Adult Neurologic Disorders

PRELIMINARY CONSIDERATIONS: SWALLOWING SYMPTOMS AND NEUROLOGIC DEFICITS

Swallowing disorders are symptoms of underlying disease processes. One implication of this perspective is that swallowing disorders in patients with neurologic disorders should manifest the characteristics of damage to different areas of the nervous system. This premise has long been accepted in the arena of motor speech disorders (dysarthria).¹ For example, spastic dysarthria results from damage to the upper motor neuron system governing speech production. Upper motor neuron damage results in specific patterns of neuromotor impairment, including spasticity, slowed movement, exaggerated reflexes, and reduced range of movement. The characteristics of spastic dysarthria are believed to be the direct result of spasticity in the corticobulbar system governing speech production. Patients with spastic dysarthria demonstrate a slow rate of speech, limited movement of the speech articulators, equalized stress patterns, and other characteristics reflecting the underlying neuromotor characteristics of spastic weakness.

Brief Overview of Functional Neuroanatomy Relative to Swallowing Functions

Motor and sensory systems work together to produce movement, including movement associated with swallowing. However, in clinical practice motor and sensory functions frequently are described separately as they may relate to impaired swallowing physiology. To facilitate a clinical perspective, a top-down approach to the nervous system is followed in which sensory and motor components are described at each level. Figure 5-1 is a simplified schematic depicting each “level” of the nervous system. Table 5-1 summarizes neurobehavioral and sensorimotor functions associated with each level.

TABLE 5-1

Basic Sensorimotor Functions Associated with Different Levels of the Nervous System

Level	Motor	Sensory
Cortical	Intent Initiation Programming Execution	Recognition Awareness Motor tuning
Subcortical (basal ganglia)	Initiation Refinement Inhibition	Motor tuning Awareness Sensory conduit
Brainstem	Junction box: upper motor neuron/lower motor neuron Motor/sensory “centers”: Swallow Respiration Heart	Reflexes Sensory conduit
Cerebellum	Refinement Inhibition	Refinement
Peripheral nerves	Lower motor neuron Drive movement	Sensory conduit
Muscles and sensory receptors	Effect movement	Sensation reception

CORTICAL FUNCTIONS

Functional control of sensorimotor behaviors in the human cortex frequently is described in reference to various areas or regions. The frontal lobe cortex is deemed responsible for multiple aspects of motor control, ranging from intent and initiation of movement to coordinating a movement in time and space to executing the movement in an organized and timely fashion. In general, parietal lobe regions are responsible for recognizing and interpreting sensory functions. These functions might include identifying the presence of a sensory stimulus or the interpretation of a sensory stimulus in reference to an appropriate motor response. Sensorimotor impairments resulting from cortical damage may vary in response to the location of neurologic deficit, extent of the deficit (larger areas of damage are believed to result in more severe or widespread behavioral impairments), and whether the neurologic damage is unilateral or bilateral.

Other important functions housed within the cortex are those of human communication and cognition. Damage to primarily the left side of the brain may result in a number of difficulties in the ability to communicate. Focal attention is frequently afforded to the area of the inferior frontal lobe and superior temporal lobe, although damage to these areas often is accompanied by damage to adjacent motor control areas of the frontal lobe and/or sensory control areas of the parietal lobe. Cognitive deficits associated with cortical dysfunction may present in various forms with different levels of severity and different clinical courses depending on the location of damage and the nature of the underlying disease process.

arriving to and leaving from the cortex are the major sensory and motor tracts within the central nervous system. Damage to the sensory tracts arriving in the primary sensory strip of the anterior parietal lobe results in loss of recognition of sensory stimuli in the corresponding body area. Damage to the motor tracts leaving the primary motor strip in the posterior frontal lobe (upper motor neurons) results in paresis or paralysis of the corresponding body area. Sensory or motor deficits are similar regardless of the location of the damage along the tracts. For example, cortical level damage to the upper motor neuron system results in the same type of motor weakness as subcortical or brainstem upper motor neuron damage.

Cortical Functions and Swallowing Impairment

If motor functions of the cortex range from intent to execution, then swallowing deficits resulting from cortical damage may range from no observable swallow activity to poorly coordinated execution of the act of swallowing. In considering these possibilities, frequent cortical pathologic conditions such as stroke, dementia, and traumatic brain injury should be reviewed.

