Disorders of the Larynx and Videostroboscopy
Source: UTMB Grand Rounds Presentation
Date: April 8, 1998
Resident: Stephanie Cordes, MD
Faculty: Anna Pou, MD
Series Editor: Francis B. Quinn, Jr., MD
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In the last 10 years, scientific and technological advances have resulted in dramatic improvements in medical treatment of voice disorders. In the past many physicians considered hoarseness as a symptom of either cancer or an insignificant problem. Patients without laryngeal masses were either likely to be treated for allergies or told that there was nothing wrong. In the last several years, attention to a more extensive history and physical examination, augmented with new equipment and better understanding of laryngeal function, have increased physiciansí awareness of subtle problems in the head and neck that adversely affect voice, as well as laryngeal manifestations of distant or systemic disease. This new knowledge has changed the standard of care for all patients with voice complaints.
The laryngeal mechanism is subject to highly complex, extensive neural control; therefore, it is not surprising that disorders of the nervous system have effects on the voice. A wide range of neurological disorders can affect the phonatory function of the larynx, as well as its role in respiration and swallowing. Except for the more common problem of recurrent laryngeal nerve paralysis and the unusual, but disabling, entity of spastic dysphonia, neurologically based voice disorders until recently have been a neglected topic for both basic and clinical research in the fields of otolaryngology, speech pathology, and neurology. It is now more apparent that laryngeal dysfunction is a component of many neurological disorders and should be a critical consideration in patient assessment and management.
The larynx is a complex organ that functions as a biological valve for regulation of phonation, respiration, and swallowing. In the adult it is located in the anterior neck and connects the hypopharynx and the trachea. It lies between the third and sixth cervical vertebra anterior to the laryngopharynx, prevertebral muscles, and fascia. The upper poles of the thyroid gland are closely related to the inferolateral part of the larynx and the great vessels are located posterolaterally. Covering the larynx are the infrahyoid or strap muscles as well as superficial cervical fascia and skin.
The larynx arises primarily from the paired branchial arches III, IV, and VI, which contribute tissue of endodermal, mesodermal, and ectodermal origin. Development of the respiratory system usually begins during the third week of embryonic growth as an endodermal outgrowth from the foregut. The foregut differentiates into the pharynx, trachea, bronchi, and lungs, with the larynx serving as the conduit for air exchange between the pharynx and trachea.
The mesodermal layer provides muscles, blood vessels, lymphatics, bones, and cartilage of the larynx. Second arch mesoderm gives rise to the lesser horns and upper portion of the body of the hyoid bone. The greater horns and lower part of the body of the hyoid, as well as the common and internal carotid arteries, originate from third arch mesoderm. The thyroid and cuneiform cartilages, cricothyroid muscles, proximal subclavian artery on the right and aorta on the left arise from fourth arch derivatives. The sixth arch contributes the cricoid, arytenoid, and corniculate cartilages, all of the intrinsic laryngeal muscles except the cricothyroid, the ductus arteriosus on the left, and the pulmonary artery on the right. From ectodermal tissues arise two primary branches of the tenth cranial nerve, the superior and recurrent laryngeal nerves, derived from branchial arches IV and VI, respectively.
The larynx is composed of four basic anatomic units: skeleton, intrinsic muscles, extrinsic muscles, and mucosa. It comprises nine cartilages: three unpaired cartilages and three sets of paired cartilages. The unpaired cartilages are the thyroid, cricoid, and epiglottis. The paired cartilages consist of the arytenoids, corniculates, and cuneiforms, of which the arytenoids are most important. Even though the hyoid is not a part of the larynx, it is involved in movement of the larynx and therefore needs to be discussed. It serves as an attachment for numerous muscles of the tongue as well as some of the extrinsic muscles of the larynx. This allows it to play an important role in the movement of both structures.
