Spectrum of cognitive impairment
Differences according to disease phase
C.L. Rodrigues, MD,
D.C. de Andrade, MD,
J.A. Livramento, MD,
L.R. Machado, MD,
R. Abraham, MD, PhD
L. Massaroppe, MSc
L.T. Lucato, MD, PhD
P. Caramelli, MD, PhD
Objectives: Cognitive decline related to neurocysticercosis (NC) remains poorly characterized and
underdiagnosed. In a cross-sectional study with a prospective phase, we evaluated cognitive
decline in patients with strictly calcified form (C-NC), the epidemiologically largest subgroup of
NC, and investigated whether there is a spectrum of cognitive abnormalities in the disease.
Methods: Forty treatment-naive patients with C-NC aged 37.6 ? 11.3 years and fulfilling criteria
for definitive C-NC were submitted to a comprehensive cognitive and functional evaluation and
were compared with 40 patients with active NC (A-NC) and 40 healthy controls (HC) matched for
age and education. Patients with dementia were reassessed after 24 months.
Results: Patients with C-NC presented 9.4 ? 3.1 altered test scores out of the 30 from the
cognitive battery when compared to HC. No patient with C-NC had dementia and 10 patients
(25%) presented cognitive impairment–no dementia (CIND). The A-NC group had 5 patients
(12.5%) with dementia and 11 patients (27.5%) with CIND. On follow-up, 3 out of 5 patients with
A-NC with dementia previously still presented cystic lesions with scolex on MRI and still had
dementia. One patient died and the remaining patient no longer fulfilled criteria for either demen-
tia or CIND, presenting exclusively calcified lesions on neuroimaging.
Conclusions: Independently of its phase, NC leads to a spectrum of cognitive abnormalities, rang-
ing from impairment in a single domain, to CIND and, occasionally, to dementia. These findings are
more conspicuous during active vesicular phase and less prominent in calcified stages.
A-NC ? active neurocysticercosis; AED ? antiepileptic drug; BCSB ? Brief Cognitive Screening Battery; BNT ? Boston
Naming Test; C-NC ? calcified neurocysticercosis; CDT ? clock-drawing test; CE ? cryptogenic epilepsy; CERAD ? Consor-
tium to Establish a Registry for Alzheimer’s Disease; CFT ? Category Fluency Test; CI ? confidence interval; CIND ? cogni-
tive impairment–no dementia; CP ? constructive praxis; DSB ? digit-span backward; DSF ? digit-span forward; DSM-IV ?
Diagnostic and Statistical Manual of Mental Disorders, 4th edition; HC ? healthy controls; NC ? neurocysticercosis;
PFAQ ? Pfeffer Functional Activities Questionnaire; SCIT ? Stroop Color-Interference Test; TMT-A ? Trail-Making Test A;
TMT-B ? Trail-Making Test B; VMT ? Verbal Memory Test.
Neurocysticercosis (NC) is a prevalent chronic parasitic disease caused by invasion of the CNS by
Taenia solium larvae.1The disease is still endemic in Latin America, Africa, and Asia, where it
develops its complete life cycle owing to poor sanitary conditions.2NC is also emerging in developed
countries,duetohumanmigration,and has been recently reported to occur by local transmission.3
NC-related cognitive impairment is one of the most frequent manifestations of the disease
along with symptomatic seizures, epilepsy, focal neurologic deficits, and headache secondary to
intracranial hypertension.4,5Recently, we reported that patients with cystic lesions were found
to present significant cognitive impairment, including dementia in some cases.6Despite the
importance of these data, patients with cystic lesions represent only a small part of the popula-
tion of NC individuals.7The largest subgroup, representing about 70% of cases, is composed
From the Departamento de Neurologia, Faculdade de Medicina (C.L.R., D.C.d.A., J.A.L., L.R.M., R.A.), Instituto do Ca ˆncer do Estado de Sa ˜o Paulo
(ICESP) (D.C.d.A.), Departamento de Engenharia (L.M.), and Departamento de Radiologia (L.T.L.), Universidade de Sa ˜o Paulo; and Departamento
de Clínica Me ´dica (P.C.), Faculdade de Medicina da Universidade Federal de Minas Gerais Belo Horizonte (MG), Brazil.