Before reviewing dysphagia characteristics in various cortical pathologies, a worthwhile question to ask is “Where is swallowing function represented in the human cortex?” Given the complexity of motor control involved in oropharyngeal swallowing, it is logical to implicate the frontal cortex, specifically areas involved in various components of motor control. In fact, results of both animal and human studies using lesion or cortical stimulation techniques implicate the importance of the lateral frontal cortex, the inferior frontal lobule, and the insula in various motor acts associated with feeding and swallowing. Recent studies using functional magnetic resonance imaging (fMRI) implicate a wide range of cortical, subcortical, and brainstem structures involved in swallowing performed by healthy volunteers.² Not surprisingly, the primary motor and sensory cortical areas consistently participated in swallowing function. In a comparison of ischemic stroke patients with dysphagia and stroke patients without dysphagia, the internal capsule emerged as the only brain region significantly associated with dysphagia. However, other areas of the sensorimotor cortex and the basal ganglia also were frequently associated with the presence of dysphagia in stroke patients.³

Although findings from many studies implicate a dysphagia based in poor motor control resulting from damage to the anterolateral and precentral frontal cortex, no consensus exists concerning the specific characteristics of these dysphagias. Still, hemispheric damage to frontal areas underpinning motor control resulting in direct movement deficits should raise significant clinical concern for the presence of dysphagia.

What about cortical or hemisphere lesions that impair sensory function? These sensory areas of the hemisphere may be important in understanding swallowing functions and impairments. In fact, some studies report that many stroke patients with dysphagia have damage to the parietal lobe with associated sensory deficits.⁴ Primary sensory areas of the cortex have extensive interconnections with the motor areas of the cortex. Sensory function is deemed important in the control of voluntary movement. Beyond direct sensory loss, we should consider conditions in which the patient cannot interpret sensory information, for example, neglect. Patients with neglect may not respond to a stimulus in the swallowing tract (food or liquid bolus), not because of direct sensory loss, but because of a cortical deficit in processing and interpreting sensory information. In at least one study, hemispatial neglect was related to nonoral intake of food and liquid, but not severity of dysphagia, in patients evaluated 3 days after hospital admission for stroke.⁵ Unfortunately, these investigators did not interpret the association between neglect and nonoral intake. As a result, the presence of neglect may be related to feeding limitations rather than swallowing deficits leading to nonoral intake.

More recently, increased systematic attention has been afforded sensory functions in swallowing and swallowing impairment.6–8 Continued emerging information and clinical observations suggest that impaired sensory functions may have a direct influence on swallowing functions. A better understanding of the role of sensory systems on swallowing function and impairment may lead to improved sensory-based interventions for dysphagia.

CLINICAL CORNER 5-1

Sensory deficits may be observed in many neurologic (and nonneurologic) diseases and disorders. They may range from a direct loss of sensory input (e.g., numbness, blindness) up to and including the inability to interpret an intact sensory signal (e.g., agnosia, cortical blindness). Depending on the nature of the sensory deficit, patients may have reduced (and at times insufficient) oral intake of food and liquid. However, this deficit level of oral intake of food and liquid may not represent a dysphagia (here meaning specific difficulty swallowing food). Rather, certain sensory deficits may contribute to feeding limitations that reduce oral intake of food and liquid. Clinical specialists in the area of dysphagia need to be able to differentiate various sensory deficits and interpret their impact on feeding versus swallowing impairments.

CRITICAL THINKING

1. What types of sensory problems might occur within the swallowing mechanism—specifically the oral and pharyngeal components of the mechanism? Consider various diseases and/or disorders that might contribute to these sensory deficits. Be sure to consider direct sensory loss versus deficit interpretation of sensory input.

2. How would you evaluate sensory functions within the swallow mechanism from direct sensory loss up to poor interpretation of sensory information?

3. What practical impact might sensory deficits have on the oral intake of food and liquid? Consider specific clinical examples.

