scholarly journals Optic Chiasm Morphometric Changes in Multiple Sclerosis: Feasibility of a Simplified Brain Magnetic Resonance Imaging Measure of White Matter Atrophy

2019 ◽  
Vol 32 (8) ◽  
pp. 1072-1081
Author(s):  
Fulvio Zaccagna ◽  
Tomasz Matys ◽  
Tarik F. Massoud
2021 ◽  
pp. 55-56
Author(s):  
Jonathan L. Carter

A 36-year-old woman with a history of relapsing-remitting multiple sclerosis was evaluated for new multiple sclerosis symptoms accompanied by new, enhancing, white matter lesions on brain magnetic resonance imaging. Her multiple sclerosis presented with L’hermitte sign when she was 24 years old. She had onset of bilateral lower extremity and left upper extremity tingling at age 26 years. Magnetic resonance imaging and cerebrospinal fluid examination at the time were supportive of the diagnosis of multiple sclerosis, and disease-modifying therapy was recommended by her neurologist. She initiated therapy with dimethyl fumarate at age 30 years after several further relapses. Surveillance magnetic resonance imaging showed new gadolinium-enhancing lesions on brain magnetic resonance imaging on each of 3 consecutive yearly scans. Urine culture and sensitivity tests were performed to rule out occult urinary tract infection; results of this testing were negative. magnetic resonance imaging of the brain concurrently showed new enhancing white matter lesions. The patient was diagnosed with clinical and radiographic breakthrough disease activity while receiving therapy for multiple sclerosis. The patient was treated with 5 days of intravenous methylprednisolone for her relapse. After discussion with the patient, it was decided to transition therapy from dimethyl fumarate to ocrelizumab infusions for her breakthrough disease activity. This decision was further supported by the patient’s concerns that she might be entering an early progressive phase of the disease. In patients with spinal-predominant multiple sclerosis, or with symptoms potentially indicating new spinal cord involvement, it may be necessary to include spinal cord imaging to assess for new disease activity.


2007 ◽  
Vol 13 (2) ◽  
pp. 186-192 ◽  
Author(s):  
José A Cabrera-Gómez ◽  
L Quevedo-Sotolongo ◽  
A González-Quevedo ◽  
S Lima ◽  
Y Real-González ◽  
...  

Background Some studies showed abnormalities in brain magnetic resonance imaging (MRI) of relapsing neuromyelitis optica (R-NMO) from 12 to 46%. These abnormalities are described as compatible/non-compatible with multiple sclerosis (MS). Objective To describe the abnormal brain MRI lesions in R-NMO with imaging studies conducted with more sensitive white matter change techniques. Methods Thirty patients with R-NMO were selected. All MRI brain studies were performed with a 1.5-T Siemens MRI system according to the Standardized MR Imaging Protocol for Multiple Sclerosis from the Consortium of MS Centers Consensus Guidelines. Results Brain MRI images were evaluated in 29 R-NMO cases because in one case the MRI images were not appropriate for the study. Of these 29 brain MRI studies, 19 cases (65.5%) had at least one or more lesions (1–57) and 10 were negative (34.4%). Brain MRI findings in 19 cases were characterized in T2/fluid-attenuated inversion-recovery (FLAIR) by the presence of subcortical/deep white matter lesions in 16 (84.2%) cases (1–50), most of them < 3 mm and without juxtacortical localization. Periventricular lesions were observed in 13 (68.4%) cases, but morphologically they were not oval, ovoid or perpendicularly orientated. Infratentorial lesions, all >3 mm, were observed in 4 (21.05%) cases without cerebellar involvement. T1 studies demonstrated absence of hypointense regions. Optic nerve enhancement was observed in 6/19 patients (31.5%). None of the brain MRI abnormalities observed were compatible with Barkhof et al. criteria of MS. Conclusions This study, based on a Cuban patient population, with long duration of disease, good sample size and detailed characterization by MRI, demonstrated the brain MRI pattern of R-NMO patients, which is different from MS. Multiple Sclerosis 2007; 13: 186–192. http://msj.sagepub.com


2016 ◽  
Vol 12 (1) ◽  
pp. 108-113 ◽  
Author(s):  
Stephanie A Ward ◽  
Parnesh Raniga ◽  
Nicholas J Ferris ◽  
Robyn L Woods ◽  
Elsdon Storey ◽  
...  

