Table 4.
Characteristics of studies describing NPSLE (n = 10) specific cohort studies
| Author and year | Study design | (n) sample | Mean age (years) | % Female |
|
aPL types (isotypes; cut-offs) | % Cognitive dysfunction | Cognitive domains | Imaging modality | Imaging biomarkers |
|---|---|---|---|---|---|---|---|---|---|---|
| NPSLE studies (n = 10) | ||||||||||
| Shulman et al. (2017) [36] | Cross-sectional, case–control | 21 (cases), 11 (controls) | 40.14 (cases), 39.6 (controls) | NR |
|
LA; aCL, anti-β2GPI (IgG/M) | 47.6 | Global, memory, information processing speed, executive function, visual spatial, verbal function, motor skills, problem solving, attention | MRI, OCT | Infarcts, UBOs, retinal nerve fiber layer thickness (biomarker for white matter damage) |
| Sarbu et al. (2015) [26] | Cross-sectional, retrospective cohort | 108 | 40.6 | 92 |
|
LA; aCL (IgG/M) | 11 | Global, simple/complex attention, memory, visuospatial processing, language, reasoning/problem solving, psychomotor speed, executive function | MRI | Inflammatory lesions, LVD, SVD |
| Steup-Beekman et al. (2013) [37] | Cross-sectional, retrospective cohort | 155 | 29.7 (median) | 90 |
|
LA; aCL (IgG/M) | 25.6 | Global, simple/complex attention, memory, visuospatial processing, language, reasoning/problem solving, psychomotor speed, executive function | MRI | WMH, infarcts, atrophy |
| Abda et al. (2013) [28] | Cross-sectional, prospective cohort | 34 | 33.2 | 94 |
|
aPL | 42.86 | Global, attention, memory, problem solving, visuospatial processing, psychomotor speed | MRI, DWI, MRA | Ischaemic brain lesions and demyelination, infarctions, diffuse brain atrophy |
| Zirkzee et al. (2012) [29] | Cross-sectional, retrospective cohort | 71 (SLE) | 42 | 90 |
|
LA; aCL | 60.5 | Global intelligence, memory, executive function, psychomotor speed | MRI | Infarction, inflammation |
| Cantú-Brito et al. (2010) [30] | Longitudinal, prospective cohort | 109 | 34 | 95 |
|
aCL (IgG) | 38.5 | Memory, language, calculation, construction, reasoning | TCD | Microembolic signals—vascular damage |
| Emmer et al. (2008) [37] | Cross-sectional, prospective case–control | 52 | 38.5 (cases), 44.7 (controls) | 90 |
|
aCL (IgG/M) | 13.5 | NR | MTI, MRS | Histogram peak height, NAA:Cr ratio |
| Cho et al. (2007) [38] | Cross-sectional, retrospective case–control | 25 (NPSLE), 18 (NBD) | 31 (NPSLE), 38 (NBD) | 67 |
|
aCL, anti-β2GPI | 25.5 | NR | MRI | WMH, infarcts, parenchymal haemorrhage, atrophy, abnormal intracranial and meningeal enhancement |
| Roldan et al. (2006) [39] | Cross-sectional, retrospective case–control | 28 (SLE), 28 (controls) | 40 (SLE), 37 (controls) | 82 |
|
LA; aCL; aPL (IgG/M/A) | 57 | NR | MRI | Infarcts, periventricular and WMH, cortical atrophy, ventricular dilation |
| Appenzeller et al. (2005) [40] | Cross-sectional, prospective case–control | 115 (SLE), 44 (controlss) | 33.5 (cases), 33.8 (controls) | 95 |
|
LA; aCL (IgG/M) | 30 | Global, simple/complex attention, memory, visuospatial processing, language, reasoning/problem solving, psychomotor speed, executive function | MRI | Cerebral atrophy, infarcts |
Anti-β2GPI: anti-β2 glycoprotein-I antibody; Cr: creatinine; DWI: diffusion-weighted imaging; LVD: large vessel disease; MRA: magnetic resonance angiography; MRS: magnetic resonance spectroscopy; MTI: magnetization transfer imaging; NAA: N-acetylaspartate; NBD: neuroBehçet’s disease; NR: not reported; OCT: optical coherence tomography; SVD: small vessel disease; TCD: transcranial Doppler; UBOs: unidentified bright objects; WMH: white matter hyperintensities.