Trigeminal nerve (CN V)
Motor innervation
Mastication—temporalis, masseter, medial and lateral pterygoid
Hypolaryngeal excursion—Mylohyoid, anterior belly digastric
Tensing velum—Tensor veli palatini
Sensory innervation
Bolus manipulation—sensation from mouth, cheeks, and anterior 2/3 of the tongue (not taste)
Facial nerve (CN VII)
Motor innervation
Lip closure: orbicularis oris, Zygomaticus
Buccal tone: buccinator
Hypolaryngeal excursion—posterior belly digastric, stylohyoid
Sensory and autonomic innervation
Taste—taste from the anterior 2/3 of the tongue.
Salivation—parasympathetic fibers to the submandibular and sublingual salivary glands
Glossopharyngeal nerve (CN IX)
Motor innervation
Pharyngeal constriction—upper pharyngeal constrictor
Pharyngeal shortening—stylopharyngeus
Sensory and autonomic innervation
Taste and sensation—sensation from the posterior 1/3 of the tongue (including taste), the velum, the fauces and the superior portion of the pharynx
Salivation—parasympathetic fibers to the parotid salivary glands
Vagus nerve (CN X)
Motor innervation
Velopharyngeal closure—levator veli palatini
Tongue base retraction—palatoglossus
Pharyngeal squeeze—pharyngeal constrictors
Airway closure—all intrinsic laryngeal muscles
UES closure and opening—cricopharyngeus
Esophageal motility—esophageal musculature, both striated in proximal 1/3 and smooth muscle in distal 2/3 of esophagus
Sensory innervation
Sensation—sensory information from the velum, posterior and inferior portions of the pharynx, all sensation in the larynx, esophagus
Hypoglossal nerve (CN XII )
Motor innervation
Tongue mobility—all extrinsic and intrinsic tongue muscles
Hypolaryngeal elevation—thyrohyoid approximation through thyrohyoid and hyoid protraction through geniohyoid
Modelling of swallowing. Of the many models used to describe the oropharyngeal swallowing, McConnel’s “Piston Model,” proposed in 1988, remains the most widely used around the world. The “Piston Model” is based on the following assumption: the primary function of the oropharynx is to generate a pressure gradient for swallowing without aspiration.
Citing McConnel: “the tongue base acts like a plunger or a ‘Piston’ to develop a propulsive bolus-driving force” [3, 5]. According to this model the bolus-driving force will depend on two somewhat interdependent elements: (1) the propulsion forces (PF) and (2) the flow resistance forces (FRF). The PF is largely dependent on two elements: (a) the tongue appearing as the major pressure-generator and (b) the resistance of the pharyngeal walls acting as a dynamic chamber for the tongue. In contrast the FRF is mainly determined by the upper esophageal sphincter (UES) behavior (hypo-relaxed, hyper-contracted, lack of passive opening, etc.) [6].
17.3 Neural Control of Swallowing
The swallowing reflex can be triggered voluntarily or involuntarily by the sensory impulses in the posterior oropharynx, larynx, and hypopharynx [7]. The swallowing reflex response is controlled by the brain stem but modulated by cortical input. Sensory feedback can modify the intensity of the pharyngeal reflex as it synapses in both the brain stem and the cortex, in particular when related to the volume of the bolus ingested. Once the bolus enters the pharynx, the afferent fibers trigger a region of the nucleus tractus solitarius that sets up a sequence of cranial motor nuclei activation.
Cognitive awareness, drive for food and nutrition plays an important role. The coordination with apnea is essential. The muscle groups involved in swallowing are represented bilaterally but asymmetrically in the premotor cortex, in a somatotopic fashion, with a dominant hemisphere independent of handedness [8, 9]. The clinical implication is that impairment of swallowing will be more prominent if the hemisphere affected is the dominant one and that there will be a possibility of rehabilitation reorganizing the swallowing areas in the non-dominant hemisphere. The cerebral cortex has an important role in swallowing initiation and strong involvement in the coordination of the normal swallow. Suppression of cortical input makes oral time longer, uncoordinated and with a prolonged triggering time of the reflexive swallow. The sensory motor cortex receives afferent information of the oral, pharyngeal, and laryngeal areas modulating the brain stem response according to the type of information received. The brainstem is responsible for the involuntary phases. Brainstem representation is both sided and they are interconnected. That means a unilateral lesion can result in bilateral pharyngeal motor and sensory dysfunction.
