Rheumatology 2004;43:15551560

Advance Access publication 1 September 2004

doi:10.1093/rheumatology/keh384

Predictors of neuropsychiatric damage in systemic

lupus erythematosus: data from the Maryland
lupus cohort
J. Mikdashi and B. Handwerger

KEY WORDS: Systemic lupus erythematosus, Neuropsychiatric damage, Risk factors.

Survival in systemic lupus erythematosus (SLE) has improved

dramatically over the past few decades [1, 2], but specic organ
damage, the most frequent of which is neuropsychiatric (NP) [36]
remains a signicant cause of morbidity in these patients. Previous
studies have described predictors of overall damage in SLE [414],
but specic predictors of NP damage have not been, otherwise,
adequately evaluated.
In the multiethnic Lupus in Minorities; Nature vs Nurture
(LUMINA) cohort [5] and similarly in the Hopkins Lupus cohort
[4], NP manifestations accounted for the greatest proportion of
organ system damage. Older age at SLE onset, higher dose of
corticosteroid used, disease activity as measured by the Systemic
Lupus Activity Measurement (SLAM), as well as psychological
and sociodemographic features, contributed independently to
overall damage measured by the Systemic Lupus International
Collaborating Clinics American College of Rheumatology
Damage Index (SLICC/ACR-DI) or SDI [15]. Rivest et al. [6],
found that damage to most systems, NP included, was associated
with older age at diagnosis of SLE and disease duration, and not
ethnicity or socioeconomic status.
The predictors of NP damage have been difcult to ascertain.
The heterogeneity of NP manifestations preceding NP damage, the
problems with adequate classication of these NP manifestations,
and the different types of NP damage (which may have different
predictors) probably explain the paucity of literature on this subject. Furthermore, the NP manifestations previously recognized

among the American College of Rheumatology (ACR) criteria for

the classications of patients with SLE [16, 17] include only seizure
and psychosis and not others that may be followed by NP damage.
Using the revised ACR nomenclature and case denitions of
NPSLE [18] as well as the individual items of the NP domains
of the SDI as endpoints, we have now reassessed the risk factors
associated with signicant NP damage in a contemporary SLE
cohort. Of note, NP damage has been considered a predictor of
mortality and serious morbidity in SLE [1922], so understanding
the factors underlying NP damage appears to be quite relevant.
Thus, we have also assessed mortality and its relationship with NP
damage in our cohort. These data are now presented.

Patients and methods

Patients
The University of Maryland (U of M) Lupus cohort includes
patients recruited between 1992 and 2002. This cohort consists of
SLE patients according with the 1982 ACR revised criteria, modied in 1997 [16, 17]; all patients are from the state of Maryland,
Baltimore city included, and most are of AfricanAmerican
ancestry. These are unselected patients who receive their care
at U of M Hospital and Clinics; they are referred to U of M by
practitioners from the private and public sectors. These patients
are monitored quarterly, their mean follow up being 7 yr at the

University of Maryland School of Medicine, Baltimore, MD, USA.

Submitted 23 March 2004; revised version accepted 23 July 2004.
Correspondence to: J. Mikdashi, Division of Rheumatology and Clinical Immunology, 10 South Pine Street, Suite 834, Baltimore, MD 21201, USA.
E-mail: jmikdash@umaryland.edu.
1555
Rheumatology Vol. 43 No. 12 British Society for Rheumatology 2004; all rights reserved

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Objective. To identify factors predictive of signicant neuropsychiatric (NP) damage in systemic lupus erythematosus (SLE).
Methods. One hundred and thirty patients with SLE were followed at the University of Maryland Lupus Clinic from 1992 until
2003. NP manifestations were dened according to the revised American College of Rheumatology (ACR) nomenclature and
case denitions for NPSLE syndromes. Disease activity was measured using the SLE Disease Activity Index (SLEDAI),
organ damage using the Systemic Lupus International Collaborating Clinics Damage Index SLICC/ACR (SDI); NP damage
(NPDI) was measured with the corresponding domain of the SDI. At end of study period, 64 patients exhibited no NP damage
(NPDI 0) and 66 patients developed signicant NP damage (dened as NPDI
1). The baseline features for these two patient
groups were compared, and variables found to be signicantly different were examined by multivariable analyses to determine
their contribution to NP damage.
Results. Signicant NP damage is common in SLE; mortality is infrequent and the cause of death is unrelated to NP damage.
Independent predictors of signicant NP damage were disease activity, Caucasian ethnicity and the presence of antiphospholipid antibodies and anti-Ro/SSA antibody. Certain clinical features at baseline predicted specic NP damage. For example,
higher disease activity at baseline was predictive of psychosis and cognitive impairment, anti-dsDNA was predictive of polyneuropathy, and antiphospholipid antibodies were predictive of seizures and cerebrovascular accidents.
Conclusions. In this longitudinal SLE cohort, signicant cumulative NP damage occurred. Early aggressive therapy targeted
towards NP manifestations may prevent the occurrence of NP damage.

