A wide range of communication and swallowing disorders result from neurologic injury. This chapter provides the physiatrist with a broad overview of some of the impairments that result from acquired neurologic conditions and how they are assessed and treated by a speech-language pathologist. In addition to providing an understanding the underlying impairment, this chapter describes the impact these impairments have on the activity and participation levels of individuals undergoing rehabilitation.
Rehabilitation of Patients with Communication Disorders
Aphasia
Aphasia is a communication disorder typically resulting from damage to the language-dominant hemisphere in the brain. Stroke is the most common cause of aphasia with approximately 20% to 40% of patients with stroke having aphasia. Aphasia, however, can occur in traumatic brain injury or dementia and other progressive neurologic disorders.
Aphasia affects an individual’s ability to express and understand language. Aphasia types include Broca, Wernicke, conduction, global, transcortical motor, transcortical sensory, anomic, and crossed and primary progressive Aphasia ( Table 3-1 ). Some individuals may have relatively intact receptive language capabilities but demonstrate significant challenges with expression, whereas others may have significant deficits in both areas. Speech-language pathologists play a primary role in teasing out these deficits and identifying strengths to capitalize on during recovery. Apraxia of speech is a common co-occurring deficit and differential diagnosis is key to appropriate intervention.
| Aphasia Type | Lesion | Expressive and Receptive Language Impairments |
|---|---|---|
| Broca aphasia | Left posterior inferior frontal cortex and underlying structures | Expressive: Nonfluent aphasia with effortful speech, anomia, and reduced utterance length. Receptive: Impaired but typically better than expressive language. |
| Wernicke aphasia | Left superior temporal region or inferior parietal cortex involving angular gyri | Expressive: Fluent with normal prosody but significant paraphasias, neologisms, and empty content. They appear unaware of these deficits. Receptive: Often severely impaired with inability to understand spoken language. |
| Conduction aphasia | Left superior temporal area or the supramarginal gyrus of the parietal lobe | Expressive: Fluent with considerable anomia, paraphasias, self-correcting behavior, and difficulty with repetition. Receptive: Relatively intact auditory comprehension of spoken language. |
| Global aphasia | Frontotemporoparietal | Expressive: Limited speech output but may exhibit ability to produce repetitive perseverative utterances. Receptive: Severely impaired ability to understand spoken and written language. |
| Transcortical motor aphasia | Occlusion of anterior cerebral artery with damage to the border zone areas in the frontal lobe superior or anterior to Broca area | Expressive: Similar to Broca aphasia, nonfluent, limited speech with dysarthric component. Receptive: Generally intact. |
| Transcortical sensory aphasia | Posterior or inferior to Wernicke area | Expressive: Similar to Wernicke aphasia but able to repeat and can exhibit echolalia. Receptive: Significant impairment understanding spoken and written language. |
| Anomic aphasia | Focal damage to the left temporal and parietal areas | Expressive: Primary challenge is word finding and naming. Speech includes pauses and circumlocutions and they typically have a good prognosis for recovery. Receptive: Generally intact. |
| Crossed aphasia | Rare incidence of right hemisphere lesion resulting in aphasia | Expressive and receptive: Mirrors aphasias of left hemisphere. Some may also have co-occurring visual-spatial deficits consistent with right hemisphere lesion. |
| Primary progressive aphasia | Insidious onset | Initial symptoms include word finding deficits similar to acute aphasia but later expands to greater difficulty with expressive and receptive language along with dementia and other cognitive communication deficits. |
Assessment by the speech-language pathologist involves identification of the specific areas of language deficit, including spoken language, auditory comprehension, reading and writing, and the severity of these deficits. Standardized assessments, such as the Western Aphasia Battery–Revised and the Boston Naming Test, are often used to identify specific areas of deficit to guide treatment planning.
Intervention with adults with aphasia is unique in that these are individuals who typically were literate before injury and have a lifetime of experiences to communicate and share. However, the language deficits associated with aphasia make it difficult for these individuals to not only communicate basic wants and needs but also to be able to maintain their previous life roles. Many become isolated, and their social networks significantly diminish after injury. Although the exact rate and extent of recovery varies, many are left with substantial communication impairments. Therefore speech-language pathologists focus their interventions on restorative as well as compensatory strategies and techniques to supplement language deficits and to facilitate participation with the greatest level of independence possible.
Early in recovery in the acute rehabilitation setting, patients may be struggling to not only express what their wants, needs, and ideas are but to also understand what is being said to them. Language deficits related to aphasia can make it challenging for the patient to fully participate in rehabilitation with all disciplines; therefore the speech-language pathologist’s intervention will focus on developing and implementing compensatory strategies and techniques and training/supporting therapy, nursing, and family in these strategies and techniques. Compensatory strategies and techniques for individuals with aphasia are also referred to as augmentative and alternative communication (AAC). AAC can take the form of low-tech (pictures, communication boards, talking photo albums, augmented input such as writing) to high-tech (computerized communication devices and software that the patient can use to communicate) options. The specific content (pictures compared with words), the complexity of the content (e.g., low tech compared with high tech, amount of communicative content represented) is determined through careful assessment and trials with the patient as well as specific feedback from the rehabilitation staff and family. For example, a patient with auditory receptive deficits may benefit from adding written words on a dry-erase board or pictures of content in addition to the auditory cues given in therapy. In another example, a patient with severe expressive deficits may benefit from photographic images presented in a communication device to communicate basic requests to staff and family as well as to support communication of biographic information (e.g., home, family, vocation, interests). These compensatory AAC strategies and techniques help the patient communicate their current needs and in the contexts in which they need to participate to the fullest extent possible. In addition, the speech therapist will often focus on attempting to restore deficit areas to a more functional level (e.g., naming, conversation, reading, writing). This combined approach is essential, particularly for those with severe impairments because their recovery of expressive and receptive language abilities may be an ongoing process. These individuals may plateau at a level where they will require compensatory tools for the long term.
There is evidence that currently supports the intensity of treatment offered to the patient with aphasia. In general, shorter bouts of intense treatment have been shown to improve communication outcomes compared with less intense treatment over longer periods. However, extended periods of therapy that include a strict regimen of intervention (2 to 4 hours daily) can also result in substantial improvements in communication. Constraint-induced aphasia therapy has been compared with multimodal aphasia therapy with comparable results.
The impact of new interventions with repetitive transcranial magnetic stimulation (rTMS) is being explored, along with the development of computerized treatment options to augment and supplement speech treatment. In addition, pharmacologic therapy modulating the activity of several neurotransmitter systems with medications, such as levodopa, donepezil, galantamine, and memantine, have been used along with language therapy for treatment of aphasia with moderate success.
Education is a key component of treatment because it is often difficult for family and friends to understand the difference between cognitive and language deficits. Family and friends must understand that individuals with aphasia are aware of what is occurring around them and that they remember who people are but that they cannot access the “language” to communicate this information. In addition, they may need to rely on modalities other than spoken language to understand what is being said to them (e.g., writing key words down may facilitate comprehension of the topic of conversation). The long-term nature of some deficits can be difficult to accept for patients and family because they have a significant impact on the patient’s ability to return to preferred life roles (e.g., work, family, and social roles). Providing education about the existing deficits and providing training on the use of compensatory strategies and techniques to facilitate full participation are essential as the patient and family begin to adjust to changes in life roles.
Special Considerations: Handedness and Language Dominance
Since the description of left hemisphere language regions in right-handed patients by Paul Broca in the nineteenth century, it has been speculated that the reverse, that is, right hemisphere language dominance, should be true of those who are left-handed. This claim has been widely accepted as the Broca rule, although Broca never explicitly postulated such a rule. Luria was among the first to point out that such an association could not be universally true because even in those who are left-handed, aphasia usually occurs after a lesion to the left hemisphere. Ninety-three percent of the population is right handed, with the left hemisphere being dominant for language in 99% of right-handed individuals. In left-handed individuals, 70% have language control in the left hemisphere, with only 15% having it in the right hemisphere, and 15% in both hemispheres, localizing the language control in the left hemisphere in approximately 97% of the population.
Even now, our knowledge about the suspected association between handedness and language dominance rests almost exclusively on studies of neurologic patients. In this population, however, there is an increased incidence of pathologic left-handedness and right language dominance because the control of both dexterity and language can shift to the right hemisphere after long-standing left hemisphere lesions.
