This article highlights the most common causes of velopharyngeal insufficiency (VPI), and discusses routine evaluation and treatment algorithms for the managment of VPI in children. VPI is a multifactorial condition that occurs commonly in syndromic and non-syndromic children. The most common features of VPI are audible hypernasal speech, facial grimacing, decreased speech intelligibility, nasal regurgitation, and nasal emission from failure to produce oronasal separation. Work-up of VPI typically involves radiologic and endoscopic testing performed with the assistance of a speech-language pathologist. Management of VPI involves initial speech therapy followed by operative repair with sphincter or pharyngeal flap pharyngoplasty, if needed.
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Velopharyngeal insufficiency (VPI) is an uncommon problem that typically manifests in patients as hypernasal speech, increased nasal resonance, nasal regurgitation, and nasal emission during phonation.
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VPI can occur sporadically but most often coexists as a syndromic finding (also known as velocardiofacial syndrome, submucosal cleft palate) or following previous operative intervention such as after cleft palate repair or adenoidectomy.
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Evaluation of VPI is multidisciplinary and revolves around initial perceptual speech evaluation by a speech-language pathologist, which is often combined with instrumental testing for confirmation.
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Treatment of VPI often initially involves a course of speech therapy for about 3 to 6 months before consideration of operative intervention as well as following most operative interventions to correct learned maladaptive speech patterns. However, most children are referred to the otolaryngologist after receiving prolonged speech therapy for hypernasal speech that fails to improve despite intensive therapy.
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Instrumental testing typically allows the surgical approach to be tailored based on the velopharyngeal (VP) gap size, location, and pattern of VP closure (VPC) that can involve of a superior-based pharyngeal flap versus sphincter pharyngoplasty versus posterior wall augmentation versus double-apposing Furlow Z-plasty versus prosthetic obturation.
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Operative repair of VPI is often undertaken after age 3 or 4 years when the patient is more cooperative with instrumental testing, which allows confirmation of the diagnosis and cause of VPI. Often, the earlier VPI is repaired, the fewer long-term speech problems and need for therapy exist. Occasionally, secondary repair is required, and this is successful in most children.
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Individual operative approaches may be used solely or in combination for VPI repair depending on the results of instrumental testing and the clinician’s experience.
Video of videofluoroscopy for the evaluation of palatal function during speech accompanies this article at http://www.Oto.theclinics.com.
VP function
The soft palate is commonly referred to as the velopharynx (VP). It is attached anteriorly to the hard palate via the palatal aponeurosis and is composed of multiple structures and muscles acting in a concerted fashion to produce VPC. These muscles include the paired muscles of the levator veli palatini and (LVP) tensor veli palatini (TVP), musculus uvulae, superior constrictor, palatopharyngeus, and palatoglossus muscles. Contraction of the VP elevates and retracts it posterosuperiorly in conjunction with simultaneous contraction of the lateral and posterior pharyngeal walls that move medially and anteriorly about 10 mm, respectively. Closure occurs at the level of the VP isthmus, whose location varies among individuals. Within the isthmus, sphincteric contraction with subsequent apposition of all structures within the nasopharynx functions to produce VPC, and this is typically located along the inferior aspect of the adenoid bed. VPC is required during attempted phonation, deglutition, and sucking, and serves to prevent nasal regurgitation of fluids or solids that are normally delivered to the oropharynx (OP). In addition, it functions to channel exhaled airflow and pressure from the vocal tract to the articulators of the oral cavity (tongue, teeth, lips) for normal resonant speech production. Coupling and uncoupling of the oral and nasal cavities occurs through rapid opening and closing of the VP valve, which permits regulated entry of sound pressure and energy into either the nasal or oral cavities during phonation. VPC also allows oral pressure development of 5 to 7 mm Hg to produce oral plosives or fricatives by the articulators.
