International Psychogeriatrics (2011), 23:7, 1051–1060 

C International Psychogeriatric Association 2011

doi:10.1017/S1041610210002449

Prevalence, incidence and risk factors of paratonia in patients

with dementia: a one-year follow-up study
.........................................................................................................................................................................................................................................................................................................................................................................

Johannes S. M. Hobbelen,1,2,3,4,5 Frans E. S. Tan,2,6 Frans R. J. Verhey,3,8

Raymond T. C. M. Koopmans7 and Rob A. de Bie2,4
1
Dutch Institute of Allied Health Care, Amersfoort, The Netherlands
2
Maastricht University, Research School CAPHRI, Maastricht, The Netherlands
3
The Maastricht Institute of Mental Health and Neurosciences/Alzheimer Center Limburg, Maastricht University, Maastricht, The Netherlands
4
Department of Epidemiology, Maastricht University, Maastricht, The Netherlands.
5
Institute for Human Movement Studies, Department of Physiotherapy, University of Applied Sciences Utrecht, The Netherlands
6
Department of Methodology and Statistics, Maastricht University, The Netherlands
7
Department of Primary and Community Care. Center for Family Medicine, Geriatric Care and Public Health, Radboud University Nijmegen Medical
Center, Nijmegen, The Netherlands
8
Maastricht University Hospital / Alzheimer Center, Limburg, The Netherlands

ABSTRACT

Background: Paratonia is a progressive motor problem that is observed in individuals with dementia and is not
a well-known phenomenon. This study explores the development and risk factors of paratonia in moderate
stage dementia patients.
Methods: A multi-center, longitudinal, one-year follow-up cohort study was performed. Patients with an
established diagnosis of dementia, with a score of 6 or lower on the Global Deterioration Scale (GDS) were
included. The participants were assessed using the Paratonia Assessment Instrument (PAI), the Timed Up
and GO test, the Qualidem, the Global Deterioration Scale (Reisberg et al., 1982) and the Mini-mental State
Examination. Information about each patient’s diagnosis of dementia, comorbidities and use of medication
were obtained from the participant’s medical file. The PAI was assessed every three months, the other variables
at baseline and after 12 months. Cross-tabulation χ 2 and logistic regression tests were used for the statistical
analyses.
Results: Baseline measures were assessed in the 204 participants – 111 (54%) female and 93 (46%) male, with
a mean age of 79.8 years (56–97). Seventy-one patients (34.8%) were diagnosed with paratonia at baseline,
and 51 patients developed paratonia over one year. The highest hazard ratio (3.1) for developing paratonia
within one year was observed in the vascular dementia group. The logistic regression analysis revealed that
the presence of diabetes mellitus (OR = 10.7) was significantly related to the development of paratonia (Wald
χ 2 p-value < 0.01).
Conclusions: Diabetes mellitus and likely vascular damage are risk factors for the development of paratonia.

Key words: movement disorders, paratonia, dementia, diabetes mellitus

Introduction rigidity and impaired balance and gait are frequently

reported in patients with these disorders (Kurlan
Alzheimer’s disease (AD), dementia with Lewy et al., 2000; Prehogan and Cohen, 2004). The
bodies (DLB) and vascular dementia (VaD) are development of motor disturbances has been shown
the most common causes of dementia (Stevens to vary within and between the types of dementia
et al., 2002). In addition to cognitive decline, ac- (Román et al., 1993; O’Keeffe et al., 1996).
companying motor dysfunctions such as slowness, Paratonia is a form of hypertonia that is defined
as an active unintentional resistance against passive
movement. Paratonia is a motor problem that is
Correspondence should be addressed to: Hans Hobbelen, PhD, PT, PO
Box 616, 6200 MD Maastricht, The Netherlands. Phone: +31-43- frequently observed in individuals with dementia
3882366; Fax: +31-43-3884128. Email: Hans.Hobbelen@EPID.unimaas.nl and results in a loss of mobility and the development
and hhobbelen@iae.nl. Received 22 Jul 2010; revision requested 15 Sep 2010; of contractures (Souren et al., 1997; Hobbelen
revised version received 14 Dec 2010; accepted 14 Dec 2010. First published
online 27 January 2011. et al., 2006). The prevalence of paratonia increases
1052 J. S. M. Hobbelen et al.