1556

J. Mikdashi and B. Handwerger

SDI and denition of damage (overall and NP)

The SDI measures cumulative damage accrued since disease
onset. The SDI includes 41 non-reversible items encompassing
nine organ systems: diabetes, malignancies and infertility are the
three additional domains of SDI. Each item must be present for at
least 6 months to be scored. For a repeated event to be scored (e.g.
a new stroke) it has to occur at least 6 months apart from the rst;
the same item cannot be scored twice. The SDI was scored
according to the denitions outlined in the corresponding glossary
and it was obtained in all patients 6 months after disease onset
and biannually thereafter. Patients with an SDI score
1 are said
to have accrued overall damage.
The NP damage index (NPDI) was ascertained 6 months after
the occurrence of an acute NP event (Appendix 1, available as
supplementary data at Rheumatology Online). An NPDI score
1
was felt to be clinically signicant; thus an increment of
1 was
considered as NP damage worsening.

Mortality and causes of death

The causes of death in this SLE cohort were categorized as
follows in accordance with previously published work [31]: (i) SLErelated causes, including active disease [particularly nephritis,
vasculitis leading to NPSLE syndromes, and end-organ failure
(renal, cardiac or pulmonary)], infections, and others (particularly
vascular events); (ii) unrelated to SLE (particularly malignancies,
suicide); and (iii) unknown.

Statistical methods
First, the baseline features of those patients accruing and those not
accruing any NP damage were examined. Comparisons were done

using the 2 test and analysis of variance (ANOVA) for categorical

and continuous variables respectively. Subsequently, patients were
divided into three groups as follows: (i) no NP damage, NPDI 0;
(ii) mild damage, NPDI 1 or 2; and (iii) severe damage,
NPDI
3. Baseline features were compared among these three
groups. Given that damage tends to accrue over time, disease
duration was included in these analyses as a covariate.
Demographic features, such as ethnicity, gender, age at onset,
socioeconomic status, including the type of health-care delivery
system that is available, clinical manifestations frequently occurring in SLE, including arthritis, skin rashes, fever, pleurisy,
pericarditis, nephritis (dened as mesangial, focal proliferative,
diffuse proliferative or membranous glomerulonephritis according to the WHO classication on histopathology, or persistent
proteinuria of >0.5 g/day, or proteinuria of >3.5 g/day, or cellular
casts of any kind according to the ACR criteria), alopecia,
vasculitis, Raynauds phenomenon, adenopathy, splenomegaly,
myositis, myocarditis, anaemia, leucopenia, thrombocytopenia
and immunological abnormalities, including anti-dsDNA, antiphospholipid, anti-Ro/SSA, anti-La/SSB and anti-Smith antibodies, as well as disease activity, were examined in relation to
NP manifestations according to the ACR nomenclature. The
possible relationship between NP damage and mortality was also
examined.
Multivariable analyses were performed using logistic regression
with NP damage as the dependent variable in one of them. In other
regression analyses, the dependent variable was mild or severe
damage. Finally, an attempt was made to examine the variables
associated with the occurrence of specic NPDI items. In a
separate regression, the factors associated with mortality were
examined. In all regressions, P<0.05 was considered signicant.
All analyses were done with SPSS for Windows, version 11.0
(SPSS, Chicago, IL, USA).
Informed consent was obtained from all patients prior to
enrolment into the study. This clinical research followed the code
of ethics approved by the Institutional Review Board at the
University of Maryland.

