Sam-Yeol Ha

25-Hydroxyvitamin D Status Is Associated With Chronic Cerebral Small Vessel Disease

Background and Purpose— The aim of this study was to determine the association between 25-hydroxyvitamin D (25(OH)D) and neuroimaging correlates of cerebral small vessel disease. Methods— We identified 759 consecutive patients with acute ischemic stroke or transient ischemic attack. Lacunes, white matter hyperintensity, and cerebral microbleed (CMB) were assessed using MR images. Deep CMB was defined as the presence of CMB in basal ganglia, thalamus, or brain stem. The association between 25(OH)D and small vessel disease was tested using linear and logistic regression analyses. Results— Mean age was 68 (±13) years. Mean level of 25(OH)D was 34.1±17.8 nmol/L. On bivariate analysis, a 25-nmol/L decrease in 25(OH)D was associated with lacunes (regression coefficient, 0.23; 95% confidence interval [CI], 0.02–0.45), severe white matter hyperintensity (odds ratio, 2.05; 95% CI, 1.41–3.08), and deep CMB (odds ratio, 1.28; 95% CI, 1.01–1.63). Also, 25(OH)D deficiency (⩽25 nmol/L) was associated with lacunes (regression coefficient, 0.5; 95% CI, 0.04–0.95), severe white matter hyperintensity (odds ratio, 2.74; 95% CI, 1.31–6.45), and deep CMB (odds ratio, 1.68; 95% CI, 1.03–2.78). The association remained significant even after multivariable adjustment and in the subgroup of previously healthy patients. Conclusions— 25(OH)D is inversely associated with lacunes, white matter hyperintensity, and deep CMB. Our findings suggest that 25(OH)D is linked to small vessel disease, and in future trials it should be tested whether 25(OH)D supplementation can prevent small vessel disease.

Voxel-based morphometric study of brain volume changes in patients with Alzheimer’s disease assessed according to the Clinical Dementia Rating score

We evaluated the volume reduction of gray matter (GM) and white matter (WM) in patients with an Alzheimers disease (AD) assessment based on the Clinical Dementia Rating (CDR) score. Patients with AD (n=61), with no subcortical WM ischemia, and healthy control patients (n=33) underwent T1-weighted spoiled gradient echo sequences, which were analyzed using voxel-based morphometry. Global GM volume reduction was observed in patients with a CDR score of 1 or a CDR score of 2, and WM volume reduction was observed in patients with a CDR score of 2. Regional GM volume reduction was found in the right inferior frontal gyrus, bilateral dorso-lateral and medial temporal lobes; WM volume reduction was found in the bilateral temporal subcortex (family-wise error, p<0.01). A CDR score of 0.5 was associated with volume reduction in the left olfactory gyrus. The peak z-score and spatial extent of volume reduction increased with increasing CDR score and were higher on the left side. GM volume reduction increased with increasing CDR scores and suggests a possible pathomechanism of AD.

A voxel-based morphometric study of cortical gray matter volume changes in Alzheimer's disease with white matter hyperintensities.

White matter hyperintensity (WMH) is commonly detected in patients with Alzheimers disease (AD), but its role in cortical impairment is unclear. This study investigated the effects of WMH on gray matter (GM) volume in patients with AD. We consecutively enrolled 84 patients with AD and 35 normal controls, who underwent brain MRI and were then classified according to WMH grade, based on a combination of deep white matter hyperintensity (DWMH) and periventricular white matter hyperintensity (PVWMH). The volume changes in GM were observed using voxel-based morphometry. It was found that global GM volume decreased with increasing WMH. Regional atrophies were in the dorsolateral frontal lobes, orbitofrontal gyri and insula (false discovery rate [FDR], p<0.01). After controlling for PVWMH, DWMH affected cortical atrophy in the frontal lobe, insula and precuneus (FDR, p<0.05), but PVWMH did not. Thus, WMH in AD is associated with GM volume reduction, especially in the frontal lobe, and DWMH is independently related to cortical atrophy.

Sulcal Effacement on Fluid Attenuation Inversion Recovery Magnetic Resonance Imaging in Hyperacute Stroke Association With Collateral Flow and Clinical Outcomes

