Imaging Differences between Neuromyelitis Optica Spectrum Disorders and Multiple Sclerosis: A Multi-Institutional Study in Japan.

BACKGROUND AND PURPOSE: Both clinical and imaging criteria must be met to diagnose neuromyelitis optica spectrum disorders and multiple sclerosis. However, neuromyelitis optica spectrum disorders are often misdiagnosed as MS because of an overlap in MR imaging features. The purpose of this study was to confirm imaging differences between neuromyelitis optica spectrum disorders and MS with visually detailed quantitative analyses of large-sample data. MATERIALS AND METHODS: We retrospectively examined 89 consecutive patients with neuromyelitis optica spectrum disorders (median age, 51 years; range, 16-85 years; females, 77; aquaporin 4 immunoglobulin G-positive, 93%) and 89 with MS (median age, 36 years; range, 18-67 years; females, 68; relapsing-remitting MS, 89%; primary-progressive MS, 7%; secondary-progressive MS, 2%) from 9 institutions across Japan (April 2008 to December 2012). Two neuroradiologists visually evaluated the number, location, and size of all lesions using the Mann-Whitney U test or the Fisher exact test. RESULTS: We enrolled 79 patients with neuromyelitis optica spectrum disorders and 87 with MS for brain analysis, 57 with neuromyelitis optica spectrum disorders and 55 with MS for spinal cord analysis, and 42 with neuromyelitis optica spectrum disorders and 14 with MS for optic nerve analysis. We identified 911 brain lesions in neuromyelitis optica spectrum disorders, 1659 brain lesions in MS, 86 spinal cord lesions in neuromyelitis optica spectrum disorders, and 102 spinal cord lesions in MS. The frequencies of periventricular white matter and deep white matter lesions were 17% and 68% in neuromyelitis optica spectrum disorders versus 41% and 42% in MS, respectively (location of brain lesions, P < .001). We found a significant difference in the distribution of spinal cord lesions between these 2 diseases (P = .024): More thoracic lesions than cervical lesions were present in neuromyelitis optica spectrum disorders (cervical versus thoracic, 29% versus 71%), whereas they were equally distributed in MS (46% versus 54%). Furthermore, thoracic lesions were significantly longer than cervical lesions in neuromyelitis optica spectrum disorders (P = .001), but not in MS (P = .80). CONCLUSIONS: Visually detailed quantitative analyses confirmed imaging differences, especially in brain and spinal cord lesions, between neuromyelitis optica spectrum disorders and MS. These observations may have clinical implications.

Relationship between sudden natural death and abdominal fat evaluated on postmortem CT scans.

OBJECTIVE: This study examined the association between sudden natural death and abdominal fat using postmortem computed tomography (CT) scans. SUBJECTS AND METHODS: Postmortem CT images at the umbilical level of 241 subjects were used to measure abdominal areas of subcutaneous- and visceral fat, the rate of visceral fat and the waist circumference. Of the study subjects, 174 died of sudden natural death (130 men and 44 women), and 67 died of different causes (46 men and 21 women). All were between 40 and 75 years of age. Logistic regression analysis was performed to identify independent abdominal parameters associated with sudden natural death. RESULTS: By univariate analysis, the areas of subcutaneous and visceral fat were significantly larger in sudden natural death than who died of different causes (subcutaneous fat, odds ratio [OR] = 1.004, 95% confidence interval [CI] = 1.000-1.007, p = 0.03; visceral fat, OR = 1.008, 95% CI = 1.003-1.013, p < 0.01). Multivariate analysis showed that the area of visceral fat was an independent factor associated with the risk of sudden natural death (OR = 1.008, 95% CI = 1.002-1.015, p = 0.02). CONCLUSIONS: Postmortem CT revealed that sudden natural death was related to abdominal fat deposits.

Orbital Fat Volumetry and Water Fraction Measurements Using T2-Weighted FSE-IDEAL Imaging in Patients with Thyroid-Associated Orbitopathy.

BACKGROUND AND PURPOSE: The quantitative evaluation of orbital fat proliferation and edema and the assessment of extraocular muscles are useful for diagnosing and monitoring thyroid-associated orbitopathy. To evaluate therapy-induced quantitative changes in the orbital fat of patients with thyroid-associated orbitopathy, we performed volumetric and water fraction measurements by using T2-weighted FSE iterative decomposition of water and fat with echo asymmetry and least-squares estimation (FSE-IDEAL) imaging. MATERIALS AND METHODS: Orbital FSE-IDEAL images of 30 volunteers were acquired twice within 1 week. Nine patients with thyroid-associated orbitopathy underwent FSE-IDEAL imaging before and after methylprednisolone pulse therapy, and the treatment results were assessed by using their pre- and post-methylprednisolone pulse therapy clinical activity scores. We performed volumetric and water fraction measurements of orbital fat by using FSE-IDEAL imaging and evaluated interscan differences in the volunteers. In patients with thyroid-associated orbitopathy, we compared pre- and posttherapy orbital fat measurements and assessed the correlation between the pretherapy values and clinical activity score improvement. RESULTS: The reproducibility of results obtained by the quantitative evaluation of orbital fat in volunteers was acceptable. After methylprednisolone pulse therapy, the water fraction in the orbital fat of patients with thyroid-associated orbitopathy was significantly decreased (P < .001). There was a significant positive correlation between the pretherapy water fraction and clinical activity score improvement (right, r = 0.82; left, r = 0.79) and a significant negative correlation between the pretherapy volume and clinical activity score improvement (bilateral, r = -0.84). CONCLUSIONS: Volumetric and water fraction measurements of orbital fat by using FSE-IDEAL imaging are feasible and useful for monitoring the effects of therapy and for predicting the response of patients with thyroid-associated orbitopathy to methylprednisolone pulse therapy.

