الفهرس 
IntroductionOnly 14 pages are availabe for public view
 |  | from | 157 |  |  |
| | | from | 157 | | |
Abstract
SLE is a prototypic autoimmune disease characterized by production of autoantibodies against cell nucleus giving rise to diverse clinical manifestations that almost affect all organ systems.
Central nervous system involvement in SLE is characteristic of severe disease as it drives most of SLE disease morbidity and mortality. It leads to a heterogeneous group of neurological and psychiatric (neuropsychiatric) symptoms. Any of these neuropsychiatric (NP) events can be directly attributed to SLE (NP SLE) or to an alternative etiology (non-NP SLE).
NP SLE is frequently reported in 75% of SLE patients and that varied from mild subtle signs: headache or mood disturbance to life threatening conditions: acute confusional state, major fits, stroke or transverse myelitis. The wide range of presentations and differential diagnosis often pose a difficult diagnostic challenge for clinicians.
Routine and quantitative EEG was used to determine whether there is a lateralized pattern of electrophysiologic dysfunction in SLE patients with diverse neuropsychiatric manifestations or not. Epileptiform discharges were observed in some SLE patients. These EEG abnormalities were mostly observed in patients with clinical NPSLE and that abnormal EEG may be an indicator for subclinical NPSLE.
The aim of the present study was to describe the prevalence and clinical associations of abnormalities on electroencephalography (EEG) in a cohort of Egyptian patients with systemic lupus erythematosus who have neuropsychiatric symptoms (NP SLE) and its possible correlation with any of the disease activity parameters.
The present study included 60 SLE patients who fulfilled the 2015 ACR/SLICC Classification Criteria for SLE. The patients were recruited from the Rheumatology Outpatient Clinic and Internal Medicine and Rheumatology Department at Ain Shams University Hospitals. The patients were classified into 2 groups: 30 patients with neuropsychiatric manifestations (NP SLE) as cases and 30 patients without neuropsychiatric manifestations (Non-NP SLE) as controls. SLE patients with end stage renal disease were excluded from our study.
All patients were subjected to detailed medical history taking together with full clinical examination including rheumatological and neurological examination. Calculations of SLE disease activity was done for all patients using the SLE disease activity index (SLEDAI) score. Laboratory investigations including CBC, ESR, CRP, BUN, creatinine, urine analysis, P/C ratio, C3, C4, LAC and ACL antibodies were done for all patients. MRI brain was done for patients with NPSLE and EEG was done for all patients.
Our study included 60 SLE patients 50 females (83.3%) and 10 males (16.7%). There were 30 patients with NPSLE, 24 females (80.0%) and 6 males (20.0%), and 30 patients without NPSLE, 26 females (86.7%) and 4 males (13.3%).
NPSLE group age ranged from 18 to 55 years, with a mean±SD of 30.87 ± 9.61 while non-NPSLE group age ranged from 19 to 44 years, with a mean±SD of 25.97 ± 7.39 years. There was a statistically significant difference between the two groups as regard the Mean±SD of age being higher in NPSLE group (30.87 ± 9.61) than non-NPSLE group (25.97 ± 7.39) (P<0.05).
In this study, oral ulcers, fever and hematological manifestations were all more common in group I (Non-NPSLE) than group II (NPSLE) (P=0.003, 0.000, 0.032 respectively).
Our study showed that there were 6 neuropsychiatric manifestations in the NPSLE group. The commonest was seizure disorders in 13 patients (43.3%), followed by psychosis in 6 patients (20.0%), cerebrovascular disease (stroke syndromes and sinus thrombosis) in 5 patients (16.7%), acute confusional state in 4 patients (13.3%), headache in 3 patients (10.0%) and lastly demyelinating syndrome in 2 patients (6.7%).
In our study, there was a statistically highly significant difference between the two studied groups as regard the SLEDAI score being higher in NPSLE group (Median=16) than non-NPSLE group (Median=4) (P<0.01). Percentage of neurological manifestations directly correlated with disease activity. It was also observed that the higher the score the more severe was the NP manifestations. 31 patients had mild disease (SLEDAI<10) with 6 of them had NPSLE, 15 patients had moderate disease (SLEDAI 10-20) with 13 of them had NPSLE and 14 patients had severe disease (SLEDAI>20) with 11 of them had NPSLE. The median SLEDAI score was 12 for those with cerebrovascular disease, 15 for those with demyelinating syndrome, 24 for those with headache, 16 for those with seizure disorder, 25 for those with acute confusional state and 22.5 for those with psychosis.
