the axon distal to the injury. Following this breakdown, there= is regrowth as the proximal stump sends out nerve fibers to reconnect. However= , in this step, fibers from the proximal neuron may reach any distal site, imply= ing that adductor nerves may innervate abductors (PCA) and abductor nerve fibers may innervate adductors. While the TVF will remain paralyzed, the reinnerva= tion helps by providing neurological stimulation in order to maintain muscle ton= e. At this point, the level of regeneration and subsequent strength of the abductors and adductors helps determine the final position.

On the final note regarding anatomy, there are generally 4 terms used to refer to = the position of the TVF. They are the following:

· median (midline),

· abducted (lateral),

· paramedian (halfway), and

· intermediate (any position between the midli= ne and halfway).

&nb= sp;

Etiology of TVF Paralysis

TVF paralysis has many causes, but five causes c= over nearly 75% of cases. In order of frequency, these are Malignancy (25%), Surgical Trauma (25%), Non-surgical Trauma (11%), Intubation, (7%) and Neurological Disorders (7%). In approximately 20% of cases, the cause is technically listed as Idiopathic, although often a future cause is often discovered. Now, we will go through each of these topics with some in more complex detail.

Malignancies

As otolaryngologists, laryngeal and thyroid canc= ers are readily encountered and easily remembered as causes for TVF paralysis. However, several other cancers can cause paralysis, usually through compres= sion from mass effect. The Left TVF is most affected due to its descent into the mediastinum as it loops around the Arch of the Aorta. Pulmonary cancers, especially bronchogenic carcinomas, which invade into the mediastinum are t= he most common of malignancy-related causes of TVF paralysis. Other malignanci= es causing paralysis include the following: Mediastinal (Thymoma, Teratoma, Lymphoma), Carotid Body Tumors, and a Paraganglioma near the skull base.

Iatrogenic Surgical Trauma

Surgical trauma can arise following a number of operations that occur in the neck where the RLN is at risk. The most common Otolaryngologic surgery during which trauma occurs is a Thyroidectomy. While all surgeons aim to trace the path of the nerve prior to removal of the thyroid, it is not uncommon for the route of the RLN to be altered and tort= uous in the case of a large Goiter. While this injury can occur during removal o= f a thyroid for Thyroid cancer, anecdotal evidence tends to believe in the idea that a large goiter removal is more difficult and has an increased risk of damage to the RLN.

Typical rates of injury of the RLN in Thyroid su= rgery can range anywhere from 0.3% to 13.2%. This rate make Thyroidectomies the surgery with the second highest rate of damage to the RLN. Anterior Cervical Spine Surgery is currently viewed as the most common surgical cause of inju= ry to the RLN. Rates for injury following this neurosurgical procedure range f= rom 2% - 21.6%. Thoracic Surgery, including Aortic Arch Repair, Esophagectomy, Pulmonary Resection, and Mediastinoscopy, poses a significant risk to the R= LN, although these percentages are quite low. Finally, vascular surgery in the neck, namely Carotid Endarterectomies, can also cause damage to the RLN, bu= t again, the rate of injury in these procedures is minimal at best.

Intubation

Intubation can also serve as a cause for RLN inj= ury, although this damage occurs through different means. Referring to a cross-section of the larynx, remember that the Anterior Rami of the RLN pie= rce the larynx in the subglottis just at the level below the TVFs. Injury throu= gh intubation is though to occur secondary to excessive cuff inflation along w= ith placement of the cuff in this area. Further, it is likely that this compres= sion only truly leads to damage following lengthy surgeries, those upwards of at least 1-2 hours.

Neurovascular Diseases

At this point, we will touch on a couple of neurovascular syndromes which may present as TVF paralysis in addition to o= ther findings. At this point, refer to a picture of the brainstem. Reviewing anatomy, the Vertebral arteries proceed superiorly where they unite to form= the Basilar artery. Along the way, they branch off into several vessels which supply the brainstem – the Superior Cerebellar Artery, Anterior Infer= ior Cerebellar Artery (which runs just inferior to the pons), and the Posterior Inferior Cerebellar Artery (which runs at the level of the medulla). These vessels being quite miniature are easily susceptible to strokes.