The brainstem swallowing center, called the central pattern generator (CPG), is formed by two groups of interneurons: one located in the nucleus tractus solitarius (NTS), called the dorsal swallowing group (DSG), which is a primary sensory nucleus from the afferent stimuli and the other one located in the ventrolateral medulla (VLM), called ventral swallowing group (VSG), adjacent to the nucleus ambiguus (Fig. 17.1). The interneurons in the DSG are involved in the triggering, shaping, and timing of swallowing, and modulate the VSG premotor neurons which distribute the swallowing drive to the motorneurons of the different cranial nerves involved in swallowing [10]. The CPG is activated by either peripheral afferent input such as the ones conducted by the superior laryngeal nerve (SNL) or by supramedullary inputs, conducted by the cerebral cortex in the case of a voluntary swallow [11]. Sinclair et al. [12] demonstrated that electric stimulation of SLN elicits swallowing more readily than stimulation of the IX cranial nerve alone. SLN impairment greatly affects deglutition specially related to aspiration risk.
Fig. 17.1
Nonexhaustive list of different screening/assessments tests
17.3.1 Neurophysiology of the Protective Function of the Larynx
The most basic action of the larynx is to provide sphincteric protection of the lower airway. Protective vocal fold adduction is mainly due to thyroarytenoid (TA) contraction and is elicited by stimulation of the internal branch of the superior laryngeal nerve. Therefore, if the larynx is locally anesthetized the adductor response is not elicited.
Anesthesia dependency of the contralateral adductor reflex:
In humans under general anesthesia, response to the internal branch of the SLN stimulation elicits two types of responses, one with a short latency of 10–18 msec that produces the adduction of the ipsilateral VF and a second one, with a longer latency of 50 to 80 msec that produces a bilateral vocal fold adduction. In anesthetized cats this bilateral cross reflex reaction is already present at the short latency response. Sasaki et al. [13] suggested that “whereas the contralateral short latency response in humans is supported by central facilitation in the awake state, anesthesia suppression of facilitative mechanisms restricts the response to an only ipsilateral one.” These findings could explain the greater incidence of aspiration in sedated patients.
In other words, awake patient would benefit of a short lasting internal branch of the SLN mediated bilateral closure of their laryngeal sphincter whereas anesthetized patients would only benefit of a unilateral reflex of this kind.
17.4 The Effect of Aging in Swallowing
Changes associated with aging can impact swallowing and have to be differentiated from dysphagia from other neurolaryngological causes.
There is evidence that suggests that the aging larynx suffers structural and functional changes [14–16]. Saliva production is decreased. Oral time is longer as muscles are weaker. The pharynx becomes larger and more dilated. The UES relaxation is altered due to neurologic impairment and to decreased hyolaryngeal elevation. The incidence of CP bar is higher. Pooling in pyriform sinuses is common, although aspiration does not seem to occur. Increased effort is necessary to swallow and pharyngeal transit becomes longer. This exposes the airway to the risk of aspiration. The laryngeal adductor reflex decreases with age in relationship to decreases in SLN sensitivity. The decline in the rest of sensory end organs capabilities and cortical function further impair normal swallowing ongoing adaptations in the elderly are necessary to accommodate these changes.
17.5 Signs and Symptoms of Abnormal Swallow
Dysphagia is defined as a sensation of difficulty with swallowing that can occur anywhere from the mouth to the stomach. Dysphagia symptoms are summarized in Table 17.2.
Table 17.2.
Symptoms of dysphagia
Dysphagia symptoms |
|---|
Difficulty chewing |
Drooling |
Difficulty initiating swallowing |
Food retained between the cheeks and teeth |
Coughing, laryngospasm |
Choking with liquid or solid food, before, during or after swallowing |
Increased saliva |
Frequent throat clearing |
Wet voice after eating |
Sensation of food stuck in the throat |
Pain when swallowing |
Regurgitation of food or liquids |
As compensation mechanisms may have taken place, detailed questioning about dietary behaviors is necessary: chewing more, liquid ingestion after solids, cutting food in smaller pieces, double swallowing, etc. to find asymptomatic dysphagia patients.
Based on McConnel’s modelization mentioned above, one can infer from it, some clinical signs and diagnostic hints. Table 17.3 summarizes the link between McConnel’s postulated swallowing issues, clinical signs, and a non-exhaustive list of diagnostic possibilities.
