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Delirium in Parkinson’s disease patients. A five-year follow-up study
Marcos Serrano-Duenasa,b,*, Marıa J. Bledac,d
aAbnormal Movement Disorders Unit, Neurological Service, Hospital Carlos Andrade MarınbFacultad de Medicina, Pontificia Universidad Catolica del Ecuador, P.O. Box: 17-03-1694, Quito - Ecuador
cNational Center of Epidemiology, Carlos III Research Institute, Madrid - SpaindDepartment of Statistics, Universidad Carlos III de Madrid
Received 23 July 2004; revised 10 May 2005; accepted 11 May 2005
Abstract
Objective: To assess the significance of delirium in parkinsonian patients in a 5-year follow-up case-control study with three groups of
patients: Parkinsonian and Delirium (PDG), Parkinsonian (PG) and Control (CG). Methods: Comparisons of Short Test of Mental Status
(STMS) and Unified Parkinson’s Disease Rating Scale-motor section (UPDRS(m)) between groups were performed using analysis of
variance with repeated measurements. Comparisons of survival functions and Cox regression models were used to analyse the time until
death. Results: STMS and UPDRS(m) mean scores were statistically different between PDG group and the other two groups (p!0.001) and
between PDG and PG groups (p!0.001), respectively. Including all groups, PG’s patients (HRZ0.29; 95% C.I.Z0.09–0.93) and CG’s
patients (HRZ0.13; 95% C.I.Z0.03–0.60) had less hazard to die than PDG’s patients; patients with a STMS basal score O33 (HRZ0.37;
95% C.I.Z0.13–0.99) had less hazard to die than patients with a score %33. Finally, including PDG and PG groups, patients with basal
UPDRS(m) score O17 (HRZ4.88; 95% C.I.Z1.11–21.48) had higher hazard to die than patients with a score %17. Conclusion: For patients
with Parkinson’s, delirium is an increased risk factor for developing dementia, to have a more severe motor impairment and to death.
q 2005 Elsevier Ltd. All rights reserved.
Keywords: Parkinson’s disease; Delirium; Survival analysis; Repeated measurements
1. Introduction
Delirium is an acute organic brain syndrome presenting
with whole cognitive impairment, attention disorders,
reduced level of consciousness, increased or decreased
psychomotor activity, and wake-sleep rhythm disorders [1–
5]. The prevalence of delirium is variable due to the
difference in population studied and distinct diagnostic
criteria used [5], but there is consensus that this increases
with aging [6], with rates as high as 60% reported in
hospitalised elderly patients [7].
On the other hand, Parkinson’s Disease (PD) mostly affects
older people [8], and risk for postoperative delirium varying
between 2.8 and 8.1 among patients with PD against controls
[9], and occurrence of delirium in 5–25% of Parkinson patients
treated with levodopa have been reported [10].
1353-8020/$ - see front matter q 2005 Elsevier Ltd. All rights reserved.
doi:10.1016/j.parkreldis.2005.05.002
* Corresponding author.
E-mail address: serranom@pi.pro.ec (M. Serrano-Duenas).
The mesocortical dopaminergic system has been
involved in the physiopathology of delirium. This proposal
has been supported by the fact that neuroleptics are useful in
treating delirium [5], and additionally because dopamin-
ergic medications are known to be likely to cause delirium
[10], which determines the great complexity in handling
delirium in parkinsonian patients, in which neuroleptics
aggravate the disease [11].
While delirium has traditionally been considered as
temporary and reversible [12], recent evidence has
associated it with increased morbidity, mortality and as a
risk factor for developing dementia, i.e., it can lead to
catastrophic consequences [2,3,6].
This 5-year prospective comparison observational study
was conducted to identify behavior in patients with PD
developing delirium against a group of patients with PD and
a control group.
