7.Causal disease : Stroke

Explanation

This module will cover the following areas.

Explanation

Among various causes, stroke is the most common and important cause of dysphagia. Stroke-related dysphagia¹is caused by impaired functional movement or sensation of the organs and tissues involved in eating and swallowing (functional causes); it is not associated with pathway obstruction due to anatomical/structural abnormalities (organic causes), although prolonged functional impairment may lead to disuse atrophy and/or inflammation, causing structural abnormalities and resulting pathway obstruction (e.g. insufficient opening of the esophageal entrance). Here, iatrogenic dysphagia is also included in a separate category, which is another important group of causes of dysphagia defined from a different point of view and includes both functional and organic disorders. Both types of disorders are causes of dysphagia that need to be differentiated from "diseases". We also see CT images of typical causes of stroke, including multiple cerebral infarction, subarachnoid hemorrhage, and intracerebral hemorrhage.

Explanation

Stroke is essentially synonymous with cerebrovascular disorder. Blood flow is interrupted either due to bleeding in the brain from a ruptured vessel (cerebral hemorrhage) or due to lack of flow from a clogged vessel (cerebral infarction). Many people fall when having a stroke and, interestingly, in the local dialect of Akita Prefecture in Japan, stroke is expressed as "ataru", which means to fall or hit something. Cerebral hemorrhage is divided into intracerebral hemorrhage, which occurs in the parenchyma of the brain (commonly occurring in the putamen, thalamus, cerebellum, and pons), and subarachnoid hemorrhage, which occurs on the surface of the brain. Cerebral infarction is divided into cerebral thrombosis resulting from arteriosclerosis (further divided into atherothrombotic infarction caused by embolization of thicker vessels, and lacunar infarction caused by embolization of thinner vessels) and cerebral embolism caused by thrombi cast off from distant organs such as the heart. The therapeutic and prophylactic treatments of stroke vary depending on its pathogenesis.

Explanation

For the different types of stroke, symptoms depend on which part of the brain is damaged. Cerebral infarction and cerebral hemorrhage can manifest similar symptoms if the same part of the brain is damaged, and also a single cerebral infarction can result in different symptoms if different parts of the brain are damaged.

We should also remember that symptoms of stroke in the acute phase can change over time. This is because of expansion of the affected area and development of cerebral edema, as shown. Even with the same affected site, different symptoms may develop depending on age, underlying disease, and other systemic factors such as blood pressure, respiratory condition, and electrolyte balance.

In general, a damaged brain does not undergo regeneration and manifests sequelae. Still, a certain extent of functional recovery can be expected from treatment and rehabilitation. The area called an ischemic penumbra (see the next slide) is where cells are considered to be alive but not functioning, and this area has potential for functional recovery. Recent evidence on plasticity of the brain now suggests that lost brain function, which used to be considered unrecoverable, can be restored to some extent by appropriate rehabilitation.

Explanation

As mentioned earlier, the symptoms of stroke in the acute phase can change over time. Extra care is needed especially during the first week after onset. Many cases have been reported where screening examinations on admission showed no abnormalities and regular meals were prescribed, but the patient presented with a clearing cough and developed pneumonia 3 days after admission. The development of pneumonia delays the start of rehabilitation, affecting survival outcome. Special attention is needed during the first 3-4 days after stroke onset, when cerebral edema is likely to develop. Cerebral edema may be accompanied by consciousness disturbance, which has an adverse effect on swallowing, as described later. When encountered, patients with recurrent disease (bilateral injuries) and elderly patients should be considered "always at risk".

Explanation

Frequency
It is very important to know the morbidity and prevalence of dysphagia, but these are very difficult to determine. For example, healthy individuals can experience choking and some patients experience aspiration without choking. For these reasons, the diagnostic criteria for dysphagia remain ambiguous. A Japanese study that surveyed the incidence of dysphagia using a questionnaire form²showed that 13.8% of 1313 healthy elderly individuals aged ≥ 65 years (575 men and 738 women) had swallowing-related problems³.

The incidence of stroke-related dysphagia varies at different times after onset. The incidence is as high as 30%-100% (varying among reports) in acute-phase patients (within 1 week after onset), while that in patients in the recovery or chronic phase is as low as 5-10%. This indicates the importance of acute-phase treatments for the prevention of dysphagia-related complications and that patients who have survived the acute phase without complications are likely to experience improvement in their symptoms without special intervention for dysphagia. We should also remember that during the acute phase of stroke, dysphagia can be caused by consciousness disturbance and drugs (eg, anticonvulsants and psychotropics).

There are three types of stroke-related dysphagia: major injuries causing consciousness disturbance, false bulbar palsy, and bulbar palsy. We look at each type in the following slides.

Explanation

There are three types of stroke-related dysphagia: major injuries causing consciousness disturbance, false bulbar palsy, and bulbar palsy. We look at each type in the following slides.