Issues of Unilateral versus Bilateral Hemispheric Lesions

The issues previously raised regarding hemispheric contribution to swallowing control also raise the question of whether such control is unilateral or bilateral. A traditional perspective is that patients with bilateral lesions often demonstrate the most severe and persistent dysphagia characteristics.⁹ Still, patients with unilateral hemisphere lesions may demonstrate dysphagia to varying degrees. Recent research using the technique of transcranial magnetic stimulation has suggested an interesting point of view on the hemispheric representation of swallowing function. Transcranial magnetic stimulation involves sending a magnetic current across the cranium over discrete hemisphere regions. These magnetic currents stimulate motor activity that is measured in various muscles by electromyography. This interesting work on the hemispheric control of swallowing function can be summarized as follows:

1. Swallowing motor functions are bilaterally represented in the hemispheres.

2. If the dominant hemisphere is impaired, a contralateral “backup” area may be available to facilitate recovery.

3. A form of cortical plasticity may occur over time, increasing the utility of the intact, nondominant hemisphere to control swallowing motor functions.

4. Bilateral strokes would result in the most tenacious dysphagias.10–13

In some respects, this perspective is consistent with traditional clinical observations; bilateral strokes produce the most severe dysphagias, and many patients with unilateral strokes often recover the ability to swallow after a period of dysphagia.

SWALLOWING DEFICITS IN HEMISPHERIC STROKE SYNDROMES

Several issues must be addressed when considering dysphagia secondary to hemispheric strokes. These issues may be simplified into two general considerations: location of damage and functional consequences of the damage. These considerations are not mutually exclusive. Location of the damage may be important in understanding sensory and/or motor impairments and in understanding the severity and potential for recovery based on unilateral versus bilateral lesions. In clinical practice, information on lesion location often is not available at the time of the dysphagia evaluation. Therefore a strong reliance on the clinical examination of functional impairment after stroke may provide the best “road map” to understanding and perhaps predicting dysphagia characteristics. Table 5-1 provides a basic orientation to some of the functional impairments that may be clinically observed after impairment to various levels of the nervous system. At the hemisphere level, intent to swallow may be an important consideration. If the patient indicates such intent, a subsequent consideration would be motor initiation of the swallow. Patients with damage to premotor areas (e.g., supplemental motor cortex) may have generalized difficulty with motor initiation. The clinical picture may be that of a patient who holds a bolus in the mouth for an abnormally long period with associated movements that indicate the intent to swallow but without initiating a swallow.

Practice Note 5-1

The difference between intent to swallow and poor initiation of the swallow may be difficult to differentiate clinically. Some patients may hold food or liquid material in the mouth but not make any overt attempt to swallow. When this situation is encountered, one strategy is to observe differences in swallows when the patient self-feeds versus when the clinician provides the material to be swallowed.

Several years ago we encountered a young woman who had a severe stroke. Details of the stroke were sparse other than it was large and involved the frontal areas of the brain. She was nonverbal but did produce some vocalizations and demonstrated a very hypokinetic appearance. She was receiving all nutrition and hydration by gastrostomy tube. During the fluoroscopic swallowing study a clinician placed materials in the patient’s mouth by spoon. No overt reaction was noted to the placement of liquid or pudding material in the mouth. A colleague who was observing the examination suggested having the patient self-feed. We did not believe this was viable because of the paucity of spontaneous movement demonstrated by this patient, but we placed a spoon in the patient’s hand and assisted her through the movements of filling the spoon with a liquid and then placing it in her mouth. The difference in swallow was dramatic. The woman swallowed the liquid material almost immediately. She demonstrate little residue and no airway compromise. This pattern was repeated for all materials presented in this manner. This simple change in feeding strategy was subsequently used in her daily rehabilitation program and she eventually returned to total oral feeding.

Refer to Videos 5-1, A and B on the companion Evolve site for an example of fluoroscopic swallowing differences in a single patient. This patient had a large right hemispheric middle cerebral artery stroke. In her initial fluoroscopic swallowing examination the clinician “fed” the patient barium contrast materials. A week later, the fluoroscopic examination was repeated because the reported results did not match the clinical profile. In this second examination we asked the patient to self-feed. The differences were dramatic.

Patients with sensory deficits may demonstrate a variety of dysphagia characteristics, including retention of a portion of a bolus in the mouth, oropharynx, or hypopharynx with no attempt to clear the residue. These patients also may be more susceptible to aspiration of material into the upper airway as a result of the sensory deficit. Another category of sensory deficit may be seen in the patient with neglect. Such patients may not recognize material presented to one side of the swallowing tract. These patients may hold material in the mouth with no apparent intent to swallow, but in fact they are unaware of the material in the mouth.