Table 17.3
Types of swallowing issues
Type of swallowing issues | Clinical signs | Example of diagnostic related to clinical signs |
|---|---|---|
Orality issues | 1. Improper bolus conditioning 2. Defect of mouth water tightness (a) Anterior: drooling (b) Posterior: posterior spillage/anticipated pharyngeal phase triggering 3. Absence of pharyngeal phase triggering | 1. Edentate/masticator muscle issues/xerostomy 2.a Facial palsy 2.b Velar incompetence/myasthenia gravis/ skull base tumor (IX) 3. Dementia |
Propulsive issues | 1. Pressure leaks (a) Soft velar leaks (b) Pharyngeal hypotonia dilatation, pouching (c) UES pouching 2. Tongue plunger issues (a) Weakness (b) Stiffness 3. Pharyngeal weakness | 1.a Lesion of the IX/myasthenia gravis 1.b Post stroke 1.c Zenker’s diverticulum 2.a Myasthenia/myositis 2.b Parkinson’s disease 3. Post-stroke/oculo-pharyngeal dystrophy/myasthenia/post-stroke/post-radiotherapy |
Resistive issues | Lack of UES opening 1. Stiffness 2. Impaired neuromuscular control of EUS tone/ lack of UES relaxation 3. Lack of anterosuperior excursion of the larynx 4. EUS tone setting reflex conflict | 1. Post-radiotherapy 2. Post-stroke/recurrent/superior laryngeal nerve injury 3. Myasthenia/myositis/dystrophies/frailty syndrome/ tracheostomy 4. GERD/hiatal hernia |
Mixed issues (resistive & propulsive | 1. Global defect and/or incoordination of neuromuscular inhibitory and excitatory control 2. Global muscular weakness impeaching pharyngeal contraction and superior laryngeal anterior–superior excursion | 1. Post-stroke 2. Myotonic dystrophy/post radiotherapy |
Esophageal issue | 1. Mechanical 2. Lack of esophageal motility | 1.a Tumor 1.b Nutcracker esophagus 1.c Eosinophilic esophagitis 2. Achalasia |
17.6 Evaluation of Swallowing
Dysphagia screening and repeat objective testing in patients with NM diseases are essential to reduce the risk of aspiration pneumonia, malnutrition, or dehydration. There are two groups of diagnostic methods: (1) screening tests and bedside assessment tests and (2) the instrumental tests: Flexible endoscopic examination of swallowing (FEES), Videofluoroscopy or modified barium swallow (MBS), manometry and electrophysiological studies in between others.
17.6.1 Screening Tests and Bedside Assessment Tests
Multiple screening and bedside assessment tests have been published these last decades [17–26]. By definition a screening test should have a high sensibility, be rapid and easily performed. They are mainly used in short length-of-stay institutions such as acute care hospitals. On the other hand, bedside assessment tests have a high specificity and can be time and effort consuming in order to orient a treatment plan or assess the degree of impairment. These are more likely to be used in long length-of-stay institutions such as speciality department, rehabilitation centers, or nursing homes.
Figure 17.1 shows a non-exhaustive list of different screening/assessments tests that are available in the recent literature. They are classified on an analogical scale regarding their screening or assessment characteristics, Fig. 17.1.
Bedside assessment tests consist of a quick medical history and clinical observation of how the patient manages oral intake and saliva swallowing.
17.6.2 Dysphagia ENT Assessment
The objective is to find the alterations that lead to the dysphagia encountered in the previous tests, assess the type of diet to follow, and plan an initial treatment.
17.6.2.1 Clinical Examination
Detailed directed medical history will focus on neurological impairments, dietary restrictions, pneumonia suffering, nutritional state, and the presence of tracheostomy or feeding tubes. As compensation mechanisms may have taken place detailed questioning about dietary behavior is necessary.
Observe mental state, general appearance, posture, conversation, affective response, intellectual ability, temporospatial orientation, and possibility of cooperation in the rehabilitation.
General ENT examination will include facial mobility, lip sealing, dental health, tongue movement and strength, pharyngolaryngeal sensation, phono-respiratory coordination, and patient ability to follow directions. Sensory motor assessment of the cranial nerves involved in swallowing: V, VII, IX, X, and XII [27] will follow.
17.6.2.2 Instrumental Dysphagia Assessment
The two gold standards of oropharyngeal instrumental examination are FEES and MBS. They are complementary tests that yield different information and both can detect silent aspiration. Patient complaints and test availability will dictate the choice of test. They both assess the effect of therapeutic strategies: postural changes, sensory or dietary modifications, or therapeutic maneuvers. Comparison between FEES and MBS is shown in Table 17.4.