Study funding: Supported by Neurology Division of Sa ˜o Paulo University, Conselho Nacional de Desenvolvimento Científico e Tecnolo ´gico (CNPq),
and Coordenac ¸a ˜o de Aperfeic ¸oamento de Pessoal de Nível Superior (CAPES).
Disclosure: Author disclosures are provided at the end of the article.
Correspondence & reprint
requests to Dr. Caramelli:
*These authors contributed
equally to this work.
Copyright © 2012 by AAN Enterprises, Inc.
of patients with calcified lesions, which is the
final common pathway of the disease and is
not responsive to antiparasitic treatment.7
The occurrence of cognitive decline and de-
mentia in patients with calcified NC (C-NC)
would have a major negative socioeconomic
impact in endemic areas and would provide
us insight on the mechanisms of NC-related
We conducted a thorough cognitive and
functional evaluation in patients with C-NC
and compared them with age- and education-
matched healthy controls (HC) and with
matched patients presenting active NC (A-
NC). Patients fulfilling criteria for dementia
were reassessed after 24 months.
METHODS Participants. All participants were evaluated by
2 blinded experienced neurologists (C.L.R. and D.C.A.). All in-
dividuals underwent neurologic examination, alcohol abuse
screening through the CAGE and Alcohol Use Disorders Identi-
fication Test questionnaires,8,9and appropriate blood tests (com-
plete blood cell count, electrolytes, thyroid function tests,
vitamin B12 levels, syphilis, and HIV immunology).10Individu-
als from the HC groups presenting altered blood tests, current
alcohol abuse, or depression were excluded from the study. The
presence of current high blood cholesterol, hypertension, diabe-
tes mellitus, thyroid dysfunction, depressive symptoms, stroke,
and history of head trauma were assessed in all participants.
All individuals fulfilled definitive criteria for NC at some
point of disease course, according to current definitions.11Pa-
tients with definite disease and presenting at least 1 calcified NC
lesion on a recent CT of the skull were included in the C-NC
group. They had only strict calcified lesions at the moment of
the cognitive evaluation. Patients with at least 1 intact cystic
lesion with scolex (also called a vesicular lesion) on a recent MRI
were included in the active group of NC (A-NC).
Patients fulfilling all the inclusion criteria from the C-NC
and A-NC groups were screened for depression (DSM-IV crite-
ria12). Depressed patients with NC (both C and A groups) were
treated with fluoxetine and were only evaluated after being
asymptomatic for at least 2 months. Nondepressed patients with
C-NC or A-NC underwent cognitive assessment only if 1) they
had been seizure-free for at least 2 weeks preceding consultation;
2) they had been on a fixed dose of AED treatment during the
last 30 days before evaluation; 3) they presented no clinical signs
of AED intoxication (blood levels of AEDs were determined in
cases of suspected intoxication and cognitive evaluation was only
performed if they were within normal limits); and 4) they pre-
sented no signs of delirium on examination, based on the Delir-
ium Rating Scale.13Patients not fulfilling these criteria had their
cognitive evaluation postponed for 2 months and had a new
MRI (A-NC group) performed to assess the presence of degener-
ating cysts. Patients with transitional lesions on MRI (i.e., de-
generating cysts) or delirium symptoms had their cognitive
evaluation withdrawn from the analysis.
Standard protocol approvals, registrations, and patient
consents. Approval was obtained from the institutional review
board of the participating institution (Hospital das Clínicas,
University of Sa ˜o Paulo) and written informed consent was ob-
tained from all study participants.
