Moo-Seok Park

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.

The cortical contrast accumulation from brain computed tomography after endovascular treatment predicts symptomatic hemorrhage.

The prognostic value of contrast accumulation from non‐contrast brain computed tomography taken immediately after endovascular reperfusion treatment in acute ischaemic stroke patients to predict symptomatic hemorrhage was studied.

Anti-Ma2 Antibody Encephalitis Manifesting as Cognitive Impairment and Psychosis

To the Editor: Anti-Ma2 antibody encephalitis is a rare autoimmune disease and is a paraneoplastic syndrome related with systemic cancers. The literature includes a few case reports in which anti-Ma2 antibody encephalitis involved the brainstem and limbic system; these patients showed neuropsychiatric manifestations, including neuro-ophthalmologic abnormalities, dizziness, headache, ataxia, seizure, and drowsiness. Given the rarity of the condition and the need to test levels of specific antibodies, diagnosing anti-Ma2 antibody encephalitis is a very difficult and challenging process. Therefore, a physician’s knowledge of and experience with autoimmune encephalitis are important for proper diagnosis and treatment. This report describes a patient with anti-Ma2 antibody encephalitis and a hidden malignant neoplasm who initially manifested acute cognitive impairment and psychosis.

Subcoracoid bursitis presenting with brachial plexopathy involving the posterior cord

Department of Neurology, Chung-Ang University Hospital, Chung-Ang University College of Medicine, Seoul, Republic of Korea Department of Neurology, Inha University Hospital, Inha University College of Medicine, Incheon, Republic of Korea Department of Neurology, Kyung Hee University Hospital, Kyung Hee University College of Medicine, Seoul, Republic of Korea. Department of Orthopaedic Surgery, Chung-Ang University Hospital, Chung-Ang University College of Medicine, Seoul, Republic of Korea Address for correspondence: Suk-Won Ahn, MD., PhD., Department of Neurology, Chung-Ang University Hospital, Chung-Ang University College of Medicine, 224-1 Heukseok-dong, Dongjak-gu, Seoul, Republic of Korea.. Tel: +82-2-6299-3153 Fax: +82-2-6299-3153 E-mail: icandr@hanmail.net

Relapsing Polychondritis Presented with Encephalitis Followed by Brain Atrophy

Relapsing polychondritis (RP) is a rare autoimmune disease that is characterized by inflammatory reaction of unknown etiology and destruction of cartilaginous structures. Characteristic symptoms of this disease include cartilage inflammation of the ear, nose, larynx, trachea, bronchi, joints, eyes, heart and skin. Concomitance with neurologic symptom is very rare in RP, and the detailed underlying mechanism of neurological involvement associated with RP is not fully understood. We herein described an unusual recurrent case of inflammatory brain lesions associated with RP, with attention to clinical manifestations, autoimmune disease involvement, and therapeutic effects.