Results
Patient population, NP manifestations and NP damage
The U of M lupus cohort consists of 130 SLE patients; 121 (93%)
are women and 83 (64%) are AfricanAmericans. The average age
at disease onset in these patients was 37 yr. NPSLE manifestations occurred at any time during the course of SLE along with
other features of SLE or as isolated events as part of the NPSLE
syndromes. Seventy-four of the 130 patients with SLE had NP
manifestations, including psychosis, seizures, polyneuropathy,
cerebrovascular accidents (CVA), myelitis and headache.
Seven years from enrolment into the cohort, on the average,
nearly half the patients have yet to accrue any damage, NP
included. Some SLE manifestations, particularly headaches related
to SLE, have been common but they have not been followed by NP
damage. Nonetheless, individual NP damage items accrued with
variable frequency, cognitive impairment being the most common
(27.3%); other NP damage items were as follows: CVA, 25.7%;
polyneuropathy, 18.2%; psychosis, 15.1%; seizures, 7.6%; and
transverse myelitis, 6.1%. Some patients have accrued more than
one NP damage item.

Neuropsychiatric damage
Baseline demographic and clinical features of patients with and
without NP damage are shown in Table 1. The two patient groups
had comparable disease durations and numbers of ACR criteria
for the classication of SLE. Likewise, other socioeconomic
features, including education, health insurance and access to

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time the analyses to be presented were done (range 110 yr). Data
on demographic variables, clinical and laboratory manifestations,
including age at disease onset, symptom duration at disease onset,
duration and types of NP events and therapies received for these
events, are collected, as are all comorbidities, and recorded on
standard forms.
Disease onset was dened as the time at which a patient met
four ACR criteria for the classication of SLE; patients were then
enrolled into the study. SLE patients with NP manifestations prior
to enrolment were excluded from the analyses. NP manifestations
were clinically ascertained and classied into distinct syndromes
as per the ACR nomenclature. Cognitive function was assessed,
if indicated, using the ACR-recommended battery for neuropsychological testing plus the Mini-Mental State Examination
[23]. Disease activity was measured with the SLE activity index
or SLEDAI [24]. Imaging studies were performed if clinically
indicated.
Antinuclear antibodies (ANA) were measured with an immunouorescent test using rat liver as the substrate and following the
World Health Organization (WHO) recommendations [25]. AntidsDNA antibodies were examined with the Crithidia luciliae assay
[26]; anti-Ro/SSA and anti-La/SSB antibodies were tested using
the traditional Ouchterlony double immunodiffusion method [27].
Anti-Smith (Sm) and anti-RNP antibodies were detected using
a commercial enzyme-linked immunosorbent assay (ELISA), and
if these antibodies uctuated over time on repeated testing an
immunoprecipitation test was done to conrm these antibodies
[28]. The lupus anticoagulant (LAC) was ascertained using the
guidelines established by the 1991 Scientic Subcommittee criteria,
later simplied by Exner [29]; anti-IgM and IgG anticardiolipin
(aCL) antibodies were measured using a commercial ELISA [30].
Anti-ribosomal P antibodies were determined in selected patients
using a commercial ELISA method.

Predictors of neuropsychiatric damage in SLE

TABLE 1. Baseline sociodemographic and clinical features of SLE patients
as a function of the later occurrence of NP damage
NPDI
1
(n 66)

35.6
21.955.1
73.4
96.8

39.7
26.060.4
54.5
90.9

7.2
2.611.8

8.5
3.413.6

0.100

0.0
3.1
3.1
0.0
0.0
0.0

37.8
30.3
30.3
36.4
33.3
10.6

0.001
0.001
0.001
0.001
0.018
0.010

17.2

33.3

0.030

15.6
1.6
3.0

37.8
13.6
45.0

0.050
0.030
0.001

6.3
4.5

25.7
12.0

0.003
0.001

4.8
28

15.4
921

0.001

1.0
03

3.8
25

0.001

P
0.020
0.030
0.320

immunosuppressive therapy. The presences of anti-Ro/SSA and

of the antiphospholipid antibodies, particularly LAC and IgG
aCL, were also associated with severe NP damage.
Patients with severe NP damage had accrued more organ
damage overall, but the most frequent damage was NP damage.
Severe NP damage was attributed to multiple documented NP
events/manifestations, in particular CVA. Musculoskeletal, renal
and pulmonary manifestations were more frequent in the severe
NP damage group than in the non-severe NP damage group, but
the differences did not reach statistical signicance.