Recruitment and matching strategy. The C-NC patients
were consecutively recruited from January 2006 to November
2009 from the neuroinfectious diseases outpatient clinic of the
“Hospital das Clínicas” from the University of Sa ˜o Paulo School
of Medicine. Based on previous studies14,15we considered that 40
patients in the calcified phase of NC would be enough to test our
hypothesis. Matching was performed in blocks of 10 patients: for
every 10 patients with C-NC included, age and level of educa-
tion were ranked (age: 5-year, and level of education: 4-year
intervals), and this information was used to recruit the next
block of individuals from the HC and A-NC groups.
Patients with C-NC. Forty-four consecutive patients younger
than 60 years presenting in the calcified phase of NC were in-
cluded in the study. These patients initially met criteria for defi-
nite NC on the initial evaluation but developed exclusively
calcified lesions during follow-up. CT was also used to assess
disease burden, i.e., lesion number, general localization (right/
left side, cortical/subcortical), according to an optimized proto-
col.16All C-NC patients were submitted to MRI to exclude other
causes of epilepsy (such as hippocampal sclerosis). Four patients
with C-NC did not undergo cognitive evaluation because of re-
fractory depression (n ? 2), chronic psychotic disorder (n ? 1),
or postoperative frontal gliosis (n ? 1). Depression was present
initially in 12 patients (27.2%) with C-NC and was successfully
treated in 10 (83.3%) of them. Thus, 40 patients in NC calcified
phase underwent cognitive and functional evaluation.
Comparison groups. Forty patients presenting with A-NC
(i.e., at least 1 cystic lesion with scolex on MRI) were included in
the study and underwent cognitive and functional evaluation.
Forty HC fulfilled the inclusion criteria and underwent cog-
nitive examination, mostly members of the hospital staff or pa-
tient relatives, with no personal history of epilepsy, chronic
intestinal infections, or neurologic disease. They all underwent a
Cognitive and functional evaluation. All participants un-
derwent cognitive and functional evaluations, including Mini-
Mental State Examination,17,18digit-span forward (DSF) and
backward (DSB),19clock-drawing test (CDT), 10-word list re-
call, Constructive Praxis Test and Category Fluency Test (CFT),
Boston Naming Test (BNT), and the Trail-Making Test
(TMT-A and -B) from the Comprehensive Battery of the Con-
sortium to Establish a Registry for Alzheimer’s Disease
(CERAD),20,21the Brief Cognitive Screening Battery (BCSB),22
and the Stroop Color-Interference Test (SCIT).23Functional
status was assessed by the Pfeffer Functional Activities Question-
naire (PFAQ) scored by a close relative. PFAQ scores ?5 were
considered indicative of functional impairment.24
Dementia was diagnosed according to DSM-IV criteria,12
with memory impairment defined by scores below the 95% con-
fidence interval (CI) of HC performance in the delayed recall
sections of both the CERAD and the BCSB, in conjunction with
altered scores in at least 1 additional cognitive test and functional
impairment. Cognitive impairment–no dementia (CIND) was
diagnosed in patients fulfilling these same criteria, except for
functional impairment. The patients with dementia were reas-
sessed after 24 months using the same protocol.
Statistical analysis. Group data without normal distribution
under the Shapiro-Wilk test were compared using the non-
parametric Kruskal-Wallis test followed by Mann-Whitney
Neurology 78 March 20, 2012
test within groups, whenever indicated. Correlation analyses
were performed using the Spearman correlation test. Multiple
regression analyses were performed to study independent
variables potentially related or not to cognitive performance.
Cognitive scores for each patient with C-NC were compared
with performance of controls. Scores below the 95% CI (sig-
nificance level: ? ? 5%) were considered abnormal, except
for timed ones (TMT-A, TMT-B, and SCIT), where values
higher than the 95% CI were considered as altered. Data
obtained from cognitive tests were grouped by cognitive do-
mains and expressed as z scores. Categorical variables were
compared by Fisher exact test. The p values shown below are
from 2-tailed tests.