2. Patients, materials, and methods
A consecutive series of 21 patients with PD (recorded on
the Abnormal Movements Clinic, Neurology Service,
Parkinsonism and Related Disorders 11 (2005) 387–392
www.elsevier.com/locate/parkreldis
Table 1
Demographic and clinical patients’ characteristics by groups
Variables PDG (nZ21)
PG (nZ21) CG (nZ21) P
Age (years) 67.7 (5.3) 67.5 (5.4) 67.1 (5.9) 0.9a
STMS 34.5 (2.0) 34.7 (1.6) 34.4 (2.1) 0.9a
Gender (M/
F)
14/7 16/5 11/10 0.3b
Variables PDG (nZ21) PG (nZ21) p
Disease dur-
ation (years)
6.05 (1.4) 6.0 (1.5) 0.8a
UPDRS(m) 18.4 (2.8) 19.2 (2.6) 0.4a
H and Y (1.5/2) 11/10 13/8 0.5b
S and E (70/80/
90)
3/12/6 3/12/6 1b
Daily levodopa
(mg)
n (%) n (%)
500 5 (23.8%) 2 (9.5%)
625 11 (52.4%) 12 (57.1%)
750 5 (23.8%) 7 (33.3%) 0.4b
x(y), mean (standard deviation); x/y, absolute frequency of first class/
absolute frequency of second class.a Means comparison (ANOVA test); p!0.05 as significant.b Pearson chi-square test; p!0.05 as significant.
M. Serrano-Duenas, M.J. Bleda / Parkinsonism and Related Disorders 11 (2005) 387–392388
‘Carlos Andrade Marın’ Hospital, a third level reference
hospital) who met criteria for delirium according to the
Confusion Assessment Method of Inouye et al [7], (the
Confusion Assessment Method requires the presence of (i)
Acute onset and fluctuating course;(ii) Inattention; (iii)
Disorganized thinking; and (iv) Altered level of conscious-
ness. The diagnosis of delirium requires the presence of
features (i) and (ii) and either (iii) or (iv)).
The patients were assessed by one of the authors (MS-D),
between January 1994 until December 1999 and designated
as Parkinson and Delirium Group (PDG). Only those with a
previous assessment (up to 3 months before the occurrence
of delirium) of their higher mental functions (using the
Short Test of Mental Status STMS) [13] that ruled out
dementia were included; and an assessment of either the
presence or absence of depression using the Hamilton scale
[14] that excluded those with depression (the cut-off score
was 12/13). Those in which a previous evaluation (within
the last 3 months) of their parkinsonian condition through
the UPDRS motor section [15] was not available were
excluded as well.
Additionally, two control groups were used, one formed
by 21 patients with PD, called Parkinson Group (PG), and
the other one including 21 relatives (husbands or wives of
patients with PD), referred to as the control Group (CG).
Both patients in the PG and CG were excluded if they had,
as in the case above, a score of 28 or lower on the STMS or
scored with depression under the Hamilton scale (with a
similar cut-off score of 12/13). For patients in the PG, those
without an assessment within the last 3 months of the
UPDRS motor section were excluded. The general health
status in the PG, in the CG, and pre-delirium in the PDG,
was similar without severe disease.
Relevant demographic and clinic variables were collected
in all of them; the three groups had a total of 11 assessments:
the so-called Basal Evaluation (BE) and other 10 assess-
ments performed every 6 months. All assessments included
the STMS for the three groups, the UPDRS(m), Hoehn and
Yahr (H and Y) [16], Schwab and England Scale (SES) [17]
for those within the PDG and PG. The BE of the PDG was the
last recorded immediately before development of delirium.
The Analysis of variance (ANOVA) [18] was used to
compare age mean and STMS basal scores mean between
the 3 groups, and also to compare disease duration mean and
the UPDRS(m) mean between PDG and PG groups. The
Pearson chi-square test [19] was used to evaluate differences
of proportions by gender (between all groups) and, by H and
Y, SES and daily levodopa between PDG and PG groups. A
p-value lower than 0.05 was accepted as statistically
significant.
Comparison of the eleven assessments of STMS and
UPDRS(m) mean scores collected through the five years of
follow-up were performed using an ANOVA with repeated
measurements [20].
To analyse the time until death between groups we
compare these groups’ survival functions estimated by
the Kaplan-Meier method using the log-rank test [21]. We
also compared the three pairs of survival functions and then
we corrected the global-aZ0.05 for multiple comparisons
using Bonferroni’s method (aBonferroniZ0.017). Finally, to
identify which of these factors: gender, basal age, group,
basal STMS, years of illness, basal H and Y and basal
UPDRS(m) were related to the time until death, we
performed a first Cox regression model including the three
groups and a second Cox regression model including only
PDG and PG groups [21].
All statistical analysis were performed using Stata
8.0 [22].
