Acute-Onset Chronic Inflammatory Demyelinating Polyradiculoneuropathy Mimicking Miller-Fisher Syndrome

A 77-year-old man developed diplopia, gait ataxia, and paresthesia. A clinical examination also revealed ophthalmoplegia, facial palsy, ataxia of the limbs and trunk, and reduced deep tender reflexes. Laboratory and electrophysiological studies revealed albuminocytological dissociation and demyelination. He was diagnosed as Miller-Fisher syndrome and received intravenous immunoglobulin therapy. His clinical symptoms deteriorated at 12 weeks after onset. We diagnosed acute-onset chronic inflammatory demyelinating polyradiculoneuropathy, and which the patient recovered from following corticosteroid therapy.

Acute-Onset Chronic Inflammatory Demyelinating Polyradiculoneuropathy Mimicking Miller-Fisher Syndrome

A 77-year-old man developed diplopia, gait ataxia, and paresthesia. A clinical examination also revealed ophthalmoplegia, facial palsy, ataxia of the limbs and trunk, and reduced deep tender reflexes. Laboratory and electrophysiological studies revealed albuminocytological dissociation and demyelination. He was diagnosed as Miller-Fisher syndrome and received intravenous immunoglobulin therapy. His clinical symptoms deteriorated at 12 weeks after onset. We diagnosed acute-onset chronic inflammatory demyelinating polyradiculoneuropathy, and which the patient recovered from following corticosteroid therapy.

Acute Symptomatic Seizures in Patients with Acute Ischemic Stroke: Incidence and Predictive Factors

BACKGROUND: The aim of this study was to establish the incidence, predictive factors, characteristics, and clinical outcomes of acute symptomatic seizures (ASS) after acute ischemic stroke (AIS). METHODS: In total, 2,528 consecutive patients with first-ever AIS were included. Patients with a history of epilepsy or provoked seizures due to tumor, head trauma, brain surgery, or high fever were excluded. Onset seizure (OS) and ASS were defined as seizures occurring within 24 hours and 7 days after AIS, respectively. The incidence of ASS, type of seizures, presence of late unprovoked seizure (LUS), MRI, and electroencephalogram were analyzed. RESULTS: ASS and OS occurred in 23 patients (0.9%) and 15 patients (0.6%), respectively; 20 of the patients with ASS (87.0%) had partial seizures and 4 (17.4%) developed status epilepticus. The incidence rates of ASS were 1.3%, 0.3%, and 0.2% in AIS caused by large-artery atherosclerosis, small-vessel occlusion, and cardioembolism, respectively. Of the 23 patients with ASS, the cortex was involved in 19 (82.6%), 16 patients (69.6%) had medium-sized to large lesions, the anterior circulation territory was involved in 21 patients (91.3%), and 4 patients (17.4%) developed MRI-confirmed hemorrhagic transformation of the lesions. Epileptiform discharges were observed in 9 (45%) of the 20 patients with ASS. Three of the 23 patients with ASS (13.0%) developed LUS. CONCLUSIONS: The incidence of ASS was 0.9% and was highest in the large-artery atherosclerosis group. The development of ASS was significantly associated with cortical involvement, medium-sized to large lesions, and lesions in the anterior circulation territory. Three of 23 patients (13%) developed LUS.