Cognitive Communication Disorders
Cognitive communication disorders is a term used to describe a cluster of deficits that impair the processes of memory, new learning, awareness, problem solving, organizing, planning and execution, and all areas of executive function. The causes of these impairments vary as does the approach to intervention. In addition, whether the condition is severe and whether the condition is recovering or degenerative affect the exact focus of treatment. The following sections describe the management of cognitive communication disorders that result mostly from right hemisphere stroke, traumatic and nontraumatic brain injury, and Alzheimer disease and other dementia.
Right Hemisphere Stroke
Cognitive communication disorders that result from right hemisphere strokes include a range of deficits, including memory, attention, problem solving, decreased awareness/insight into severity of deficits, processing and expressing higher level/abstract language concepts, decreased or flat affect, organizing, planning, and other executive functions. Visuospatial neglect is often a co-occurring deficit and affects scanning and attention for reading, writing, and functioning safely in all environments. The most commonly reported cognitive communication deficits in patients who have had right hemisphere damage include attention, neglect, perception, and learning/memory. Speech-language pathologists formally assess these deficits with a variety of standardized tests, including the Ross Information Processing Assessment (RIPA), the Cognitive Linguistic Quick Test (CLQT), or the Scales of Cognitive Assessment Test Battery (SCATBI).
Specific treatment goals and intervention strategies vary on the basis of severity of deficits. However, increasing insight into deficits can be a particularly challenging barrier in rehabilitation. Coupled with a common left neglect, more severely affected patients require significant cues and support to safely navigate and participate in all environments. Research has indicated that those without neglect tend to have reduced cognitive communication deficits compared with patients with left visual field neglect. Education of family on how to manage these deficits and provide the level of cueing and supervision necessary for the patient is essential.
Intervention with the speech-language pathologist might focus on activities related to home, community, and work reentry. Taking the specific deficits into account and how these deficits affect reintegration back into these environments is essential. For example, if a patient is expected to return to work, the ability to perform daily work functions (e.g., reading, writing, problem solving, time management) is assessed, and specific interventions are designed to compensate for deficits and to restore certain areas that were affected by the stroke.
Traumatic and Nontraumatic Brain Injury
Individuals who have sustained a brain injury demonstrate a range of neurobehavioral and cognitive disorders. Brain injuries are typically classified as traumatic (e.g., resulting from impact, translational pressure, or rotational forces to the brain) or nontraumatic (e.g., tumor, anoxia, aneurysm). Traumatic injuries include penetrating (open) head injury that often causes focal damage and closed head injuries that often result in diffuse axonal damage. Brain injury recovery typically occurs in stages, and speech-language intervention goals and objectives vary by stage.
The cognitive communication disorders associated with brain injury are often described with the Rancho Los Amigos Levels of Cognitive Functioning ( Table 3-2 ). For clinical intervention, these levels are often grouped into stages and treatment goals focus on supporting and optimizing the progressions through these stages. The stages of recovery include early (Rancho Levels I-III), middle (Rancho Levels IV-V), and late (Rancho Levels VI-VIII).
| Rancho Level | Communication/Behaviors |
|---|---|
| Unresponsive to any stimuli and there is no evidence of language processing. |
| Reacts inconsistently and unpurposefully to stimuli in nonspecific manner. Receptively and expressively there is no evidence of processing or verbal or gestural expression. |
| Reacts specifically, but inconsistently, to stimuli. May follow simple commands in an inconsistent, delayed manner. Language begins to emerge (e.g., automatic verbal and gestural responses, yes/no head nodding, single words, limited reading). |
| Behavior may appear bizarre and outbursts may be common. Attention to environment is very short and recall is limited. Disinhibition is common with inability to self-monitor behavior. Literal paraphasia may be present and incomplete expression of thoughts. Marked disruptions in auditory and visual processing may be apparent. |
| Able to respond to simple commands with consistency. Disoriented/confused with limited short-term recall. May be able to sustain short bursts of appropriate automatic social behavior. Verbalizations may be bizarre with many confabulatory statements. Semantic and syntactic confusion may be impaired. |
| Shows goal-directed behavior, follows simple commands, and demonstrates some increases in short-term memory. Processing of receptive language is delayed with some difficulty in retaining and synthesizing information. Difficulty with new learning is evident. Speech may be characterized by monopitch, monostress, and monoloudness. |
| Appropriate and oriented to immediate environment, able to follow daily routine with structure/support. Ability to process and retain receptive language improves for simple/concrete information. Expressive language may be tangential, concrete, and self-oriented. Judgment remains impaired. |
| Increasing memory/recall and ability to learn and retain new information. May demonstrate higher level cognitive-language deficits that become more apparent under new or stressful situations. |
Early Stage of Recovery: At this level, the speech-language pathologist focuses on stimulating and shaping responses for basic communication and will look for consistency of ability to respond, follow basic commands, and helping the team identify when the patient is transitioning from generalized to localized responses. Most patients at this level are nonspeaking and in the early stages of demonstrating consciousness.
Middle Stage of Recovery: As the patient transitions from early to the middle stage of recovery, they may be very agitated and treatment generally focuses on structuring the environment to reduce agitation so that the patient can continue to participate as fully as possible in rehabilitation. The patient transitions from an agitated to a nonagitated state, but confusion and disorientation are still evident. Evidence has shown that this stage of recovery is particularly important with regard to speech recovery. As a patient begins to cognitively “clear” at this stage, many will become verbal communicators. For those who remain nonspeaking through this middle phase of recovery, it is a long-term disability attributable to either significant motor speech impairment/or aphasia/apraxia. If a patient remains nonspeaking at this level, AAC will be implemented by the speech-language pathologist. Because of the significant cognitive challenges that are still apparent at this stage, a variety of AAC systems will likely be developed and implemented over time. Some examples may include the use of a single message switch that has recorded messages to make basic requests, eye-gaze boards to communicate yes/no, or simple digitized message devices with a small number of messages to communicate basic needs or personally relevant information. The particular device, access method, and types of messages to be communicated are individualized per patient and dependent on the physical capabilities of the patient, his or her cognitive and language status, and the needs of the family and rehabilitation team. If AAC is a long-term recommendation for a patient with a brain injury, it may evolve and gradually change into consistent use of a more sophisticated computerized communication device once the patient has reached the late stages of recovery.
For patients who regain their ability to speak at this stage, the focus of intervention is to increase orientation and insight, short-term and prospective memory, new learning, processing auditory and visual information, managing language of confusion and confabulations, and ability to learn new information, following directions, and processing and increasing functional participation in rehabilitation.
Late Stage of Recovery: At this level, speech intervention focuses on increasing orientation, memory, carryover of new learning, and eventually higher-level executive functions for home, school, and community reintegration.
Mild Brain Injury.
Some individuals sustain mild brain injuries that are not easily detectable through brain imaging, and many may bypass an acute inpatient hospital stay. However, high-level cognitive communication disorders associated with these injuries can affect work, home, and community reintegration. Impairments of executive function (e.g., planning, organization, attention, self-monitoring, prospective memory, insight) are common. Many of these individuals receive therapy on an outpatient basis. Intervention focuses on increasing awareness of deficits, education, and the development and application of a range of compensatory strategies (e.g., organizational systems, memory logs, planners, specific recall strategies, electronic reminders, reorganization of work environment to facilitate recall and organization). Some may be struggling to maintain their employment and driving given the deficits they are experiencing; therefore intervention focuses on compensating for these losses so that the individual can maintain employment and life roles. Over time, many report a lessoning or resolution of impairments. For those with lasting deficits, compensatory strategies developed during intervention become lifelong habits that enable these individuals to fully participate in work and life roles as independently as possible.
Alzheimer Disease and Other Dementia
The pathophysiologic features of dementia can vary by person and can be caused by neurodegenerative changes in the brain, vascular in origin, the result of toxic reactions, infections, or repeated head injury. Diagnosis is based on extensive patient history and excludes other associated issues, cognitive and neuropsychological testing, psychiatric evaluation, and brain scanning. Definitive diagnosis hinges on evidence of short- and long-term memory impairment in addition to at least the presence of aphasia, apraxia, agnosia, or impaired executive functioning. Speech-language pathologists can assist in identifying specific cognitive communication disorders, the severity of these disorders, and the presence of other conditions.
