Cortical lesions are a interesting field of study, because demyelination happens without autoimmune infiltration. In this article the authors compare several cases of cortical lesions, and find a difference in the microglia activation.
http://www.neurology.org/content/79/13/1369.short
Abstract
Objective: Autopsy cases show that cortical lesions (CLs) in multiple sclerosis (MS) lack lymphocyte/macrophage influx, blood-brain barrier breakdown, and complement activation. However, some CLs were demonstrated to harbor activated microglia. Here, we assessed the clinical significance of microglia activation in CLs in a large autopsy sample, and we investigated possible interrelationships with other pathologic characteristics.
Methods: We cross-sectionally investigated the clinicopathologic characteristics of 22 patients with MS with extensive subpial demyelination (CL group) and 19 patients with MS with only little demyelination of the cerebral cortex (non-CL group).
Results: A subset of the patients in the CL group (12 patients) showed rims of activated microglia (RAM) at the border of the CLs (RAM-CL group), whereas the other 10 patients in this group did not show microglia activation (non−RAM-CL group). A subsequent comparison between groups showed that patients with MS harboring RAM-CLs were significantly younger at the time of their death (53.5 years) than patients harboring mainly non–RAM-CLs (68.7 years; p < 0.05) or patients without extensive numbers of CLs (66.9 years; p < 0.01). In addition, a significantly shorter disease duration was found for the RAM-CL group (mean 20.9 years) than for the non-CL group (mean 34.5 years; p < 0.05). We also found that the presence of RAM-CLs is associated with a higher number of chronic active white matter (WM) lesions (Spearman ρ = 0.74; p < 0.0001).
Conclusions: RAM-CLs were found in a subset of patients with MS who also have more active WM inflammation and a less favorable disease course.
Heterogeneity of cortical lesions
If it's on your mind and it has to do with multiple sclerosis in any way, post it here.
Return to “General Discussion”
Jump to
- Multiple Sclerosis
- ↳ General Discussion
- ↳ Introductions
- ↳ Drug Pipeline
- ↳ Regimens
- ↳ Undiagnosed
- ↳ MS Etiology and Pathogenesis
- Treatments
- ↳ Chronic Cerebrospinal Venous Insufficiency (CCSVI)
- ↳ Low Dose Naltrexone
- ↳ Tysabri (Antegren, Natalizumab)
- ↳ Copaxone
- ↳ Glatopa
- ↳ Avonex
- ↳ Rebif
- ↳ Betaseron
- ↳ Plegridy
- ↳ Novantrone
- ↳ Aimspro
- ↳ Diet
- ↳ Stem Cells
- ↳ Antibiotics
- ↳ Campath (Lemtrada, Alemtuzumab)
- ↳ Gene Therapy
- ↳ Natural Approach
- ↳ Biotin (Qizenday, Cerenday, MD1003)
- ↳ Coimbra High-Dose Vitamin D Protocol
- ↳ Statins
- ↳ Tcelna (Tovaxin)
- ↳ Revimmune (Cyclophosphamide, Cytoxan)
- ↳ Medical Devices
- ↳ Rituxan (Rituximab)
- ↳ Ocrevus (Ocrelizumab)
- ↳ Kesimpta (Ofatumumab)
- ↳ Briumvi (Ublituximab-xiiy)
- ↳ General Medications
- ↳ Tecfidera (BG-12, Dimethyl fumarate)
- ↳ Vumerity (Diroximel fumarate)
- ↳ Bafiertam (Monomethyl fumarate)
- ↳ Gilenya
- ↳ Aubagio (Teriflunomide)
- ↳ Mayzent (Siponimod)
- ↳ Zeposia (Ozanimod)
- ↳ Ponvory (Ponesimod)
- ↳ Mavenclad (Cladribine)
- ↳ Ampyra (Dalfampridine)
- ↳ Medical Marijuana
- ↳ Sativex
- ↳ Chiropractic Treatment
- Life
- ↳ Daily Life
- ↳ Veterans and MS
- ↳ Trigeminal Neuralgia in MS
- ↳ Reading Nook
- ↳ Humor
- ↳ Shopping
- ↳ Friends and Family
- ↳ Mental & Spiritual Health
- ↳ Exercise and Physical Therapy
- ↳ Under 25 with MS
- ↳ MS in the Golden Years
- ↳ Parenting Kids With MS
- ↳ Parents with MS
- ThisIsMS.com
- ↳ Site Support
- ↳ Suggestions