Damage in the other domains of the SDI and NP damage

Although renal and pulmonary manifestations occurred with
increased frequency in the NP damage group, the overall SDI or
damage in these particular organs did not associate with NP
damage accrual. Likewise, none of the other damage items
associated with NP damage but osteoporosis, alopecia, cataracts
and vascular damage were more frequent among patients in the NP
damage group than in the group with no NP damage, but the
differences were not statistically signicant (data not shown).

Mortality and NP damage

NPDI 0, NP manifestations not fullling damage glossary denitions. P value <0.05.

Disease duration was a covariate in these analyses.
MRI magnetic resonance imaging.

health-care, were comparable between the two groups (data

not shown).
The occurrence of NP damage (any) was more frequent among
patients of non-AfricanAmerican ethnicity and of older age at
diagnosis. Renal (but not cardiovascular) involvement was more
frequent in patients with NP damage than in those without it.
Cutaneous vasculitis, arthritis and, not surprisingly, NP manifestations were more frequent in patients who later developed NP
damage than in those without it. Autoantibodies were present with
comparable frequency in the two groups, with the exception of
antiphospholipid antibodies, particularly LAC and IgG aCL,
which were more frequent in the NP damage group. Abnormal
magnetic resonance imaging (MRI) of the brain [including focal
lesions in white matter, white matter hyperintensity, increased
intensity in grey matter, uid-attenuated inversion recovery
(FLAIR) lesions, areas of infarction, intracerebral bleed, demyelination and cortical atrophy] was more frequent in patients who
later developed NP damage. Of importance, patients in the NP
damage group were also more likely to have active disease and be
treated more aggressively, as evidenced by a higher dose of
corticosteroids and the more frequent use of immunosuppressive
therapy.

At the time these analyses were conducted, eight deaths had

occurred; all eight patients had developed NP damage, death
occurring 5 yr after NP damage ensued. The cause of death in these
patients was unrelated to NP damage and NP damage was not
retained in a logistic regression model in which mortality was the
dependent variable (data not shown).

Neuropsychiatric damage: multivariable analyses

NP damage. Variables independently associated with the
occurrence of NP damage (any) were disease activity, nonAfricanAmerican ethnicity, age at disease onset and the presence
of antiphospholipid antibodies, particularly LAC and IgG aCL.
After adjusting for age at onset in the multivariate analysis, the
variables retained in the model were the same. These data are
shown in Table 3.
Severe damage. Male gender, vasculitis and anti-Ro/SSA
antibodies were independently associated with severe NP damage.
These data are also shown in Table 3.
Specic NP damage. The variables independently associated
with specic NP damage items are shown in Table 4. Seizures were
associated with CVA and the presence of antiphospholipid
antibodies, particularly LAC and IgG aCL. Polyneuropathy was
associated with the presence of serum anti-dsDNA antibodies.
Psychosis was associated with greater disease activity and the
presence of the anti-dsDNA antibodies. CVA was associated with
the presence of antiphospholipid antibodies. Cognitive impairment
was associated with greater disease activity and older age at SLE
diagnosis.
Discussion

Severity of NP damage
Baseline demographic and clinical manifestations as a function
of the severity of NP damage are presented in Table 2. Features
associated with more severe damage included disease duration,
non-AfricanAmerican ethnicity, older age at diagnosis, male
gender, disease activity, cutaneous vasculitis and the use of

During the past two decades, a great deal has been written
about the frequency and clinical presentations of NP features
in SLE. However, the relationship of various clinical variables
with NP damage has not been adequately examined. Thus, we
have reviewed our experience with NP damage in SLE, paying
particular attention to the socioeconomic, demographic and
clinical predictors of NP damage.