The intrinsic laryngeal muscles are those that have both their origin and insertion within the larynx, where they play an important role in respiration and phonation. These muscles include the cricothyroids, the posterior cricoarytenoids, the lateral cricoarytenoids, the transverse arytenoid, the oblique arytenoids, and the thyroarytenoids. The cricothyroids are paired muscles that when contracted raise the pitch of the voice because the vocal folds are tensed. The posterior cricoarytenoids are paired muscles that when contracted open the glottis. These are the only muscles that abduct the vocal cords. The lateral cricoarytenoids are also paired muscles that act to pivot the vocal bands by rotating the arytenoids. They act as a vocal cord adductor. The unpaired transverse arytenoid approximates the two arytenoid cartilages and assists in closing the posterior portion of the glottis. The oblique arytenoids are paired muscles that also bring the arytenoids together for phonation. The paired thyroarytenoids compose most of what is known as the vocal fold. Their action is to allow the tight closure of the glottis and are probably active in raising the pitch and increasing vocal volume during phonation. The intrinsic muscles of the larynx serve to make possible the fine adjustments within the larynx that produce the various valving activities necessary for life preservation and voice production.
The extrinsic laryngeal muscles connect the larynx to other structures of the body. These muscles act to raise, lower, stabilize, and anchor the larynx, depending upon the requirements for speech at any precise moment. The omohyoid, sternohyoid, and sternothyroid act to anchor the larynx and lower it when necessary. The thyrohyoid, stylohyoid, digastric, mylohyoid, and geniohyoid act in conjunction with the middle and inferior constrictor and stylopharyngeous to elevate the larynx.
The vagus nerve, which contains motor, sensory, and secretory fibers innervate the larynx. At the level of the inferior ganglion of the vagus nerve, the superior laryngeal nerve originates and descends towards the larynx medial to the carotid arteries. The nerve divides into the internal and external branches. The internal branch pierces the thyrohyoid membrane along with the superior laryngeal artery to supply the mucosa of the epiglottis, the aryepiglottic folds, and the cavity of the larynx as inferior as the vocal cords. The external branch remains outside the larynx lying on the inferior constrictor muscle in close relationship with the superior thyroid artery and ends in the cricothyroid muscle, which it innervates. The rest of the cavity of the larynx as well as the remaining muscles is supplied by the recurrent laryngeal nerve. It enters the larynx posterior to the cricothyroid joint just inferior to the attachment of the inferior constrictor muscle. The nerve on both sides divides into an anterior and posterior branch either outside or inside the larynx. The anterior branch supplies the lateral cricoarytenoid, thyroarytenoid, and vocalis muscles. The posterior branch supplies the posterior cricoarytenoid and the interarytenoid muscles. The infraglottic space receives both sensory and secretory innervation via the recurrent laryngeal nerve.
The blood supply to the larynx arises from both the carotid and subclavian arteries. The superior thyroid artery gives rise to the superior laryngeal artery, which enters the larynx through the thyrohyoid membrane with the superior laryngeal nerve. It is always inferior to the nerve and may pass through a foramen in the thyroid cartilage. The inferior thyroid artery enters the larynx with the recurrent laryngeal nerve at the inferior border of the inferior constrictor muscle. These two arteries anastomose.
The human adult vocal fold consists of an overlying mucosa layer and a deeper thyroarytenoid muscle complex. The mucosa includes an outer stratified, nonkeratinizing squamous epithelium and an inner lamina propria. The superficial layer of the lamina propria, often referred to as Reinkeís space, consists mainly of amorphous material and few fibroblasts or elastic or cartilaginous fibers. The intermediate and deep layers of the lamina propria form the thickened tissue located at the free edge of the conus elasticus, known as the vocal ligament. These deeper layers consist of a higher density of fibroblasts and elastic and collagen fibers. This formation of layers allows for fluency of vibration of the epithelial cover over the vocal fold body. The activity generated resembles traveling waves of mucosa from the inferior to the superior surface of the vocal fold.