3. Results
Delirium causes were: prostatectomy (benign hyperpla-
sia), 4 patients; hip surgery, 8 (5 men, 3 women);
dehydration, 3 (1 man, 2 women); pneumonia, 5 (3 men, 2
women); and finally, use of anti-flu medication (this patient
take 4 pill (each with 2,5 mg of loratadine, 60 mg of
pseudoefedrine and 500 mg od acetaminophen), 1 male
patient. Delirium was the agitated type in 16 patients; in 6
patients do not have altered level of sensorium.
There were no statistically significant differences on
mean age, on mean STMS basal scores and on gender
between the three groups. There were no differences
between PDG and PG groups on mean disease duration,
on mean UPDRS(m) basal score, on H and Y, on SES and
on daily doses of levodopa (Table 1).
Analysing variables collected during 5-year follow-up,
values were correlated. We performed an ANOVA with
M. Serrano-Duenas, M.J. Bleda / Parkinsonism and Related Disorders 11 (2005) 387–392 389
repeated measurements to analyse data. The first result was
a statistically significant decreasing trend in the STMS mean
score and the UPDRS(m) mean scores through time. Taking
this trend into account, there was a statistically significant
difference in STMS mean scores between the PDG group
and the other two groups (p!0.001); nevertheless, there
was no difference in STMS mean scores between PG and
CG groups (p0.769). Comparing UPDRS(m) mean scores
only between PDG and PG groups, there was also a
statistically significant difference (p!0.001) (Table 2).
Analysing the time until death, we estimated survival
functions using the Kaplan-Meier method. We compared
the three survival functions using the log-rank test which
showed a statistically significant difference between groups
(p!0.05). To identify which pairs of survival functions
were different, we performed three pairs of comparisons:
PDG versus PG, PDG versus CG and PG versus CG. There
were statistically significant differences only between
survival functions of PDG and CG groups (p!0.017)
(Fig. 1).
Table 2
Comparison of short test of mental status (SMTS) and unified Parkinson’s diseas
Groups BASALa 1 (6 m)b 2 (12 m) 3 (18 m) 4 (24 m) 5 (30 m
STMS
Parkin-
son’s and
delirium
(PDG)
34.5 (2.
0)c
31.8 (2.2) 31.0 (2.3) 29.8 (2.8) 27.4 (3.3) 26.3 (3.2
nZ21d nZ21 nZ21 nZ19 nZ18 nZ17
Parkin-
son’s
(PG)
34.7 (1.6) 34.4 (1.9) 34.1 (2.1) 33.8 (1.9) 33.3 (1.8) 32.6 (2.0
nZ21 nZ21 nZ21 nZ21 nZ21 nZ21
Control
(CG)
34.4 (2.1) 34.0 (2.0) 33.3 (2.2) 33.2 (2.3) 32.8 (2.3) 32.6 (2.5
nZ21 nZ21 nZ21 nZ21 nZ21 nZ21
Group differences
adjusting by repeated
measures
PDG versus PG PDG ve
P !0.001 !0.001
UPDRS(m)
Parkin-
son’s and
delirium
(PDG)
18.4 (2.
8)c
22.1 (2.8) 25.4 (2.7) 28.8 (2.9) 32.8 (3.0) 33.7 (3.1
nZ21d nZ21 nZ21 nZ21 nZ18 nZ17
Parkin-
son’s
(PG)
19.2 (2.6) 19.4 (2.5) 19.9 (2.2) 20.8 (2.0) 21.9 (1.8) 23.3 (1.9
nZ21 nZ21 nZ21 nZ21 nZ21 nZ21
Group
differ-
ences
adjusting
by
repeated
measures
p
a No significant differences between means at basal time (p O 0.10).b First assessment at 6 months.c Mean (standard deviation).d Number of subjects in this time.
To identify factors associated with the time until death,
we performed a Cox regression model including all cases
and controls (nZ63). The statistically significant factors in
the model were associated negatively, indicating higher
survival (less hazard to die) for: PG group (Hazard Ratio
(HR)Z0.29; 95% C.I.Z0.09–0.93) and CG group (HRZ0.13; 95% C.I.Z0.03–0.60) compared with PDG group;
patients with a STMS basal score O33 compared with
patients with a STMS basal score %33 (HRZ0.37; 95%
C.I.Z0.13–0.99) (Table 3).