Speech Production
Within the English language, all phonemes with the exception of /m/, /n/, and /ng/ are produced with oral airflow that requires VPC to exclude nasopharyngeal airflow. The presence of airflow leaking into the nasopharynx during normal oral speech or swallowing creates hypernasal speech, as well as excess nasal resonance, regurgitation, and audible emission, which occurs when a VP gap of greater than 10 mm 2 is present during attempted VPC. Only the /m/, /n/, and /ng/ phonemes require an open nasopharyngeal portal/valve and nasal airflow to produce these sounds. Hyponasality is a reduction in nasal resonance during phonation, especially of nasal phonemes such as /m/, /n/, and /ng/. It typically results from either partial or complete blockage of the nasal cavity or nasopharynx from mucosal edema associated with viral upper respiratory infection (URI), hypertrophic tonsils/adenoids, allergic rhinitis, hypertrophic turbinates, or anatomic obstruction from a deviated nasal septum or choanal atresia. Hyponasality can be referred to diminished nasal resonance that occurs during the height of a URI when nasal mucosal congestion and obstruction are maximal. However, hyponasality and hypernasality may coexist in the same patient and make diagnosis of VPI difficult if hyponasality masks the hypernasal speech component. Referral to an otolaryngologist is advisable if hyponasal or hypernasal speech exist.
VP Anatomy and Action
Anatomically, contraction of the LVP provides posterosuperior elevation of the VP.
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The LVP derives its origin from the petrous portion of the temporal bone and from the medial lamina of the eustachian tube (ET).
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It descends with the ET from the temporal bone through the foramen of Morgagni to the level of the soft palate.
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It is innervated from the pharyngeal plexus of cranial nerve (CN) X and possesses muscle fibers that are oriented in a transverse fashion at the level of the VP. The pharyngeal plexus is also innervated via minor contributions from CN IX and CN VII.
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At the level of the VP, LVP fibers interdigitate in the midline with the contralateral LVP to form the VP sling.
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Anteriorly, the TVP originates from the base of the medial pterygoid plate, sphenoid spine, and lateral cartilaginous hook of the ET, and is innervated by CN V.
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Its tendinous fibers hook around the hamulus to insert into the anterior fibrous palatal aponeurosis of the soft palate, anterior to the LVP muscle. Contraction of this muscle serves to tense and stabilize the soft palate. In addition, given its origin from the ET, contraction of the TVP functions to open and close the ET via a pumping action.
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The musculus uvulae is a paired muscle that arises from the tendinous palatal aponeurosis anterior to the LVP and courses dorsal to the LVP to insert into the mucosa of the uvula. It functions to elevate the uvula as well as to shorten and add bulk to the VP to occlude the VP port during speech and deglutition. Absence of this muscle, especially in children with occult cleft palates or neuromuscular dysfunction, often results in VPI.
VPC is also obtained with the use of the palatopharyngeus and superior constrictor muscles primarily, which are innervated by the pharyngeal plexus. The palatopharyngeus muscles serve to elevate the pharynx and larynx during bolus transmission from the oral cavity to the hypopharynx. They also function to narrow the oropharyngeal aperture during swallowing. Contraction of the superior constrictor muscle produces anterior and medial displacement of the posterior and lateral pharyngeal wall during deglutition, at the level of the first cervical vertebra. Within the area of the VP isthmus, 20% of all individuals may show development of a discrete transverse muscular ridge, also known as the Passavant ridge, which is produced during superior constrictor muscle contraction. However, it is controversial whether the Passavant ridge participates in VPC or is even located within the VP isthmus.
Classification of VP disorders
Disorders of the VP have been classified and/or named according to the underlying pathologic mechanism suspected to cause VPI. Within the literature, the nomenclature, including VP incompetence, insufficiency, inadequacy, and dysfunction, have been described, but are confusing as result of terminology used interchangeably without distinction or respect to the pathologic mechanism. With regard to children, the cause of VPI is typically anatomic, iatrogenic, or neuromuscular. VPI can also be classified as resulting from structural, functional, mechanical, or dynamic palatal (neuromuscular) abnormalities.
Neuromuscular Abnormalities
Historically, VP incompetence has typically denoted a structurally intact VP affected by an underlying neurologic or musculoskeletal injury such as neuromuscular incoordination. This condition may be associated with an acute neurologic injury (CVA), intracranial processes, palatal paralysis, or progressive neurologic deterioration of the pharyngeal plexus (Amyotrophic Lateral Sclerosis, Parkinson disease, cerebral palsy, Möbius syndrome, Down syndrome). Neural injury may result in asymmetric weakness of the velopharynx and constrictor muscle if unilateral, or symmetric weakness in more severe cases. This condition can be associated with gross hypotonia and dysarthria. In more severe cases, weakness of the recurrent laryngeal nerve may also occur, resulting in dysfunction of vocal fold mobility, and the inability to generate adequate subglottic pressure for development of speech. Protective and reflexive acts such as gagging and swallowing may be impaired depending on the nature and the level of the lesion. This impairment includes lesions at CNs IX, X, XI, or the cerebellum. VP incompetence may also result from a primary muscular disorder, although this is less common. It can occur in disorders such as muscular dystrophy. The velum and superior constrictor muscles may show evidence of gross hypomobility or immobility during voluntary speech and swallowing that result in dyscoordination of sphincteric closure and flaccid dysarthria.