RESULTS Participants from the 3 groups (C-NC,
A-NC, and HC) had similar age (37.6 ? 11.3;
39.2 ? 10.5; 40.3 ? 12.2 years; p ? 0.600) and
educational level (7.0 ? 3.6; 6.2 ? 4.0; 7.2 ? 3.7
years; p ? 0.395). The C-NC group presented with
significantly lower monthly seizure frequency than
the A-NC group (0.2 ? 0.3 and 5.1 ? 2.3, respec-
tively; p ? 0.001). The majority (90%) of patients in
both A-NC and C-NC groups presented with focal
seizures as the main or unique seizure type. AED
regimen was not significantly different between the
groups (table 1). Most patients from C-NC and
A-NC groups had at least 1 epileptic seizure in their
clinical history and 60% of them developed epilepsy
during follow-up. Thirty-one individuals from the
A-NC group also presented other lesions types con-
comitantly on the first image study, such as transi-
tional or calcified lesions.
Cognitive evaluation. Between-group analysis. There
were no statistically significant differences between per-
formance of C-NC and HC groups in any cognitive
tests and subtests assessed (p ? 0.05). However, the
the A-NC group in tests assessing naming (BNT), ver-
bal fluency (CFT), and nonverbal memory (BCSB and
delayed recall of constructive praxis of the CERAD)
(p ? 0.001, p ? 0.006, p ? 0.027, p ? 0.001, respec-
tively) (table 2 and appendix e-1 on the Neurology®
Web site at www.neurology.org).
Within-group analysis. All patients with C-NC
showed lower scores on at least one cognitive test com-
pared with the HC group. Patients with C-NC pre-
sented an average of 9.4 ? 3.1 altered test scores out of
the 30 in our battery when compared to HC, while
A-NC patients presented a significantly higher number
ory, attention, executive functions, language, and visu-
ospatial skills were altered in more than 50% of C-NC
patients (table 4 and appendix e-2).
No patient in the C-NC group showed functional
impairment, thus no patient fulfilled the diagnostic
criteria for dementia. Ten patients (25%) presented
CIND. The A-NC group had 5 patients with de-
mentia (12.5% of the sample) and 11 patients with
CIND (27.5% of the sample) (table 3). The A-NC
patients with and without dementia did not differ
significantly in relation to age (44.4 ? 10.0 and
38.5 ? 5.4 years; p ? 0.26), education (4.2 ? 3.9
and 6.2 ? 3.6 years; p ? 0.23), presence of success-
fully treated depression (20% and 28%; p ? 0.97),
and monthly seizure frequency (6.2 ? 1.7 and 5.3 ?
2.5; p ? 0.58, respectively).
We found no correlation between cognitive scores
and age, education, monthly seizure frequency, and
number of AEDs for each patient in the C-NC and
A-NC groups, either when the groups were analyzed
separately or pooled (total of 80 patients).
The C-NC group had significantly fewer lesions
than the A-NC group (table 3). C-NC patients with
Table 1Main sociodemographic data, seizure frequency, and antiepileptic drug regimen of the participants
Age, y, n (%)Education, y, n (%)
mean ? SD18–30 31–40 41–5051–60 Illiterate1–4 5–88–12
11 (27.5)12 (30.0) 11 (27.5)5 (17.0) 1 (2.5) 11 (27.5)13 (32.5)14 (35.0)1 (2.5)47.2 33.325.0 0.22 ? 0.36
11 (27.5)13 (32.5) 9 (22.5)7 (17.5)2 (5.0) 16 (40.0)10 (25.0) 10 (25.0) 2 (5.0)62.518.7 25.85.15 ? 2.63a
9 (22.5) 12 (30.0)9 (22.5)10 (25.0) 1 (2.5)14 (35.0)8 (20.0) 16 (40.0) 1 (2.5)————
Abbreviations: A-NC ? active neurocysticercosis; C-NC ? calcified neurocysticercosis; CBZ ? carbamazepine; HC ? healthy controls; PB ? phenobarbital;
PHT ? phenytoin.
ap ? 0.001.