Treatment focuses primarily on patient, family, and caregiver education and compensatory strategy implementation. Some direct intervention strategies have been identified as potentially beneficial, such as spaced retrieval (specific memory intervention where recall is systematically lengthened). In the early stages, when impairments are mild/moderate, treatment may focus on developing strategies to compensate for memory loss to maintain the greatest level of independence possible. If co-occurring expressive language deficits exist, strategies to supplement communication would be addressed. Actively engaging family and caregivers in treatment is necessary to provide them with the skills to support the patient over time as the dementia progresses and the patient becomes more dependent on others for daily needs. Treatment often occurs in bouts at crucial times during the patient’s disease progression to develop new strategies and provide education for the patient and caregivers.
Motor Speech Disorders
Dysarthria
Dysarthria is a motor speech disorder resulting from a wide range of acquired injuries, including (but not limited to) stroke, brain injury, and neurodegenerative conditions (e.g., amyotrophic lateral sclerosis, Parkinson disease, multiple sclerosis). Dysarthria, present in many disorders, is a major source of disability because of its impact on communication. Dysarthria can be categorized into types based upon the Darley, Aronson, and Brown dysarthria classification system and include the following: flaccid, spastic, ataxic, hypokinetic, hyperkinetic, and mixed ( Table 3-3 ). Dysarthria involves all or some of the speech subsystems, including respiration, phonation (laryngeal), resonance (velopharyngeal), and articulation (tongue, lips).
| Type of Dysarthria | Site of Lesion | Neuromuscular Symptoms | Speech Characteristics |
|---|---|---|---|
| Flaccid | Peripheral nervous system or lower motor neuron system | Weakness, decreased muscle tone | Hypernasal, imprecise articulation, slurred speech, breathiness |
| Spastic | Pyramidal and extrapyramidal systems | Weakness, increased muscle tone | Harsh voice quality, imprecise articulation, strain-strangled voice quality, hypernasality |
| Ataxic | Cerebellum | Slow and inaccurate movement | Prolonged speech, slow rate, imprecise articulation, irregular articulatory breakdowns |
| Hypokinetic | Basal ganglia and subcortical structures | Slow movements, limited range of movements | Rapid speech, low volume, reduced articulatory movements |
| Hyperkinetic | Basal ganglia and subcortical structures | Quick, unsustained, involuntary movements | Harsh and/or strain-strangled vocal quality, voice stoppages associated with dystonia, involuntary speech movements |
| Mixed | Upper and lower motor neuron | Varies depending on level of motor neuron involvement | Variable, example: harsh but breathy vocal quality |
In addition to determining the dysarthria type and the specific subsystems involved resulting in speech impairment, the speech-language pathologist has a range of tools to quantify the impairment to guide treatment planning. Objective intelligibility testing can be accomplished with a range of possible measures, including the Word Intelligibility Test or the Speech Intelligibility Test . These assessments quantify the impact of the dysarthria on phoneme production and serve as a general measure of how the dysarthria affects the patient’s ability to be understood in day-to-day environments. Computerized aerodynamic assessment allows for quantification of intraoral pressure (centimeters of water) and the amount of nasal airflow (cubic centimeters per second) present, with identification of potential timing of soft palate closure. Endoscopy can also assist in visualization of the velopharyngeal function. Computerized voice analysis programs, such as the Visi-Pitch IV, also assist in quantifying specific vocal characteristics that may be impaired, including pitch, shimmer, and jitter. Along with bedside assessment and initial motor speech examination, these tools can provide a comprehensive analysis of the type, severity, and functional impact of the dysarthria and guide the speech-language pathologist in the specific targets for remediation.
Management of dysarthria depends on subsystem involvement and severity. For example, poor respiratory support may be managed with specific exercises, binders, abdominal paddles, biofeedback tools, such as respiratory induction plethysmography (Respitrac), and voice amplification devices. If velopharyngeal dysfunction is a prominent feature, immediate management of hypernasality is warranted because it affects respiratory drive for speech. A nasal obturator and palatal lift prosthesis are common interventions in cases of velopharyngeal incompetence. Opportunities for extensive practice are necessary to make functional changes in speech.
Some types of dysarthria have been documented to respond particularly well to specific treatments. For example, the Lee Silverman Voice Treatment program has been shown to be a highly effective treatment for those with hypokinetic dysarthria common in Parkinson disease. New treatments, including the SpeechVive, have had promising results for even those with significant cognitive impairment along with hypokinetic dysarthria. Other strategies, such as alphabet supplementation, have been documented as effective interventions for some that greatly increase functional intelligibility.
For those with moderate to severe dysarthria or for those who have degenerative conditions, such as amyotrophic lateral sclerosis, AAC is often a warranted intervention. Evidence supports the assessment for and implementation of a high-tech AAC system for individuals with amyotrophic lateral sclerosis once their speaking rate reaches 120 words per minute. Ball and colleagues have found that although intelligibility may be relatively high (90% or above), once a patient’s speaking rate reaches 120 words per minute, or half of the normal speaking rate, there is a precipitous drop in intelligibility that typically follows shortly thereafter. Using this guideline in intervention helps speech-language pathologists make timely decisions for ordering and implementing high-tech devices to ensure that these patients can continue to communicate effectively throughout their course of illness. AAC devices and strategies can be semitemporary or long-term communication tools used by individuals with dysarthria even as they continue to work on regaining speech. Studies have shown that some individuals can make functional improvements in speech production many years after injury, demonstrating the need for ongoing speech practice support and the need for technologies and strategies to supplement or augment speech over time.
Apraxia
Apraxia of speech (AOS) is a motor speech disorder that is caused by a disturbance in the planning and programming of movements for speech despite normal muscle functioning. AOS can occur simultaneously with aphasia and dysarthria or, although infrequently, can occur as a “pure” apraxia. The neurologic insult resulting in AOS has been suggested to be in the left cerebral hemispheres in the premotor and motor cortices, although Broca area and the insula have also been implicated. In addition to AOS, other ideomotor apraxias can include limb apraxia and nonverbal oral motor apraxia. In all ideomotor apraxia, individuals know what they need to do but cannot sequence the movements. This typically affects voluntary movements, with automatic movements remaining intact. The primary clinical characteristics of acquired AOS include slow speaking rate, lengthened sounds and durations between sounds, sound distortions, consistent errors, and abnormal prosody. Although not discriminatory of AOS, other characteristics may include articulatory groping, perseverative errors, increased errors with increased word length, difficulty initiating speech, and a preference for automatic speech instead of novel speech. In those with a severe AOS, their speech may be limited to only a few words. A speech-language pathologist typically assesses for AOS by completing an oral mechanism examination, which includes a physical examination to look at the structure and function of the speech mechanism, as well as a motor speech examination to assess performance across various speech tasks, including single word repetitions, repetitions of words of increasing length, alternating motion rates (single syllable repetitions), sequential motion rates (syllable sequence repetitions), a comparison of automatic and volitional speech, and assessment of speech in reading and conversation. A formal assessment that may be used for adults includes the Apraxia Battery for Adults , second edition (ABA-2). Formal assessments used with children include the Kauffman Speech Praxis Test, the Verbal Motor Production Assessment for Children, as well as the Dynamic Evaluation of Motor Speech Skills (DEMSS) (in development). Therapy typically involves intense, repetitive behavioral therapy, most frequently an articulatory-kinematic approach that focuses on the position or movement of the articulators, and is based on principles of motor learning. Articulatory-kinematic approaches use integral stimulation (i.e., “watch me, listen to me, say it with me”) for cueing and work through a hierarchy of steps to increase accuracy of speech production, such as Sound Production Treatment. Individuals with AOS need intensive practice and benefit from blocked, consistent practice and immediate, frequent feedback early on to lead to initial success, while progressing to random, variable practice and delayed, infrequent feedback later to lead to greater generalization. Treatment approaches may use visual feedback, such as watching video self-recordings or using the VAST application developed for the iPad. Other treatment approaches, such as script training, work on personalized, core phrases and sentences to develop automaticity. Treatment approaches that focus on rate and rhythm control are also being explored. Progression through therapy for AOS can be lengthy; therefore it is vital to ensure that the individual with AOS has a means of communication while working on improving speech. Low-tech and high-tech AAC should be established early to provide an effective means of communication.