The most common brainstem stroke is of the Poste= rior Inferior Cerebellar Artery. The manifestation of the patient is known as PI= CA syndrome, Wallenberg’s syndrome, or Lateral Medullary Syndrome. It of= ten presents as Vertigo, Ipsilateral Hemiataxia, Dysarthria, Ptosis, Miosis, an= d/or Hoarseness. These patients are often more disturbed by the Vertigo and Hemiataxia, but rarely, hoarseness can be the first symptom noted.

The second most common brainstem stroke is that = of the Anterior Inferior Cerebellar Artery. This usually manifests as Vertigo, Unilateral Ipsilateral Deafness (secondary to Laryrinthine Artery Ischemia), Ipsilateral Facial Weakness and Ataxia, and hoarseness. Again, Hoarseness is not likely their first manifestation, but one should be prepared to note th= is syndrome can present in this way.

Neurological Diseases

A vast array of neurological disorders can prese= nt with voice changes and may cause vocal fold paresis and paralysis. While th= is list of diseases is extensive, in the following paragraphs, we will discuss= a few of these diseases and their presentation.

Multiple Sclerosis is an autoimmune disorder whi= ch occurs secondary to a response directed against Myelin, the protein which f= orms the sheath around nerves. It typically affects women in their 20s-40s. While not uncommon, the disease remains a mystery with regards to several aspects. First, the exact cause is unknown, but viral, genetic, and environmental factors have been implicated. It typically presents with either vision chan= ges or muscle weakeness of the extraocular muscles. It eventually progresses to include complete loss of muscle control and function. There are two general forms, a relapsing episodic form and chronic progressive form. It is import= ant to realize this as patients may present in between episodes or may notice s= ome symptoms between episodes of worsening. Hoarseness is often associated and = may even be the first symptom.

Amyotrophic Lateral Sclerosis, or Lou GehrigR= 17;s Disease, is one that affects upper and lower motor neurons. As such, it cau= ses complete atrophy of muscles due to the loss of neurological stimulation. It tends to affect breathing and swallowing functions first with several of th= ese patients requiring a tracheotomy tube early in the disease process. Again, these patients may also present with voice changes and demonstrate paresis = and paralysis of the laryngeal musculature.

Syringomyelia is a fairly rare disease which occ= urs secondary to the formation of a cyst in the spinal cord. While this cyst may arise at any location of the spinal cord, it has more devastating effects w= hen located high in the cervical region or even in the brain stem. Due to mass effect, patients can develop TVF paralysis, ipsilateral tongue wasting, and ipsilateral facial sensory loss secondary to compression of cranial nerve 5. When the cyst is located in the brainstem, it is also referred to as syringobulbia. It is typically a disease that spares proprioception, pressu= re, vibration, and touch intact.

Myasthenia Gravis is an autoimmune disorder occu= rring secondary to antibodies directed against Acetylcholine receptors at the post-synaptic junction. It often presents as fluctuating muscle weakness and fatigability. It typically affects muscles that are small and used repetitively. As such, extraocular muscle weakness is prominent and often t= he first sign. As with most autoimmune disorders, it is typically seen in fema= les who present with complaints that begin to occur in the afternoon. There are five classes for MG ranging from minimal eye weakness to severe with associ= ated limb abnormalities or bulbar abnormalities affecting the cranial nerves. Of clinical note, a thymoma, if present, should be excised as there is a strong correlation between MG improving if a thymectomy.

Guillain-Barre disease, also known as Acute Inflammatory Demyelinating Polyneuropathy, is a disease of ascending paraly= sis which begins in the lower extremities. It is named for Georges Guillain and Jean Alexandre Barre – two French Neurologists. Usually, the disease = does not reach the facial muscles; however if cranial nerves are involved, it involves the lower cranial nerves. By attacking, the disease causes demyelination. It often follows a respiratory or gastrointestinal infection with several bacteria (ex. Campylobacter) and viruses implicated. 30% of affected patients require mechanical ventilation due to loss of respiratory capacity.