The physiology of voice production is complex. Volitional production of voice begins in the cerebral cortex. The command for vocalization involves complex interaction among brain centers for speech and other areas. The idea of the planned vocalization is conveyed to the precentral gyrus in the motor cortex, which transmits another set of instructions to the motor nuclei in the brain stem and spinal cord. These areas send out the complicated messages necessary for coordinated activity of the larynx, thoracic and abdominal musculature, and vocal tract articulators. Auditory and tactile feedback act to fine tune the vocal output.
During phonation, the infraglottic musculature must make rapid, complex adjustments because the resistance changes almost continuously as the glottis closes, opens, and changes shape. At the beginning of each phonatory cycle the vocal folds are approximated and the glottis is obliterated. This permits the infraglottic pressure to build up. The subglottic pressure then pushes the vocal folds progressively farther apart from the bottom up until a space develops and the air begins to flow. The upper portion of the vocal folds has strong elastic properties which tend to make the folds snap back to the midline. This force becomes more dominant as the upper edges are stretched and the opposing force of the air stream diminishes because of approximation of the lower edges of the vocal folds. The upper portions of the vocal folds are then returned to the midline completing the glottic cycle. Subglottic pressure then builds up again and the cycle repeats. The frequency of vibration is dependent on air pressure and mechanical properties of the vocal folds, which are regulated in part by the laryngeal muscles.
There are three primary parameters of voice: quality, loudness, and pitch. The quality or overall pleasantness of voice is largely dependent upon the extent to which the vocal folds vibrate symmetrically and completely at the midline of the glottis. Excess noise is the consequence of escape of unphonated air through leaks in the glottis. When noise mixes with voice, the result is abnormal vocal quality. Vocal loudness or intensity is directly influenced by subglottic air pressure, glottal resistance force created by the myoelastic properties of the vocal folds, transglottal airflow rate, and amplitude of vocal fold vibration. Increasing these parameters will result in a louder voice. Pitch or frequency is directly influenced by alterations in the length, tension, and cross-sectional mass of the vocal folds. The speed of vibration is faster when the vocal folds are lengthened whereas when they are shortened, thickened, or more lax the speed of vibration is slower. The speed of vibration determines pitch.
The proper diagnostic workup for a patient with dysphonia should always begin with a through review of the history of the complaints, followed by a comprehensive physical examination of the head and neck region. During the interview, the astute physician directs the line of questioning and permits the patient to do most of the talking. This yields a good voice sample and at the same time allows for efficient extraction of valuable information regarding the presenting complaints. To allow complete coverage of the patientís background, Dworkin and Meleca developed an easy-to-remember acronym: "I MADE A SPEECH." Each letter represents in sequence 1 of 12 separate interview steps. These are:
Every patient with a voice complaint should have a complete otolaryngologic examination, vocal fold visualization at least by indirect mirror laryngoscopy, and more general medical examination as indicated. Examination of the ears should include assessment of hearing acuity. The conjunctiva of the eyes should be assessed for signs of allergy, anemia, jaundice, and other abnormalities. The nose should be assessed for patency. Nasal obstruction necessitates mouth breathing, which may lead to mucosal irritation and drying. Oral cavity examination should include special note of xerostomia, dental wear patterns, and transparency of enamel. Neck examination should include special attention to the thyroid gland and to the posterior portion of the neck for excessive muscle tension or limitation in the range of motion. Cranial nerve examination should be performed with special attention to the gag reflex, deviation of the palate, or other deficits. Laryngeal exam begins when the patient enters the office. The range, ease, volume, and quality of the speaking voice should be noted. The current standard of medical care requires that indirect laryngoscopy be performed on every patient with a voice complaint. It allows assessment of the symmetry of vocal fold abduction and adduction, laryngeal color, and the presence of substantial masses or lesions. It does not allow the evaluation of the many important lesions that impair vibration and produce hoarseness and breathiness.