Brain MR findings in patients with systemic lupus erythematosus with and without antiphospholipid antibody syndrome.

BACKGROUND AND PURPOSE: Antiphospholipid syndrome may affect the incidence and pathogenesis of cerebrovascular diseases in patients with systemic lupus erythematosus. We compared the spectrum of MR findings in patients with systemic lupus erythematosus with and without antiphospholipid syndrome. MATERIALS AND METHODS: We identified 256 patients with systemic lupus erythematosus (45 with, 211 without antiphospholipid syndrome) who underwent MR studies; in 145 (57%), we detected abnormalities. These were categorized as large territorial, lacunar, localized cortical, and borderzone infarctions and as microembolisms, basal ganglia lesions, callosal lesions, hemorrhages, and white matter hyperintensity on T2-weighted and/or FLAIR images, and as stenotic arterial lesions on MR angiograms. Logistic regression analysis was performed to compare the MR findings in patients with systemic lupus erythematosus with and without antiphospholipid syndrome, with patient age and antiphospholipid syndrome as the covariates. RESULTS: Abnormal MR findings were more common in patients with systemic lupus erythematosus with antiphospholipid syndrome (73% versus 53%). Large territorial (P = .01), lacunar (P = .01), localized cortical (P < .01), borderzone infarcts (P < .01), basal ganglia lesions (P = .03), stenotic arterial lesions (P = .04), and the rate of positive findings on MR imaging (P = .01) were significantly associated with antiphospholipid syndrome. Irrespective of age, significantly more patients with antiphospholipid syndrome manifested lacunar infarcts in the deep white matter (P < .01), localized cortical infarcts in the territory of the MCA (P < .01), bilateral borderzone infarcts (P < .01), and anterior basal ganglia lesions (P = .01). CONCLUSIONS: Abnormal MR findings were more common in patients with systemic lupus erythematosus with than in those without antiphospholipid syndrome. Large territorial infarctions, lacunar infarctions in the deep white matter, localized cortical infarctions in the MCA territory, bilateral borderzone infarctions, anterior basal ganglia lesions, and stenotic arterial lesions are common MR findings in patients with systemic lupus erythematosus with antiphospholipid syndrome.

Dopamine D3 receptor binding by D3 agonist 7-OH-DPAT (7-hydroxy-dipropylaminotetralin) and antipsychotic drugs measured ex vivo by quantitative autoradiography.

Because the dopamine D3 receptor is primarily expressed in regions of the limbic system of brain, it was proposed that it may represent a target for antipsychotic drugs that is free of extrapyramidal side effects. An ex vivo receptor binding technique employing [3H]7-OH-DPAT was used to evaluate in vivo occupancy of dopamine D3 receptors in the rat nucleus accumbens by selective D3 agonist 7-OH-DPAT (7-hydroxy-dipropylaminotetralin) and various antipsychotic drugs. With an ID50 value of 0.07 mg/kg, the selective D3 agonist (+)-7-OH-DPAT had the most potent inhibitory effect on ex vivo binding of [3H]7-OH-DPAT among all drugs tested. Clinical doses of phenothiazine drugs, such as chlorpromazine and levomepromazine, induce binding to D3 receptors in vivo, while atypical antipsychotic drugs, such as clozapine, pimozide, and sulpiride, are very weak in inhibiting ex vivo binding of [3H]7-OH-DPAT, indicating that the role of D3 receptors as targets of antipsychotic drugs free of extrapyramidal side effects may not be important.

Effect of chronic amitriptyline administration on serotonergic receptors in rats with methylazoxymethanol-induced microencephaly.

Methylazoxymethanol (MAM)-induced cortical hypoplasia resulted in a 20% decrease in the Bmax of 5-HT2A receptors in the frontal cortex with no change in the Bmax of 5-HT1A receptors. Chronic treatment with amitriptyline did not further decrease the Bmax of 5-HT2A receptors in the MAM-lesioned cortex, suggesting that the persistent down-regulation of cortical 5-HT2A receptors in MAM-lesioned rats was induced by serotonergic hyperinnervation.