Parkinson’s disease is a degenerative cent= ral nervous system disease which occurs secondary to the loss of Dopamine. It w= as initially presented by Dr. Parkinson in an essay on Shaking Palsy. The typi= cal traits of Parkinson’s disease are the shuffling gait, muscle rigidity, and resting “pill-rolling” tremor. However, patients may present initially with a weak and breathy voice along with sluggish articulation. T= his is characterized as laryngeal bradykinesia. When performing flexible laryngoscopy, one may note weak vocal fold adduction. Further, the vocal fo= lds may be thinned and bowed (similar to a paretic view) secondary to atrophy of the vocalis. Patients may also have strained voices similar to that seen in spasmodic dysphonia.

Patient Work-Up

The patient work-up begins as with any disease &= #8211; a thorough history and physical. Due to knowledge of the aforementioned diseases, it is important to question a patient on all symptoms and complai= nts in order to rule out any neurological disorders. Also, patients should be questioned for having rheumatoid arthritis or gout as these can cause depos= its or changes in the joints. To rule out he major cause of TVF paralysis, one should ask all patients with regards to smoking/alcohol use, past surgical history, trauma, and recent infections.

When speaking with patient, it is important to t= ake mental note of the patient’s voice. Features that suggest neurological involvement include vocal fatigue, vocal tremor, weak or breathy voice, voc= al strain, vocal stoppage, altered resonance, acquired dysarthria, and associa= ted dysphagia.

After a thorough history, the physical exam alon= g with flexible laryngoscopy is extremely important. While all parts of the physic= al exam are relevant, evaluation of the cranial nerves is particularly relevan= t as several of the aforementioned diseases present as a constellation of various issues. As a quick reminder, evaluating the vagus nerve can be performed by checking for palate elevation and uvular deviation – uvula will devia= te away from the side of the lesion. Flexible laryngoscopy is integral in evaluating the patient’s vocal cord function. In addition to viewing = the entire larynx for obviouc pathology, one should also view the movement of t= he vocal folds. This is done by having the patient say “ee” then having them sniff. The position of the arytenoids is also important during = the exam.

Another exam which can be performed in the clini= c to help in the work-up of vocal fold paralysis is the Laryngeal EMG. This test, laryngeal electromyography, aids the physical by demonstrating the level of muscle activity. Due to easier access, the thyroarytenoid muscle is often selected and tested. Three principles are important to remember when viewei= ng the EMG. First, spontaneous activity detected is a sign of fibrillarion and implies denervation. Second, recruitment is a principle of muscle with nerve innervation. Muscle that is repetitively stimulated responds with an increa= se in the number and rate of the motor units. This is a sign of normal functio= ning muscle or reinnervated muscle. Lastly, motor units on the EMG can occur in small groups but usually less than 3 in one group. If more than 3 are prese= nts, this is a sign of an injury. The value of the Laryngeal EMG, while indicati= ng the activity of the muscle, is to also rule out cartilage or joint dysfunct= ion as a cause for the lack of movement of the vocal fold.

As a quick aside, we will touch on arytenoid car= tilage dislocation here. This is often noted in fiberopticl laryngoscopy by viewin= g an anteriorly overhanging arytenoid. This is an uncommon diagnosis but does oc= cur following neck trauma or intubations. Another thing noted on exam is the changes in the level of the vocal folds when the patient phonates. Finally,= it is also noted by the absence of the “jostle” sign. The jostle s= ign refers to the movement of one arytenoid cartilage which occurs secondary to being “jostled” by the opposite arytenoid cartilage during clos= ure of the TVFs. Again, this diagnosis can be ruled in or out by findings on the Laryngeal EMG.