A slow motion evaluation is now possible routinely with the use of videostrobolaryngoscopy (VSL). Stroboscopic light allows routine, slow-motion evaluation of the mucosal cover layer of the leading edge of the vocal fold. This improved physical examination permits the detection of vibratory asymmetries, structural abnormalities, small masses, submucosal scars, and other conditions that are invisible under ordinary light. Stroboscopy does not provide a true slow-motion image, as obtained through high-speed photography. The stroboscope actually illuminates different points on consecutive vocal fold waves, each which is retained on the retina for 0.2 seconds. The stroboscopically lighted portions of the successive waves are visually fused. Having the stroboscopic light desynchronized with the frequency of vocal fold vibration by approximately 2 Hz creates the slow-motion effect. When vocal fold vibration and the stroboscope are synchronized exactly, the vocal folds appear to stand still, rather than move in slow-motion. Coupling the stroboscopic light with the camera allows later reevaluation by the laryngologist, or by other physicians. Characteristics assessed include fundamental frequency, symmetry of bilateral movements, periodicity, glottal closure, amplitude, mucosal wave, the presence of non-vibrating segments, and other unusual findings. The other means of evaluating laryngeal function include electroglottography, photoglottography, aerodynamic measures, and laryngeal electromyography.
The etiologies of neurological voice disorders are varied. Any damage or disease of the components of the peripheral or central nervous system that control laryngeal function can affect voice production. The most common etiologies of neurological voice disorders include trauma, cerebral vascular accidents, tumors, and diseases of the nervous system.
Flaccid neural laryngeal disorders involve damage or disease to one or more components of the motor unit (nucleus ambiguus, vagus nerve, myoneural junctions, or laryngeal muscles). Viral infections, trauma, stroke, tumor, or degeneration of the cell bodies in the nucleus ambiguus or an injury to the recurrent laryngeal branch of the vagus nerve could result in laryngeal muscle paralysis. The type and extent of dysphonia depends upon the lesion site, and whether the damage is unilateral, bilateral, partial, or complete. Bilateral complete lesions, involving both recurrent and superior laryngeal branches of the nerve, result in total weakness, hypotonicity, atrophy, and paralysis of the vocal folds. The patient is aphonic and the risk for aspiration pneumonia is high. Bilateral incomplete lesions often cause partial paralysis of the vocal folds. Breathy-hoarse, wet-gurgly vocal quality, increased jitter and shimmer values, and low harmonics to noise ratio are predictable. Shortness of breath and vocal fatigue are common presenting complaints, as glottal incompetency and reduced glottal resistance results in air wastage during phonation and taxing respiratory compensation. Bilateral lesions of the recurrent laryngeal nerves only often produce bilateral abductor paralysis, wherein the vocal folds are fixed in the median position and can not be abducted. In these patients, the voice features are near normal, as are swallowing abilities. However, the airway at the glottic level is compromised due to the midline position of the paralyzed vocal folds. These patients have inspiratory stridor and dyspnea and require a tracheotomy for respiratory relief.
Unilateral recurrent nerve paralysis causes hoarse-breathy voice quality, as the affected vocal fold hangs motionless in the paramedian position. The findings on examination are suggestive of a large posterior glottic chink and glottic incompetence. Once atrophic changes take place, the free edge of the affected fold thins out and becomes bowed. The vocal folds vibrate asymmetrically and aperiodically. Excursions away from the midline on the involved side are usually limited, and the mucosal wave may be completely absent.
Myasthenia Gravis is caused by autoimmune mechanisms that reduce available acetylcholine receptors at the neuromuscular junction and reduce laryngeal neuromuscular transmission. It produces severe muscular deterioration. In females, the onset of MG is typically in the third decade of life, whereas in males onset frequently occurs in the sixth decade. These patients reach a maximum level of weakness in 3 years. Inhalatory stridor, breathy voice, hoarseness, flutter, and tremor have characterized MG. Loudness is reduced, and there is a restriction in pitch range. Also can have dysphagia, hypernasality, and velopharyngeal insufficiency. Similar findings occur in patients with the progressive disorder of myotonic muscular dystrophy.
