Kazushi Yamane

Eicosapentaenoic acid (EPA) induces peroxisome proliferator-activated receptors and ameliorates experimental autoimmune encephalomyelitis

Eicosapentaenoic acid (EPA), one of the n-3 polyunsaturated fatty acids, is a neuroprotective lipid with anti-inflammatory properties. We investigated the possible therapeutic effect of EPA on experimental autoimmune encephalomyelitis (EAE). EAE mice were fed a diet with or without EPA. The clinical EAE scores of the EPA-fed mice were significantly lower than those of the non-EPA mice. In the EPA-treated mice, IFN-γ and IL-17 productions were remarkably inhibited and the expression levels of peroxisome proliferator-activated receptors were significantly enhanced in the CNS-infiltrating CD4T cells. Thus EPA shows promise as a potential new therapeutic agent against multiple sclerosis.

Postural Abnormality as a Risk Marker for Leg Deep Venous Thrombosis in Parkinson’s Disease

Background Pulmonary thromboembolism is a common cause of death in patients with autopsy-confirmed Parkinsonism. This study investigated the incidence of leg deep vein thrombosis in Parkinson’s disease and relationships between deep vein thrombosis and clinical/laboratory findings, including postural abnormalities as assessed by photographic measurements. Methods This cross-sectional study assessed the presence of deep vein thrombosis using bilateral leg Doppler ultrasonography in 114 asymptomatic outpatients with Parkinson’s disease. Results Deep vein thrombosis was detected in 23 patients (20%) with Parkinson’s disease. Deep vein thrombosis was located in the distal portion in 18 patients and in the proximal portion in 5 patients. No significant differences in age, sex, body mass index, disease duration, Hoehn-Yahr stage, anti-Parkinson’s drugs, or daily levodopa-equivalent dose were seen between deep vein thrombosis-positive and -negative groups. Univariate analysis for developing deep vein thrombosis in patients with Parkinson’s disease identified the following markers: long-term wheelchair use, bent knee, bent spine, and D-dimer elevation. Bending angles were significantly greater in the deep vein thrombosis-positive group at the knee and spine than in the deep vein thrombosis-negative group. Half of Parkinson’s disease patients with camptocormia had deep vein thrombosis. Among diabetes mellitus cases, long-term wheelchair use, bent knee over 15°, camptocormia, D-dimer elevation, the more risk markers were associated with a higher incidence of DVT. The presence of risk markers contributed to the development of deep vein thrombosis. On multivariate logistic regression analysis, a bent knee posture was strongly associated with an increased risk of deep vein thrombosis. Conclusion Presence of leg deep vein thrombosis correlated with postural abnormalities in Parkinson’s disease. We recommend non-invasive ultrasonographic screening for leg deep vein thrombosis in these high-risk patients with Parkinson’s disease.

Optic perineuritis associated with antineutrophil cytoplasmic autoantibody-related hypertrophic pachymeningitis: a case report

Hypertrophic pachymeningitis is an inflammatory disease that causes various neural symptoms, including headache and cranial neuropathy, presenting as pachymeningeal hypertrophy with contrast enhancement on imaging. The cause of this disease is classified as idiopathic, in which the underlying disease is unknown, and is associated with autoimmunity, such as antineutrophil cytoplasmic autoantibody (ANCA)-related vasculitis, IgG4-related disease and infections [1]. Here, we describe a patient with ANCArelated hypertrophic pachymeningitis that developed with visual impairment caused by optic perineuritis. Although optic perineuritis closely resembles optic neuritis, it is a different condition. Thus, it is important to ascertain the condition after hypertrophic pachymeningitis diagnosis and to provide appropriate treatment. An 87-year-old woman underwent surgery for a cataract of the left eye; however, immediately after the surgery, blurred vision occurred in the eye. Thereafter, she developed headaches and loss of vision. Visual acuity of the left eye was 0.4, and 3 days later, only light perception was possible, and she was admitted to our hospital. However, on identifying a high inflammatory response and abnormal findings through magnetic resonance imaging (MRI) of the head, she was admitted to our department. On admission, she had right visual acuity of 0.8 with left light perception, no difference in left–right pupil size, normal eye movement. She was negative for neck stiffness, and no other neurological deficit suggesting neuromyelitis optica spectrum disorders was detected. Blood tests revealed a high inflammatory response with white blood cell counts of 10,970/mm, C-reactive protein (CRP) levels of 9.25 mg/ dL, anti-nuclear antibodies 1:640, proteinase 3 (PR3)ANCA levels of 7.1 U/mL, and high myeloperoxidase (MPO)-ANCA levels of 5.1 U/mL. However, IgG4 level was normal at 108 mg/dL. Anti-aquaporin 4 antibody was negative. Examination of the cerebrospinal fluid revealed a cell count of 13/mm and protein and glucose levels of 107.3 and 54 mg/dL, respectively. PCR revealed the absence of herpes simplex virus, varicella zoster virus, and tuberculosis bacterial DNA in cerebrospinal fluid. There were no abnormalities on fundoscopy, and no papilledema was observed; however, visual field test on the Goldmann perimeter revealed central scotoma with concentric narrowing of the visual field in the left eye. MRI of the optic nerve on T2-weighted fat-suppressed imaging revealed linear high signal intensity and tram-track signs [2] that were believed to be an enlargement of the cerebrospinal fluid cavity surrounding the left and right optic nerves (Fig. 1a). The left optic nerve showed increased enhancement of the gadolinium contrast medium surrounding the optic nerve (Fig. 1b, c). These visual field test and MRI findings were believed to be signs of left optic perineuritis. Cerebral MRI revealed increased enhancement of the pachymeninx extending to the entire cerebral hemisphere with left-side predominance (Fig. 1d–f), and positive results for PR3-ANCA and MPO-ANCA on blood testing led to the consideration of ANCA-related hypertrophic pachymeningitis. Furthermore, diffusion-weighted imaging & Hideto Nakajima in1045@poh.osaka-med.ac.jp

Acute Cerebellar Ataxia Associated with Anti-glutamic Acid Decarboxylase Antibodies Mimicking Miller Fisher Syndrome: A Case Report

We herein report the case of a 53-year-old man with cerebellar ataxia with anti-glutamic acid decarboxylase antibody (GAD-Ab) who mimicked Miller Fisher syndrome (MFS). He developed ophthalmoplegia, diplopia, and gait ataxia for one week. The serum and cerebrospinal fluid GAD-Ab titers were greatly increased, and the GAD-Ab index suggesting intrathecal antibody synthesis was elevated, while GQ1b-Ab was negative. After steroid pulse therapy and following prednisolone, his symptoms dramatically improved over the course of 11 months with the simultaneous decline of GAD-Ab titers. This case indicates that cerebellar ataxia with GAD-Ab can present with acute neurological findings mimicking MFS, and that steroid therapy has an excellent therapeutic effect.