Table 2.
Reported cases of corticobasal syndrome associated with antiphospholipid syndrome.
| Case | Authors | APS | Age/sex | Imaging studies | Treatment | Follow-up (period) |
|---|---|---|---|---|---|---|
| 1 | Lees and Morris [5] | primary | 44/F | MRI: multiple infarcts in the cerebral hemispheres and basal ganglia with prominent lesions in the right parietal lobe and head of the left caudate nucleus | Warfarin and aspirin | Moderate improvement in apraxia (3 years) |
|
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| 2 | Martino et al. [6] | primary | 56/F | MRI: extensive white matter changes, marked diffuse cerebral corticosubcortical atrophy, and several infarcts in both hemispheres involving multiple vascular territories, including the striatum bilaterally | Aspirin and warfarin were separately tried | Progressive deterioration (2 years) |
|
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| 3 | Lee et al. [7] | primary | 47/M | MRI: only diffuse brain atrophy without evidence of cerebral infarction, and dopamine transporter imaging studies using [18F] FP-CIT PET: normal |
Warfarin | No change (6 months) |
|
| ||||||
| 4 | Our case | secondary | 53/F | MRI: marked cortical atrophy, several small infarctions in the deep white matter, and mild white matter changes, no infarction nor atrophy in the striatum 99mTc-ECD SPECT: decreased cerebral blood flow in the bilateral central area extending into the frontal and parietal areas |
Aspirin | No significant change (8 years) |
APS, antiphospholipid syndrome; [18F] FP-CIT PET, positron emission tomography using 18F-fluorinated N-3-fluoropropyl-2-β-carboxymetholxy-3-β-(4-iodophenyl) nortropane; 99mTc-ECD SPECT, single photon emission tomography using technetium-99m-L, L-ethyl cysteinate dimer.