Recent clinical and experimental studies suggest that ischemic strokes may play an important role in the pathogenesis of Alzheimer's disease (AD). Beta amyloid (Abeta), a major component of senile plaque in AD, is known to be derived from ischemic brain or activated platelets. We prospectively enrolled 62 patients with acute ischemic stroke and 27 age-matched controls. The serum Abeta and P-selectin levels were determined using the Sandwich-ELISA. We divided ischemic strokes into subgroups according to the clinical syndrome, pathogenesis, and infarct size, and compared the Abeta level between each subgroup. The Abeta1-40 level was markedly elevated in ischemic stroke patients, as compared to controls (140.2 +/- 54.0 vs 88.44 +/- 34.96 pg/ml, p<0.001). Cardioembolic and larger artery atherosclerotic infarcts had higher Abeta1-40 level than small vessel disease (p = 0.001). Both infarct size and the initial NIHSS score had significantly positive correlations with the serum level of Abeta1-40 (r = 0.539, p<0.001 and r = 0.425, p = 0.001, respectively). However, the P-selectin level was not significantly correlated with serum Abeta1-40. Our data suggest that elevated circulating Abeta1-40 in ischemic stroke patients may be derived from brain as a consequence of ischemic insults.

Background: Apart from diffusion-weighted imaging (DWI) lesion volume and diffusion-perfusion mismatching, there is limited information about neuroradiological predictors of early prognosis after an ischaemic stroke. This study sought to identify specific DWI lesion patterns that would help prediction of early prognosis of three different endpoints: unstable hospital course, recurrence of stroke, and poor neurological outcome at 90 days after ischaemic stroke. Methods: A total of 426 patients with acute cerebral infarcts within the middle cerebral artery territory were prospectively studied. Using the DWI data the patients were divided into six groups (territorial, other cortical, small superficial, internal border zone, small deep, and other deep infarcts), and any recurrent strokes and prognosis over the following 90 days were recorded. Results: DWI lesion pattern was a stronger and more consistent independent outcome predictor than DWI lesion volume. The specific DWI lesion patterns associated with each endpoint differed. An unstable hospital course was frequently observed in patients with internal border zone infarcts, whereas recurrent strokes after the index stroke were commoner in those who had small superficial infarcts (p,0.05 in both cases). Similarly, poor outcome after stroke was associated with older age, severe neurological deficits at admission, and a DWI lesion pattern showing internal border zone infarcts. Conclusions:The results of the present study indicate that the DWI lesion pattern may help in recognition of the likely differences in the early prognostic endpoints after ischaemic stroke, and DWI analysis may guide targeted interventions to prevent negative outcomes.

Although LS on examination, SDIs on diffusion-weighted imaging, and a stable hospital course suggest lacunar stroke of benign course, our results indicate that the PAD group represents an intracranial type of LAD.

Astasia, inability to stand unsupported despite good strength, resembles the marked balance impairment of patients with vestibulocerebellar disease. We describe a patient with unilateral thalamic infarct that presented with astasia. A 76-year-old hypertensive woman was admitted to our hospital because of marked unsteadiness. On neurological examination, she could not stand unsupported and the woman's body swayed back and forth markedly. The swaying was not compensated for by her taking a step forward or backward, and she frequently collapsed when support was withdrawn. Diffusion-weighted magnetic resonance image revealed a discrete infarct within the right posterolateral thalamus. Brain single photon emission computerized tomography revealed markedly decreased regional cerebral blood flow within in the right thalamus with concomitant left superior cerebellar region. We discuss the possible pathomechanisms of thalamic astasia.

Since Balint originally described a patient with striking disturbances in vision and movement, 1 this syndrome has been reported to result from stroke, metastatic lesions, demyelinating disorders, carbon monoxide poisoning, corticobasal ganglionic degeneration, Alzheimer disease, and HIV infection. 2 We report a patient with Balint syndrome resulting from Creutzfeldt-Jakob disease (CJD).Case report. A 65-year-old man with no medical history developed personality changes during a 3-week period. He experienced visual hallucinations and paranoid delusion of neighbors stealing his money and Internet identity. Initial brain MRI revealed T2 hyperintensities within the parietal and occipital lobes. Progressive neuropsychiatric decline required hospitalization. On admission he had disorganized perseverative behavior, fixation on guilt, mild apraxia, and a Mini-Mental State Examination (MMSE) of 26 of 30 with errors in orientation and recall. MRI at admission showed T2 hyperintensities within the parietal and occipital lobes, whereas diffusion-weighted imaging (DWI) revealed confluent lesions in the cortical ribbon of the parietal, occipital, and frontal lobes. Lumbar puncture was unremarkable. EEG demonstrated spike and wave discharges in the left frontal and right parietal lobes. The patient was treated with antiepileptic medications but continued to become more withdrawn.Twelve days after admission, the patient exhibited features consistent with Balint syndrome. When presented a complex visual scene, such as the cover of a magazine, he could not recognize more than one item at a time. He could not recognize two adjacent unlinked drawings ("simultagnosia"). He had difficulty reaching for objects under visual guidance with either arm and often missed objects ("optic apraxia"). However, he could rapidly grab an object when presented auditory clues (i.e., shaking keys). He had full extraocular movements and a normal oculocephalic reflex but could not voluntarily saccade to an object of regard ("oculomotor apraxia"). MMSE was 16 of 30 with significant errors in orientation, attention, registration, recall, and copying. Twenty days after admission, repeat EEG demonstrated generalized 1-Hz periodic sharp and wave complexes (PSWCs) lasting for Ͼ10 seconds. 3 At this time, PET and SPECT demonstrated decreased metabolism and blood flow within the parietal and occipital lobes. Further laboratory tests, including antithyroglobulin antibodies, antithyroid microsomal antibodies, erythrocyte sedimentation rate, and antinuclear antibodies, were normal, whereas CSF 14 -3-3 protein levels were qualitatively elevated (National Prion Disease Pathology Surveillance Center). The patient was prescribed quinacrine for compassionate use 24 days after his admission. He developed startle myoclonus, could not perform activities of daily living, and had an MMSE of 10 of 30 with errors in all categories by 35 days after admission. He experienced visual hallucinations and developed cortical blindness (Anton syndrome) and died 2 months after his adm...