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Age at SLE diagnosis (yr)

Mean
Range
Ethnicity AfricanAmerican, (%)
Gender: women (%)
Duration of SLE (yr)
Mean
Range
NPSLE manifestations (%)
Confusional state
Psychosis
Seizures
Cerebrovascular accident
Polyneuropathy
Demyelinating disease
Other SLE manifestations (%)
Glomerulonephritis
Autoantibodies (%)
Anti-cardiolipin IgG
Lupus anticoagulant
Abnormal brain MRI (%)
Therapy used
Cyclophosphamide (%)
Prednisone (mg/day): mean
SLEDAI
Mean
Range
SDI
Mean
Range

NPDI 0
(n 64)

1557

J. Mikdashi and B. Handwerger

1558

TABLE 2. Demographic and clinical features of SLE patients with different degrees of NP damage score

Damage variable

Mild (NPDI 1 or 2)
(n 55)

Severe (NPDI
3)

(n 12)

35.6
21.955.1
73.4
96.8

38.2
26.060.4
58.2
94.5

38.3
27.460.4
33.3
66.6

7.2
2.611.8

8.3
3.413.6

10.0
3.913.6

0.100

0.0
3.1
3.1
0.0
0.0
0.0

36.3
25.4
23.6
29.1
29.1
3.6

41.6
50.0
58.3
66.7
50.0
41.6

0.020
0.020
0.040
0.001
0.001
0.040

9.5

14.5

41.6

0.050

1.6
17.4
3.0

12.7
21.8
36.4

25.0
8.3
91.7

0.005
0.040
0.001

6.3
4.5

21.8
5.9

41.6
15.6

0.001
0.001

4.8
28

8.3
313

20.0
1326

0.020

1.0
03

3.0
24

6.0
57

0.001

P
0.050
0.013
0.050

MRI magnetic resonance imaging.

Disease duration was a covariate in these analyses.

TABLE 3. Multivariable analysis of factors associated with signicant NP damage (NPDI>1), and severe NP damage (NPDI>3) according to the SDI
Multivariable-adjusted OR
Predictor
Any NP damage
Disease activity
Caucasian ethnicity
Autoantibodies
Anticardiolipin
Severe NP damage
Male gender
Vasculitis
Autoantibodies
Anti-Ro/SSA

Age-adjusted OR

OR (95% CI)

OR (95% CI)

2.7 (1.06.7)
3.0 (1.019.5)

0.001
0.020

3.0 (0.914.8)
2.0 (1.07.9)

0.001
0.040

4.8 (1.023.0)

0.040

1.0 (0.91.1)

0.020

5.8 (1.820.0)
4.9 (1.317.9)

0.008
0.030

1.6 (1.314.2)
1.9 (1.210.4)

0.020
0.040

2.2 (1.07.9)

0.020

1.7 (0.823.9)

0.016

Disease duration was a covariate in all analyses.

Only signicant variables are shown.
OR odds ratio.

In this longitudinal cohort, signicant NP damage was present

in 51% of SLE patients with mean disease duration of 7 yr; the
most frequent NP damage was cognitive impairment. The strongest risk factors for the development of signicant NP damage
was the presence of greater disease activity at the NPSLE event.
Signicant NP damage (any) was particularly noted among
Caucasian patients, patients who were older at SLE onset, and
having antiphospholipid antibodies, particularly LAC and IgG
aCL. Severe NP damage was greater among male patients having
vasculitis and anti-Ro/SSA antibodies.
Prior studies [19, 20, 32, 33] have shown that signicant overall
damage, NP included, is more common in patients with evidence of

clinical activity, particularly vasculitis [33], diffuse glomerulonephritis [14] and multiple autoantibodies [34, 35], including antidsDNA, anti-Smith antibodies and antiphospholipid antibodies.
Similarly, we showed that NP damage was associated with greater
disease activity particularly NP manifestations, but also manifestations in other organ systems. Of importance in this regard,
most patients with mild disease activity at time of NP events
developed only mild NP damage. Furthermore, subsequent NP
damage occurred more frequently in patients with greater or
persistent disease activity.
The clinical relevance of autoantibodies in SLE is well
recognized for the diagnosis, and in some cases, the prediction of

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Age at SLE diagnosis (yr)

Mean
Range
Ethnicity: AfricanAmerican (%)
Gender: women (%)
Duration of SLE (yr)
Mean
Range
NPSLE manifestations (%)
Confusional state
Psychosis
Seizures
Cerebrovascular accident
Polyneuropathy
Demyelinating disease
Other SLE manifestations (%)
Vasculitis
Autoantibodies (%)
Lupus anticoagulant
Anti-Ro/SSA
Abnormal brain MRI (%)
Therapy used (%)
Cyclophosphamide
Prednisone (mg/day): mean
SLEDAI
Mean
Range
SDI
Mean
Range

None (NPDI 0)
(n 64)