Rehabilitation of Patients with Swallowing Disorders
Oropharyngeal swallowing is a complex sensorimotor behavior involving the precise selection and sequencing of many paired muscle systems, which are regulated by the central and peripheral nervous systems, and modified by sensory mechanisms. The safe and efficient passage of food items allows nutritional and hydration needs to be met without the risk of airway compromise. Swallowing disorders, or dysphagia, affect more than 6 million individuals with acquired and congenital disorders and 22% of individuals older than 55 years. The successful management of swallowing disorders is best accomplished through evaluation and treatment with an interdisciplinary team of professionals who are involved with the delivery of clinical services for patients with dysphagia. The most effective teams typically involve a speech-language pathologist, occupational therapist, physiatrist, dietician, and psychologist. In most clinical situations, the speech-language pathologist is typically the principal provider of dysphagia diagnostic and treatment services. A physiatrist requires a strong working knowledge of all rehabilitation modalities (e.g., physical therapy, occupational therapy, and speech-language pathology) and, more specifically, swallowing disorders to guide dysphagia services as the physician assumes ultimate responsibility for directing the overall care of a patient. This section of the chapter provides an overview of neurophysiology, an overview of common assessment tools, and a brief overview of disorders and treatment.
Physiology
The normal swallow is typically divided into four stages: oral preparatory, oral transit, pharyngeal transit, and esophageal. During the oral preparatory stage, liquids and solids are prepared for transport to the pharyngeal cavity. Sucking is one of the very first motor behaviors a human infant will perform in life. There are several muscles that converge lateral to the oral angle to form a semitendinosus node known as the modiolus. The movements of the modiolus are central to the actions of lip rounding and spreading, as well as sucking and swallowing.
The mammalian suck is primarily generated by a neuronal network called the suck central pattern generator (sCPG). Central pattern generators (CPGs) are bilateral networks of premotor interneurons that direct output to lower motoneurons to activate and sequence rhythmic, patterned motor outputs. Although CPGs can generate motor patterns in the absence of descending or sensory inputs, these inputs play a highly significant role in modulating and shaping the motor output of CPGs. The sCPG is located within the brainstem pontine and medullary reticular formation, is highly responsive to peripheral inputs, and adapts its patterned motor output to changes in task dynamics and manipulations in the local environment.
From a clinical perspective, the ability to safely feed depends on a coordinated suck, swallow, and breathe pattern regulated by a swallow central pattern generator (swCPG) consisting of a network of pontomedullary premotor internuncial circuits, which influence the firing patterns among trigeminal, facial, glossopharyngeal, ambiguous, and hypoglossal lower motor neurons. In mammals, fluids are transported through the oral cavity by consecutive cycles of rhythmic oral activity, which accumulates as a bolus primarily in the valleculae of the oropharynx and periodically empties into the esophagus. The process of emptying the valleculae corresponds to the pharyngeal stage of the classical swallow, and this action is periodically integrated into one of the fluid transporting cycles to form a combined transport/swallow cycle. After liquids enter the oral cavity, the bolus is collected by the tongue and positioned between the surface of the tongue and the palate in a “swallow-ready” position. The lips maintain a seal to prevent anterior spillage. Premature leakage of food from the oral cavity to the pharynx is prevented by tongue-palate contact behind the bolus.
For solids, when food enters the mouth, it is positioned to allow for mastication. As with many other vital life functions, such as breathing, sucking, and swallowing, mastication is a rhythmic movement. It is characterized by cyclic jaw movements that vary among animal species and the types of food they consume and in humans requires coordination of more than 20 orofacial muscles, in concert with breathing and swallowing. Similar to sucking, rhythmic mastication is primarily under the control of internuncial circuits within the brainstem and is modulated by descending inputs from a putative cortical masticatory area. In fact, it is still unclear whether the masticatory CPG (mCPG) is an evolution of the sCPG that transforms its intrinsic properties and network connectivity during development or whether the mCPG emerges as its own separate network during weaning.
The natural masticatory sequence has been divided into three functionally different, consecutive series based on the jaw movement trajectory and jaw muscle activity: (1) the preparatory series , where the food in the anterior portion of the mouth is transported back between the molar teeth; (2) the reduction series , where the food is broken down between the teeth; and (3) the preswallowing series , where the food is transported posteriorly toward the pharyngeal region for the swallow to occur. During rhythmic mastication, there is a disproportionately high level of jaw-closing activity relative to jaw-opening activity. This is necessary for the breakdown of food, and it is common across many species (including humans) that mastication often occurs on one favored side. During mastication, the lips are sealed, and the tongue mixes the food particles with saliva to form a bolus for transportation to the pharynx. The cheeks or buccal walls are also compressed to prevent the bolus from pocketing in the lateral sulcus. Similar to liquids, the bolus is placed in the swallow-ready position immediately posterior to the tongue tip. The lips and cheeks remain compressed, as the tongue flattens anteriorly to posteriorly along the roof of the mouth propelling the bolus into the pharynx.
The pharyngeal stage involves multiple simultaneous muscular events to prevent airway compromise and allow safe passage of the bolus to the esophagus. The soft palate elevates and retracts, with the pharyngeal wall compressing along the soft palate to achieve a velopharyngeal seal. As the bolus passes into the pharynx, the base of tongue retracts posteriorly to contact the posterior pharyngeal wall, which has stiffened and shortened. The pharyngeal wall contracts superiorly to inferiorly, compressing the bolus toward the esophagus. The upper esophageal segment (UES) opens to allow the bolus to pass into the esophagus. As the bolus passes through the pharynx, multiple events occur to protect the airway. The true vocal folds adduct, the arytenoids tilt to the base of the epiglottis, and the hyolaryngeal mechanism is pulled upward and forward by contraction of the suprahyoid and thyrohyoid muscles.
The cricopharyngeus muscle is typically contracted between swallows, opening briefly during the swallow. The opening is influenced by hyolaryngeal elevation, relaxation of the cricopharyngeus muscle, and pressure of the bolus against the UES.
The esophagus is quite different from the pharynx because it is primarily composed of striated muscle in its cervical portion and smooth muscle in its thoracic portion. Because the thoracic esophagus is a largely smooth muscle, it has intrinsic contractile activity that can be increased or inhibited by autonomic nerves. Once the bolus has passed through the UES, it is propelled down the esophagus by peristalsis (defined as a wave of inhibition followed by a wave of excitation that propels material down a hollow viscus). In the upright position, gravity assists peristalsis. The lower esophageal sphincter (LES) is held closed by tonic muscle contraction between swallows. It relaxes during a swallow and is pushed open by the pressure of the descending bolus.
Central “Cortical” Representation of Swallowing
Recent evidence on deglutition and swallowing supports the notion of reciprocal or heterarchical control among cerebral cortex, forebrain, cerebellum, and brainstem loci. Functional neuroimaging in humans indicates an elaborate network of cortical areas participating in the volitional swallow. The blood oxygen level–dependent (BOLD) response associated with the functional magnetic resonance imaging (fMRI) technique during reflexive swallows reveals a cerebral network localized bilaterally to the lateral primary somatosensory and motor cortex. Voluntary swallows produced by healthy young adults show a more elaborate bilateral activation in the insula, prefrontal (Brodmann area [BA] 24, 32, 33), anterior cingulate, parietooccipital (BA 7, 17, 18, 19, 26, 30, 31), and primary somatosensory and motor cortices (BA 1, 2, 3, 4) with an asymmetry favoring the right brain. This pattern of asymmetry is reversed during reflexive swallows. The expanded representation during volitional swallows is likely to be related to motor planning and the urge to swallow when presented a small water bolus. Transcortical magnetic stimulation studies in humans indicate the presence of multiple cortical areas, including oral motor, pharyngeal motor, and esophageal motor cortex, in BA 4. The face sensorimotor cortex, cortical masticatory area (CMA), and cortical swallowing area (CSA) are active during deglutition in awake primates with intracortical microstimulation. Swallowing can be evoked by electrical stimulation of face primary motor cortex (M1), face primary somatosensory cortex (S1), CMA, and an area deep to CMA.
Pathophysiology
Dysphagia can lead to malnutrition, dehydration, inability to safely protect the airway resulting in respiratory compromise, and a decrease in quality of life. Swallowing disorders are frequently described in terms of stage affected: oral, pharyngeal, or esophageal. Regardless of site, it is useful to consider whether a given impairment of swallowing affects food transport (preparation and propulsion of the bolus), airway protection (prevention of laryngeal aspiration), or both, because these have implications for treatment.
