Figure 23.5. Patterns of activation (a) before and (b) after electrical stimulation in normal swallowers. Activation increased bilaterally (Fraser C. et al., 2002 reprinted with permission).

Figure 23.5. Patterns of activation (a) before and (b) after electrical stimulation in normal swallowers. Activation increased bilaterally (Fraser C. et al., 2002 reprinted with permission).

has not been studied, but it should be. A typical pattern of managing the dysphagic person is tube feeding. Unlike the case of limb paralysis where movement is never performed, in dysphagia even a tube-fed person will continue to swallow saliva unless the dysphagia is profound in which saliva is suctioned or spit into a container. Nonetheless the number of swallows is drastically reduced. As some tube-fed persons are not systematically followed, this reduced rate of swallowing may persist long after some additional swallowing of food and drink is possible. Thus tube feeding presents the researcher with a natural laboratory for studying cortical effects of non-use. A priority would be to determine if a period of tube feeding changes cortical representation of swallowing structures. Next it would be important to test the effects of treatment in cases of learned non-use.

23.9 Negative effects of treatment

The potential negative effects of inappropriately timed or intense treatments especially in relation to severity of neurologic deficit (Kozlowski et al., 1996; Kozlowski and Shallert, 1998; Shallert and Kozlowski, 1998; Shallert et al., 2000) warrants research. It is known that the wrong intensity of electrical stimulation can inhibit cortical functioning. It may well be that such inhibition is a function of lesion size. Smaller lesions may have what Shallert and colleagues (2000) call a "penumbra of vulnerable yet potentially salvageable tissue surrounding the core of the infarct" (p. 159). The wrong treatment intensity and this vulnerable tissue can be further degraded. The tradition in speech-language pathology is to intervene early but possible negative effects of early intervention require further study. Dysphagia clinicians are not used to thinking about harm; that attitude may need to change.

23.10 Alternative explanations of treatment effects

In addition to plasticity, other explanations, especially for immediate effects of treatment can be posited. These include what Moerman and Jonas (2002) call an information effect, more popularly known as a placebo effect. Indeed, as in all treatments, a placebo effect is anticipated in dysphagia management. Another possible explanation, which is probably distinct from the placebo effect, is that patients merely increase attention, concentration, or effort, thereby enhancing performance. The effect is to use more of what might be called the residual support for swallowing. Like the information or placebo effect, this effort effect is to be understood on the way to a fuller appreciation of how rehabilitation changes performance. An issue to be resolved by research is to discover if these influences are different from what are called short-term mechanism of plasticity (Nudo et al., 2000). These authors describe short-term plasticity as "an immediate reorganization in response to altered afferent inputs" (p. 182). The implication is that these short-term changes reflect differences in "synaptic efficacy." Presumably placebo effects and - if they are different - effects resulting from increased attention would be supported by changes in nervous system activity remote from the cortical swallowing centers. Short-term plastic changes are likely to be supported by perilesional changes.

Peripheral and central effects

Huckabee and Cannito (1999) have observed that the relationship among peripheral changes from treatment by which they mean a variety of performance and muscle level changes and central or plastic changes in the nervous system should be investigated. Doubtless these relationships will be complex. A variety of hypotheses can be tested. Early peripheral changes may precede changes in the nervous system. They may follow changes in the central nervous system (Hamdy et al., 1998). They may be associated simultaneously with widely distributed, even bilateral, alterations in brain activity. Late in treatment, the alterations may be more focal involving subcortical regions, perilesional areas, or homologous areas on the brain's side opposite the lesion. These and other permutations, based on underlying pathophysiology of the swallow; locus of damage; and type, intensity, and duration of treatment are yet to be tested. However, a beginning in the understanding of plastic changes with dyspha-gia treatment has been made.

23.11 Conclusions

Clinicians are convinced most dysphagia management is successful in restoring safe, adequate, pleasurable eating and drinking. The evidence on which this conviction rests is taken from single case and small N studies, however, so the probability of Type II errors is high. Randomized clinical trials will address this shortcoming. In even shorter supply is evidence for experience-dependent plasticity in dysphagia. The early data are promising for electrical stimulation, especially of the pharynx, but are non-existent for all other methods. These data need to be collected. As the science of dysphagia matures, the "why" questions will be more frequently asked. The relationships of peripheral and central changes will be elucidated and ways of maximizing both will be developed. In the interim, clinicians will continue to practice in ways guided by the extant data and their professional experience. Clinical-scientists will continue working to provide a firmer database. Both groups can afford to be confident because the reality of plasticity, even in the damaged adult brain, is now widely recognized.

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