Eye Movement Abnormalities and Neuroimaging Findings of Disequilibrium of Unknown Origin / 대한평형의학회지

BACKGROUND AND OBJECTIVES: Although disequilibrium is common type of dizziness in older people, it is sometimes difficult to identify a specific cause for this problem. The diffuse brain pathology including subcortical ischemia and atrophy can be a cause for patients with disequilibrium of unknown cause. Aim of this study is to identify the eye movements and neuroimaging features in patients with disequilibrium. MATERIALS AND METHODS: We performed a prospective investigation in patients with disequilibrium of unknown cause. We collected information on demographic characteristics and clinical features of disequilibrium. The impact of dizziness on everyday life was assessed by 25-item dizziness handicap inventory (DHI). Vestibular function test (VFT) includes smooth pursuit, saccade, optokinetic nystagmus, and rotatory chair test. Subcortical white matter lesions and brain atrophy were graded from brain magnetic resonance image (MRI). RESULTS: This study included 14 patients (12 female and 2 male), aged between 64 and 84 years, mean age 74.01+/-6.02 years. The score of DHI was 39.4+/-11.8 (20-58). Eye movements were abnormal in 13 patients and normal in only one patient. The degree of subcortical ischemia was mild in 7, moderate in 4, and severe in 3 patients. Ventricular brain ratio was 0.23+/-0.03. However, there was no significant relationship between MRI findings and the degree of oculomotor alterations (result of VFT). CONCLUSION: Patients with disequilibrium of unknown cause are usually elderly women. Alterations in oculomotor movements and diffuse brain pathology including white matter lesions and atrophy were observed in patients with disequilibrium of unknown cause.

Guillain-Barre Syndrome Following Acute Cerebral Infarction

Guillain-Barre syndrome (GBS) is an autoimmune polyneuropathy that presents with acute onset and rapid progression of ascending quadriparesis and hyporeflexia, which can be triggered by various conditions. However, GBS following cerebral infarction is very rare. We describe herein a patient with facial diplegia, ophthalmoplegia, and areflexia that occurred during acute cerebral infarction. The symptoms were improved after intravenous immunoglobulin treatment. The details of this case suggest that GBS is triggered by immune dysregulation after acute cerebral infarction.