Table 2Results from abnormal cognitive test scores in comparison among
healthy controls, calcified neurocysticercosis, and active
mean ? SD
mean ? SD
BCST delayed recall,
mean ? SD
CP delayed recall,
mean ? SD
13.72 ? 1.58 16.52 ? 4.35 9.00 ? 1.266.85 ? 2.41
11.90 ? 2.25a,d
13.72 ? 4.29a,c
8.30 ? 1.57a,b
4.85 ? 2.45a,d
13.10 ? 2.14 17.27 ? 5.429.20 ? 0.85 6.42 ? 2.54
Abbreviations: A-NC ? active neurocysticercosis; BCSB ? Brief Cognitive Screening Bat-
tery; BNT ? Boston Naming Test; C-NC ? calcified neurocysticercosis; CFT ? Category
Fluency Test; CP ? Constructive Praxis; HC ? healthy controls.
aStatistical significance on the Mann-Whitney test between A-NC and HC: 0.01.
bStatistical significance on the Mann-Whitney test between A-NC and C-NC: 0.05.
cStatistical significance on the Mann-Whitney test between A-NC and C-NC: 0.01.
dStatistical significance on the Mann-Whitney test between A-NC and C-NC: ?0.001.
Neurology 78March 20, 2012
CIND did not differ from C-NC patients without
CIND in median number of lesions (10.7 ? 16.1
and 8.1 ? 12.3; respectively; p ? 0.363).
We found no correlation between cognitive scores
and the number and localization of lesions for each
patient in the C-NC and A-NC groups, either when
they were analyzed separately or pooled (total of 80
In multiple linear regression analysis, no correla-
tion was found between cognitive scores and age, ed-
ucation, monthly seizure frequency, and number of
lesions simultaneously for each patient in C-NC and
A-NC groups, either when they were analyzed sepa-
rately or pooled (total of 80 patients) (R2? 13.4%
and p ? 0.05).
Long-term follow-up. No C-NC patients developed
dementia on follow-up of 24 months. Three out of
the 5 A-NC patients with dementia on the first as-
sessment still fulfilled these diagnostic criteria in the
re-evaluation performed 24 months later, still pre-
senting cystic lesions with scolex (active disease) on
the follow-up MRI. One patient died due to unre-
lated causes and 1 patient no longer fulfilled criteria
for either dementia or CIND. In the second
MRI/CT scan, this patient presented exclusively
with calcified lesions.
DISCUSSION We performed a controlled study to
compare the cognitive profile of different phases of
NC. NC irrespective of its phase (calcified or active)
was associated with significant cognitive decline
when compared with age- and education-matched
healthy controls. Interestingly, dementia was present
exclusively in patients with active disease, although
CIND was present in both calcified and active
groups. Our findings show that patients with NC
exhibit a wide range of cognitive decline, going from
impairment in at least one cognitive test through an
amnestic pattern without functional impairment in
both C- and A-NC, and finally reaching full-blown
dementia in some individuals with A-NC. All cogni-
tive domains could be affected. Cognitive perfor-
mance of these patients, albeit below normal, was
superior to those of patients with A-NC.
Since cystic lesions go through different evolu-
tionary stages (i.e., cystic, transitional, and calcified),
irrespective of the presence of specific treatment,25
one single patient may present lesions in different
phases of their natural history. One approach to
overcome this challenge is to assess more homoge-
nous subgroups of patients. We decided to evaluate
the extremes of the continuum: patients with active
lesions and those with exclusive chronic calcified le-
Psychiatric manifestations related to NC are well
described in previous studies and have been reviewed
elsewhere.26,27The high frequency of initially de-
pressed patients in our sample was similar to the
works previously mentioned.26,27Since the presence
of depression or delirium is known to influence the
Table 3 Cognitive diagnoses in NC groups
No. (%) of patients
mean ? SDa
No. of lesions,
mean ? SDDementiaCIND
0 (0)10 (25.0)9.4 ? 3.1 8.8 ? 3.2
5 (12.5) 11 (27.5)11.6 ? 3.9b
18.7 ? 23.3c
Abbreviations: A-NC ? active neurocysticercosis; C-NC ? calcified neurocysticercosis;
CIND ? cognitive impairment–no dementia; NC ? neurocysticercosis.
aIn comparison with healthy controls from a total of 30 tests.
bp ? 0.012.
cp ? 0.001.