Background and Purpose— The clinical significance of sulcal effacement has been widely investigated in CT studies, but the results are controversial. In this study, we evaluated the presence of perisylvian sulcal effacement (PSE) on fluid attenuation inversion recovery MRI and hypothesized that PSE may be related to collateral flow status together with hyperintense vessels on fluid attenuation inversion recovery in hyperacute stroke. In addition, we investigated whether an association between PSE and clinical outcome could be found in these patients. Methods— Consecutive patients with acute middle cerebral artery infarcts within 6 hours of symptom onset were included. All patients had internal carotid artery or middle cerebral artery occlusion and underwent MRI including FLAIR. The presence of PSE and hyperintense vessels on fluid attenuation inversion recovery and the collateral status and occurrence of early recanalization (ER) on conventional angiography were evaluated. Results— Of 139 patients, 79 (56.8%) had PSE. Multivariate testing revealed PSE was independently associated with collateral status. The association between hyperintense vessels and collaterals was different depending on PSE. Compared to PSE-positive and ER-negative patients, PSE-negative and ER-negative patients (odds ratio, 4.11; 95% confidence interval, 1.12–15.17) and PSE-negative and ER-positive patients (odds ratio, 34.62; 95% confidence interval, 5.75–208.60), but not PSE-positive and ER-positive patients, were more likely to experience favorable clinical outcomes (modified Rankin Scale score ⩽2 at 3 months). Conclusions— PSE is independently associated with collateral status in patients with acute middle cerebral artery stroke. Moreover, PSE in conjunction with recanalization status can predict clinical outcomes in these patients.

Hypermetabolism in the left thalamus and right inferior temporal area on positron emission tomography–statistical parametric mapping (PET–SPM) in a patient with Charles Bonnet syndrome resolving after treatment with valproic acid

Charles Bonnet syndrome (CBS) is characterized by the occurrence of complex visual hallucinations in visually impaired patients who understand that what they see is unreal. The pathophysiologic mechanism of CBS is poorly understood. However, hypermetabolism of the thalamocortical pathway as a result of deafferentation was recently proposed as a possible mechanism. A 69-year-old patient with CBS presented with a 5-year history of visual hallucinations after bilateral visual impairment, which had progressed to troublesome images of many unreal people and animals. Positron emission tomography-statistical parametric mapping (PET-SPM) imaging studies initially revealed hypermetabolism in the right inferior temporal area and left thalamus, which disappeared after treatment with valproic acid. This case, using PET-SPM analysis, supports the thalamic hypermetabolism theory of CBS.

Carotid Artery Calcification Is Associated with Deep Cerebral Microbleeds

Background/Aims: The aim of the present study was to determine the association between arterial calcification and cerebral microbleeds (CMB) relative to their distribution. Methods: We identified 834 consecutive patients with acute ischemic stroke or transient ischemic attack who underwent CT angiography and susceptibility-weighted imaging. Results: Internal carotid artery (ICA) calcification and CMB were found in 660 patients (79.1%) and 335 patients (40.2%), respectively. ICA calcification was independently associated with CMB of any location (odds ratio, OR, 2.86, 95% CI 2.01-4.08, p < 0.0001). The association between calcification and deep CMB was stronger (OR 3.51, 95% CI 2.39-5.14, p < 0.0001). However, ICA calcification was not associated with CMB in a strictly lobar area. Conclusion: ICA calcification is an independent risk factor for deep CMB but not for a strictly lobar CMB. Our findings might contribute to the elucidation of the pathogenesis of cerebral small vessel disease.

Steroid-Responsive Recurrent Encephalopathy Associated with Subacute Thyroiditis

BACKGROUND Steroid-responsive encephalopathy associated with subacute thyroiditis has, to our knowledge, not been reported previously. CASE REPORT A 49-year-old woman was found collapsed and brought to our institution with decreased mentality, dysarthria, and gait disturbance. Brain magnetic resonance imaging and angiography were normal but blood tests revealed thyroid-autoantibody-negative thyrotoxicosis. Results of a (99m)technetium-pertechnetate scan were compatible with the thyrotoxic phase of subacute thyroiditis. 14-3-3 proteins were detected in cerebrospinal fluid. Her mental status began to improve from the day following steroid administration. Recurrent encephalopathy was found 2 months after the initial admission, which was also effectively treated with steroid. CONCLUSIONS We speculate that steroid-responsive recurrent encephalopathy associated with subacute thyroiditis is a subtype of Hashimotos encephalopathy, and consider that steroid treatment should not be delayed in suspected patients.

Conduction aphasia as an initial symptom in a patient with Creutzfeldt–Jakob disease

We report a 59-year-old woman who presented to our facility with conduction aphasia as an initial symptom which, within 3months, was followed by generalized myoclonus and global aphasia. She had difficulty repeating words during the Korean-Western Aphasia Battery test. Diffusion-weighted MRI demonstrated ribbon-like hyperintensities in the bilateral temporal, parietal and occipital cerebral cortex. An electroencephalogram showed periodic discharges over the bilateral hemispheres, while single photo emission CT revealed diminished perfusion. After a positive finding of the 14-3-3 protein in her cerebrospinal fluid, she was diagnosed as having probable sporadic Creutzfeldt-Jakob disease.