Finally, patients with hemispheric stroke may have significant communication deficits or cognitive deficits that reduce their ability to relate to the clinical examiner the nature of the dysphagia complaints. Patients who are asleep, lethargic, have waxing and waning alertness, or difficulty participating in the swallowing evaluation because of cognitive deficits present significant challenges to a valid evaluation of swallowing abilities. Also, the inability to describe swallowing difficulties may delay or hinder clinical evaluation and/or implementation of rehabilitation strategies. Figure 5-2 depicts general hemisphere areas that may be associated with various sensorimotor functions associated with swallowing. The left hemisphere is shown for descriptive purposes only. Box 5-1 presents various swallowing characteristics that may be associated with sensorimotor deficits after hemispheric stroke.

BOX 5-1 General Sensorimotor Considerations for Various Swallowing Deficits in Hemisphere Stroke

• Volitional motor control

• Initiation difficulties

• Paresis/paralysis

• Transport difficulties

• Sensory recognition

• Residue

• Aspiration

• Communication deficits

• Inability to describe difficulties

Practice Note 5-2

Acute stroke patients may present a variety of clinical signs and certainly are at risk for a variety of morbidities. One issue that seems obvious but may not be apparent to all health care providers is the level of alertness presented by the patient. Some stroke patients may be generally lethargic, whereas others may demonstrate a waxing and waning level of alertness.

A few years ago, I was working on the inpatient service in our hospital when I received a request for a consultation from a neurologist whom I knew well. The consult was to “evaluate and treat” dysphagia in a patient who had survived a recent stroke. On entering the patient’s room I found her asleep. I tried to gently awaken her by speaking close to her ear, then by speaking louder, then by washing her face and hands with a cloth rinsed in cold water. Nothing worked. I entered a note in the chart that the patient could not be aroused and that the service should reconsult when her status improved. The next day I received another consultation request from the same neurologist. I visited the patient at a different time during the day with the same result. In fact, I went back at different times on the same day with the same result. I called the neurologist and arranged to be with him when he next saw this patient. Together we agreed that this patient could not realistically participate in a swallowing examination and we would wait and watch. In another few days she “woke up” and we evaluated her swallow and began small amounts of oral intake.

A variety of swallowing deficits have been reported after hemispheric stroke. In general, hemispheric lesions (including both cortical and subcortical damage) contribute to many swallowing deficits (Box 5-2), including (1) poor initiation of saliva swallows (sometimes termed the dry swallow); (2) delay in initiation of the pharyngeal component of the swallow; (3) incoordination of the oral components of swallowing; (4) increased pharyngeal transit time and reduced pharyngeal constriction and clearing; (5) aspiration; (6) dysfunction of the pharyngoesophageal segment (cricopharyngeal muscle); and (7) poor relaxation of the lower esophageal sphincter. These collective observations indicate that hemispheric stroke can impair swallowing functions from the mouth to the stomach. Furthermore, a wide spectrum of swallowing deficits has been noted, ranging from impaired initiation of the swallow to poor transport of the bolus to aspiration into the airway. To date no report has emerged comparing specific sensorimotor stroke sequelae with specific swallowing impairments. However, the above list suggests that the array of potential swallowing deficits after stroke is extensive and may relate to the spectrum of poststroke sensorimotor impairments.

BOX 5-2 Swallowing Deficits in Patients After Hemisphere Stroke

• Reduced ability to initiate a saliva swallow

• Delayed triggering of pharyngeal swallow

• Incoordination of oral movements in swallow

• Increased pharyngeal transit time

• Reduced pharyngeal constriction

• Aspiration

• Pharyngoesophageal segment dysfunction

• Impaired lower esophageal sphincter relaxation

Practice Note 5-3

Recently I saw two patients within a short time frame who had similar histories and clinical presentations. Both patients were stroke survivors and at least 6 months past the stroke event. Both were deemed medically stable. Both were dependent on nonoral percutaneous esophageal gastrostomy (PEG) feedings. And both had difficulty managing their oral secretions; they drooled and carried a towel to “mop up the problem.” Finally, neither patient had functional speaking ability, but both could vocalize and phonate simple vowels. These patients were referred for evaluation and treatment of pharyngeal dysphagia.