Table 4 Number (%) of C-NC patients with abnormal results in different cognitive domains after z scores
analysis of the testsa
General AttentionMemoryLanguage Executive
No. (%) of C-NC patients
with abnormal scores
22 (55)22 (55)22 (55) 22 (55)23 (57.5)21 (52.5)19 (47.5)
Abbreviation: C-NC ? calcified neurocysticercosis.
aThe final scores in the table represent the sum of all the altered z scores for each cognitive domain of all patients in the
C-NC group: for each cognitive domain, each patient’s subscore was transformed into z scores and averaged using healthy
that cognitive domain for each given patient, while zero was given for normal results.
bCognitive domains included the following subscores from the cognitive evaluation: general (Mini-Mental State Examina-
tion); attention (digit-span forward, incidental memory of Brief Cognitive Screening Battery and Trail-Making Test A); mem-
ory (immediate recall 1 and 2; delayed recall from the Brief Cognitive Screening Battery, immediate recall and delayed
recall of 10-word list of Consortium to Establish a Registry for Alzheimer’s Disease ?CERAD?, delayed recall of Con-
structive Praxis); language (Category Fluency Test and Boston Naming Test); executive functions (digit-span back-
ward, clock-drawing test, Category Fluency Test, Stroop Color-Interference Test, and Trail-Making Test B);
visuospatial function (clock-drawing test and constructive praxis of CERAD); and Praxis (constructive praxis of CERAD).
Neurology 78 March 20, 2012
results of cognitive tests, we only evaluated nonde-
pressed patients who were not under delirium in or-
der to overcome this source of bias.6
In the longitudinal phase of a landmark study,15
the authors showed that most patients with active
NC lesions treated with a regular pharmacologic reg-
imen experienced cognitive improvement, no longer
fulfilling the diagnosis of dementia in some cases.
Despite the lack of a control group, these findings
have a major impact on the decision of when to start
antiparasitic treatment in NC patients, especially in
those with cognitive decline or dementia. However,
in some clinical scenarios, especially in rural areas
where no public education programs exist and pa-
tients are exposed to reinfection, patients may pres-
ent with multiple lesions, most often in different
phases of evolution. The present study was per-
formed in a tertiary university hospital that receives
patients from general practitioners and secondary
hospitals. The vast majority of these patients had
more than 5 active lesions when they were first as-
sessed. Based on our clinical experience and on previ-
ous reports, we did not offer antiparasitic treatment
to patients presenting multiple brain lesions, due to
the high risk of encephalitis and uncontrolled sei-
zures due to the synchronous degenerations of all the
lesions.28,29Instead, we use AED when indicated and
steroids to control for excessive vasogenic edema. If
on one hand we ended up with a group of patients
with a relatively more severe form of the disease, on
the other hand, we had the unique possibility to
study the clinical presentation of the disease in
Three out of 5 patients who initially presented
with dementia remained so after 2 years. Interest-
ingly, the only patient who no longer fulfilled criteria
for dementia during follow-up initially had active ve-
sicular lesions that evolved to exclusively calcified
forms after 2 years. We hypothesize that major cog-
nitive dysfunction may occur as long as active cystic
lesions are present in these patients. As the lesions
become calcified, patients would move to a less se-
vere form of cognitive impairment. This hypothesis
needs to be confirmed by further prospective studies.