Work-up here should also continue with a few radiological tests. An MRI of the brain, CT Neck, CT Chest, and CXR would n= ot be unreasonable in trying to identify the cause. However, several authors suggest that a CT Neck/Chest would be adequate unless one feels that a neurological issue is present and in that case a CT Neck and MRI brain woul= d be recommended.

True Vocal Fold Paralysis in Children

Following laryngomalacia, TVF paralysis is the #2 cause of stridor and #2 most common congenital anomaly in children. It is typically not bilateral, but if so, then there is often a central nervous system cause. An example of bilateral TVF paralysis is a child is Arnold Ch= iari malformation, where herniation of the cerebellum and brainstem can cause compression of the Vagus Nerve. Other causes of hydrocephalus in children m= ay also cause compression of the nerve.

In children, causes are typically secondary to b= irth trauma, with blunt trauma, surgical injury, mediastinal masses, and iatroge= nic causes also linked. Surgical causes are predominantly following cardiothora= cic surgeries – especially Patent Ductus Arteriosus Ligation and Tracheo-Esophageal Fistula Repair. Children often present with stridor, bre= athy cry, feeding difficulties, and aspiration. Also, it has been reported that somewhere from 16 to 64% of children recover from paralysis. Therefore, watchful waiting is often the best course with possible placement of a tracheotomy if needed.

Surgical Management

First, there are several decisions to address pr= ior to surgery. As stated, many cases of unilateral TVF paralysis resolve so a fair amount of waiting is needed prior to deciding to perform a case. While the amount of time to wait is debated, most authors suggest 12 months after inj= ury to being an acceptable amount of time. Further, children tend to heal even after delayed periods.

The occurrence of the recovery is greater in chi= ldren, and some reports say as high as 50% recover. The range for recovery in chil= dren is quite long with some case reports demonstrating recovery after 10 years. However, the mean tends to be within 12 months with another peak around 2 y= ears if the paralysis is secondary to neurological causes. In children, injectio= ns are favored as this will give the most hope in case there is future recover= y. Most injection materials last for several months – with calcium lasti= ng the longest – upto about 1 year.

Surgical management can be broken into three main categories of procedures:

· = Injection Thyroplasty

· = Framework procedures

· = Reinnervation procedures

Injection thyroplasty is often chosen due= to the fact that is temporary, done easily, can be repeated, and does not prec= lude the chance for recovery. Many materials can be used. Teflon was initially u= sed but is no longer in use due a granulomatous inflammatory reaction that it caused. Collage and Gelfoam have also been used but also have fallen out of favor. Fat grafts remain frequently used for several factors. Fat is easily re-absorbed in 3-4 months causing minimal trauma, and re-absorbtion can lea= d to some long-lasting effects. Also, fat is easily harvested.

Calcium Hydroxyl Apatite is a biologically inert material created by Radiesse and in use since 2003. In comparison to fat, collagen, or fascia, this substance lasts for a much greater amount of time with no studies showing negative scarring or permanent complications. A stu= dy from 2010 by Carroll and Rosen showed that in 22 patients with UVFP, approximately 0.5 mL was needed for injection and this persisted for an ave= rage of 18 months as noted by voice testing.

Hyaluronic acid gels are either animal or bacter= ial derived versions of naturally occurring extracellular matrix GAGs. This same material is found in the TVF lamina propria. While it is believed that it should be able to replace the lamina propria, it has shown poor results. Studies suggest that it actually worsens vocal fold vibration if placed superficially. It tends to last from an average of 6 months to even 1 year = in some studies.

Carboxymethylcellulose can be used a preview mat= erial because as an injection it only lasts for 2-3 months but can give an idea of what can be achieved by an injection. It does not cause any scarring. Also,= it has no risk of biologic infection transmission. It can sometimes be coupled with calcium hydroxyl apatite.

Indications for injection thyroplasty are severa= l. First, their temporary nature is good for patients in whom there is uncerta= inty regarding the state of paralysis. This is also an easy procedure that can be done in the office as an out-patient. It benefits those patients with mild glottic gap (1mm). Finally, it requires less patient compliance. Contraindications include a posterior gap and glottic gaps greater than 3 m= m. While an injection thyroplasty can help these patients, there is not as muc= h of an effect posteriorly.