On the surface, this clinical presentation may make sense. However, the basic problem for both patients was not pharyngeal dysphagia, but rather oral apraxia. Admittedly, oral apraxia was quite severe in both patients. Both presented with a persistent open-mouth posture but in the absence of overt weakness within the facial or oral musculature. Both could close the mouth in response to intraoral sensory stimuli and both spontaneously swallowed, though infrequently. A key feature of the clinical examination in both cases was the absence of overt cranial nerve deficits. Also, each patient had the ability to close the mouth, but this was context dependent (e.g., they did not close the mouth on command, but when liquid was placed in the posterior mouth they did close and a spontaneous swallow was observed). As part of the clinical swallow examination, liquid was placed in the oropharyngeal area with a straw as a pipette. As this liquid trickled into the hypopharynx, we occasionally observed a swallow. Under endoscopic inspection we delivered additional liquid to the oropharynx in this fashion. I also learned that both patients protected their airway and that no residue remained after these volume-dependent swallows.

Based on these clinical and endoscopic findings I did not enroll these patients in therapy for pharyngeal dysphagia. The dysphagia was primarily the result of a severe oral apraxia that limited oral motor control for voluntary tasks, including swallowing.

I did make simple recommendations that I hoped would improve oral functions for feeding and oral control for swallowing. Because I observed intermittent spontaneous swallows when liquid was placed in the posterior part of the mouth, I recommended this technique in an attempt to stimulate improved oral swallow initiation. I suggested to the local therapist that if the frequency of spontaneous swallowing improved, she should vary the type and amount of material used in this fashion and gradually place the material more forward within the mouth. Later I heard from one of the local therapists that her patient had increased the frequency of spontaneous swallowing and was taking more oral intake. Sometimes success comes in small steps.

Refer to Videos 5-2, A and B on the Evolve site for endoscopic and fluoroscopic examples of a single patient who demonstrated significant oral apraxia in the presence of preserved pharyngeal swallowing function.

Dysphagia is highly prevalent in acute stroke, with estimates that well over 50% of all patients are affected. However, the majority of acute stroke patients recover functional swallowing ability within the first 1 to 6 months after stroke, whereas swallowing problems develop in a small percentage of patients during the postacute period.14–16 These observations emphasize the importance of accurate identification and management of swallowing deficits in acute stroke patients. Furthermore, it is important to understand the factors that might predict persistent swallowing problems beyond the acute recovery period. The importance of this perspective is highlighted by the observation that acute and chronic swallowing problems in stroke patients are associated with many complications, including dehydration, malnutrition, aspiration, chest infections and, in some cases, death. Furthermore, dysphagia during acute stroke is associated with poor long-term outcome, including death and an increased rate of institutionalization.¹⁷

Treatment Considerations

Perhaps the most obvious statement about dysphagia in stroke is that it changes over time. From that perspective, dysphagia intervention strategies should also change over time. Table 5-2 presents clinical considerations and decisions that may affect treatment planning over time. Early in the course of a stroke, focus should be given to basic decisions such as the safety of oral feeding versus the need for nonoral feeding routes, the presence of comorbid conditions such as pneumonia, malnutrition, or dehydration, and the overall medical condition of the patient.

TABLE 5-2

Treatment Considerations and Decisions for Dysphagia After Stroke *

Considerations	Decisions
Acute (0-1 Month)
Most comorbid conditions	How to avoid or minimize complications
Resolving dysphagia	Need and readiness for therapy
Malnutrition	How to maintain and improve nutrition
Improving (1-6 Months)
Patient more stable with better endurance	Need and readiness for therapy
Comorbid conditions often under medical control	Type of therapy
Feeding routes established for most
Malnutrition may still be a factor
Chronic (After 6 Months)
Feeding routes more established	Therapy or no therapy (prognosis?)
Patients eating orally may have impaired swallow	Type of therapy
Compensations that interfere with swallow
Impact of prior therapy

^*Changing issues with time after onset.