Spastic (pseudobulbar) neural laryngeal disorders are associated with bilateral upper motor neuron damage. Such damage may occur with multiple, bilateral cerebral vascular accidents, any lesion of the corticobulbar tracts bilaterally, and vascular and degenerative diseases involving motor cortical areas bilaterally. In addition, vascular diseases and tumors of the internal capsule or brainstem, degenerative diseases involving the entire corticobulbar tract system, infectious diseases, and the congenital disorder of spastic cerebral palsy may also be etiologies. Consequent release of inhibition of excitatory nerve impulses to vagal nuclei may result in hyperadduction of the true and false colds observed in these disorders. The voice may be low-pitched with little variation in either pitch or volume. Characteristically, the voice quality will be strained-strangled. So much effort may accompany the speech attempt that a grunt can sometimes be heard after each utterance. In pseudobulbar palsy there are articulation disorders, and frequently, hypernasality. These vocal changes frequently occur in the presence of accompanying dysarthria. Aronison suggests that the voice disorder accompanying spastic dysarthria is caused by hyperadduction of the true and false folds. VSL may reveal normal appearing vocal folds and surrounding soft tissue structures. During respiratory tasks, movements to and from the midline may be mildly to moderately slow-labored. Phonation events are characterized by prolonged glottic closure time and squeezing, hyperactive supraglottic activities. A less severe form involves a unilateral lesion of the corticospinal and corticobulbar tracts. The speech effects these unilateral tract damage produce are either mild or transient.
Ataxic neural laryngeal disorders may occur following cerebellar damage resulting from strokes, traumas, toxins, tumors, or diseases such as Friedreichís ataxia. This is an autosomal recessive cerebellar disorder that has its onset between the ages of 8 - 15. A disruption of the fine coordination of movement is a major symptom. Equilibrium and gait are likely to be impaired. Ataxic dysarthric patients typically struggle with uncontrollable loudness and pitch outbursts. They may occasionally exhibit a coarse vocal tremor overlay as a consequence of clumsy, uncoordinated, and tremorous laryngeal musculature contractions. Laryngoscopy may reveal mild to moderate tremors of the laryngeal inlet upon phonation, but not at rest. No discernible anatomic abnormalities are evident when examining the status of the vocal folds.
Hypokinetic neural laryngeal disorders have been most commonly related to the degenerative neurological disorder idiopathic Parkinson disease. The etiology of this disease of the extrapyramidal system is unknown; however, it has been associated with both genetic and environmental factors. In Parkinson disease, degenerative changes in the substantia nigra result in depletion of the neurotransmitter dopamine. Parkinsonism is a term for other disorders that have some of the characteristics of idiopathic Parkinson disease, but are the result of a virus, head trauma, carbon monoxide poisoning, toxic build-up, or historic influenza epidemic. It has been reported that 1.5 million Americans have idiopathic Parkinson disease with 89% of these patients having a voice disorder. The physical pathologies of rigidity, tremor, reduced range of movement, and slowness of movement are observed together with the classic symptoms of mask-like face and micrographia. Hypokinetic dysarthric vocal symptoms vary greatly, depending on the medication given for the other symptoms that are present and how much the disease has progressed. Most patients with Parkinsonís disease exhibit hoarse-harsh vocal quality, with limited pitch and volume range, because of laryngeal musculature involvement. Other voice characteristics include breathiness, roughness, hoarseness, and tremulousness. Although the appearance of the vocal folds may be normal, recruitment of the vocal folds is not uncommon during laryngoscopy. The findings of bowing and greater amplitude of vibration and laryngeal asymmetry have also been described in Parkinson patients. The most striking videostroboscopic findings in these patients were abnormal phase closure and phase symmetry. Amplitude and mucosal wave were essentially within normal limits in these patients.