with the progression of dementia and is estimated to Methods

reach 100% in patients with later stages of dementia
(Souren et al., 1997). The effect of paratonia on Design
a patient’s quality of life is devastating, and the We performed a multi-center, longitudinal, one-
caregiver’s burden increases substantially with time year follow-up cohort study in which the
(Souren et al., 1997). participants were visited at their center every three
In early-stage dementia, paratonia has been months.
associated with the development of apraxia, and in
late-stage dementia, it has been associated with the Study population
reappearance of neonatal reflexes that are known
Dementia day-care centers in nursing homes
as frontal release symptoms (Franssen et al., 1993;
and residential homes with dementia special
Beversdorf and Heilman, 1998; Vahia et al., 2007).
care units (DCUs) in the regions of Eindhoven,
The pathogenesis of paratonia is not well
Helmond and Tilburg in the Netherlands were
understood. The increased prevalence in patients
randomly selected as recruitment facilities. The
with neurodegenerative disorders suggests a central
participants were considered to be eligible for
cerebral pathology, possibly in the substantia nigra
inclusion in the present study when they met the
(Risse et al., 1990; O’Keeffe et al., 1996). However,
following criteria: (1) an established diagnosis of
positron emission tomography (PET) scan analyses
dementia according to DSM-IV criteria (American
and autopsy studies have provided no evidence
Psychiatric Association, 1994); (2) a score of
for dopaminergic nigrostriatal dysfunction in AD
stage 6 or lower on the Global Deterioration Scale
patients with paratonia (Tyrrell et al., 1990). Altern-
(GDS; Reisberg et al., 1982); and (3) the ability
atively, peripheral biomechanical changes have been
to walk at least 10 meters without assistance (a
hypothesized (Hobbelen et al., 2003). Previous re-
walking aid was allowed), which was necessary for
search has reported that diabetes mellitus (DM) and
the assessment of functional mobility. Participants
general multimorbidity are risk factors for muscle
were excluded from the study if they had unstable
rigidity in non-dementia patients (Arvanitakis et al.,
health owing to an interfering comorbidity.
2004; Mourey et al., 2004). In addition, studies have
The staff of the participating day-care centers
shown that antipsychotic medication may induce
and DCUs were asked to identify eligible parti-
paratonia-like rigidity in dementia patients (Risse
cipants, after which an information brochure about
et al., 1990; Soininen et al., 1992).
the study and a written consent application form
Most previous studies on paratonia have focused
was sent to the eligible participants and their legal
on patients in the late stages of dementia with
representatives. A participant was only included in
severe paratonia, making it difficult to investigate
the present study if written informed consent was
retrospectively the factors that contributed to the
received from their representative. The patients’
development of paratonia. To date, no longitudinal
general practitioners (GPs) were notified about
studies exist that examine the contributing factors
the study and were mandated by the participants
to the development of paratonia.
to provide information from their records. Those
Recently, a consensus definition was established,
participants who initially agreed to participate
and a new, valid and reliable assessment instrument
but refused further collaboration during the study
for paratonia became available, stimulating new
were excluded. The local ethical committee of the
research in this field (Hobbelen et al., 2006; 2008).
Arnhem/Nijmegen region approved the study.
In the present study, we performed a one-
year longitudinal study among dementia day-care
patients to explore the possible contributing factors Assessments
to the development of paratonia in dementia The primary outcome measure in the present study
patients. The specific research questions included was the Paratonia Assessment Instrument (PAI)
the following: (1) Do differences exist in the (Hobbelen et al., 2008). The PAI is a dichotomous
profiles of the participants with and without assessment instrument with which an examiner can
paratonia? (2) During what stage of dementia establish the presence (or absence) of paratonia
does paratonia develop? (3) Do differences exist by successively moving all four limbs passively in
in the course and the development of paratonia flexion and extension while the participant is in
between the different types of dementia? (4) Is a sitting position (Hobbelen et al., 2008). The
decreased functional mobility an early indicator of examiner starts with a slow movement of the limb,
the development of paratonia? (5) Does diabetes after which the movement is accelerated. The PAI is
mellitus, multimorbidity or the use of antipsychotic a construct of five criteria that allow for a categorical
medication contribute to the development of diagnosis of paratonia, i.e. paratonia can only be
paratonia? diagnosed when the following five criteria are all