We also performed a second Cox regression model
including only cases from PDG and PG groups (nZ42).
There were two factors associated negatively: PG (HRZ0.11; 95% C.I.Z0.03–0.41) compared with PDG and a
HY basal scoreZ2 compared to HY basal scoreZ1.5
(HRZ0.19; 95% I.C.Z0.05–0.70); and one factor
associated positively, indicating less survival (high
hazard to die): basal UPDRS(m) score O17 compared
to basal UPDRS(m) score %17 (HRZ4.88; 95% C.I.Z1.11–21.48) (Table 3).
e rating scale (motor section) (UPDRS(m)) by groups
) 6 (36 m) 7 (42 m) 8 (48 m) 9 (54 m) 10 (60 m) Trend
differ-
ences
) 25.4 (2.9) 24.4 (3.0) 22.9 (3.2) 21.6 (3.4) 21.1 (3.3) p!0.001
NZ15 nZ14 nZ13 nZ11 nZ11
) 32.6 (2.0) 32.3 (1.9) 32.0 (1.9) 31.8 (2.1) 31.6 (2.1) p!0.001
NZ21 nZ20 nZ20 nZ18 nZ17
) 32.4 (2.4) 32.3 (2.3) 32.1 (2.1) 32.0 (2.0) 32.1 (2.1) p!0.001
NZ21 nZ20 nZ20 nZ20 nZ19
rsus CG PG versus CG
Z0.769
) 35.3 (3.6) 38.2 (4.4) 40.2 (4.1) 41.8 (3.7) 44.5 (4.1) p!0.001
NZ15 nZ14 nZ13 nZ11 nZ11
) 24.9 (1.9) 26.2 (2.0) 27.6 (1.9) 28.7 (2.4) 30.3 (2.1) p!0.001
NZ20 nZ20 nZ20 nZ18 nZ17
PDG versus PG
!0.001
19
11
17
21 21 21
0.00
0.25
0.50
0.75
1.00
0 12 24 36 48 60Time analysis: months
PDG PGCG
Kaplan-Meier survival estimates by groups
pLog-rank test for equality of survivor functions 0.0045a
Comparisons PDG versus PD 0.031PDG versus CG 0.0046b
PG versus CG 0.38a p < 0.05 as significantb Applying Bonferroni correction, p < 0.017 as significant
Fig. 1. Estimated survival functions by groups.
M. Serrano-Duenas, M.J. Bleda / Parkinsonism and Related Disorders 11 (2005) 387–392390
Related to survival analysis, there were no differences of
survival functions by gender; the Cox’ regression model
showed that there were no evidences of a by gender effect.
At the end of follow-up, 10 deaths were recorded for the
PDG group, 4 deaths for the PG and 2 deaths for the CG.
Table 3
Time until death analysis
Variables
included
ALL GROUPS (nZ63) PDG and PG (nZ42)
Hazard
Ratio
(95% C.I.) Hazard
Ratio
(95% C.I.)
Gender
(Female)
0.85 (0.29–2.50) 0.26 (0.05–1.30)
Male
Basal age 1.02 (0.93–1.12) 1.11 (0.98–1.25)
Group
(PDG)
PG 0.29a (0.09–0.93) 0.11a (0.03–0.49)
CG 0.13a (0.03–0.60) –
Basal
STMS
(!Z33b)
0.37a (0.13–0.99) 0.56 (0.14–2.26)
O 33
Years of
disease
1.30 (0.84–2.03)
Basal Hand
Y (1.5)
0.19a (0.05–0.70)
H and YZ2
Basal
UPDRS(m)
(!Z17b)
4.88a (1.11–21.
48)
O17
Reference categories are in brackets. Results of Cox’s regression models.a p!0.05 as significant.b !Z25th percentile.
4. Discussion
This study confirms the outcomes from previous
publications where patients with increased risk for
developing delirium are shown to be: the elderly hospital-
ised patients [12], with a previous central nervous system
(CNS) disease [5], patients with Parkinson’s disease [9] and
those using antihistaminic medications [23]. Additionally,
and according to the vulnerability schema proposed by
Inouye et al. [24], the elderly and patients with a previous
CNS disease require less heavy noxas to develop delirium.