Hyperkinetic neural laryngeal disorders are generally associated with the diseases of the extrapyramidal system and include a range of diseases such as Huntingtonís disease, organic essential tremor, orofacial dyskinesia, dystonia, athetosis, palatopharyngolaryngeal myoclonus, and Gilles de la Touretteís. The abnormal choreiform movements (abrupt, jerky, purposeless) accompanying the autosomal dominant disease of Huntingtonís disease are associated with the loss of neurons in the caudate nucleus. The voice of Huntingtonís chorea is characterized by irregular pitch fluctuations and voice arrests. Other characteristics that have been found include: sudden forced inspiration or expiration, harsh voice quality, excess loudness variations, strained-straggled phonation, monopitch, monoloudness, reduced stress, and transient breathiness. Endoscopic descriptions of one individual with Huntingtonís disease revealed adductory movements at rest and termination of phonation seemingly by adductory laryngospasm.
Mixed neural laryngeal disorders occur from damage or disease to multiple neural subsystems. For example, both lower motor neurons and bilateral upper motor neurons may be affected in amyotrophic lateral sclerosis ( ALS) which is considered a flaccid and spastic dysarthria. This is a progressive disease with an unknown etiology. The ALS patient may experience dysphagia and dangerous airway obstruction. The initial manifestations of ALS include muscle weakness, cramps, and fasciculations. The specific profile of voice characteristics in ALS is dependent on the site of lesion. Aronson described the dysphonia of ALS as a harsh, strain-strangle sound with the degrees of breathiness, reduced loudness, audible inhalation, and wet hoarseness. The wet gurgling sound is due to pooling of secretions in the piriform sinuses and around the glottis. Endoscopic reports of patients with ALS reveal that, if there is spastic involvement, patients may adduct normally or may hyperadduct with the false cords. If there is flaccid involvement, there is less abductory, adductory excursion.
Demyelination of both the upper motor and cerebellar neurons occurs in Multiple Sclerosis (MS) which is considered a spastic and ataxic dysarthria. Etiologies of MS include environmental agent in a genetically susceptible host. The onset and course of MS varies. Classic signs of MS are varied: optic neuritis and sensory or motor disturbance of the limbs may e common presentations. Approximately two thirds of the patients have exacerbation and remission of symptoms. Impairment of speech described as scanning speech has been considered a hallmark symptom of MS. The reports of dysarthria and dysphonia accompanying MS are varied. When the voice was affected, the main perceptual findings were impaired loudness control and hoarseness, described as a spastic-ataxic dysarthria. Less frequently observed were impaired pitch control, inappropriate pitch level, breathiness, and hypernasality. This variety of vocal symptoms suggests that the MS patients with voice abnormalities may be found to have problems in both laryngeal adduction and phonatory stability. Although endoscopic reports on MS are limited, the voice characteristics of breathy or pressed suggested that hypo- or hyperadduction might be observed.
Essential tremor is the most common movement disorder. It is found in all age groups but generally increases with advancing age. The voice is affected in 4 to 20 % of the cases, but more frequently the hands or head are involved. This disorder has been placed in the category of hyperkinetic disorders by some authors. Vocal tremor has been described perceptually as quavering or tremulous speech. The symptoms are most noticeable on vowel prolongation. There is pitch breaks and voice arrests from the large amplitude tremor of laryngeal structure that interrupt airflow or allow excess air to escape. On laryngeal examination the larynx is usually reported to move both at rest and with increased movement during phonation. Electromyographic studies of eight patients with vocal tremor found predominant involvement of the thyroarytenoid muscles as well as other extrinsic muscles.
Focal laryngeal dystonia is a slow movement disorder, which commonly results in spasmodic dysphonia, of which there are three types: adductor, abductor, and mixed. The adductor type is most prevalent. Some authors place this into the category of hyperkinetic disorders, however this is controversial. Numerous reports in the literature describe a psychogenic basis for the disorder. However, an increasing body of evidence supports as organic cause. It is characterized by excessive or inappropriate contraction of laryngeal muscles during speech. The signs and symptoms of the adductor type include strained-strangled voice quality, periodic arrests of phonation, limited pitch control, and limited volume control. Glottal resistance measurements may reveal three to four times the normal degree of vocal fold compression forces during phonation efforts. Prolonged vocal fold closure, reduced amplitude of vibration, and limited mucosal wave dynamics are often evident during VSL.