During the oral preparatory and transit stages, the lips, tongue, cheeks, and jaw are active in completing mastication, bolus preparation, and transportation from the oral to the pharyngeal cavity. Weak or uncoordinated oral movements may result in retention of the bolus in the oral cavity. An impaired labial seal can result in spillage anteriorly. Pocketing in the lateral sulcus can occur as a result of buccal weakness or lingual incoordination resulting in difficulty with forming a cohesive bolus. Posterior spillage from the mouth to the throat can occur secondary to posterior lingual weakness or incoordination with the bolus falling prematurely into the pharynx during mastication.
Pharyngeal disorders are difficult to visualize during the clinical assessment and should be evaluated through instrumentation. There are many signs and symptoms that can be observed during a meal, such as coughing, choking, multiple swallows, but the cause of these behaviors is unknown until instrumental assessment is completed. Disorders at this stage may include impaired swallow initiation, ineffective bolus propulsion, retention of a portion of the bolus in the pharynx after swallowing, and aspiration of the bolus. Nasal regurgitation may be noted when the soft palate does not elevate and the pharyngeal wall contraction is incomplete around the soft palate. When tongue base retraction is weak, pharyngeal propulsive force can be inadequate, resulting in retention of all or part of the bolus in the pharyngeal recesses after swallowing. Similar findings can be produced by weakness of the pharyngeal constrictor musculature. Epiglottic inversion is a passive movement reliant on bolus pressures, base of tongue retraction, and hyolaryngeal elevation. If the epiglottis does not invert during swallowing, it might act as a physical barrier, resulting in retention of part of the bolus in the valleculae after swallowing.
Another cause of food retention in the pharynx after swallowing is impaired opening of the UES. This can be caused by increased stiffness of the UES, as in fibrosis or inflammation, or failure to relax the closing muscle of the sphincter (primarily the cricopharyngeus muscle). Because UES opening is an active process, failure of opening can also be caused by weakness of the muscles of sphincter opening, particularly the anterior suprahyoid musculature. Dyscoordination of the swallow can also lead to failure of UES opening. Because the UES is ordinarily closed between swallows, its opening is obligatory for swallowing to occur. This means that failure of UES relaxation and opening can produce obstruction of the food pathway.
Airway protection is a critical function of swallowing; however, airway protection mechanisms are not always effective. Failure of laryngeal protective mechanisms can reflect reduced laryngeal elevation, incomplete closure of the laryngeal vestibule, or inadequate vocal fold closure caused by weakness, paralysis, or anatomic fixation. For the purpose of dysphagia rehabilitation, laryngeal penetration is defined as passage of material into the larynx but not through the vocal folds. Aspiration is defined as passage of material through the vocal folds. Laryngeal penetration can be observed in healthy individuals. Aspiration of microscopic quantities occurs in healthy individuals, but aspiration that is visible on fluoroscopy or endoscopy is pathologic and is associated with an increased risk of aspiration pneumonia or airway obstruction. The normal response to aspiration is a strong reflex coughing or throat clearing. Laryngeal sensation is often abnormal, however, in individuals with severe dysphagia. Silent aspiration, or aspiration in the absence of visible response, has been reported in 25% to 30% of patients referred for dysphagia evaluations. The effects of aspiration are highly variable, and some individuals tolerate small amounts of aspiration without apparent ill effects. Several factors determine the effect of aspiration in a given individual, including the quantity of the aspirate, the depth of the aspiration material in the airway, the physical properties of the aspirate (acidic material is most damaging to the lung), and the individual’s pulmonary clearance mechanism. Predictors of aspiration pneumonia risk include diagnoses of chronic obstructive pulmonary disease and congestive heart failure, presence of a feeding tube, oral/dental status, bedbound status, and presence of dysphagia.
Dysphagia can result from a wide variety of disorders. A major cause of dysphagia is stroke. Dysphagia is found in approximately half of individuals with a recent stroke. Most recover within the first 2 weeks, but dysphagia can be severe and persistent. Brainstem lesions can result in particularly severe dysphagia, given their proximity to the major swallow centers.
Reduced laryngeal elevation, insufficient UES opening, vocal fold weakness, and severe weakness of oropharyngeal muscles are common in patients with stroke. Cerebral lesions can result in dyscoordination of the swallow, with impaired oropharyngeal bolus propulsion and airway protection. Swallow dysfunction is typically more severe in bilateral cerebral lesions because there is bilateral cortical representation for swallow function. By contrast, the brainstem motor nuclei innervate only ipsilateral muscles, so lesions of cranial nerves or their nuclei can result in unilateral sensory or lower motor neuron dysfunction.
In neurodegenerative disorders, dysphagia can be the first symptom. Oral-stage dysphagia is common in Parkinson disease, characterized by tremor, dyskinesia, and bradykinesia in lips, tongue, jaw, and larynx, which hamper oral and pharyngeal food transport. Medication for Parkinson disease does not improve swallowing, even when it is effective for improving other aspects of motor function. Alzheimer disease can result in agnosia for food within the oral cavity, characterized by oral holding and incoordination of swallowing. In motor neuron disease, progressive degeneration of motor neurons in the brain and spinal cord results in weakness in the muscles of mastication, respiration, and swallowing. Inflammatory muscle diseases, including dermatomyositis and polymyositis, commonly affect striated muscles, resulting in weakness of the pharynx. By contrast, progressive systemic sclerosis affects smooth muscle and commonly produces esophageal dysfunction, including reduced peristalsis, dilatation of the lower esophagus, and gastroesophageal reflux disease (GERD).
Tumors of the oral cavity, pharynx, and larynx can be treated with surgical excision, deletion of anatomic structures, chemotherapy, or radiation therapy. Dysphagia occurs from tissue loss or dysfunction. Oral cavity cancer often requires partial or complete glossectomy and mandibulectomy, which can limit lingual and mandibular function for bolus formation and propulsion, and significantly increase aspiration risk. Pharyngeal tumor excision can require removal of structures critical for swallowing, including the faucial arches, hyoid bone, epiglottis, and pharyngeal constrictors. Ineffective laryngeal protection and reduced pharyngeal transport are common. Supraglottic laryngectomy, a common cancer surgery, spares the true vocal cords but eliminates the epiglottis, laryngeal vestibule, and false vocal folds. Without these laryngeal protective mechanisms, individuals are at increased aspiration risk. Pharyngeal transport problems are also common. Total laryngectomy separates the airway from the pharynx with a permanent tracheostomy. Although there is no risk for aspiration, pharyngeal transport problems resulting from weakness, tissue fixation, and cricopharyngeal dysfunction are common.
Radiation therapy can cause fibrosis of the oral cavity, pharynx, and larynx immediately after radiation or, in some cases, years later. Xerostomia (dry mouth) and edema are common when salivary glands are within the radiation field, hampering bolus formation and timing of oral and pharyngeal transport. The salivary changes are often permanent. Fibrosis can result in delayed swallow initiation, decreased pharyngeal transport, and ineffective laryngeal protection.
Structural abnormalities, whether congenital or acquired, can impair swallow function. Birth defects, such as clefts of the lip and palate often produce inadequate labial control for sucking and bolus control, or velopharyngeal insufficiency with nasal regurgitation. The resulting dysphagia can lead to malnutrition, requiring surgical repair of the defect during infancy.
Structural abnormalities can impair pharyngeal transport and airway protection. Cervical osteophytes are common in the elderly and can impinge on the pharynx. This can also be seen with edema or hematoma after anterior cervical fusion. Webs and strictures can obstruct the food pathway. Diverticula can form along the pharyngeal or esophageal walls. The Zenker diverticulum is a pulsion diverticulum of the hypopharynx. Its mouth is located just above the cricopharyngeus muscle, but the body of the pouch can extend much lower. Food or liquid collects in the diverticulum and can be regurgitated to the mouth or result in aspiration.
Esophageal dysfunction is common and is often asymptomatic. Webs, rings, or strictures of the esophagus can obstruct the lumen and might require dilatation. Esophageal motor disorders include conditions of either hyperactivity (e.g., esophageal spasm) or hypoactivity (e.g., weakness) of the esophageal musculature. Either of these can lead to ineffective peristalsis with retention of material in the esophagus after swallowing. Retention can result in regurgitation of material from the esophagus back into the pharynx, with aspiration of the regurgitated material. Patients who complain of discomfort or the food sticking in the chest almost always have an esophageal problem.