Framework procedures include medialization laryngoplasty and arytenoid adduction or arytenoid pexy. Medialization laryngoplasty is a procedure in which a small window in created in the thyr= oid cartilage. An implant of some sort – examples include GoreTex Strips, Silastic strips or blocks, or hydroxyapatite – is placed through the window to create stability and medialize the TVF. The benefits of this procedure are that it is reversible, can be “fine-tuned”, and augments the TVF in all 3 dimensions (anterior-posterior, superior-inferior, and medial-lateral). This procedure is performed under local anesthesia so = fine adjustements can be made the size of a block that is inserted to increase t= he Gore Tex strip. There has been no differences shown as far as patient outco= me with regard to use of different materials although many surgeons tend to be= gin the operation with a block and then use strips for adjustment.

Arytenoid surgery is done as an adjunct to other procedures are rarely if ever alone. Arytenoid pexy consists of the placeme= nt of a suture anchoring the muscular process of arytenoid to thyroid cartilag= e. This procedure achieves 3 things with respect to Vocal Process – lowe= rs position, medializes & stabilizes the TVF, and

Discussant’s Rem= arks 2011-02-25 Vocal Cord Paralys= is by Dr. Underbrink

That was a ve= ry good presentation Dr. Venkatesan, very thorough and included a discussion of a l= ot of causes for paralysis other than the most common which was nice because we tend to focus on or have tunnel vision with respect to what we see on exam = and not necessarily incorporate what we see among the more unusual findings. With respect to the treatment of t= hese, I like to think of it along the lines you did. There are temporizing procedures s= uch as injection medialization and there’s permanent: when you’re manipulating the framework, doing an arytenoid pexy which is what you described, or arytenoid adduction which is a little bit different.

And then there’s of course re-innervation where you actually know that you’re going to sacrifice a nerve, and so you have no place to go. The thyroplasty is sort of inbetween. It’s a rever= sible procedure. You can place a bl= ock and the patient that might recover, who’s a professional voice user who w= ants something more permanent doesn’t necessarily have to be removed and w= ill recover and not lose too much function with just a block as long as you don’t manipulate the joint.

It’s al= so interesting that you bring up laryngeal EMG. That’s also very relevant in= that as you showed some of the more subtle presentations that you’re looki= ng at an arytenoid is sort of overhanging and the level of which you can’= ;t really make out on a two-dimensional picture endoscopy but that’s also similar to what happens on a dislocation and you’re right, I have a patient that’s recent to the clinic that’s going to have a laryngeal EMG because that can be easily diagnosed and that would indicate a different procedure.

I agree that = I like to use injection medialization in children that have a problem that hasn’t recovered or if they’re having some sort of dysphagia. Usually kids recover completely or recover some function like swallowing and don’t necessarily present w= ith the same symptoms as an adult with regard to dysphagia or difficulty feedin= g, sometimes not much of an issue. Generally they maintain hoarseness and might need a better functional outcome which is the reason to go ahead and do injection medialization.

Many times wi= th respect to the re-innervation procedure, it’s a great procedure for w= hen you know you’re going to cut the nerve and you have a paraganglioma.<= span style=3D'mso-spacerun:yes'> Many times when you’re doing thyroid surgery which is a much more common surgery, and you close area, wh= en you go back to do the re-innervation, you almost can never find the stump of that nerve. It’s imposs= ible. So that the most common procedure I’ve been associated with or that I’ve done is taking a small c= up of muscle from where the ansa has innervated one of the strap muscles and actually implanting that through a thyroplasty and it usually takes as long= as you can implant it into the bed of the thryroarytenoid muscle. That provides just the tone and it’s amazing that after about three months the patient has to be will= ing to undergo three months of breathiness with no recovery until re-innervation occurs.

Yours was a v= ery good talk, overall very thorough. = Thank you.

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