Lumbar puncture performed and revealed the following: WBC=25. RBC=250. Lymphocytes= 89. Monocytes=11. Protein=69. Glucose=29. Results were interpreted by rheumatology and ID as an inflammatory process.
CT brain demonstrated curvilinear calcifications bilaterally in basal ganglia and jagged calcifications in the temporal lobe, cerebellum, and brainstem (Figures 1 and 2). Brain MRI revealed chronic small vessel disease with lacunar infarcts, superficial siderosis of the left frontal lobe, and multifocal intracranial calcifications.
The differential diagnosis for intracranial calcifications includes neurocysticercosis, congenital cytomegalovirus, toxoplasmosis, Fahr disease, Primary Familial Brain Calcification, SLE and other rare etiologies. After an extensive workup including VDRL CSF screen, HIV and hepatitis panels, Quantiferon gold assay, family history review for neurodegenerative or genetic disorders and evaluation of PTH and thyroid hormone for metabolic causes of Fahr syndrome was negative, it became clear that the cause of the calcifications was likely SLE.
Furthermore, MRI revealed atrophy of the cervical, thoracic, and lumbar spine. The progressive myelopathy was then attributed to SLE, B12 and copper deficiency.