Poor consciousness is associated with poor biological responses. This also implies that poor consciousness may prevent the protective clearing cough normally triggered by aspiration. Because the status of consciousness changes, it is important to always check the consciousness level immediately before eating and to be reminded that decreased consciousness level may occur during eating. For example, some patients are awake when they start eating but become sleepy while eating. This is attributable to reduced cerebral blood flow resulting from increased blood flow in the digestive tract when food enters it or from the parasympathetic nervous system becomes dominant. It may also be attributable to aspiration or consciousness disturbance due to reduced oxygen saturation resulting from swallowing apnea. When decreased consciousness is apparent, we need to identify its cause so that appropriate measures can be taken.

Explanation

Dysphagia can also occur in the acute phase of unilateral cerebral injury without consciousness disturbance⁴. This type of dysphagia can be classified as false bulbar palsy and manifests with relatively mild symptoms that do not last as long as several months⁵. Robbins⁶ et al. investigated differences between right and left hemisphere damage and found that right hemisphere damage is often associated with a delayed pharyngeal reflex and liquid aspiration/penetration. Daniels et al.⁷ reported that the anterior insular cortex plays an important role in the development of dysphagia caused by unilateral cerebral injury. Hamdy et al.⁸ have reported that about one-third of patients with acute stroke have dysphagia and that dysphagia is associated with increased mortality, although the dysphagia usually resolves within 1 week. They speculate that there is hemispheric dominance for swallowing and that even with unilateral cerebral injury, damage to the dominant hemisphere can lead to prolonged dysphagia.

In unilateral cerebral injury, the function of the contralateral hemisphere may be impaired due to diaschisis². In this case, dysphagia may also occur as a common symptom of false bulbar palsy. Regardless, the fact is that dysphagia can be caused by unilateral cerebral injury and we must keep this in mind when treating stroke patients. The involvement of the cerebrum in dysphagia and the mechanism by which dysphagia resolves continue to be interesting topics of investigation.

Explanation

Pseudobulbar palsy is caused by injury of bilateral upper motor neurons in the medulla oblongata. There are various possible combinations of injured sites, including the cortex and subcortex, the basal nucleus, and the brainstem (mesencephalon, pons). Cortical and subcortical injuries often cause higher brain dysfunction, such as aphasia and hemispatial neglect, depending on the affected area of the brain. Severe facial nerve palsy, which is often encountered in clinical practice, is characterized by oral stage disorders often accompanied by severe dyslalia. The swallowing reflex rarely occurs, but it can be induced with a normal reflex pattern by dry swallowing after ice massage or K-point stimulation. Applying a slice of jelly to the back of the tongue or directly to the pharynx can induce the swallowing reflex (pharyngeal phase) quite smoothly, usually allowing the jelly to be swallowed. However, in patients with muscular weakness, a food bolus can remain in the pharynx even after onset of the swallowing reflex. There is no right/left difference (ie, differences in laterality) in the movements of organs or tissues during the oral and pharyngeal stages. Significant oral stage disorders, as well as marked dysarthria, are observed. Dysarthria is spasmodic and exertional. Insufficient lip closure and increased salivation are evident.

Bulbar palsy is caused by damage to the swallowing centers in the medulla oblongata (ambiguous nucleus, solitary nucleus, and central pattern generator [CPG]). The swallowing reflex rarely occurs and if it does, its pattern is disturbed. The most common clinically encountered type of bulbar palsy is Wallenberg syndrome, also known as lateral medullary syndrome, which is caused by lateral medullary lesion. Dysphagic patients with this syndrome tend to be independent in activities of daily living. The syndrome is characterized by a laterality of pharyngeal wall, arytenoid cartilage, and vocal cord movements (poor motility on the affected side). Laterality of UES opening (cricopharyngeal muscle) and laterality of bolus passage through pharynx are particularly evident; these affect the rehabilitation progress. ⁹. Dysarthria is relatively mild, ataxic, flaccid, and hypernasal. Patients tend to be unable to swallow saliva and constantly spit into a tissue. See slide 12 for more information on Wallenberg syndrome and slide 14 for other types of bulbar palsy caused by medullary injury.

Explanation

Damage to part of the brainstem higher than the medulla oblongata usually leads to pseudobulbar palsy, although major damage to the mesencephalon or pons can lead to a condition similar to bulbar palsy with no swallowing reflex during the acute phase. This is likely to be due to dysfunction of the whole brainstem. Patients who have survived have an intact medulla oblongata and so can have severe pseudobulbar palsy.

Explanation

We see here typical VE and VF findings of false bulbar palsy, with VF shown in the clip on the left. One of the distinct features of pseudobulbar palsy compared to true bulbar palsy, as discussed later, is that the entire pharynx can be visualized relatively clearly without saliva accumulation. As shown in the clip, some pudding introduced to the back of the tongue is transported weakly to the pharynx and swallowed. Poor tongue movement is evident, with the bolus being swallowed without chewing. Initially, we seen no aspiration or pharyngeal pooling, but pooling becomes evident after the jelly changes form to thickened liquid. As we can see, in patients with pseudobulbar palsy, increased fatigability tends to result in pooling or aspiration in the later phase of swallowing.