The acute stroke patient is at greatest risk for dysphagia and morbidities associated with dysphagia. During the acute phase of stroke, patients are likely to demonstrate significant weakness contributing to reduced stamina and perhaps reduced mental status, including alertness and attention. These factors significantly limit any meaningful clinical (or other) evaluation of swallowing ability. Thus a conservative strategy would be to observe the patient’s status and postpone any in-depth assessment or intervention until the patient is more alert and has better endurance. Acute stroke patients also are at risk for respiratory abnormalities. Respiratory abnormalities range from basic weakness in expiratory muscles that might reduce cough effectiveness,¹⁸ to increased episodes of oxygen desaturation,^19,20 to deviations in the respiratory rate,²¹ to alterations in the coordination between respiration and swallowing.^22,23 Collectively, these respiratory deviations noted in acute stroke patients suggest an increased risk of aspiration of swallowed materials and pooled secretions and potential limitations in clearing aspirated secretions as a result of reduced cough efficiency. Given these potential risks, respiratory functions in the acute stroke patient should be evaluated as part of the comprehensive swallowing examination.

Pneumonia is commonly noted in acute stroke patients. Pneumonia is a significant morbidity because it is related to both an increased number of hospital readmissions ²⁴ and short-term and long-term mortality.²⁵ Causes of pneumonia in the poststroke patient are multifactorial; however, dysphagia, especially dysphagia accompanied by aspiration, is significantly related to the presence of pneumonia.¹⁶ In fact, dysphagia screening leading to early identification and treatment of swallowing deficits in acute stroke patients has been associated with a reduction in pneumonia rates.²⁶

The presence of dysphagia after stroke may contribute to pneumonia in various ways. Although the focus is often on aspiration of orally ingested food and liquid, aspiration of pooled pharyngeal secretions also may contribute to chest infection. Aspiration of secretions may be especially problematic in the acute stroke population because oral bacteria colonization is prominent in these patients.²⁷ Patients dependent on tube feeding, specifically nasogastric tube feeding, may have a higher degree of bacterial colonization than patients who feed orally.²⁸ In fact, at least one study has reported that stroke patients who were completely dependent on nonoral feeding (e.g., nothing by mouth) demonstrated higher rates of respiratory infections than did stroke survivors who were feeding orally.²⁹ One implication of these findings is that reduced frequency of swallowing contributes to an increased risk of aspirating pharyngeal secretions in the presence of higher rates of bacterial colonization within the swallowing mechanism. This premise is supported by treatment studies demonstrating that swallowing therapy³⁰ and strategies to improve oral hygiene³¹ reduce the incidence of pneumonia in stroke patients. Thus the dysphagia clinician should consider more than aspiration of food and liquid when providing swallowing interventions to patients after acute stroke.

Nutritional deficits are prevalent among stroke patients on admission and may worsen during hospitalization. On admission, the prevalence of such deficits has been estimated at approximately 16%; this figure increases to 22% to 26% through discharge from acute care.32–34

Nutritional decline continues beyond acute care. The prevalence of nutritional deficits in stroke patients at admission to rehabilitation approximates 50%.³⁵ At approximately 1 month after stroke, nutritional status begins to improve and continues to improve up to 4 months after stroke. In the acute stroke patient nutritional deficits are not overtly linked to dysphagia.^33,36 However, later during the rehabilitation period and thereafter, swallowing and/or feeding difficulties may contribute to the maintenance or increase in poor nutritional status.³⁷ Still, some suggest that poor nutrition during the acute phase of stroke contributes to poor longer term functional outcomes.³⁸ Nutritional evaluation and intervention are outside the scope of practice for most dysphagia clinicians. However, all dysphagia clinicians should be aware of the potential impact of swallowing and feeding abilities on nutritional status and participate in multidisciplinary health care teams, including nutritional specialists.

As the patient’s condition improves and more active rehabilitation is initiated (usually well within the first month after stroke), dysphagia treatment strategies also may change. One consideration is spontaneous resolution of dysphagia as the patient recovers from the effects of acute stroke. Although many stroke patients have some degree of recovery in swallowing ability, estimates of persisting dysphagia range from 11% to 50% at 6 months after stroke.14,39 During this period of improvement the patient with persistent dysphagia is likely to be engaged in active swallowing rehabilitation. By this time a decision about oral or nonoral feeding has already been established and comorbid conditions are often under medical control. Of importance to active dysphagia rehabilitation are various patient issues and the nature of the swallowing deficit. If the patient is able to participate in active rehabilitation and is motivated, direct and intense swallowing therapy is expected to produce significant benefit. Benefits from swallowing therapy extend beyond improved swallowing abilities to include reduced pneumonia rates and improved nutritional status.^29,40–42 Decisions about therapy technique(s) selection depend in large part on the specific dysphagia characteristics demonstrated by individual patients (see Chapter 14).

