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Brain calcification in patients with cerebral lupus
A A Raymond1, A A Zariah, S A Samad
1Department of Medicine, Faculty of Medicine, National University of Malaysia, Kuala Lumpur, Malaysia.
Insights
Cerebral lupus (CL) can cause brain abnormalities like atrophy and infarcts in Systemic Lupus Erythematosus (SLE) patients. Intracerebral calcification, particularly in the basal ganglia, is a notable finding in CL, warranting its inclusion in differential diagnoses.
Area of Science:
- Neurology
- Radiology
- Rheumatology
Background:
- Cerebral lupus (CL) is a significant cause of neurological complications in patients with Systemic Lupus Erythematosus (SLE).
- Understanding the neuroimaging findings in CL is crucial for diagnosis and management.
Purpose of the Study:
- To review brain CT findings in adult patients with SLE presenting with neurological symptoms.
- To characterize the types and prevalence of brain abnormalities, including intracerebral calcification, in this cohort.
Main Methods:
- Retrospective review of brain CT scans from 27 adult SLE patients with neurological presentations.
- Categorization of CT abnormalities into cerebral atrophy, calcification, infarcts, and combinations thereof.
Main Results:
- 41% of patients had normal CT scans.
- Abnormalities included cerebral atrophy, calcification, and infarcts.
- 30% of patients exhibited intracerebral calcification, predominantly in the globus pallidus, with no correlation to age or symptom duration.
Conclusions:
- Cerebral lupus can manifest with diverse neuroimaging findings, including atrophy, infarcts, and calcifications.
- Intracerebral calcification, especially in the basal ganglia, is a key feature in some CL patients.
- Cerebral lupus should be considered in the differential diagnosis for patients with intracerebral calcification.
Abstract:
Cerebral lupus (CL) is a common cause of morbidity and mortality in patients with SLE. The brain CTs of 27 consecutive adult patients with SLE and various neurological presentations were reviewed. The median age and duration of neurological symptoms at the time of the brain CT were 30 years (range = 14-51 years) and six days (range = 1 day-22 years), respectively. Eleven patients (41%) had normal CTs. The abnormalities in the remaining patients could be divided into six categories: (a) cerebral atrophy alone (two patients); (b) calcification alone (three patients); (c) infarct(s) alone (five patients); (d) cerebral atrophy and calcification (three patients); (e) cerebral atrophy and infarct(s) (one patient) and (f) cerebral atrophy, calcification and infarct(s) (two patients). Altogether eight patients (30%) (age range = 17-47 years) had intracerebral calcification: the globus pallidus was involved in all, putamen in two, head of the caudate nucleus in one, thalamus in one, centrum semiovale in two and cerebellum in three patients. Two patients had extensive calcifications of most of the basal ganglia, centrum semiovale and cerebellum. There was no relationship between the presence/degree of calcification and age of patients/duration or type of neurological presentation. The pathogenesis of cerebral calcification in CL is unknown. Cerebral lupus must now be included in the differential diagnosis of intracerebral calcification.