Patients suspected of having esophageal dysphagia should be referred to a gastroenterologist because there may be structural disorders, including strictures or even cancer. Persistent pain on swallowing (odynophagia) is suggestive of esophageal cancer. In esophageal cancer, early detection and treatment can save lives. Another possibility is achalasia of the esophagus; this also requires prompt evaluation and treatment. When there is structural narrowing of the esophagus, dilatation is often effective but generally must be repeated periodically because narrowing can recur. Esophageal dysphagia can also be due to physiologic disorders, even when the anatomy is normal. These include spasm and ineffective peristalsis and may be amenable to pharmacotherapy.
GERD can affect swallowing indirectly. In GERD, the LES has insufficient tone, rendering it ineffective for preventing gastric contents from passing back through the LES into the esophagus. Because the esophageal lining is not resistant to acid (as is the stomach lining), reflux of highly acidic stomach contents can result in inflammation (esophagitis) or scarring (stricture) of the esophagus. This can lead to pain or obstructive symptoms. In severe cases, the refluxate can pass all the way up the esophagus and into the pharynx, passing through the UES. The individual with severe GERD is particularly vulnerable at night, when protective reflexes are less effective. Under these conditions the refluxate can be aspirated, causing inflammation or scarring of these vital airway structures. Although GERD is not a swallowing disorder per se, it can be an underlying cause of dysphagia or aspiration pneumonia.
Dysphagia is often iatrogenic. Several drugs can impair swallowing, including anticholinergic drugs and benzodiazepines. Neuroleptic agents, also called antipsychotic drugs, can cause movement disorders affecting the face and mouth, such as tardive dyskinesia, especially after long-term use. These can impair eating and swallowing. Any medication that causes sedation can have an adverse effect on swallowing and potentially impair airway clearance (e.g., cough) in response to aspiration.
Postoperative dysphagia is a common complication of anterior cervical fusion, occurring in approximately half of patients. Individuals with multiple cervical surgical levels demonstrate a higher risk of having dysphagia when compared with those undergoing survey at one level. The mechanism is unclear, but it might be related to injury of the pharyngeal constrictor muscles or their innervation. Most patients recover within the first 2 months. Compromised and altered respiratory function increases the risk for dysphagia. Chronic obstructive pulmonary disease alters the coordination of respiration and deglutition. Patients who have undergone lung transplantation may demonstrate dysphagia, with a high risk of silent aspiration.
Exacerbations can lead to aspiration. Endotracheal intubation and ventilator dependency can cause decreased laryngeal sensation, pooling of secretions in the pharynx and larynx, impaired swallow initiation, and aspiration. The presence of a tracheostomy tube alters normal pharyngeal aerodynamics, eliminating the positive subglottic pressure normally associated with swallowing and hampering laryngeal protective reflexes. An inflated cuff does not fully eliminate aspiration, because secretions can still leak around the cuff into the trachea. A cuffless tracheostomy tube is often better tolerated. A unidirectional tracheostomy speaking valve prevents expiratory airflow through the tracheostomy tube, providing expiratory flow through the larynx and upper airway, and restoring positive subglottic air pressure thereby reducing laryngeal penetration and aspiration.
Evaluation
To effectively treat swallowing disorders (i.e., providing appropriate dietary recommendations, behavior management strategies, and rehabilitation exercises) and decrease risk for dysphagia-associated medical complications, the health care team first needs to correctly identify the specific biomechanical aspects of the swallowing function through the appropriate use and interpretation of a diagnostic swallow procedure. The purpose of the swallowing evaluation is to assess dysphagia and, when appropriate, make recommendations for diet, swallow safety strategies, and rehabilitation interventions. Swallowing evaluations can be divided into two main categories of bedside/clinical assessments and instrumental assessments.
Instrumental swallowing assessments include evaluation procedures, such as the videofluoroscopic swallow study (VFSS), the fiberoptic endoscopic examination of the swallow (FEES), high-resolution manometry (HRM), and ultrasonography. Regardless of the type of assessment used to evaluate the swallow, the examiner should recognize that the results represent only a snapshot picture of a patient’s swallow function at any moment in time. Many variables, such as the underlying medical condition, medication timing, distractions, or even unknown factors potentially influence swallow function in either a positive or negative manner. Furthermore, it is not unusual for a person with dysphagia to demonstrate variable swallowing performance depending on the time of day because of fatigue or timing of medications. The variability of swallowing performance throughout the day may be especially prominent in patients with progressive neurologic diseases or with elderly patients. Therefore it is imperative to interpret the results of the swallowing assessment in conjunction with the overall clinical picture of the patient.
Bedside/Clinical Swallow Assessments
Swallow Screenings.
The swallow screening is usually the first step to identify the risk of dysphagia and is often completed by the nurse or the physician. The screening protocols may take on a variety of forms, and although the most valid screening protocol remains to be determined, it is generally agreed that the screening protocol should be quick and minimally invasive. The purpose of the swallow screen is to accurately identify individuals who present a risk of dysphagia and to expedite a referral to speech-language pathologist for further evaluation. The swallow screening may identify risk factors for dysphagia by means of self-report, by clinical history, or by direct clinical observation.
One type of swallow screen available is the Yale Swallow Protocol, or as it is more commonly known, the 3-ounce water challenge. The Yale Swallow Protocol has three components: a brief cognitive screen, an oral mechanism examination, and the 3-ounce water challenge. To pass the Yale Swallow Protocol, the individual must consume the 3 ounces of water uninterrupted without any overt signs of aspiration (e.g., cough, wet voice quality). If a person is unable to drink the entire amount uninterrupted or demonstrates coughing during or immediately after consuming the water, then this is considered a fail on the Yale Swallow Protocol.
Other swallow screenings reported in the literature also use water with volumes ranging from 5 to 90 mL and with different criteria for pass/fail. Direct assessment of the swallow by having the individual actually swallow something has been associated with higher quality screenings. Furthermore, the use of water as part of a screening makes the screening relatively easy to administer. Questions regarding the safety of allowing a patient to self-administer 3 ounces of water during the screening remain, and further research is required to determine which water-screening protocol is the most valid along with defining the most appropriate algorithm to identify dysphagia risk factors.
Clinical Swallow Examination.
The clinical swallow examination (CSE) is often conducted after the individual fails the swallow screening and is usually completed by a speech-language pathologist. Although the CSE does not allow for any direct observation of the physiology of the swallow, other pertinent information can be obtained related to swallow function. The CSE is used in settings, such as nursing homes, and in home health where access to an instrumental assessment of the swallow (e.g., VFSS or FEES) may not be readily available.
The CSE has five basic components: (1) medical history and current medical status; (2) cognitive/mental status function; (3) oral motor function; (4) laryngeal and pulmonary function; and (5) trial swallows. Medical history and current medical status include a review of the individual’s nutritional status, hospital treatments, laboratory values, medications, and respiratory status. The cognitive/mental status evaluation may include an assessment of alertness, orientation, memory (i.e., long-term, immediate, delayed), ability to follow directions, and reasoning/problem-solving skills. The oral motor assessment includes primarily an evaluation of the lips, tongue, dentition, and hard/soft palatal structures. The oral mechanism structures are evaluated for abnormalities with strength, tone, symmetry, or movement (e.g., apraxia) of the structures, as well as any structural deviations related to surgical/acquired condition or congenital factors. Preliminary studies are beginning to emerge demonstrating potential objective measures of oral strength and range, which may be beneficial during the initial evaluation for predictors of swallowing outcomes. Dentition and condition of the oral mucosa are also evaluated during the oral motor assessment. Laryngeal function is indirectly assessed by evaluating strength of the cough and vocal quality. Pulmonary status is assessed by the observation of the individual’s respiratory rate at rest.
Depending on the results for the cognitive/mental status function, oral motor function, and laryngeal/pulmonary function, the clinician may then attempt trial swallows. Usually the clinician will have the individual attempt a saliva swallow, followed by an ice chip, and then other bolus sizes and consistencies as deemed appropriate. The clinician can observe for oral phase deficits as evident by labial spillage, buccal pocketing, or prolonged mastication. It is also helpful for the clinician to place his or her fingers gently on the patient’s neck to assess submandibular movement, hyoid bone movement, and laryngeal movement during the swallow trials. The correct placement of the fingers will further assist the clinician with making additional observations related to the timeliness and strength of the swallow response. Furthermore, the clinician observes for any overt signs of aspiration with the presence of a cough, throat clear, or “wet” vocal quality either during or immediately after the swallow. If the patient demonstrates any clinical signs of aspiration during the swallow trails, this usually triggers a referral for an instrumental assessment of the swallow.