Structural Abnormalities
VPI has been used to describe a neurologically intact VP that is structurally or anatomically deficient with respect to either position, size, soft tissue volume, or all of these variables. Examples include iatrogenic causes, such as following hard palatal advancement or adenoidectomy. In addition, it can occur in association with short palate syndrome, hard and soft cleft palate, nasopharyngeal disproportion, and so forth. Similarly, VPI may be produced from mechanical obstruction impairing VP mobility during speech and swallowing. This condition can occur secondary to tonsillar hypertrophy or tethering of the velum resulting from tonsillectomy, pharyngoplasty, or pharyngeal flap surgery that scars and stiffens the velum. It may also result from a palatal fistula complicating palatoplasty repair that allows airflow to escape from the oral to the nasal cavities.
Articulation Abnormalities
VPI may arise from the presence of compensatory misarticulation that persists long after surgical repair of the palate. As described by Dworkin and colleagues, this includes greater use of nasals, glides, glottal stops, pharyngeal stops and fricatives, posterior nasal fricatives, and fewer stop plosives that constitute articulatory avoidance behaviors and linguapalatal valving constraints. This condition can also manifest as facial grimacing and low speech volume that act to reduce nasal airflow during oral phoneme speech. Ultimately, this can impair speech intelligibility and is difficult to correct, even with intense speech therapy. Similarly, mislearned errors of articulation or dialectical influences may also masquerade as VPI in a neuromuscularly intact child. Although rare, this can occur in an atmosphere in which a child is exposed to mispronounced/misarticulated speech that is subsequently learned and replicated, leading to faulty speech patterns and behaviors. In addition, phoneme-specific misarticulations can occur when nasal emission is present with fricatives and affricatives in the absence of any hypernasal resonance. In these instances, there is typically not a role for surgical intervention but instead speech therapy may be more beneficial. Thus, work-up for VPI must consider multiple causes during the diagnostic process. To simplify the frequent use of incorrect terminology, the term VP dysfunction or inadequacy is now more commonly used to describe abnormal VPC.
Classification of VP disorders
Disorders of the VP have been classified and/or named according to the underlying pathologic mechanism suspected to cause VPI. Within the literature, the nomenclature, including VP incompetence, insufficiency, inadequacy, and dysfunction, have been described, but are confusing as result of terminology used interchangeably without distinction or respect to the pathologic mechanism. With regard to children, the cause of VPI is typically anatomic, iatrogenic, or neuromuscular. VPI can also be classified as resulting from structural, functional, mechanical, or dynamic palatal (neuromuscular) abnormalities.
Neuromuscular Abnormalities
Historically, VP incompetence has typically denoted a structurally intact VP affected by an underlying neurologic or musculoskeletal injury such as neuromuscular incoordination. This condition may be associated with an acute neurologic injury (CVA), intracranial processes, palatal paralysis, or progressive neurologic deterioration of the pharyngeal plexus (Amyotrophic Lateral Sclerosis, Parkinson disease, cerebral palsy, Möbius syndrome, Down syndrome). Neural injury may result in asymmetric weakness of the velopharynx and constrictor muscle if unilateral, or symmetric weakness in more severe cases. This condition can be associated with gross hypotonia and dysarthria. In more severe cases, weakness of the recurrent laryngeal nerve may also occur, resulting in dysfunction of vocal fold mobility, and the inability to generate adequate subglottic pressure for development of speech. Protective and reflexive acts such as gagging and swallowing may be impaired depending on the nature and the level of the lesion. This impairment includes lesions at CNs IX, X, XI, or the cerebellum. VP incompetence may also result from a primary muscular disorder, although this is less common. It can occur in disorders such as muscular dystrophy. The velum and superior constrictor muscles may show evidence of gross hypomobility or immobility during voluntary speech and swallowing that result in dyscoordination of sphincteric closure and flaccid dysarthria.