Furthermore, delirium becomes a risk factor for
developing dementia and death [6]. For patients in this
study (PDG), SMTS mean scores since the fourth evaluation
(corresponding to the 24 months) was 27.5 (scores below 29
are considered as dementia); likewise, a significant
difference in cognitive response is already found after the
first evaluation (at six months of the event), which increases
and persists over the remaining follow-up.
This study shows that PDG patients have a significant
trend for having their higher functions impaired as measured
by the STMS, compared with both PG and CG group
patients. The primary role of delirium is confirmed since no
differences were seen for this variable between the PG and
CG groups. Similarly, the damaging role of this acute
confusion syndrome is seen by comparing the UPDRS(m)
score between PDG and PG groups. Patients with delirium
had a significant impairment as compared with those that
did not develop this complication.
In comparing the survival curves for the three groups,
overall significant differences were found suggesting that
there were at least two different survival functions (PDG
and CG group functions). This implicate that Parkinson’s
disease per se has no mayor repercussions.
The Cox regression model, including all groups, showed
that a basal STMS rating between 33/38 scores significantly
increases the risk to die, whereas there was no influence
from gender or age. Let us remember that on the STMS a
score %29 implies dementia cognitive impairment. The
presence of predictors for developing psychotic disorders
(delirium has been assumed as part of this syndrome) [25,
26] has been shown in other studies. Cognitive impairment
[27] is among these recognized predictors; our findings are
in agreement with this recognition.
Likewise, cognitive impairment was been associated to
an increased mortality risk [28]. Accordingly, our PDG
patients showed increased development of cognitive
impairment and dementia (STMS score !29) as shown in
Table 2.
Relating to the development of dementia and death, our
patients with Parkinson’s disease were not different from
other elderly patients. In our opinion, the newest fact is
verifying that patients go through a significant impairment
of their motor function as measured by the UPDRS motor
section. From the second evaluation (corresponding to the
M. Serrano-Duenas, M.J. Bleda / Parkinsonism and Related Disorders 11 (2005) 387–392 391
twelve months of the event), impairment is significant,
which persists over the 60-month follow-up carried out.
We believe this impairment is not the only consequence
of cognitive impairment but rather the direct cause of
delirium that would behave as a process, while the UPDRS
motor section may be influenced by dementia-associated
concurrent morbidity [29]. When the same factors of
previous Cox’s model were included, but only with patients
of PDG and PG groups, this analysis did not found that the
basal disease level (measured by H and Y) or the years of
disease become elements of risk; only the basal punctuation
of UPDRS(m) %17 become it. The involved motor degree
also has been considered as risk factor to develop dementia
[28], as delirium [6].
In that way, motor impairment measured by the
UPDRS(m) and the low STMS scores are present as
elements to increase mortality. A base line score O17,
implying increased motor involvement, was in our patients a
mortality risk factor.
Delirium is acute by definition [7] and it was mentioned
above that the dopaminergic mesocortical system is
involved in its physiopathology, which would become
hyperfunctioning [5]. But if it is considered to predispose or
start a demential picture, it should be assumed that delirium
stops being an event to become a process, and acting as such
it would condition an aberrant cerebral reparation or
become a marker of the physical frailty notion [6].
It is necessary to clarify whether these notions may be
applied to Parkinson’s disease, i.e. if delirium promoted an
aberrant neurological regeneration involving the striatoni-
gral circuitry and caused a greater affectation of the same,
patients with Parkinson’s without delirium would have a
more favourable evolution in both cognitive impairment and
mortality.
Finally, this study show the fact that delirium is a risk
factor for dementia and death for patients with Parkinson’s
disease; thus, preventing its appearance should be intended
particularly in subjects with planned elective surgeries;
Golden et al. [9] state a relative risk between 2.8 and 8.1 for
these patients to develop delirium, thus, we must insist on
the need for an early diagnosis [30].
On the other hand there is a need for relying on
harmonized diagnosis criteria so that we are able to be fully
aware of the prevalence of this major complication as well
as extrapolate results from the various studies on delirium
available.
5. Conclusions
Delirium is a syndrome that should be prevented,
particularly in patients likely to develop it such as
Parkinson’s patients. Delirium is per se a risk factor to
develop dementia and motor impairment. Both, cognitive
and motor impairment, in turn interact with and potentate
each other influencing finally in an early mortality.
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