Blue Dye Clinical Swallow Examination.
When a CSE is conducted with an individual with a tracheostomy tube, the use of food coloring (e.g., FD&C Blue Dye No. 1) mixed with the food and liquid is done to enhance the visualization of the bolus to assist the examiner with the detection of tracheal aspiration. If blue-tinged secretions are present in or around the tracheostomy tube or suctioned through the tracheostomy tube after the swallow trials, then the examination result is considered positive for aspiration. The amount of blue dye added to the food and liquid during the blue dye clinical swallow examination (BDCSE) is relatively small (1 to 2 mL). There has been some reported potential risks related to the use of blue dye or food coloring with patients with increased gastrointestinal permeability (e.g., sepsis, burns, trauma, shock, renal failure, celiac sprue, and inflammatory bowel disease), and caution may be warranted with these patient populations.
The usefulness of the BDCSE has been questioned by many researchers. Several studies with rehabilitation patients who had a tracheotomy revealed that the BDCSE had sensitivity rates ranging from 38% to 79% for the detection of aspiration by the BDCSE as compared with the VFSS. The accuracy of aspiration detection of the BDCSE has also been compared with the FEES procedure. During simultaneous BDCSE and FEES, the BDCSE again only had a 50% sensitivity rate for the detection of aspiration when compared with the FEES.
Given the relatively poor sensitivity of the BDCSE to detect aspiration in patients with a tracheostomy tube, it is recommended in cases where the patient has a negative BDCSE (i.e., no aspiration detected) that further workup either by means of a VFSS or an FEES be conducted to confirm the results before the initiation of oral feedings. In cases where the BDCSE result is positive for aspiration, the examiner may then want to defer the instrumental swallow assessment of either the VFSS or FEES until the BDCSE is negative. The BDCSE is designed to only detect the presence or absence of tracheal aspiration in patients with a tracheostomy tube (with only a 50% false-negative error rate), and the BDCSE cannot determine why the patient is aspirating or whether strategies may be used to eliminate or reduce the aspiration. Therefore in some cases where the patient has a positive BDCSE result, a VFSS or FEES may be indicated if it is suspected that the instrumental examination at that time would provide additional diagnostic information that would allow the individual to successfully advance to oral feedings.
Cervical Auscultation.
Cervical auscultation is a noninvasive technique used during a CSE and involves a listening device (i.e., stethoscope) usually placed at the lateral aspect of the neck above the cricoid cartilage to evaluate swallow and airway sounds during the pharyngeal phase of swallow. On the basis of the sounds the examiner hears, judgments are made as to whether the “swallowing sounds” were considered normal or abnormal. An abnormal swallowing sound would suggest the presence of aspiration. The clinical efficacy of using cervical auscultation during a CSE to detect aspiration has been mixed. Criticism of this technique include limited interrater reliability related to how the swallowing sounds correlate with various physiologic events during the swallow and the presence or absence of aspiration.
Instrumental Swallow Assessment
Videofluoroscopic Swallow Study.
The VFSS is the most commonly performed instrumental swallow assessment and is known by several different names, such as the “modified barium swallow,” the “cookie swallow,” or the “pharyngogram with video recording.” The arrival of cinefluorography (i.e., motion picture x-ray film) in the 1950s allowed for the examination of the swallow as a dynamic process. As technology advanced, the use of video recordings for the fluoroscopic images began to replace the cine recordings as radiation exposure were less for the video recordings as compared with the cine recordings and thus lead to the introduction of the VFSS.
The VFSS involves the use of a fluoroscopic x-ray image along with various consistencies of barium sulfate to evaluate the physiology of the swallow function during the oral, pharyngeal, and esophageal phases. The VFSS allows the examiner to identify normal and abnormal anatomy and physiology; evaluate the integrity of airway protection before, during, and after the swallow; and evaluate the effectiveness of bolus modifications, postural changes, and swallowing maneuvers used to improve swallow safety and efficiency. The VFSS is recorded to allow further analysis with a frame-by-frame review of the film. At most facilities, the VFSS is completed in the radiology department with a radiologist, radiology technologist, and a swallowing clinician (usually a speech-language pathologist); however, at some facilities, the VFSS is completed with a physiatrist or other physician specialist with an interest in swallowing disorders instead of a radiologist. For members of the health care team conducting the VFSS, they should receive additional training and education regarding radiation protection, wear protective lead shielding (e.g., thyroid collar, full lead apron, protective eye goggles), and/or stand behind a glass lead shield or barrier during the examination.
There are several standardized VFSS protocols available in the literature, and in clinical practice there are even additional variations to these standard VFSS protocols. The basic components of most VFSS protocols involve assessing various bolus consistencies (e.g., thin liquids, nectar-thick liquids, honey-thick liquids, puree, semisolids, and solids), bolus sizes (e.g., 1 mL, 3 mL, 5 mL, uncontrolled large bolus), and presentation methods (e.g., cup sip, straw sip, patient-administered, clinician-administered). Further, most VFSS protocols involve the introduction of compensatory strategies (e.g., positioning, swallowing maneuvers, and bolus modifications) to identify the most optimal conditions for swallowing performance. The challenge when performing a VFSS is to determine when it is necessary to perform a standardized protocol versus performing a tailor-made study designed to match typical eating behaviors. Additionally, when conducting the VFSS protocol for clinical practice, the examiner must take into account how to obtain as much information about the swallow function with the minimum amount of radiation exposure. Finally, a particular bolus consistency or size should be deferred during the VFSS protocol if it is judged that advancing the patient to test the item would be unsafe.
Assessment of the esophageal phase is not a major component of the VFSS protocol; however, some examiners may choose to scan the esophagus when clinical indications (e.g., globus) are present. Patients who complain of discomfort or the food sticking in the throat or neck may have a problem in either the pharynx or the esophagus (including the thoracic esophagus). For this reason and others, it is wise to image esophageal swallowing as well as oral and pharyngeal when performing a VFSS. This is one of the advantages of fluoroscopy over FEES. Currently, there are no practice guidelines available on the proper performance of an esophageal screen. The patient’s position (e.g., upright versus supine), viewing position (lateral versus anteroposterior view), bolus size, and bolus consistency may all influence the esophageal screen.
FEES Procedure.
The FEES is the second most common instrumental assessment of the swallow and allows for an evaluation of the anatomic structures of the larynx and pharynx, accumulated oropharyngeal secretion levels, swallowing ability, and sensory ability with a flexible laryngoscope with a halogen or xenon light source. During the FEES, the oral phase and the height of the swallow during the pharyngeal phase cannot be directly observed, and the examiner must make inferences based on the preswallow and postswallow components of the FEES. The examiner (i.e., endoscopist) visualizes the images of the pharynx directly through the eyepiece or with a chip camera attached to the laryngoscope. The use of a chip camera allows viewing of the images on a monitor and can be recorded for further analysis.
The FEES protocol includes an assessment of the anatomic structures of the larynx at rest and in movement, the accumulated oropharyngeal secretion level, and bolus flow of various foods and liquids while swallowing. If difficulty with swallowing is observed during the FEES, then similar to the VFSS protocol, compensatory swallow safety strategies (e.g., positioning, swallowing maneuvers, and bolus modifications) may be introduced to identify the most optimal conditions for swallowing performance.
The main advantage of the FEES not only includes the ability to identify the signs and symptoms of dysphagia but also provides a view of the anatomy and physiology of the swallow and accumulated oropharyngeal secretion levels. A common physiologic abnormality observed during the FEES is the presence of reduced vocal fold mobility, which has been associated with increased risk of aspiration. Before any bolus presentation, the FEES clinical protocol involves an observation of secretions including describing the amount and location. The evaluation of secretion levels is important because the examiner uses this information to quickly differentiate between safe levels of accumulated secretions and those that are dangerously high because the presence of endolaryngeal secretions are highly predictive of subsequent aspiration on the FEES.