However, it opens the debate on how to deal with
patients presenting with cognitive decline and multi-
ple active lesions who cannot tolerate antiparasitic
In our 80 patients, cognitive scores did not corre-
late with the number of lesions or with their localiza-
tion on CT or MRI. Two previous studies also found
no correlation between neuroimaging and neuropsy-
chiatric and cognitive findings.6,14Despite the high
number of lesions of our patients, this lack of corre-
lation emphasizes that cognitive impairment in NC
seems not to be determined by disease burden mea-
sured by lesion number alone, but rather the syner-
gistic interaction among number, localization,
different evolutionary phases, and the local produc-
tion of varying degrees of inflammation and brain
edema.30These processes seem to be attenuated in
the calcified phase, leading to more subtle cognitive
The results of our controlled study show that NC,
independently of its phase, leads to a spectrum of
cognitive abnormalities, ranging from impairment in
a single domain to CIND and, occasionally, to de-
mentia. Major cognitive impairment is more con-
spicuous during the active vesicular phase, less
prominent in the calcified stages, and seems to persist
while active lesions are present.
Dr. Rodrigues: drafting/revising the manuscript, study concept or design,
analysis or interpretation of data, acquisition of data, statistical analysis.
Dr. Ciampi de Andrade: drafting/revising the manuscript, study concept
or design, analysis or interpretation of data, acquisition of data, statistical
analysis, study supervision. Dr. Livramento: drafting/revising the manu-
script, study concept or design. Dr. dos Ramos Machado: drafting/
revising the manuscript, study concept or design, study supervision. Dr.
Abraham: study concept or design, acquisition of data. Dr. Massaroppe:
drafting/revising the manuscript, analysis or interpretation of data, statis-
tical analysis, interpretation of data. Dr. Lucato: analysis or interpretation
of data, acquisition of data. Dr. Caramelli: drafting/revising the manu-
script, study concept or design, analysis or interpretation of data, study
supervision. Dr. Rodrigues, Dr. Andrade, and Dr. Caramelli had full ac-
cess to all the data in the study and take responsibility for the integrity of
the data and the accuracy of the data analysis. All authors gave final ap-
proval of the version to be published.
The authors thank Prof. Milberto Scaff and Prof. Manoel Jacobsen Teix-
eira for institutional support, including imaging studies and blood analy-
ses. This study was made possible thanks to logistical help from Dr. Luiz
Henrique Martins Castro, Dr. Claudia Porto, Maria de Lurdes P. Santos,
Ma ´rcia Benetti, Valdenira dos Santos Silva, Vanessa Ramos, Ivete Cop-
pola A. Fernandes, Sipriana S.A. Santos, Sueli Martins, Reiko Uchizono
Simomura, Vera Lucia Pereira, Elisabete da Silva B. Malagodi, Vera Maria
de Paula dos Santos, Sandra Celidonia da Silva, Daniela Cristina N. dos
A. Rosa, Rita de Cassia, and Adriana Fonseca.
Dr. Rodrigues received a PhD scholarship from the Coordenac ¸a ˜o
de Aperfeic ¸oamento de Pessoal de Nível Superior (CAPES). Dr. Ci-
ampi de Andrade received a PhD scholarship from the Conselho Nacional
de Desenvolvimento Científico e Tecnolo ´gico (CNPq), Brazil. Dr. Livra-
mento serves as an Associate Editor for Arquivos de Neuro-Psiquiatria. Dr.
Machado serves as an Associate Editor for Arquivos de Neuro-Psiquiatria.
Dr. Abraham, Dr. Massaroppe, and Dr. Lucato report no disclosures. Dr.
Caramelli receives research grants from Conselho Nacional de Desenvol-
vimento Científico e Tecnolo ´gico (CNPq) and Fundac ¸a ˜o de Amparo a `
Pesquisa do Estado de Minas Gerais (FAPEMIG), Brazil; has received
speaker honoraria from Janssen-Cilag, Novartis, and Pfizer Inc; and has
received research support from Janssen-Cilag.
Received August 1, 2011. Accepted in final form November 4, 2011.
Neurology 78March 20, 2012
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