We showed that there was a statistically significant difference between the group I and group II as regard the ACL IgM positivity which was higher in group II (NPSLE) than group I (Non-NPSLE) (P<0.05). Collectively, in the 30 patients of NPSLE group, 14 patients had positive lupus anticoagulant (46.7%), 13 patients had positive ACL IgG (43.3%), and 12 patients had positive ACL IgM (40.0%). It indicates that there was higher incidence of antiphospholipid antibodies in patients with the NPSLE.
The present study showed that 16 patients out of 30 (53.3%) of NPSLE group had abnormal MRI brain findings, 12 patients out of 30 (40.0%) of NPSLE group had abnormal EEG. Only 6 patients with abnormal MRI brain had abnormal EEG and the remaining 10 had normal EEG. The most common MRI finding was periventricular white matter lesion (7 patients - 6 of them had abnormal EEG), followed by infarction (4 patients - normal EEG), subcortical white matter lesion (2 patients - normal EEG), demyelinating lesion (2 patients - normal EEG), sinus thrombosis (1 patient - normal EEG), cerebral edema (1 patient - normal EEG) and encephalomalacia (1 patient - normal EEG). Of the previous patients, one had both periventricular and subcortical white matter lesions and one had both infarction and sinus thrombosis.
Regarding EEG, our study showed that 12 patients out of 30 (40.0%) with NPSLE had EEG abnormalities, while the remaining 18 patients with NPSLE and all 30 patients with non-NPSLE had no EEG abnormalities. The most common EEG abnormalities in our study were diffuse slowing (6 patients=20.0%), followed by generalized epileptiform activity (4 patients=13.3%), and lastly temporal epileptiform activity (2 patients each=6.7%) and there was no association between EEG abnormalities and the presence of antiphospholipid antibodies.
In this study, 50% of SLE patients with NP manifestations and abnormal EEG (6/12 patients) had normal MRI brain study, and this means that EEG may show abnormalities early before the appearance of MRI lesions. On another way, 55.6% of patients with normal EEG (10/18 patients) had abnormal MRI brain.
We reported that the most common EEG abnormality in the NPSLE patients with abnormal EEG was periventricular white matter lesion (50.0%) with only 5.6% in NPSLE patients without EEG abnormalities, there was a statistically highly significant difference (P<0.01) between the two groups.
The present study showed that all 3 patients with headache had both normal MRI brain and EEG, only one patient out of 6 with psychosis had both periventricular white mater lesion in MRI and diffuse slowing in EEG. All 4 patients with acute confusional state showed both periventricular white mater lesion in MRI and diffuse slowing in EEG. We found also that 13 patients out of 30 with NPSLE had clinical history of seizure disorders (43.3%), 8 of them had abnormal EEG (61.5%). 4 patients (30.8%) out of 13 with seizure disorders had incidence of generalized epileptiform activity in EEG, 2 patients (15.4%) had diffuse slowing and 2 patients (15.4%) had temporal epileptiform activity.
On testing validity of EEG, we found that EEG is not sensitive nor specific test for detecting NPSLE with sensitivity (37.5%), specificity (57.1%), PPV (50.0%), NPV (44.4%) and overall test accuracy (46.7%). So, it is not an accurate screening test for detecting NPSLE and cannot be used alone without supplementary neuroimaging studies for diagnosis of NPSLE.
We conclude that not all patients with NPSLE have abnormal EEG or brain MRI. NPSLE patients may have abnormal EEG while the MRI is still normal and the reverse is true, some NPSLE patients with abnormal MRI findings have normal EEG pattern. So, both EEG and MRI are complementary investigations in assessment of NPSLE patients.
EEG is a useful assistant tool in diagnosing and studying the different manifestations of NPSLE especially seizure disorder and acute confusional state, but it cannot be used alone as a screening test for detecting NPSLE and must be supplemented by neuroimaging studies (MRI) for diagnosis of NPSLE.