Another important clinical component of the FEES protocol is identifying the relationship among sensory input, airway protection, and swallowing ability. With the FEES protocol, sensation as it relates to swallow function may be either directly assessed with light touching of the endoscope to the pharyngeal/laryngeal structures or indirectly assessed on the basis of the patient’s response to the presence of pharyngeal residue, laryngeal penetration, or aspiration. The FEES protocol may also be enhanced with a specialized endoscope with a side instrument channel that allows for the delivery of calibrated puffs of air to the mucosa of the larynx. The calibrated puffs of air during the FEES protocol is known as the fiberoptic endoscopic evaluation of swallowing with sensory testing (FEESST). During the FEESST protocol, laryngeal sensation is inferred through observation of the laryngeal adductor reflex elicited after the delivery of the puffs of air. The degree of sensory deficit is inferred by the amount of calibrated puffs of air required to elicit the laryngeal adductor reflex during the FEESST. The inclusion of the calibrated puffs of air during the FEESST is not a required element for the FEES.
Comparison of VFSS and FEES.
Many authors have stated that the VFSS is the “gold standard” to evaluate swallow function; however, evidence in the literature supports that both the VFSS and FEES are valuable procedures to evaluate the swallow. During simultaneous VFSS and FEES, findings related to laryngeal penetration, tracheal aspiration, and pharyngeal residue between the two procedures have demonstrated excellent agreement. Furthermore, recommendations for diet level and compensatory swallow safety strategies have been reported as similar between the two examinations. The selection of either the VFSS or FEES procedure is usually driven by specific patient characteristics (i.e., the field of view necessary to best identify the pathophysiologic condition of the swallowing dysfunction) or availability of equipment and personnel at the facility to perform the procedure.
High-Resolution Manometry.
HRM is a relatively new procedure and uses 36 circumferential sensors placed 1 cm apart to measure pressure events during the pharyngeal and esophageal phases of the swallow. HRM accurately captures the complex pressure events along the entire length of the pharynx and esophagus that provides a more comprehensive picture of how bolus volumes may affect swallow physiologic function. HRM is promising as an emerging technology because its use may reveal subtle findings that perhaps were not detectable with traditional manometry.
Ultrasonography.
Ultrasonography has been used to evaluate swallowing physiologic function for a long time; however, the clinical efficacy of this procedure in standard clinical practice has been inconclusive. When ultrasonography is used to evaluate swallow function, a submental placement is often used to visualize bolus transport during the oral phase of swallow and to also measure hyoid bone displacement in the pharyngeal phase of the swallow. The advantages of ultrasonography include no exposure to radiation, noninvasiveness, and portability. The limitations of ultrasonography are the limited use in clinical practice and training opportunities available. Finally, further studies are required to evaluate the reliability of aspiration detection with ultrasonography.
Electromyography.
Electromyography (EMG) of the muscles of the pharynx and larynx is a reliable method for detecting lower motor neuron dysfunction and aberrant central motor patterning. EMG is not a sufficient test for demonstration of swallow physiologic function, however, and should be used only as an adjunct to other instrumental assessments. EMG can be used in biofeedback as an adjunct to dysphagia therapy.
Treatment of Dysphagia
Similar to the earlier description of treatment for communication disorders, treatment approaches are described in terms of restorative (exercise) or compensatory (posture, diet modification, swallowing maneuvers, surgery). Early treatment of dysphagia has been shown to reduce the patient’s risk for aspiration pneumonia, to reduce medical complications related to malnutrition and dehydration, and to reduce the length of the hospital stay. Equally important is the amelioration of barriers that decrease an individual’s ability to participate in and enjoy the pleasures of eating orally. Small physiologic improvements in swallowing that do not result in an increase in quality of life miss the true goal of rehabilitation.
Restorative: Exercise Training and Plasticity Considerations
The oropharyngeal system exhibits considerable plasticity in the adaptation of new tasks or sensory experiences in health and disease. For example, during daily tongue training, the proportion of neurons in the primary somatosensory cortex (S1) and the primary motor cortex (M1) correlated with tongue protrusion increased with training. Additional studies have shown the importance of task-related specificity among tongue motor representations and the CMA. The specificity in orofacial gestures and swallowing for targeted neuroplasticity interventions suggest that consideration be given for stimulus salience (nonswallow task training compared with swallow-specific task training) to affect beneficial behavioral change and adaptive plasticity for swallowing and oral motor behaviors.
The strength training principles of overloading and specificity have been successfully applied to swallowing training. Following the principle of specificity, it is best to select exercises that are similar to the target behavior. The Mendelsohn and Masako exercises apply this principle as the individual is attempting swallowing function during these exercises. Overloading involves competing exercises at resistance levels higher than typically used. During the Mendelsohn maneuver, the swallow is prolonged longer than the normal duration. For Masako, the anterior tongue is anchored, resulting in increased pharyngeal constrictor activity. Examples of exercise training that incorporate increased intensity of resistance are the isometric lingual exercise, expiratory muscle strength training (EMST), effortful swallow, Mendelsohn maneuver, Masako maneuver, and Shaker exercise.
Pharyngeal and esophageal motor cortical representations undergo expansion and suppression, respectively, following brief periods (approximately10 minutes) of 10-Hz electrical pharyngeal sensory stimulation in healthy adult participants. The swallowing motor cortex can be altered for a sustained period of time after sensory stimulation of the pharynx. Pharyngeal stimulation appears to produce a larger effect on potentiation of the swallowing network compared with voluntary swallowing in adult patients with dysphagia; thus peripheral stimulation is favored over volitional exercises. Sensory interventions are logical targets of neuroplasticity research. Pulse trains or repetitive peripheral stimulation is more effective than single pulse stimulation. Low-frequency (<1 Hz) stimulation induces inhibition, whereas high-frequency stimulation (>5 Hz) generally results in excitatory effects. rTMS at 5 Hz positioned over the swallowing motor cortex increases the excitability of the corticobulbar projection to the pharyngeal musculature. The suppression of the pharyngeal motor representation with rTMS is both intensity dependent and frequency dependent in the control of swallowing. The feature of transference is demonstrated by the finding that pharyngeal stimulation can lead to a suppression and decrease in the central representation of the esophageal motor cortex. It logically follows that peripheral sensory stimulation represents an important neurotherapeutic intervention in swallowing rehabilitation.
The application of electrical stimulation to improve muscle function is not new in rehabilitative medicine and is biologically plausible in theory for dysphagia treatment. In a neuromuscular electrical stimulation typical treatment session, surface electrodes are taped to the skin overlying the submental or anterior cervical strap muscles. With a commercial device marketed specifically for dysphagia therapy, pulsed electrical stimulation is delivered in a controlled, structured manner (59 seconds on, 1 second off, for 60 continuous minutes daily).
Studies have demonstrated that electrical stimulation results in depression of the hyolaryngeal complex. Electrical stimulation can put patients with severe dysphagia at risk for penetration as the hyolaryngeal complex descends. Electrical stimulation should only be used with patients who can overcome the hyolaryngeal lowering.
Compensatory Strategies in Swallowing Rehabilitation
Compensatory strategies are designed to increase safe swallowing in the presence of abnormal physiology. These can be divided into posture, maneuvers, and diet modification. They are to be performed with every swallow or just before a meal, as in the case of a novel approach pioneered by Japanese physiatrists. Patients are taught to perform self-dilatation of the UES when the sphincter does not relax satisfactorily during a swallow. This is accomplished by patients inserting a balloon catheter into their UES before each meal. Another compensatory strategy that is performed before eating is thermal tactile stimulation. This strategy is recommended when delayed pharyngeal swallow is observed. A chilled laryngeal mirror is used to stroke the anterior faucial pillars five to six times before a meal and intermittently throughout the meal. Improved timing of swallow initiation has been demonstrated to occur for up to three swallows after application, but long-term benefits of thermal tactile stimulation have not been observed. This treatment should be viewed as a short-term compensatory strategy.
Postural strategies have been reported to successfully address 80% of all swallowing disorders. These strategies involve use of gravity or changes in anatomy to assist in propelling bolus of improving airway protection. Examples include collapsing pharyngeal space by turning the patient’s head toward the impaired side, having the patient do a chin tuck to widen the vallecula, and positioning the epiglottis in a more protective position posteriorly to prevent laryngeal penetration or aspiration. For a description of compensatory interventions and purpose, refer to Table 3-4 .
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