Proposal for a New Exercise Method for Dysphagia with Velopharyngeal Inadequacy: A Case of Bickerstaff's Brainstem Encephalitis.

Bickerstaff's brainstem encephalitis is an autoimmune disease with the primary lesion situated in the brainstem and three cardinal signs: ophthalmoplegia; ataxia; and impaired consciousness. A 68-year-old man was started on rehabilitation exercise 3 months after onset of Bickerstaff's brainstem encephalitis, due to remnant dysarthria and dysphagia (Functional Oral Intake Scale, level 5) after the cardinal signs of Bickerstaff's brainstem encephalitis resolved. Exercise involved using a straw in the anterior midline between the dorsal tongue and hard palate. While the patient was inhaling through the straw, the straw was blocked. After strengthening suction as much as possible, the patient was asked to immediately dry swallow at the same time that suction was stopped. Effects of exercise were examined using videofluorographic swallowing studies before and after 6 weeks of training to compare posterior and superior velar displacements and the presence of nasopharyngeal reflux. No adverse effects of exercise were encountered, and Functional Oral Intake Scale improved to level 7, with significant increases in posterior and superior velar displacement during swallowing compared with before training. In addition, nasopharyngeal reflux that had consistently been seen on swallowing before training was absent after 6 weeks of exercise. This exercise method may prove useful.

Increase in plasma malondialdehyde-modified low-density lipoprotein in patients with atherothrombotic cerebral infarction.

Oxidized low-density lipoprotein cholesterol (Ox-LDL) is considered to play a critical role in the pathogenesis of atherosclerosis. We investigated the role of malondialdehyde-modified LDL (MDA-LDL), an indicator of Ox-LDL, in cerebral infarction. We also investigated the relationship between MDA-LDL and atherosclerotic change of the carotid artery. Subjects were 30 patients with lacunar infarction (LA), 19 patients with atherothrombotic infarction (AT) and 48 controls. Carotid arteries were evaluated with B-mode Doppler ultrasonography. The intima-media thickness (IMT) was considered to be increased if its value was more than 1.1 mm. The level of MDA-LDL concentration was significantly (P < 0.05) elevated in AT patients (129.96 +/- 27.88 U/I) than in LA patients (99.35 +/- 34.06 U/l) and controls (97.65 +/- 32.61 U/l). Among AT patients, plasma level of MDA-LDL concentration was statistically significantly elevated in the group with increased IMT (139.7 +/- 24.5 U/l) than in the group without increased IMT (102.7 +/- 17.2 U/l). No statistically significant difference was found among LA patients. However, there was no difference in LDL-C concentration between the patients with and without IMT thickening among LA or AT patients. The concentration of MDA-LDL was significantly decreased (P < 0.05) after statin administration for 5-6 months. MDA-LDL, namely degraded or qualitatively changed LDL-C, appears to be related to atherosclerotic change of the carotid artery in AT patients.

Apoptosis occurs in the penumbra zone during short-duration focal ischemia in the rat.

To investigate the appearance of apoptosis in short-duration focal ischemia, the authors induced left middle cerebral artery (MCA) occlusion in male rats by insertion of an intraluminal suture. The total number of apoptotic cells was determined by hematoxylin-eosin staining and TUNEL labeling and confirmed by gel electrophoresis. The data indicate that the total number of apoptotic cells increased with ischemia duration (P = 0.0006), with most apoptotic cells located in the striatum of the ischemic hemisphere. As the duration of ischemia lengthened, necrosis became more prevalent and apoptosis receded to the periphery of the infarct. Using iodo[14C]-antipyrine to correlate the distribution of apoptosis to regional CBF (rCBF), the authors found that rCBF in the ischemic dorsolateral striatum was compatible with penumbra flow and significantly lower than the ventromedial striatum and frontoparietal cortex. This difference disappeared after 45 minutes of reperfusion. The authors conclude that focal ischemia of short duration results in changes compatible with apoptosis in regions of low rCBF, and this can occur without necrosis. This model is relevant to transient ischemic attack in the human and may suggest that, in addition to being a harbinger of stroke, transient ischemic attacks may cause histopathologic changes not yet clinically detectable.