Chronic dysphagia is reported in some stroke survivors, although no study has documented the prevalence of dysphagia in stroke patients beyond 6 months after stroke. Typically, if the swallowing deficit persists beyond 6 months, it is considered chronic. Available reports indicate that stroke patients with chronic dysphagia can benefit from intense therapy.43–45 Such therapies are typically active and directed at changing specific physiologic features of the swallowing deficit.

In summary, dysphagia is highly prevalent after stroke and may be related to pneumonia, nutritional deficits, and other health complications. Dysphagia does resolve to varying degrees in the poststroke period, but the few estimates available suggest that up to 50% of stroke patients demonstrate some degree of persistent dysphagia. Dysphagia therapy has been shown to improve swallowing ability, reduce pneumonia rates, and improve nutritional status in stroke patients. Even stroke survivors with chronic dysphagia can experience functional benefit from intensive swallowing therapy.

SWALLOWING DEFICITS IN DEMENTIA

Another form of cortical impairment that can affect swallowing ability is the category of progressive diseases known as dementia. Several types of dementias have been described; the most frequent is Alzheimer’s disease. Other forms of dementia include dementia caused by cerebrovascular disease, Lewy body dementia, frontotemporal dementia, alcoholic dementia, and metabolic and/or nutritional dementia.⁴⁶ The hallmark of all dementias is a progressive deterioration in cognitive abilities, including memory, judgment, abstract reasoning, and personality changes. Other cortical disturbances such as apraxia and/or aphasia might be noted.

Swallowing deficits are well documented in advanced dementia.47–50 Persistent weight loss may be the first indication that patients with dementia have a significant swallowing problem; however, weight loss may not be directly related to feeding or swallowing difficulties.^49,51 As a result, such individuals are at significant risk for nutritional deficits that may further compromise their health status. Pneumonia is a common cause of death in patients with dementia.⁵⁰ Although dysphagia, including aspiration, is associated with pneumonia in this population,⁵¹ it is not the only contributing factor and may not be the critical contributing factor.^49,50,52

General characteristics of swallowing deficits in dementia are listed in Box 5-3. Prominent on this list is the presence of oral-stage dysfunction. It has been suggested that certain oral aspects of swallowing are under volitional motor control. The generalized cognitive impairments in dementia may contribute to deficits in volitional motor control and hence oral aspects of dysphagia. These may be characterized by lack of initiation of the swallow in which the patient holds food in the mouth, has incoordinated oral control of food and liquid, and/or delayed initiation of the oral component of the swallow, thus prolonging mealtimes.

BOX 5-3 Swallowing Deficits Seen in Patients with Cognitive Decline (Dementia)

• Unexplained weight loss *

• Oral-stage dysfunction *

• Pharyngeal-stage dysfunction

• Combined oral and pharyngeal dysfunction

• Minor aspiration

• Major aspiration

• Feeding limitations

^*More commonly observed characteristics.

Although the majority of dysphagia information in dementia is derived from studies of patients in advanced stages of the disease, patients with mild-stage dementia also demonstrate feeding and swallowing deficits.⁵³ Box 5-4 summarizes the salient findings regarding feeding and swallowing abilities in mild-stage dementia. These impairments are similar to, though not as severe as, those reported in more advanced stages of the disease. Specifically, patients with dementia demonstrate an overall slowing of the swallowing process from the oral aspects of food manipulation through the response of the pharynx accepting the bolus. This slowing of the swallowing process can have direct consequences for longer mealtimes and hence increase the risk of declining nutritional status. In addition, slowing of the pharyngeal response in swallowing may reduce airway protection, resulting in an increase of coughing and choking behaviors during mealtimes.

BOX 5-4 Examples of Swallowing and Feeding Deviations in Mild-Stage Dementia

SWALLOWING DEVIATIONS