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Figure 23.4. Location of regions of cortical control for (a) mylohyoid, (b) pharyngeal, (c) esophageal, and (d) all three states of swallowing in the left hemispheres of normal subjects, as determined by TMS (Hamdy et al., 1996, reprinted with permission).

Figure 23.4. Location of regions of cortical control for (a) mylohyoid, (b) pharyngeal, (c) esophageal, and (d) all three states of swallowing in the left hemispheres of normal subjects, as determined by TMS (Hamdy et al., 1996, reprinted with permission).

appeared to be sited predominantly on primary motor cortex, whereas the pharyngeal locus was sited both on primary motor cortex and premotor cortex, and the esophageal locus was sited predominantly on the premotor cortex, but extended onto the primary motor cortex" (p. 1220). The locus of these areas is similar in the two hemispheres but largest in the swallowing dominant hemisphere for the pharyngeal response. The oral stage as represented by the mylohyoid tends to be symmetric. The cortical representation of these three stages is shown in Fig. 23.4.

Dysphagia after cortical insult

Estimates of the proportion of patients with dysphagia after unilateral hemispheric lesion vary, with 30% being a reasonable estimate (Hamdy et al.,

1997). The best extant hypothesis about why is that dysphagia is most likely if the stroke is in the swallowing dominant hemisphere. However, the notion of hemispheric dominance remains controversial (Kelly and Huckabee, 2003). Hamdy and colleagues (1997) studied 20 stroke patients, 8 of whom had dysphagia, in reaching this conclusion. One subtlety in these data is the difference in oral and pharyngeal stage control. They consider mylohyoid control to be bilateral and symmetric, whereas pharyngeal control is asymmetric. If they are correct, their hemispheric dominance hypothesis explains the presence of pharyngeal dysphagia in their sample. Deficits in the oral stage such as preparation, formation, and movement of the bolus may be equally likely from damage to either hemisphere. Studies using VFSE will be needed to resolve this issue.

Recovery from dysphagia

Recovery from the dysphagia resulting from cortical stroke is usually faster and more complete than for that resulting from bilateral cortical, and unilateral and bilateral brain stem lesions (Horner et al., 1991). Hamdy and colleagues (1998) explored the mechanisms of recovery in 28 stroke patients. The participant's swallowing was measured with serial VFSEs at 1 week, 1 month, and 3 months. Bilateral swallowing center control was measured by TMS on the same schedule. Most of these patients had recovered by 1 month and only the severely dysphagic patients had persisting dysphagia at 3 months. In the recovered patients, the size of the cortical swallowing areas for the pharynx increased in the healthy hemisphere. The expansion was in an anterolateral direction. In some instances this expansion occurred before changes in swallowing performance, suggesting that changes in brain are influential in recovery rather than merely reflecting recovery that occurs for some other reason. These findings lead the authors to conclude: "there remains in the intact hemisphere the capacity for reorganization, which can then develop sufficient control over brain stem centers for swallowing recovery to occur" (p. 1112). A review of the individual patient data reveals one other observation critical to thinking about treatment. A small number of patients did not recover, despite having large pharyngeal control areas in the intact hemisphere. This suggests that a patient with dysphagia but a normal region of pharyngeal modulation in the intact hemisphere be given a high treatment priority because there is a low probability for that patient's recovery.

Recovery with treatment

Enhanced sensory input is a traditional treatment for enhancing the swallowing response (Rosenbek et al., 1991, 1996, 1998). The Manchester group (Hamdy et al., 1998; Fraser et al., 2002) has published their experience with electrical stimulation to the pharynx in normal and dysphagic subjects. The method requires each subject to swallow a small diameter catheter to which electrodes are attached for delivery of the stimulation to the pharynx at the midline. A variety of stimulus intensities and durations were studied. TMS was completed prior to, immediately after, and 30 min after stimulation. Ten minutes of stimulation at 5 Hz resulted in increased cortical excitability and an expansion of the area of cortical representation for the pharyngeal stage of swallowing which persisted for 30 min, accompanied by improved swallow. Said another way, the effects of the electrical stimulation produced changes in brain similar to those seen in spontaneously recovering persons. See Fig. 23.5 for cortical representation before and after pharyngeal stimulation in normal swallowers.

In another study (Power et al., 2004), electrical stimulation was administered to the anterior faucial pillars of normal swallowers. Stimulation at 5 Hz at this site inhibited the cortical response and decreased the responsiveness of the functional swallow. Stimulation at 0.2 Hz facilitated the cortical response but had no effect on the functional swallow. These findings are especially interesting to swallowing scientists because faucial pillar stimulation with touch, cold, pressure, and now electrical stimulation has been a staple of clinical practice for three decades (Lazzara et al., 1986; Rosenbek et al., 1991, 1998). For the first time in the swallowing literature data suggesting that negative effects are possible have appeared. These data do not mean that treatments should cease, of course. Indeed it appears that electrical stimulation applied at the right site, intensity, and duration can cause plastic changes in the brain that correlate with changes in function. Similarly, the wrong site, duration, and intensity may inhibit plastic changes.

23.8 Learned non-use

Learned non-use can occur when a behavior is not performed for a period of time extending into the interval when performance is actually possible physiologically (Taub et al., 1993; Miltner et al., 1999; Liepert et al., 2001). Learned non-use in dysphagia

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