Structural Abnormalities
VPI has been used to describe a neurologically intact VP that is structurally or anatomically deficient with respect to either position, size, soft tissue volume, or all of these variables. Examples include iatrogenic causes, such as following hard palatal advancement or adenoidectomy. In addition, it can occur in association with short palate syndrome, hard and soft cleft palate, nasopharyngeal disproportion, and so forth. Similarly, VPI may be produced from mechanical obstruction impairing VP mobility during speech and swallowing. This condition can occur secondary to tonsillar hypertrophy or tethering of the velum resulting from tonsillectomy, pharyngoplasty, or pharyngeal flap surgery that scars and stiffens the velum. It may also result from a palatal fistula complicating palatoplasty repair that allows airflow to escape from the oral to the nasal cavities.
Articulation Abnormalities
VPI may arise from the presence of compensatory misarticulation that persists long after surgical repair of the palate. As described by Dworkin and colleagues, this includes greater use of nasals, glides, glottal stops, pharyngeal stops and fricatives, posterior nasal fricatives, and fewer stop plosives that constitute articulatory avoidance behaviors and linguapalatal valving constraints. This condition can also manifest as facial grimacing and low speech volume that act to reduce nasal airflow during oral phoneme speech. Ultimately, this can impair speech intelligibility and is difficult to correct, even with intense speech therapy. Similarly, mislearned errors of articulation or dialectical influences may also masquerade as VPI in a neuromuscularly intact child. Although rare, this can occur in an atmosphere in which a child is exposed to mispronounced/misarticulated speech that is subsequently learned and replicated, leading to faulty speech patterns and behaviors. In addition, phoneme-specific misarticulations can occur when nasal emission is present with fricatives and affricatives in the absence of any hypernasal resonance. In these instances, there is typically not a role for surgical intervention but instead speech therapy may be more beneficial. Thus, work-up for VPI must consider multiple causes during the diagnostic process. To simplify the frequent use of incorrect terminology, the term VP dysfunction or inadequacy is now more commonly used to describe abnormal VPC.
VPI assessment
The diagnosis of VPI is typically ascertained by :
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Routine historical intake
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Physical examination
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Combination of perceptual speech, instrumental evaluation, and reliance on the trained ear.
The physical examination focuses on detailed inspection of the oral and nasal cavities with attention to the velar height, mobility, and symmetry, and palatine tonsil size, tongue mobility and symmetry, oral competence, palatal and uvular appearance, as well as the nasal mucosa, turbinates, septum, and so forth. As is frequently described, attention to the OP searching for signs of a submucosal cleft palate (bifid uvula, zona pellucida, posterior palatal notching), as well as any anatomic or neuromuscular abnormality, is frequently undertaken. However, physical examination always overlooks an occult cleft palate and thus other instrumental evaluation is needed to make this diagnosis.
In addition, inquiry about any prior surgical intervention within the oral cavity or pharynx is discussed with the patient/family and is corroborated with examination findings of postoperative sequelae. These findings could include the presence of a palatal fistula, scarring, or mechanical obstruction of the VP valve. In the absence of findings, a detailed history is elicited for any known syndrome or neurologic abnormalities that may exist.
Dynamic mobility of the velopharynx is also inspected with the sustained phonation of the vowels /e/ or /i/. During this phase of the evaluation, the clinician may also observe for oral competence and the patient’s ability to manage secretions, while evaluating for nasal regurgitation and presence of a gag reflex.
Perceptual Speech Evaluation
After a thorough history and examination, perceptual speech analysis is performed in conjunction with a multidisciplinary team that includes a speech-language pathologist along with otolaryngologist or plastic surgeon. Frequently, the diagnosis of VPI has been suspected previously or entertained by the patient’s family or primary care physician before referral to the otolaryngologist.
Diagnostically, perceptual analysis connotes the use of the evaluator’s unaided senses, whereas instrumental includes all evaluations that involve some type of instrumentation.