Table 17.4
Comparison between FEES and MBS
Fiberoptic endoscopic evaluation of swallowing (FEES) | Modified barium swallow (MBS) |
|---|---|
Bedside performed | Not beside performed |
Cheap with no specific setting needed | Costly setting |
Easily available | Not available everywhere |
No radiation | High volume of radiation |
Repeated examinations possible | Repeated exposure to radiation not recommended |
Blackout when swallowing. Indirect aspiration signs | Clear and quantifiable measures of penetration and aspiration |
Limited to pharyngolaryngeal lumen | Explores oral cavity, pharynx, esophagus, and stomach |
Cervical spine not seen | Cervical spine perfectly visible |
Direct view of anatomy and mucosal status | Indirect view of anatomy and mucosal status |
Indirect assessment of laryngohyoidal motion and velopharyngeal closure | Perfect quantifiable assessment of laryngohyoidal motion and velopharyngeal closure |
No objective measurements | Objective measures of interrelationship of laryngohyoidal elevation, pharyngeal constriction and UES opening |
Assesses sensory and motor integrity | Indirect sensory testing |
Can last long enough to evaluate fatigue | Restricted by radiation time |
Perfect assessment of vocal fold motion | Poor indirect assessment of vocal fold motion |
Flexible Endoscopic Evaluation of Swallowing and FEES with Sensory Testing FEEST
Introduced by Langmore and colleagues in 1988 [28–30], FEES combines the everyday fibrolaryngoscopy giving detailed insight into the anatomic and physiologic issues implicated in deglutition and a functional test with the aid of ingesting colored consistencies in different volumes, followed by performing specific head posture modifications or swallowing maneuvers that can improve swallowing. In 1993, Aviv introduced the sensory testing of the SLN with pulses of air in the aryepiglottic folds, FEEST [31].
The anatomic-physiologic assessment should note: velopharyngeal closure, appearance and symmetry of the larynx and pharynx at rest, base of tongue, pharyngeal constrictors function, pooling, handling of secretions, and swallow frequency, [30]. The location of the secretion should be noted: vallecula, pharynx, pyriform sinuses, larynx vestibule, or trachea. The ability to clear them by cough elicitation is an important indicator of sensory indemnity and a predictor of safety.
We should highlight the importance of the pharyngeal squeeze maneuver, a test that gives an insight of the recruitment of the pharyngeal musculature, elicited by producing the highest pitch possible as a formal test of pharyngeal strength. It can compare to the pharyngeal constriction ratio seen on videofluoroscopy. It is also an important predictor of swallowing safety [32–34].
The laryngeal sensory testing examines the laryngeal adductor reflex (LAR), a brisk and easy to identify closure of the vocal folds responsive to a stimulus. LAR is elicited even in patients with poor consciousness, incapacitated or in the absence of patient cooperation.
Videofluoroscopic Swallowing Studies or Modified Barium Swallow
The technique of MBS consists of a radiographic video of the rapid sequences that make a swallow, ingesting different barium consistencies in different volumes and the effect of different maneuvers and positions, usually performed by radiologists and speech language pathologists. The volumes, consistencies, positions, and maneuvers are similar to the ones used in FEES and in rehabilitation.
An anteroposterior and lateral RX projections are taken which can be replayed at very low speed for accurate objective evaluation. A recording acquisition of six images per seconds is required.
Developed by Logeman 93 [36], many standardized protocols have been proposed, although a reduced personalized assessment can be determined in each patient case.
In NM disorders, MBS is specially recommended to assess oral phase, velopharyngeal closure, pooling, speed and time of each phase and the interrelationship between laryngohyoid elevation, pharynx contraction, and UES opening. It identifies and quantifies the presence of aspiration during swallowing and its severity.
The Penetration aspiration scale by Rosenbeck [37] and the Dysphagia severity rating by Waxman [38, 39] would complete the assessment of food intake safety, and would recommend dietary modifications for the dysphagia severity.
One has to take into account that even though objective examinations are the gold standard to assess aspiration risk, they only examine a discrete moment of deglutition with food that may not taste or feel pleasant. Therefore one has to be cautious when recommending dietary modifications or suppression of oral intake. Barium swallow and thickened water is not palatable and swallowing is highly dependent on cognitive sensory inputs, moreover, during FEES. The endoscope also slightly impairs physiological deglutition and breathing coordination.
The volumes used for testing should not be higher than 15 ml at a time, and we should consider 2.5 ml as a more physiological volume that resembles normal saliva reflex deglutition.
