Objectives: We investigated the incidence, clinical characteristics, outcome and factors associated with aphasia and early improvement in acute ischemic stroke. Methods: We consecutively studied 855 patients with acute ischemic stroke who were admitted to our hospital within 48 h after onset and who were not comatose on admission. Assessment of aphasia was performed on admission (day 0) and day 10. We examined the incidence, severity, and subtypes of aphasia, and compared the clinical background of patients with and without aphasia on admission, and also those with and without early improvement by day 10. In addition, we investigated the independent factors associated with the presence of aphasia on admission and with early improvement. Results: Of the 855 patients, 130 (15.2%) had aphasia on admission. The National Institutes of Health Stroke Scale (NIHSS) on admission (OR 1.21; 95% CI 1.17–1.26) was a significant and independent factor associated with the presence of aphasia on admission. Early improvement was seen in 56 of 121 aphasic patients (46.3%) who were still alive on day 10. A history of hypercholesterolemia (OR 3.27; 95% CI 1.14–9.39) was a significant and independent factor associated with early improvement in aphasia during the acute phase and NIHSS on admission (OR 0.95; 95% CI 0.90–0.99) was marginally significant. Conclusion: It is difficult to predict the outcome of aphasia within the first few days after the onset of ischemic stroke.

TIA-related DWI abnormalities are associated with prolonged duration of TIA and disturbance of higher brain function. More sustained and extensive ischemia may contribute to DWI abnormalities in patients with TIA.

We examined galactosylceramidase (GALC) cDNA in four Japanese patients with adult onset globoid cell leukodystrophy (Krabbe disease; AO-GLD) by polymerase chain reaction/single-strand conformation polymorphism (PCR-SSCP) analysis, subsequent sequence determination, and restriction enzyme digestion of PCR products, initial symptoms were the onset of slowly progressive spastic paraplegia from the middle of the second decade, and all patients had diminished GALC activity in their leukocytes. We identified three missense mutations (I66M, G270D, L618S) and one exon-6 skipping (535-573del). Two of the patients had only the I66M mutant mRNA, and one only the G27OD mutant mRNA. The fourth patient carried a compound heterozygous mutation of 535-573del and L618S. To determine the enzymatic activities produced by these mutations, we constructed mutated GALC cDNAs and expressed them in COS-1 cells. Three mutations, viz., G270D, L618S, and exon-6 skipping (535-573del), produced diminished GALC activity as expected. The I66M mutation in the wild-type GALC cDNA(I289) had normal activity, but when this mutation and the V289 polymorphism were introduced into the same allele, it had decreased activity. Thus, the combination of a unique mutation and polymorphism causes conformational change in the GALC enzyme, resulting in low enzymatic activity. AO-GLD mutations, including those found here, are located in the N-terminus (I66M, G270D, 535-573del) or C-terminus (L618S) of the GALC enzyme, whereas the reported mutations in the infantile form (IF-GLD) are in the central domain. This difference in mutation sites may affect the clinical features of GLD.

No abstract

No abstract

No abstract

The IOE feeding method may be one of the alternatives to continuous nasogastric tube feeding in acute stroke patients with severe dysphagia, who are alert.

No abstract