Perceptual analysis
Perceptual analysis, the gold standard of VPI evaluation, includes listening to the spontaneous or prompted production of specific pressure phonemes including plosives, fricatives, and affricatives while monitoring for misarticulations, hypernasal speech, nasal rustle, and facial grimacing. It may also use articulation measurement, equal-appearing interval scales, and global ratings to assess VPI. Facial grimacing is a compensatory action used by the patient to narrow the external nares to decrease nasal air emission during non-nasal speech. Use of the dental mirror placed under the nares during vowel production, may also assist in determining the amount of visible nasal air emission as shown by fogging of the mirror.
Within the office setting, VPI screening for VP inadequacy can also be performed by having the patient count from 60 to 80 while listening for the presence of nasal emission and hypernasal speech. Repetition of characteristic phrases such as “pet the puppies,” “pick the peppers,” and “Kathy kissed the cat” are frequently used as test phrases. For these tasks, coordination with a speech-language pathologist who possesses dedicated training and interest in the area of VPI is critical given the acknowledged subjective nature of perceptual evaluation. At present, there is no standardized perceptual acoustic evaluation protocol that is uniformly used among all speech-language pathologists throughout the United States, other than the International Working Group recommendations that were developed in the 1990s. Perceptual analysis may be supplemented with the use of the Pittsburgh Weighted Speech Scale, which is used in many clinics to report the severity of VPI when attempting comparative analyses.
Instrumental assessment
Instrumental assessment is complementary to perceptual analysis during the evaluation of VPI. It is performed with two-dimensional or three-dimensional technology that uses either video-nasal endoscopy or multiview videofluoroscopy in either the presence of the surgeon, radiologist, or speech-language pathologist. In many centers, evaluation of VPI may also use pressure-flow measurements to determine the size of the VP port associated with the patient’s VPI. Video-nasal endoscopy allows direct visualization of both nasal passages and nasopharynx with inspection of all nasal structures as well as the adenoids, nasopharyngeal depth, and soft palate mobility and size. It optimally uses the largest pediatric flexible laryngoscope that the child’s anatomy and cooperation will accommodate, which is passed through the middle meatus to the nasopharynx. Endoscopic images are displayed on an attached video monitor for real-time simultaneous viewing by the speech-language pathologist who is directing the patient during the phonetic evaluation. During evaluation, VPC is assessed during multiple maneuvers, such as simulated sucking through a straw, as well as testing of oral and nasal phoneme production of fricatives, affricatives, plosives, and so forth. The patient is usually instructed to repeat key phrases during the examination. Ultimately, this allows determination of the location of VPC while scrutinizing VP gap geometry and correlating this with adjacent nasopharyngeal landmarks. Simultaneously, it also allows critical assessment of the degree of mobility or hypomobility of all VP structures, which helps guide the preoperative surgical decision-making. Nasal endoscopy also allows assessment for an occult cleft palate during visualization of the nasopharyngeal surface of the velum. Should a midline dimpled concave contour, or seagull sign, be found in the normal central convex velum, an occult cleft, representing a musculus uvulae deficiency, should be entertained as a cause for the patient’s VPI.
Videofluoroscopy in Evaluation of VPI
Multiview videofluoroscopy is a two-dimensional radiologic instrumental analysis that is frequently used in the evaluation of VPI. It uses serial radiographs that are oriented in a lateral, frontal, and base view to analyze the VP valve and assess closure. It is often preferentially used in younger children who are unlikely to cooperate for a nasoendoscopic examination. It involves instillation of barium transnasally to coat the soft palate as well as the posterior and lateral pharyngeal walls. Subsequently, serial images of VPC are acquired of the cervical vertebrae and the posterior pharyngeal wall and Passavant ridge. Limitations include oversimplification of VPC in 1 plane, underestimation of the anteroposterior pharyngeal dimension, and tendency to suggest VPC when midline unilateral or bilateral defects exist. Given the speed at which VPC occurs compared with the speed at which serial radiography can occur, videofluoroscopy has been criticized for the potential to suggest VPI when normal VPC is present. Despite this, videofluoroscopy is often used in conjunction with nasal endoscopy when it is not possible to ascertain levator orientation and VPC using only endoscopic evaluation. At our institution, we always attempt awake versus asleep nasal endoscopy performed with light sedation if possible, for reasons previously stated.
See Video 1 for an example of a Televex study incorporating videofluoroscopy for the evaluation of palatal function during speech.
Cephalometrics
Cephalometric evaluation uses principles common to videofluoroscopy that involve serial radiographs from an X-ray source during sustained speech and at rest to study various anatomic relationships obtained from multiple views of the pharynx. These views include:
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Cranial base angle
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Nasopharyngeal depth
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Velar length
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Dimpling
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Gap
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Stretch.