Other instrumental examinations of particular interest in NM diseases are:
Electrophysiological Studies
Electrophysiological studies have not widely been used in dysphagia but they can complement others in the diagnoses and follow-up. They can differentiate between myopathy and neuropathy and they will confirm muscle involvement even if the patient is asymptomatic. They also give an objective insight into the coordination of the different phases. Simultaneous dynamic studies from the different swallowing muscles: superior pharyngeal constrictors (SPC), TA, interarytenoid (IA), and CP can be recorded using hooked wired electrodes. The activity of the submandibular muscles (SM) tends to be recorded with bipolar surface electrodes. The upward and downward laryngeal movement seen on deglutition can be recorded with a piezoelectric sensor attached in the CP membrane. Different combinations of recordings can be done depending on the object of the study. An excellent review can be seen in [40].
The normal swallow starts with the contraction of the SM muscles followed by the SPC and the relaxation of the CP. During the CP relaxation period the TA and interarytenoid (IA) muscles contract. The CP activity reappears before the TA and IA relax again. The time sequence and coordination in between these muscles is essential in understanding the dysphagia events. The SM give important information of the onset and duration of the oropharyngeal swallowing since they elevate the larynx and initiate other reflexive mechanisms of the pharyngeal phase. They also support the tongue propulsion force. In neurologic dysphagic patients the SM EMG is prolonged, postulated to be related to muscle weakness, central effect or to a compensatory maneuver to overcome aspiration [41].
The CP muscle is important to study in neurogenic dysphagia. The approach can be either percutaneous or intraluminal. Percutaneously the electrode is introduced lateral and inferiorly to the posterior cricoid lamina. Intraluminally, the larynx can be topically anesthetized and the electrode is passed through the thyrocricoid membrane and advanced medially and inferiorly to the posterior cricoid lamina under endoscopic vision. The electrodes can also be introduced by direct laryngoscopy in an anesthetized patient. The CP muscle is tonically activated during rest and relaxes when swallowing with opposing phases to the other swallowing muscles [4, 42].
Ertekin has extensively described different electrophysiological tests to assess swallowing and its relationship to NM disorders [4, 41–45] (Table 17.5). Many tests could correlate to FEES or MBS ones but additional information is always obtained. We summarize the following concepts:
- 1.
Dysphagia limit. It is the maximum volume of water that you can swallow at once. Any multiplication of the number of swallows called, piecemeal deglutition, below 20 ml is considered abnormal. It is tested by placing mechanical sensors in the cricothyroid membrane, and submental surface EMG electrodes taped under the chin. The recording of both sensors indicates the beginning of laryngeal elevation. Subjects are given 3, 5, 10, 15, and 20 ml in a stepwise manner stopping if piecemeal deglutition is observed. This test is very sensitive and specific for the diagnosis of dysphagia even in dysphagic patients unaware of their condition [41, 44].
- 2.
Laryngeal movement sensors integrated with surface SM-EMG measures the coordination between the contraction of the SM and the laryngeal upward and downward movement. Different swallowing patterns of abnormalities have been observed in neurologic dysphagic patients.
- 3.
CP-EMG with simultaneous SM-EMG analyzes the coordination between end of swallowing and CP relaxation, often abnormal in neurologic disorders such as late CP opening, premature closure, or abnormal bursts.
- 4.
Tonicity of the CP muscle is also assessed. In this test, 3 ml of water is swallowed. According to the tonicity, hyperreflexic CP-EMG is the type of EMG abnormality mostly encountered in motor neuron diseases (ALS, suprabulbar palsy) due to corticobulbar involvement. This prevents any inhibitory influence on the UES. Dysphagia in these patients comes from the lack of coordination between the paretic laryngeal elevators and the hyperreflexive CP muscle. The CP-EMG pause tends to be shorter, ending prematurely before the larynx descends. Unexpected bursts of activity can occur during the swallowing pause. Therefore the bolus is retained in the pharyngeal spaces and penetration or aspiration can occur when the larynx finally descends [42].