Explanation

Wallenberg syndrome is caused by lateral medullary injury, typically manifesting as dizziness, dysphagia, Horner's syndrome, and ataxic symptoms and is characterized by the absence of motor paralysis of the tongue (hypoglossal nerve) and limbs and dissociative sensibility, where alternating loss of pain and temperature sensation in the face is observed with intact deep/tactile sensation (dorsal cord). However, not many patients exhibit all of these typical symptoms. The presence of motor paralysis of the tongue and limbs and disturbance of deep/tactile sensation indicate a more extensive unilateral medullary lesion. A difference in laterality is evident in relation to bolus passage through the UES. VE shows the characteristic finding of accumulated foamy saliva in the pharynx.

Explanation

Here we see typical VE and VF findings of Wallenberg syndrome. The upper left image shows the accumulation of foamy saliva. Patients with bulbar palsy tend to spit saliva while coughing, but they are unable to spit air-containing foamy saliva because it is too light, which results in residual saliva accumulating in the pharynx, as the clip shows. Note that saliva is suctioned and the left arytenoid cartilage shows poor motility.

The clip on the upper right shows the well-known curtain sign, where the posterior pharyngeal wall moves to the left due to poor motility of the right pharyngeal wall (ie, contraction of the left pharyngeal wall causes the right pharyngeal wall to be pulled to the left). The right nasopharyngeal wall also shows poor contraction.

The clip on the lower right is lateral view VF of bulbar palsy. The bolus does not pass through the pharynx due to poor pharyngeal contraction and laryngeal elevation

The clip on the right lower is frontal view VF of right bulbar palsy. For bulbar palsy, frontal view VF should be examined to determine whether there is any difference in laterality. This patient has poor right passage. The latter half of the movie shows bolus passage through the left esophageal entrance with the patient placed in the left recumbent position with the neck rotated to the right (unilateral swallow in left recumbency).

Explanation

Here we see typical VE and VF findings of Wallenberg syndrome. The upper left image shows the accumulation of foamy saliva. Patients with bulbar palsy tend to spit saliva while coughing, but they are unable to spit air-containing foamy saliva because it is too light, which results in residual saliva accumulating in the pharynx, as the clip shows. Note that saliva is suctioned and the left arytenoid cartilage shows poor motility.

The clip on the upper right shows the well-known curtain sign, where the posterior pharyngeal wall moves to the left due to poor motility of the right pharyngeal wall (ie, contraction of the left pharyngeal wall causes the right pharyngeal wall to be pulled to the left). The right nasopharyngeal wall also shows poor contraction.

The clip on the lower right is lateral view VF of bulbar palsy. The bolus does not pass through the pharynx due to poor pharyngeal contraction and laryngeal elevation

The clip on the right lower is frontal view VF of right bulbar palsy. For bulbar palsy, frontal view VF should be examined to determine whether there is any difference in laterality. This patient has poor right passage. The latter half of the movie shows bolus passage through the left esophageal entrance with the patient placed in the left recumbent position with the neck rotated to the right (unilateral swallow in left recumbency).

Explanation

We see here a summary of the rather complicated relationship between the location of medullary lesions and common associated symptoms (many of which are termed a "syndrome"). Wallenberg syndrome is characterized by the presence of ataxic symptoms and the absence of motor paralysis and dissociative sensibility, where alternating loss of pain and temperature sensation of the face is observed with intact deep/tactile sensation (dorsal cord). The presence of motor paralysis of the tongue and limbs and disturbance of deep/tactile sensation indicates a more extensive unilateral medullary lesion.

Medial medullary injury does cause motor paralysis of the tongue and impaired deep/tactile sensation. Although medullary lesions are associated with various syndromes, classifying them by their location into lateral, unilateral, medial and peripheral as seen here, may help us to better understand the conditions. Patients with bilateral medullary injury tend to have impairment of life support functions, such as breathing, and are usually not eligible for dysphagia treatment.

References

1. Ohkuma et al: Development of a questionnaire to screen dysphagia. JJDR 6: 3-8, 2002
2. Fujishima I:Rehabilitation for swallowing disorders associated with stroke. 2^nd edition．Ishiyaku publisher, 1998
3. Kawashima K, Motohashi Y, Fujishima I.:Prevalence of dysphagia among community-dwelling elderly individuals as estimated using a questionnaire for dysphagia screening. Dysphagia. 19(4):266-71. 2004
4. Horner J, Massey EW: Silent Aspiration following stroke. Neurology 38: 317-319, 1988
5. Ohshima F:Dysphagia caused by solitary lesion in hemispher. 12th Annual Dysphagia Research Meeting Proceeding pp231, 20036)Robbinsons J, et al: Swallowing after unilateral stroke of the cerebral cortex. APMR 74: 1295-1300,1993implications for recovery after stroke. Clin Sci (Lond):99(2):151-7, 2000
6. Daniels SK, Foudas AL: The role of the insular cortex in dysphagia. Dysphagia 12: 146-156, 1997
7. Hamdy S, et al:Organization and reorganization of human swallowing motor cortex:
8. H Yaguchi et al: Dominant bolus transport side to the phyopharynx and passage side at the cricopharyngeal portion in Wallenberg syndrome. JJDR 10: 2249-256, 2006