Anti-TNFa-associated central nervous system demyelination. A triggering factor for multiple sclerosis?

2017 ◽  
Vol 381 ◽  
pp. 784
Author(s):  
V. Mastorodemos ◽  
G. Vourakis ◽  
G. Georgiakakis ◽  
P. Mitsias
Keyword(s):  
Multiple Sclerosis ◽  
Central Nervous System ◽  
Nervous System ◽  
Central Nervous System Demyelination ◽  
Triggering Factor

scholarly journals A healthy dietary pattern associates with a lower risk of a first clinical diagnosis of central nervous system demyelination

2018 ◽  
Vol 25 (11) ◽  
pp. 1514-1525 ◽  
Author(s):  
Lucinda J Black ◽  
Charlotte Rowley ◽  
Jill Sherriff ◽  
Gavin Pereira ◽  
Anne-Louise Ponsonby ◽  
...  
Keyword(s):  
Multiple Sclerosis ◽  
Central Nervous System ◽  
Nervous System ◽  
Clinical Diagnosis ◽  
Dietary Patterns ◽  
Dietary Pattern ◽  
Conditional Logistic Regression ◽  
Standard Deviation Increase ◽  
Study Region ◽  
Central Nervous System Demyelination

Background: The evidence associating diet and risk of multiple sclerosis is inconclusive. Objective: We investigated associations between dietary patterns and risk of a first clinical diagnosis of central nervous system demyelination, a common precursor to multiple sclerosis. Methods: We used data from the 2003–2006 Ausimmune Study, a case–control study examining environmental risk factors for a first clinical diagnosis of central nervous system demyelination, with participants matched on age, sex and study region. Using data from a food frequency questionnaire, dietary patterns were identified using principal component analysis. Conditional logistic regression models ( n = 698, 252 cases, 446 controls) were adjusted for history of infectious mononucleosis, serum 25-hydroxyvitamin D concentrations, smoking, race, education, body mass index and dietary misreporting. Results: We identified two major dietary patterns – healthy (high in poultry, fish, eggs, vegetables, legumes) and Western (high in meat, full-fat dairy; low in wholegrains, nuts, fresh fruit, low-fat dairy), explaining 9.3% and 7.5% of variability in diet, respectively. A one-standard deviation increase in the healthy pattern score was associated with a 25% reduced risk of a first clinical diagnosis of central nervous system demyelination (adjusted odds ratio 0.75; 95% confidence interval 0.60, 0.94; p = 0.011). There was no statistically significant association between the Western dietary pattern and risk of a first clinical diagnosis of central nervous system demyelination. Conclusion: Following healthy eating guidelines may be beneficial for those at high risk of multiple sclerosis.

scholarly journals Central Nervous System Demyelination Associated With Immune Checkpoint Inhibitors: Review of the Literature

2020 ◽  
Vol 11 ◽  
Author(s):  
Marcos C. B. Oliveira ◽  
Marcelo H. de Brito ◽  
Mateus M. Simabukuro
Keyword(s):  
Multiple Sclerosis ◽  
Central Nervous System ◽  
Nervous System ◽  
Adverse Events ◽  
Immune Checkpoint ◽  
Immune Checkpoint Inhibitors ◽  
Checkpoint Inhibitors ◽  
Case Reports ◽  
Cell Mediated Immune Response ◽  
Central Nervous System Demyelination

Immune checkpoint inhibitors (ICI) are a novel class of antineoplastic treatment that enhances immunity against tumors. They are associated with immune adverse events, and several neurological syndromes have been described, including multiple sclerosis and atypical demyelination. We performed a systematic literature review of case reports with neurological immune adverse events that presented with central nervous system demyelination, up to December 2019. We found 23 cases: seven with myelitis, four isolated optic neuritis, one neuromyelitis optica spectrum disorder, five multiple sclerosis, and six with atypical demyelination. Ipilimumab was the most frequently used ICI (11/23). The median time to develop symptoms from the onset of ICI was 6.5 weeks [range 1.0–43.0], and from last ICI dose was 14 days [range 0–161]. Anatomopathological examination was performed in four cases, with the finding of a T-cell mediated immune response. Outcomes were generally favorable after immunosuppression: 18 patients had improvement or a full recovery, three patients did not respond to treatment, three patients died, and in one, treatment was not reported. We describe the patients' clinical presentation, treatment administered, and outcomes. We further speculate on possible pathophysiological mechanisms and discuss potential treatments that may be worth investigating.

Very early scans for demonstrating dissemination in time in multiple sclerosis

2008 ◽  
Vol 14 (5) ◽  
pp. 631-635 ◽  
Author(s):  
C Tur ◽  
M Tintoré ◽  
Á Rovira ◽  
C Nos ◽  
J Río ◽  
...  
Keyword(s):  
Multiple Sclerosis ◽  
Central Nervous System ◽  
Nervous System ◽  
Symptom Onset ◽  
Clinical Syndrome ◽  
Clinically Isolated Syndrome ◽  
Lesion Effect ◽  
T2 Lesions ◽  
Central Nervous System Demyelination ◽  
Time To Relapse

Objective To evaluate the clinical significance of the 2005 modified imaging criteria for dissemination in time in multiple sclerosis stating that detection of a new T2 lesion appearing at any time compared with a reference scan done at least 30 days after the onset of a clinically isolated syndrome implies dissemination in time. Methods We included consecutive patients younger than 50 years examined at our center within 3 months of a clinical syndrome suggestive of central nervous system demyelination of the type seen in multiple sclerosis and followed for at least 3 years. We classified patients into one of two groups, according to the timing when reference scan was performed: less than 30 days and at least 30 days after symptom onset. We analyzed the interaction in time to relapse between timing of reference scan and new T2 lesion effect. Results A total of 218 patients were included. The hazard ratio (95% confidence interval) of this interaction was 0.90 (0.31–2.62) (or 1.02 (0.27–3.91) in patients with dissemination in space). Conclusions We conclude that new T2 lesions increased relapse risk regardless of timing of the reference scan, supporting the use of scans performed at any time within 30 days of symptom onset for dissemination in time demonstration.

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