Demyelinating and Thrombotic Diseases of the Central Nervous System: Common Pathogenic and Triggering Factors

Commentary: Tumefactive Demyelinating Lesions as a First Clinical Event: Clinical, Imaging, and Follow-up Observations

“…An increased risk of venous thromboembolism in MS reported in epidemiological studies (9) and a correlation between MS relapses and prothrombotic factors, such as antiphospholipid antibody positivity (10), support the hypothesis that the activation of coagulation system plays a role in MS pathogenesis (9). Indeed, fibrin deposition precedes and regulates the inflammatory demyelination in both experimental allergic encephalomyelitis and MS (9). Antiphospholipid positivity is even greater in NMOSD than in MS (11), and it should be noted that NMOSD usually represent a more severe disease as compared to MS and at the same time frequently associate with extensive brain lesions similar to TDLs (1).…”

“…When inflammatory processes have a greater intensity and extension, they likely determine a markedly slowed venous flow with partial thrombosis in larger venules manifesting with “tumor-like” characteristics of TDLs. Demyelinating and thrombotic diseases of the central nervous system (CNS) share common predisposing factors, such as smoking, endothelial dysfunction, platelet activation, thrombophilia, and hyper-homocysteine, all representing prothrombotic conditions (9). An increased risk of venous thromboembolism in MS reported in epidemiological studies (9) and a correlation between MS relapses and prothrombotic factors, such as antiphospholipid antibody positivity (10), support the hypothesis that the activation of coagulation system plays a role in MS pathogenesis (9).…”

“…Demyelinating and thrombotic diseases of the central nervous system (CNS) share common predisposing factors, such as smoking, endothelial dysfunction, platelet activation, thrombophilia, and hyper-homocysteine, all representing prothrombotic conditions (9). An increased risk of venous thromboembolism in MS reported in epidemiological studies (9) and a correlation between MS relapses and prothrombotic factors, such as antiphospholipid antibody positivity (10), support the hypothesis that the activation of coagulation system plays a role in MS pathogenesis (9). Indeed, fibrin deposition precedes and regulates the inflammatory demyelination in both experimental allergic encephalomyelitis and MS (9).…”

Dl-3-n-butylphthalide is effective for demyelination: A case-combined study

“…Demyelinating diseases are one of the most common diseases of the nervous system in which the myelin sheath of neurons is injured [1]. Genetics [2], infectious agents [3], drugs [4], or autoimmune reactions [5] can lead to demyelinating diseases.…”

Secondary Progressive Multiple Sclerosis: Definition and Measurement

“…Histopathological similarities have been highlighted comparing the so-called type 3 MS white matter lesions [53,54] (characterized by selective loss of myelin-associated glycoprotein [MAG] and apoptotic-like oligodendrocyte changes) to acute white matter stroke [55] and likely endothelial dysfunction [56]. It has been hypothesized that the thrombotic manifestations in MS patients may be part of the activation of innate immunity [57,58], linking together these two pathological aspects of the disease. Intriguingly, highdose simvastatin (80 mg a day) has been recently demonstrated to reduce the progression of brain atrophy and to have a significant effect on clinical and patient markers of progression in a phase II trial in SPMS patients [59].…”