 |
|
||||
| Home | Login | |||||
| About | Editorial board | Articles
|
NSI Publications
|
Search | Instructions | Online Submission | Subscribe | Videos | Etcetera | Contact |
|
||||||||||||||||||||
|
|
|
Systemic lupus erythematosus causing cerebral infarction and basal ganglion calcification : a case report.
Systemic Lupus Erythematosus (SLE) is an autoimmune disease characterized by a bewildering array of antibodies. Central Nervous system involvement is found in 20% of cases. We present a case of cerebral infarction and calcification in a woman with SLE. Both these findings are occasionally found together. A 27 year old female presented with low grade fever, myalgia, arthralgia involving knees and elbows symmetrically, moderate weight loss, rash on the face, oral ulcers and three episodes of gross haematuria over a period of four months. On examination, she had an enlarged non tender liver and spleen, a subcutaneous nodule on the back of the neck, butterfly rash on face and painless oral ulcers. Her haemoglobin level was 7.6 gm%, leukocyte count 4600 cells per mm3 and ESR 100 mm/1st hr. Urinary findings included proteinuria of 0.7 gm/24 hrs and 810 RBC/HPF. Blood urea was 18mg%, serum creatinine 1.08 mg%, A/G ratio of 4/3.6, serum bilirubin 0.6 mg%. Anti ds-DNA antibodies were highly positive measuring 120 units/ml (>40 units/ml being considered as positive). Fundus examination was normal. She was started on 40 mg/day oral prednisone. After three days of admission she developed severe diarrhoea along with weakness of left half of the body which progressed over 24 hours to complete left sided hemiplegia. CT scan revealed infarction in right fronto parietal region [Figure 1a] and a ring enhancing lesion in right basal ganglia [Figure1b]. Cerebrovascular involvement in SLE is found in only 5.6% cases, among whom cerebral infarction is found in 3.4% cases.[2] 30% of patients have intracerebral calcification, 25% of these being in the basal ganglia, implying that SLE is an important cause of intracerebral calcification. Infarction and calcification together are found in only 7.5% of patients.[3] Neuropsychiatric symptoms in SLE are probably due to repeated episodes of vasculitis in small cerebral vessels, which along with concurrent thrombus formation lead to thickening and irregularities in them.[4] Antibodies against 50 kD neuronal membrane protein have also been implicated in the pathogenesis of CNS involvement in SLE.[5]
|
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
|
|||||