Table 17.5
Different electrodiagnostic tests in neuromuscular disorders
Dysphagia limit | SM-EMG (surface electrodes) | Needle EMG | Laryngeal upward/downward (piezoelectric transducer on cp membrane) | CP-EMG | Lack of coordination or abnormal opening timing | |
|---|---|---|---|---|---|---|
MG [41] | Decreased | Prolonged and decreased amplitude | Normal | Prolonged | Normal | Yes, due to slow transit, CP closes before |
Muscle disorders [41] | Decreased | Prolonged | Myotonic MUAP | Abnormal | Hyperreflexive | Yes, due to slow transit, CP closes before |
Corticobulbar: ALS and SBP, Parkinson plus [83] | Decreased | Prolonged | Denervation signs: fibrillation and positive sharp waves | Paretic | Hyperreflexive, abnormal burst in swallowing pause | Opening delayed with premature closure |
Parkinson [43] | Decreased | Prolonged | Normal | Normal | Hyperreflexive/ normal | Yes, due to slow oral and pharyngeal transit, CP closes early |
In muscular disorders, laryngeal elevators are involved but the CP is structurally intact. Coordination though can be abnormal due to the slow pharynx transit that will find the CP closed when it can no longer compensate.
Parkinson patients will have similar findings but the CP muscle will not compensate the slow bolus transport. Debate has been found whereas the CP muscle is abnormal or not in PD. Controversy still surrounds CP tonicity and its meaning.
Manometry: High Resolution Manometry and Videofluoromanometry (VFM)
Manometry consists in recording a pressure inside a lumen. It provides quantitative evaluation of the pressures and relative timing involved between the pharyngeal contraction, UES relaxation, body of the esophagus contraction, and LES opening. It is useful for patients who may benefit from CP myotomy as it sensors the pressure of the UES when contracted, relaxed, and the time it takes. Solid state or sleeve transducers disseminated along a nasogastric catheter make these recordings possible.
High-resolution manometry uses catheters with numerous transducers along them that allow an instantaneous, tridimensional graph representing time, space, and pressure signals represented by a color scale. High-resolution manometry is of particular interest in demonstrating UES relaxation.
VFM consists of simultaneous recording of radiographic images and manometric data. The reasons why pioneers combined these two techniques are rather evident. Manometry alone in the pharyngoesophageal segment is difficult to interpret without concurrent X-ray.
Recently, Rommel et al. [46] integrated data recorded by high resolution VFM associated with impedancemetry in a mathematical formula that would infer the “aspiration risk.”
To talk about “aspiration risk” rather than “aspiration events” detected at FEES or MBS is a new concept of utmost interest. Indeed, many aspiration diagnoses are done based on a couple of swallows assessed by FEES or MBS regardless of the circumstances the examination has been done. One can suspect there could be many false diagnoses. This is why talking about aspiration risk is, by far, a more robust way to assess the severity of dysphagia and thus the need for treatment [46, 47].
17.7 Neurolaryngological Diseases that Affect Deglutition
In general swallowing abnormalities are not very specific to a particular NM disorders and tend to affect multiple phases of deglutition in variable degrees and changing over time. Understanding the phase impaired and the detailed structures affected is key in planning for the best multidisciplinary treatment.
Table 17.6 summarizes the signs and symptoms of vocal and swallowing actions in NM disorders. More on the role of vocal fold immobility related to neurolaryngological diseases can be found in Chap. 6.
Table 17.6
Signs and symptoms of vocal and swallowing signs of neuromuscular disorders
Site of lesion | Neurologic symptoms | Laryngeal findings | Vocal symptoms | Swallowing findings | Swallowing symptoms | Neurologic diseases |
|---|---|---|---|---|---|---|
Upper motor neuron | Spastic paralysis Hyperreflexia Muscle weakness Slow movements | Spastic vocal fold paresis/paralysis | Strained voice, breathy voice, laryngospasm, breathing incoordination, spastic dysarthria, incoordination, altered prosody, low volume, slow speech, monotony, altered prosodic accent | Poor oral sling Increased time oral phase Reduced bolus propulsion Reduced pharyngeal constriction Insufficient larynx closure CP dysfunction Lack of coordination Decreased amplitude and precision movement | Dysphagia Silent aspiration Slow imprecise swallowing Drooling | Amyotrophic lateral sclerosis, progressive lateral sclerosis, pseudobulbar palsy CVA |
Lower motor neuron | Flaccid paralysis Hyporeflexia Muscle atrophy Fasciculations | Flaccid vocal fold paresis/paralysis, glottic insufficiency In some cases, paradoxical vocal fold motion | Weak, breathy voice, rhinolalia, flaccid dysarthria, imprecise articulation | Poor oral sling Poor tongue movement and retraction Reduced pharyngeal constriction | Dysphagia Worse silent aspiration than UMN Nasal regurgitation Drooling | Amyotrophic lateral sclerosis, progressive bulbar palsy, spinal muscle atrophy |
Extrapyramidal | Poor movement control, spasticity, tremor | Vocal fold bowing, tremor, dystonia, dysdiadochokinesia
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