Predictors of neuropsychiatric damage in SLE

1559

TABLE 4. Multivariable analysis of baseline clinical and sociodemographic predictors of specic NP damage items according to the NPDI
Odds ratio
NP damage
Seizures
Polyneuropathy
Psychosis
Cerebrovascular accidents
Cognitive impairment

Predictor

(95% CI)

Anticardiolipin antibodies
Cerebrovascular accident
Anti-dsDNA antibody
Anti-dsDNA antibody
Disease activity
Anticardiolipin antibodies
Disease activity
Older age at SLE diagnosis

4.3
5.6
2.3
22.2
9.7
16.0
13.4
2.8

(1.215.3)
(2.114.3)
(1.05.6)
(2.8177.0)
(3.526.3)
(3.866.3)
(4.036.6)
(1.26.2)

P
0.02
0.05
0.001
0.001
0.02
0.001
0.006
0.02

Disease duration was a covariate in all analyses.

Only signicant variables are shown.

assessments of damage, but they are not meant to distinguish the

underlying cause of any of the damage items.
In summary, signicant NP damage is common in SLE.
Independent predictors of signicant NP damage were disease
activity, Caucasian ethnicity, older age at SLE onset, and the
presence of anti-Ro/SSA and antiphospholipid antibodies, particularly LAC and IgG aCL. Controlling disease activity in this
subset of SLE patients may improve long-term outcome and
reduce NP damage. Further studies are needed, including randomized clinical trials to address whether the use of immunosuppressive therapy or thrombophylaxis will reduce NP damage.

Acknowledgement
We gratefully acknowledge Dr Gaciela S. Alarcon for her
invaluable critical review and comments.
The authors have declared no conflicts of interest.

Supplementary data
Supplementary data are available
at Rheumatology Online.

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disease activity [3640]; however, the relation with damage has not
been established. In this cohort, anti-Ro/SSA was associated with
severe NP damage, whereas no association with anti-La/SSB was
noted. However, whether these antibodies are implicated in NP
damage cannot be determined from the data obtained in this study.
Nevertheless, knowing of this association may be important. Our
study also supports the importance of antiphospholipid antibodies,
particularly aCL antibodies and LAC, as independent risk factors
associated with different NP manifestations, such as seizures, CVA
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NP damage, as has been shown by others [4143]. The association
of cognitive impairment with aCL antibodies and LAC at baseline
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and LAC were found to have more thrombotic events with CVA,
and this may contribute to cognitive decline.
Ethnic differences in survival have often been reported for SLE
patients, with poorer long-term outcomes/damage noted among
minority or underprivileged patient groups [5]. This is attributed
primarily to differences in exposure to environmental or other
socioeconomic factors rather than to differences in genetic predisposition [3, 4445]. In this cohort, NP damage accrued rapidly
in all ethnic groups; however, a greater proportion of Caucasian
patients exhibited more NP damage accrual. These ndings may
be attributed to the presence of advanced disease at the time of
NP events or comorbid conditions. The lack of contribution of
socioeconomic features to the occurrence of NP damage was
evident in the regression analyses.
The inuence of gender (similar to ethnicity) upon SLE is
profound. Many differences have been described, including the
greatly increased frequency of SLE in women, but also the
differences in clinical features, serology and genetics. While there
have been conicting results in the literature, males have generally
been reported to have more NP symptoms. Our study supports
the overall conclusion that men are more likely to develop NP
symptoms more rapidly, and consequently to have severe NP
damage. It remains to be determined whether gender modies
NP severity among patients with a particular autoantibody
specicity.
The limitations of our study deserve some discussion. First, the
high prevalence of NP damage in our cohort has been observed
in other studies [4, 5, 7], but may represent an overascertainment
bias, given that our patients were specically asked about their NP
symptoms and were systematically ascertained for the presence of
cognitive impairment. Secondly, the limited number of manifestations of active disease used in the analyses may have precluded
the identication of an important clinical variable. Perhaps the
addition of tests that assess functional damage, including electroencephalography, electromyography, evoked potential diagnostics, functional MR/glucose metabolism neuroimaging [14] or
markers of neuronal damage [46], will complement clinical ndings
to dene damage more accurately and at earlier stages. Thirdly, the
SLICC/ACR SDI and the NPDI are valid and reliable standard

1560

J. Mikdashi and B. Handwerger

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