present: (1) an involuntary variable resistance; (2)
a degree of resistance that varies depending on
the speed of the movement (e.g. a low resistance
to slow movements and a high resistance to fast
movement); (3) resistance to passive movement in
any direction; (4) no clasp-knife phenomenon; and
(5) resistance in two movement directions in one
limb or in two different limbs.
Baseline variables
Each patient’s functional mobility was assessed using
the Timed Up and Go (TUG) test (Podsiadlo and
Richardson, 1991; Ries et al., 2009). The TUG
measures the time in seconds that it takes a patient
to stand up from a chair (with an approximate height
of 46 cm), walk 3 meters, turn around a cone, walk
back to the chair and sit down. A score of 20 seconds
or more is associated with a higher risk of falling.
Each patient’s quality of life was assessed with the
Qualidem (Ettema et al., 2007). The Qualidem is a
40-item, caregiver-rated assessment scale that was
developed for dementia patients in residential care.
The maximum score is 120, which indicates a high
quality of life.
Each patient’s severity of dementia was classified
using the 7-point Global Deterioration Scale (GDS;
Reisberg et al., 1982). The GDS rates cognitive
deterioration in dementia patients, from normal
cognition (stage 1) to a very severe cognitive decline
(stage 7). We considered GDS 3 and 4 as mild
dementia, GDS 5 as moderate dementia and GDS
6 as severe dementia.
Each patient’s cognitive function was tested
using the Mini-mental State Examination (MMSE)
(Folstein et al., 1975). The MMSE is an 11-item
questionnaire with a maximum score of 30, which
indicates no cognitive decline, and a minimum score
of 0, which indicates a very severe cognitive decline.
The diagnosis of dementia and its subtypes
(AD, VaD and DLB) was made using regular
guidelines (McKhann et al., 1984; Román et al.,
1993; McKeith et al., 1996). The presence of
comorbidities and the use of medication were
retrieved from the participants’ medical records
and the GP files. The comorbidities were classified
according to the Dutch classification of diseases
in nursing home care. The medications were
classified according to the international Anatomic
Therapeutic Chemical (ATC) classification system
(Skrbo et al., 2004).
One experienced and well-trained assessor
administered the PAI, TUG and MMSE and
assessed all of the patients at every time point.
Trained personnel at the participating day-
care centers assessed the participants using the
Qualidem and the GDS. The PAI was assessed at
Paratonia in patients with dementia 1053
baseline and every three months after baseline. All
the other variables were assessed at baseline and
after 12 months.
Statistical analysis
The data were analyzed using SPSS 16.0 for
Macintosh. With an expected paratonia prevalence
of 25% in this population, an estimated one-
year incidence of 25% and the presence of six
factors that may influence the development of
paratonia (e.g. age, medication type, severity of
dementia, type of dementia, functional mobility
and comorbidities), the sample size calculations
indicated that 240 participants would be needed
to study the development of paratonia (with 10
participants per factor). These prevalence estimates
were derived from our development of the PAI
combined with the estimates of Souren et al.,
who used an equivalent definition of paratonia
(Hobbelen et al., 2006; Souren et al., 1997).
We first analyzed the baseline characteristics
and the different determinants of paratonia in the
baseline cohort with independent sample t-tests
or cross-tabulation chi-squared tests. Second, the,
at baseline paratonia-free cohort, was studied to
establish the hazard ratio between the different
GDS stages and the different types of dementia.
For these analyses, we performed a Cox regression
with the PAI as dependent variable in time intervals
of three months, the total number of days in the
study as the time variable, and the GDS and the
type of dementia as independent variables, in two
separate analyses. Furthermore, we analyzed the
characteristics of those participants who developed
paratonia in one year’s time at baseline and after
one year. Lastly, we analyzed the risk factors for
paratonia using a logistic regression with the PAI
after 12 months as dependent variable and with
age, gender, MMSE score, TUG score, number
of co-morbidities, diabetes mellitus, stroke/TIA
score, type of medication, use of antipsychotic
medications and the type and severity of dementia
as the independent variables. In this logistic
regression analysis, we also discarded data from
those participants who exhibited paratonia at
baseline.
For all analyses, we considered p-values <0.05
to be statistically significant.
Results
Of the 366 eligible participants, 210 (57.4%) agreed
to participate. Four participants were excluded due
to severe illness, resulting in 206 participants in
the present study. Over one year, 59 participants
were lost to follow-up: two before baseline measures
1054 J. S. M. Hobbelen et al.

Assessed for eligibility (n= 366)

Excluded (n= 4)

Not meeting inclusion criteria

Enrollment (no proxy consent, n= 160)

Included (n=206)

Paratonia (n=71) Baseline No paratonia (n=133)

Withdrawal of consent (n=2)

Developed Developed
paratonia no paratonia
Follow-Up (n=51) (n=82)
Paratonia
assessment
every 3 months

Paratonia No paratonia
Paratonia (n=44) (n=39) (n=64)
1 year
Lost to follow-up (n=27) Completion of Lost to follow- Lost to follow-
study up (n=12) up (n=18)

Figure 1. Study flow chart.