Rationale Cerebral microbleeds seen on brain magnetic resonance imaging are markers of small vessel disease, linked to cognitive dysfunction and increased ischemic and hemorrhagic stroke risk. Observational studies suggest that aspirin use may induce cerebral microbleeds, and associated overt intracranial hemorrhage, but this has not been definitively resolved. Aims ASPREE-NEURO will determine the effect of aspirin on cerebral microbleed development over three years in healthy adults aged 70 years and over, participating in the larger ‘ASPirin in Reducing Events in the Elderly (ASPREE)’ primary prevention study of aspirin. Sample size Five hundred and fifty-nine participants provide 75% power (two-sided p value of 0.05) to determine an average difference of 0.5 cerebral microbleed per person after three years. Methods and design A multi-center, randomized placebo-controlled trial of 100 mg daily aspirin in participants who have brain magnetic resonance imaging at study entry, one and three years after randomization and who undergo cognitive testing at the same time points. Study outcomes The primary outcome is the number of new cerebral microbleeds on magnetic resonance imaging after three years. Secondary outcomes are the number of new cerebral microbleeds after one year, change in volume of white matter hyperintensity, cognitive function, and stroke. Discussion ASPREE-NEURO will resolve whether aspirin affects the presence and number of cerebral microbleeds, their relationship with cognitive performance, and indicate whether consideration of cerebral microbleeds alters the risk-benefit profile of aspirin in primary prevention for older people. Trial registration Australian New Zealand Clinical Trials Registry ACTRN12613001313729.


2019 ◽  
Vol 27 (2) ◽  
pp. 235-243 ◽  
Author(s):  
N. Ziliotto ◽  
R. Zivadinov ◽  
M. Baroni ◽  
G. Marchetti ◽  
D. Jakimovski ◽  
...  

2021 ◽  
pp. 69-72
Author(s):  
Andrew McKeon

A 60-year-old woman with a history of Sjögren syndrome had an episode of painful left eye vision loss. Brain magnetic resonance imaging showed an arteriovenous malformation adjacent to the left ventricular atrium. Although this was considered an asymptomatic lesion, the patient underwent stereotactic radiosurgery to reduce the risk of future growth and hemorrhage. Within days of the surgery, speech disturbance and weakness of the right arm and leg developed. Examination indicated a subcortical language deficit and an upper motor pattern of paresis of right-sided limbs. Considered in the differential diagnosis were new hemorrhage from the arteriovenous malformation, ischemic stroke, radiation-induced necrosis, abscess, and demyelinating disease. Magnetic resonance imaging of the head with and without gadolinium contrast was used to evaluate for these possibilities. Brain magnetic resonance imaging after onset of speech and motor symptoms demonstrated new areas of confluent T2 signal abnormality in the brainstem and deep white matter of the left hemisphere, with some accompanying enhancement but without evidence of hemorrhage or acute stroke. Slow conduction was noted in the left optic nerve on visual evoked potentials. The patient was diagnosed with optic neuritis, with subsequent evolution to multiple sclerosis in the setting of radiosurgery. The patient received intravenous methylprednisolone with full recovery of language function and partial recovery of the hemiparesis, which improved with rehabilitation such that she could walk without a gait aid. Because the patient had more than 1 episode, she was treated with interferon beta-1a for further prevention of multiple sclerosis relapse. Chronic neurotoxicity leading to subcortical dementia occurs in approximately 25% of patients undergoing whole-brain radiotherapy. Histologically, demyelination, as well as necrosis, can be a prominent feature. Among patients with multiple sclerosis or a clinically isolated syndrome, the risk of demyelinating events appears to increase after brain radiotherapy, within the field of treatment.


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