Treatment of neurological voice disorders must be considered in the context of treatment for the overriding neurological disorder. Frequently, patients with neurological voice disorders are receiving medication or have had neurosurgical treatment. These previous treatments can influence their voices. Treatment for a neurological voice disorder may include neurosurgical treatment to treat the overriding neurological problem or laryngeal surgical treatment to treat the disordered larynx. For example, myasthenia gravis patients receiving a thymectomy or Parkinson patients receiving neurosurgical intervention. It has been found that Parkinson patients who are treated with neurosurgical intervention have varying results on their vocal pathology. It appears that the consistency and magnitude of the affects of the surgical intervention are not adequate to consistently impact functional communication.
Neuropharmacological treatments can be very useful in treating general motor symptoms of the neurologic condition. For example, in myasthenia gravis, the positive effects of tensilon/pyridostigmine have been documented on symptoms of the disease including the voice. Drug therapy for Parkinson disease supports general amelioration of general motor symptoms with dopamine precursors (levadopa) or agonists (bromocriptine). However, the impact of these drugs on speech or voice production has not been established. Medical treatment of Huntingtonís disease has involved pharmacological attempts to control the choreic movements with antidopamenergic agents, phenothiazines, benzodiazepines, or antiseizure medication. The effects of these drugs on the voice of Huntingtonís patients have not been documented. The neuropharmacologic treatment of essential tremor has involved various drugs (propranolol, primidone, acetazolamide, alprazolam, and phenobarbital) with mixed results. Another treatment has involved the use of BOTOX injections with good results.
Adductor spastic dysphonia can be treated with a combination of methods including BOTOX injection, implantable laryngeal stimulators, or sectioning of the recurrent laryngeal nerve, as well as speech therapy. Usually a combination of the above measures is utilized to gain the best success in treating this disorder. Further research needs to be explored in order to determine its etiology and pathogenesis as well as to search for associated deficits, which, if corrected, could improve function in these patients.
Behavioral treatment for neurological voice disorders using speech therapy has only recently been addressed. They have begun to approach each disorder by looking at the physical pathology in the laryngeal mechanism. Neurolaryngeal disorders have been classified as disorders of adduction and instability.
Certain neurological disorders are accompanied by inadequate vocal fold adduction. The particular type and extent of hypoadduction may be associated with the site and extent of the related neurological damage. The primary treatment goal in these patients is to increase loudness and reduce breathy, hoarse quality by increasing vocal fold adduction. Procedures used to accomplish this include pushing, pulling, and lifting while phonating. Other techniques used to increase adduction include hard glottal attack, digital manipulation of the thyroid cartilage, and turning the head to one side or the other to increase tension on the paralyzed vocal fold.
Hyperadduction most frequently occurs in cases of upper motor neuron system disorders characterized by spasticity and hypertonicity. The primary focus of voice therapy for patients with hyperadduction is to decrease the pressed strained voice by reducing the vocal fold hyperadduction. Procedures used to accomplish this are designed to relax laryngeal musculature and facilitate easy voice onset. Other approaches include laryngeal massage, the chewing approach, the yawn-sigh, chanting, and delayed auditory feedback. The main focus of therapy in patients with phonatory instability is to reduce the unsteady, hoarse, rough voice quality by targeting steady, clear phonation. Patients are encouraged to maximize respiratory and laryngeal coordination to sustain steady voicing with consistent good quality.
In some cases, severity of the neurolaryngeal disorder in combination with breakdowns in other parts of the speech mechanism makes a form of augmentative or alternative communication the best choice to facilitate communication. These devices range from a simple manual board to more advanced devices that offer a synthesized digitaized speech output. Some include environmental control systems, which enable the patient to maintain a higher level of independence.