Jin Sung Cheong

Tooth Loss Is Associated with Brain White Matter Change and Silent Infarction among Adults without Dementia and Stroke

Periodontal disease is a predictor of stroke and cognitive impairment. The association between the number of lost teeth (an indicator of periodontal disease) and silent infarcts and cerebral white matter changes on brain CT was investigated in community-dwelling adults without dementia or stroke. Dental examination and CT were performed in 438 stroke- and dementia-free subjects older than 50 yr (mean age, 63 ± 7.9 yr), who were recruited for an early health check-up program as part of the Prevention of Stroke and Dementia (PRESENT) project between 2009 and 2010. In unadjusted analyses, the odds ratio (OR) for silent cerebral infarcts and cerebral white matter changes for subjects with 6-10 and > 10 lost teeth was 2.3 (95% CI, 1.38-4.39; P = 0.006) and 4.2 (95% CI, 1.57-5.64; P < 0.001), respectively, as compared to subjects with 0-5 lost teeth. After adjustment for age, education, hypertension, diabetes mellitus, hyperlipidemia, and smoking, the ORs were 1.7 (95% CI, 1.08-3.69; P = 0.12) and 3.9 (95% CI, 1.27-5.02; P < 0.001), respectively. These findings suggest that severe tooth loss may be a predictor of silent cerebral infarcts and cerebral white matter changes in community-dwelling, stroke- and dementia-free adults.

Serum YKL-40 Levels Correlate with Infarct Volume, Stroke Severity, and Functional Outcome in Acute Ischemic Stroke Patients

Background and Purpose YKL-40 is associated with various neurological disorders. However, circulatory YKL-40 levels early after onset of acute ischemic stroke (AIS) have not been systematically assessed. We aimed to identify the temporal changes and clinical usefulness of measuring serum YKL-40 immediately following AIS. Methods Serum YKL-40 and C-reactive protein (CRP) levels were monitored over time in AIS patients (n = 105) and compared with those of stroke-free controls (n = 34). Infarct volume and stroke severity (National Institutes of Health Stroke Scale; NIHSS) were measured within 48 hours of symptom onset, and functional outcome (modified Rankin Scale; mRS) was measured 3 months after AIS. Results Within 12 hours of symptom onset, levels of YKL-40 (251 vs. 41 ng/mL) and CRP (1.50 vs. 0.96 µg/mL) were elevated in AIS patients compared to controls. The power of YKL-40 for discriminating AIS patients from controls was superior to that of CRP (area under the curve 0.84 vs. 0.64) and YKL-40 (r = 0.26, P<0.001) but not CRP levels were correlated with mRS. On day 2 of admission (D2), YKL-40 levels correlated with infarct volume and NIHSS. High YKL-40 levels predicted poor functional outcome (odds ratio 5.73, P = 0.03). YKL-40 levels peaked on D2 and declined on D3, whereas CRP levels were highest on D3. Conclusions Our results demonstrate serial changes in serum YKL-40 levels immediately following AIS and provide the first evidence that it is a valid indicator of AIS extent and an early predictor of functional outcome.

Site-Specific Distribution of CD68-Positive Microglial Cells in the Brains of Human Midterm Fetuses: A Topographical Relationship with Growing Axons

Using 5 fetuses of gestational age (GA) of 15-16 weeks and 4 of GA of 22–25 weeks, we examined site- and stage-dependent differences in CD68-positive microglial cell distribution in human fetal brains. CD68 positive cells were evident in the floor of the fourth ventricle and the pons and olive at 15-16 weeks, accumulating in and around the hippocampus at 22–25 weeks. At both stages, the accumulation of these cells was evident around the optic tract and the anterior limb of the internal capsule. When we compared CD68-positive cell distribution with the topographical anatomy of GAP43-positive developing axons, we found that positive axons were usually unaccompanied by CD68-positive cells, except in the transpontine corticofugal tract and the anterior limb of the internal capsule. Likewise, microglial cell distribution did not correspond with habenulointerpeduncular tract. Therefore, the distribution of CD68-positive cells during normal brain development may not reflect a supportive role of these microglia in axonogenesis of midterm human fetuses.

Ectopic choroid plexus found in fetal sections: a case report with literature consideration

We incidentally found an ectopic choroid plexus (CP) attached to the posterior side of the cervicothoracic spinal cord (C4–T6) in a 16-week aborted fetus. The cytoarchitecture of the cord and segmental nerves showed normal development. The fourth ventricle did not contain the usual CP but a red blood cell cluster due to hemorrhage, although the cause, whether spontaneous or traumatic, was unknown. The ectopic CP was associated with thick neuroepithelium that was strongly positive for glial fibrillary acidic protein, vimentin, nestin, and proliferating cell nuclear antigen, but did not contain any CD34-positive vessels. Thus, the ectopic neuroepithelium seemed not to carry growth factor for vascular development. On the inferior side of the ectopic CP, the lower thoracic cord was wavy, folded, and packed in a limited space as a folding fan. Despite the strange gross appearance, however, we found no abnormality in the dorsal root ganglion, the spinal nerve root, or the cytoarchitecture of the lower thoracic cord. Therefore, the abnormality in the lower thoracic cord seemed to be secondarily induced by trophic factor(s) from the ectopic CP and/or the associated neuroepithelium. This may be the first report on an ectopic CP associated with ectopic neuroepithelium.

Target sign in an intracranial vertebral artery dissection with isolated vertigo

Received: 13-03-2013 Review completed: 30-03-2013 Accepted: 17-03-2013 the patients developing CVT following lumbar puncture have had predisposing factors l ike hypercoagulable states. There are reports of patients with multiple sclerosis who had lumbar taps and high‐dose intravenous methylprednisolone developing CVT.[3] In our patient, there was no hypercoagulable state; the headache was possibly due to the dural tear and related leakage of cerebrospinal fluid (CSF) causing intracranial hypotension. Intracranial hypotension can induce a downward shift of the brain and the resultant traction and disruption of the veins/sinus can result in venous dilatation and thrombosis.[4]

Association of Aortic Knob Calcification with Intracranial Stenosis in Ischemic Stroke Patients

Background and Purpose Aortic knob calcification (AC) is associated with increased risks of cardiovascular and cerebrovascular events. We evaluated the clinical importance of AC in ischemic stroke patients with intracranial (IC) stenosis using simple, non-invasive and routine chest radiography. Methods The presence of AC was assessed in a chest posteroanterior view in 307 acute ischemic stroke patients admitted from May 2009 to April 2010, and who underwent magnetic resonance angiography or distal subtraction angiography. The association of AC with IC stenosis was analyzed. Results Patient age (68.3±8.7 vs. 65.9±8.27 years, P=0.04), and the prevalence of IC stenosis (70.7 vs. 41.3%, P<0.01) were higher in patients with AC than in patients without calcification. After adjusting for age, gender and vascular risk factors, logistic regression analysis showed that AC (Odds ratio, 3.54; 95% confidence interval, 1.90 to 6.61, P<0.01) and age (Odds ratio, 1.79; 95% confidence interval, 1.01 to 3.19; P=0.04) were independent factors affecting IC stenosis. Conclusions AC appears to be a reliable predictor for IC stenosis, an important mechanism of ischemic stroke.