The Antiphospholipid Syndrome as a Neurological Disease

Arnson, Yoav; Shoenfeld, Yehuda; Eisen, Ami; Amital, Howard

doi:10.1016/j.semarthrit.2009.05.001

Cited by 60 publications

(41 citation statements)

References 138 publications

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“…As seen in many studies, APS may be linked to the pathogenesis. As with SLE, APS also manifests various neurological symptoms, from psychiatric disorders and cognitive dysfunction to cerebrovascular events, and even TM similar to that seen in NPSLE 5. It has been reported that the incidence of myelitis in patients with APS is just 0.4% 6.…”

Section: Discussionmentioning

confidence: 83%

Longitudinally extensive transverse myelitis with anti-NMDA receptor antibodies during a systemic lupus erythematosus flare-up

et al. 2015

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Transverse myelitis (TM) with systemic lupus erythematosus (SLE) has been linked to the presence of autoantibodies (eg, antiaquaporin 4 (AQP4) and anticardiolipin (aCL)) and SLE-induced secondary vasculitis, but the aetiology remains incompletely understood. A 48-year-old Japanese man with a 6-year history of poorly controlled SLE had stopped glucocorticoid therapy 1 year before admission. 3 days before admission, he developed flaccid paraplegia. Spinal MRI showed a longitudinally hyperintense T2 grey matter lesion from the level of Th4 to the conus medullaris, which was considered longitudinally extensive TM (LETM). We administered steroid pulse therapy (methyl-prednisolone 1000 mg/day) for 3 days and prednisolone 50 mg/day. The patient's flaccid paralysis gradually improved. We concluded that the patient's TM was caused by SLE flare-up, even though we could not completely rule out antiphospholipid syndrome. SLE myelitis is relatively rare and many aetiologies are possible for TM in SLE.

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Section: Discussionmentioning

confidence: 83%

Longitudinally extensive transverse myelitis with anti-NMDA receptor antibodies during a systemic lupus erythematosus flare-up

et al. 2015

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“…Th e Antiphospholipid Antibodies and Stroke Study showed no diff erence between aspirin therapy and warfarin; however, in patients with severe thrombotic central nervous system manifestations, long-term treatment with warfarin has been recommended (1). Statins may be benefi cial in the reduction of aPL-induced endothelial cell activation and intracellular signaling (1,2).…”

Section: Discussionmentioning

confidence: 99%

Basilar Artery Thrombosis in the Setting of Antiphospholipid Syndrome

Saad

Nickell

Shamim

et al. 2014

Baylor University Medical Center Proceedings

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“…Ayrıca hastalarda epilepsi, migren, kore, depresyon, psikoz, demans, Guillain-Barré sendromu, transvers miyelit, multipl skleroz (MS) benzeri beyin lezyonları, polinöropati, idiopatik intrakranyal hipertansiyon, sensorinöral işitme kaybı, Sneddon sendromu, livedo retikülaris, trombositopeni, deri ülserleri, amorosis fugaks, retinal arter ve ven trombozu, miyokard enfarktüsü, kalp kapak vejetasyonları, ve otoimmün hemolitik anemi izlenebilmektedir. [39,[41][42][43] Hastaların 10 yıllık sağkalım oranı %91'dir. Her ne kadar APS sinsi seyretse de nadiren çoklu organ yetmezliği şeklinde katastrofik seyreden vakalar da bildirilmiştir.…”

Section: Anti-fosfolipid Sendromuunclassified

“…[43] Antifosfolipid antikorları (aPL) ve anti-kardiolipin antikorları nöral dokuya bağlanmaktadır. [44,45] Ayrıca aPL'nin glutamaterjik serebellar granüler hücrelerin aktivitesini NMDA glutamat reseptörle-rini fazla aktive ederek bozduğu da gösterilmiştir.…”

Section: Anti-fosfolipid Sendromuunclassified