These variables allow comparison of the velar dimpling location that relates to the most anterior insertion of the levator muscle into the soft palate, in addition to the diagnosis of platybasia and cervical spine abnormalities contributing to nasopharyngeal disproportion. With increased anterior insertion, velar stretch is inversely decreased (as seen in submucosal and occult cleft palates) with the production of a potential velar gap during phonation. Limitations include VPI evaluation performed via static two-dimensional imaging and the need for radiation exposure. However, it is reported to be greater than 90% predictive of the need for pharyngeal flap surgery, as well as reliable, quantifiable, and useful in the evaluation and treatment planning of children with velocardiofacial syndrome and isolated cleft palates. However, it cannot predict the amount of VPC required by corrective pharyngeal surgery.
MRI
In the past 5 years, MRI evaluation of the VP has also been increasingly used to study VPI because it is noninvasive, not associated with radiation exposure, and possesses reproducible imaging quality. Its role in VPI evaluation is still largely academic given its prohibitive cost and frequent need for procedural sedation during evaluation of children. Although touted as dynamic imaging, it conceptually uses static imaging during limited speech that is often nonconnected and is not performed during multiple speech contexts. It is arguably used to assess LVP mobility and function, as well as assessing LVP muscle size, distribution, and orientation/position in cases in which submucosal or occult clefting of the VP is suspected. This is achieved by following the length of the LVP from origin to insertion in multiple planes, which allows visualization of the direction and final insertion location of its distal muscular fibers into the soft palate. Ultimately, it compares favorably with nasal endoscopy and videofluoroscopy as a complementary tool for the evaluation of VPI, but its mainstream use is hampered by its prohibitive cost.
Nasometry
Nasometry is an objective, indirect test that is used to measure nasal emission. It allows the reproducible calculation of a ratio between nasal and oral sound emissions, known as nasalance, which can be compared with normative values of means and standard deviations (SDs). Preoperative and postoperative nasometric scores may be compared with postoperative success, often defined as within 1 SD from the normative mean. However, nasometry does not allow the localization or quantification of VP gap size. Large gaps may produce less high-pressure airflow detected by the nasometer and thus have an artificially depressed nasometric score compared with a small VP gap.
During instrumental assessment, the velopharynx is assessed for its unique closure pattern, which has been previously classified as either coronal, sagittal, or circular (symmetric). As described previously, coronal closure of the velopharynx involves mobility of only the posterior OP wall and VP with little contribution from the lateral OP walls. Conversely, sagittal closure refers to the active muscular contraction of the lateral OP walls with minimal contribution from the posterior OP wall, soft palate, or uvula. Circular closure refers to involvement of all structures, including the posterior and lateral OP walls, soft palate, and uvula, which contract equally to close the VP port. Endoscopic evaluation assists in determining the exact contribution of each structure either symmetrically or asymmetrically in producing VPC. Although this form of evaluation is imperfect, the benefit pertains to the lack of radiation exposure to the child during videofluoroscopic evaluation. However, a limitation to this diagnostic modality is the amount of voluntary cooperation during successive testing that is required to assess the VP port endoscopically, the pattern of VPC, and degree of contribution from all VP musculature during VPC. In addition, obstructive adenoids and the obliquity of view may hinder ideal visualization of the VP port.
At our institution, nasal endoscopic examination is occasionally accomplished in the operative setting under light sedation using nitrous oxide in the presence of the speech-language pathologist. Although suboptimal, it allows assessment of all aforementioned objectives while avoiding videofluoroscopy. Typically, evaluation under light sedation is performed in children less than 4 to 5 years of age, given the difficulty in performing endoscopic examination in this young age group. However, endoscopic assessment data often influence the decision regarding how to proceed surgically with either a pharyngoplasty versus pharyngeal flap based on the visualized closure pattern and recognized deficient or immobile segment of the velopharynx. In multiple studies, tailoring of the superior pharyngeal flap width and length to the VP gap and closure point is often accomplished and with high postoperative success. Limitations of endoscopic evaluation typically include obliquity and skewing of VP port image, parallax errors, wide-angle distortion, and variability between endoscope operators, scope technology, and the clinician’s technique.
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