due to the withdrawal of informed consent, 41 died
(cause of death not noted), and 16 were transferred
to unknown addresses or became severely ill
(Figure 1).
Baseline measures were assessed in 204
participants – 111 (54.4%) females and 93 (45.6%)
males, with a mean age of 79.8 years (range 56–
97) (Table 1). We obtained medical files for all
participants and received GP files for 54% of the
participants (n = 110). Most participants had AD
(44.6%, n = 91), VaD (24.5%, n = 50) or mixed
dementia (VaD and AD) (17.6%, n = 36).
Baseline characteristics
Paratonia was diagnosed in 71 patients (34.8%) at
baseline. The prevalence of paratonia was highest
in the patients with mixed dementia (44.4%, 16
out of 36) and in the VaD group (42%, 21 out of
50). However, when compared to the prevalence
of paratonia in the AD group (29.7%, 27 out of
91), the prevalence in the VaD group was not
significantly different. The prevalence of paratonia
increased significantly as the severity of dementia
increased: 25.2% (28 out of 111) of patients with
mild dementia (GDS 3 and 4), 44.4% (36 out of
81) of patients with moderate dementia (GDS 5)
and 58.3% (7 out of 12) of patients with severe
dementia (GDS 6) (cross-tabulation χ 2 , p < 0.01).
Patients with paratonia generally had a higher
GDS rating (χ 2 , p < 0.01), a lower MMSE score
(scores: 15.4 versus 18.2; independent sample t-
test, p <0.01) and a longer time on the TUG (cross-
tabulation χ 2 , p<0.01).
 Paratonia in patients with dementia 1055

Table 1. Baseline characteristics

PA R AT O N I A N O PA R AT O N I A T O TA L , N
............................................................................................................................................................................................................................................................

Participants, n (%) 71 (34.8%) 133 (65.2%) 204 (100%)

Male, n (%) 32 (45.1%) 61 (45.9%) 93 (45.6%)
Female, n (%) 39 (54.9%) 72 (54.1%) 111 (54.4%)
Age, mean (sd) 79.2 (7.1) 80.1 (7.7) 79.8 (7.5)
Diagnosis type of dementia, n
AD 27 (38%) 64 (48.1%) 91 (44.6%)
VaD 21 (29.6%) 29 (22.8%) 50 (24%)
Mixed AD + VaD 16 (22.5%) 20 (15%) 36 (17.6%)
DLB 5 (7%) 9 (6.8%) 14 (6.9%)
Different etiologies 2 (2.8%) 11 (8.3%) 13 (6.4%)
Comorbidities, median (range) 4 (0–7) 4 (0–9) 4 (0–9)
Diabetes mellitus n (%)a 17 (23.9%) 21 (15.8%) 38 (18.6%)
Stroke-TIA n (%)a 29 (40.8%) 37 (27.9%) 66 (32.4%)
Use of medicines, median (range) 4 (0–11) 5 (0–16) 5 (0–16)
Antipsychotic drugs, n (%)a 12 (16.9%) 23 (17.4% ) 35 (17.2%)
NSAIDs, n (%)a 4 (5.6%) 5 (3.8%) 9 (4.4%)
TUG > 20 sec, n (%)a 35 (49.3%)∗ 27 (20.3%) 62 (30.4%)
Qualidem, mean (sd)b 91.4 (15.3) 94.5 (14.6) 93.4 (14.9)
MMSE, mean (sd)c 15.5 (6.4)∗ 18.2 (6.6) 17.3 (6.7)
GDS, median (range)d 5 (3–6)∗ 4 (3–6) 4 (3–6)
GDS 3 + 4 28 (39.4%) 83 (62.4%) 111 (54.4%)
GDS 5 36 (50.7%) 45 (33.8%) 81 (39.7%)
GDS 6 7 (9.9%) 5 (3.8%) 12 (5.9%)
∗ p-value< 0.01.
a The variables diabetes mellitus, stroke/TIA, antipsychotic drugs, NSAIDS and Timed Up and Go (TUG) >
20 seconds are dichotomous.
b Qualidem score range 0–120; higher score indicates a higher quality of life.
c MMSE cognitive decline score range 0–30:, score 24–28 indicates very mild; 19–23: mild; 14–18 moderately
severe; <14 severe.
d GDS stages range from 1 (normal cognition) to 7 (very severe cognitive decline).
AD = Alzheimer’s disease; VaD = vascular dementia; DLB = dementia with Lewy bodies; TIA = transient
ischemic attack; NSAIDs = non-steroidal anti-inflammatory drugs; TUG = Timed Up and Go; MMSE =
Mini-mental State Examination; GDS = Global Deterioration Scale.

Longitudinal data indicating that the incidence of paratonia increases

One hundred and forty-seven participants com- with increasing severity of dementia (severe versus
pleted the study. Of the 71 diagnosed with paratonia mild dementia: HR = 5.34, 95% CI 1.82–15.6).
at baseline, 27 were lost to follow-up. The remaining Table 2 shows the hazard ratio of the different types
44 participants were diagnosed again with paratonia and stages of dementia.
after one year. The baseline characteristics of the 39 cases
Of the 133 participants who did not have of paratonia in comparison with the baseline
paratonia at baseline, 51 participants (38.3%) characteristics of the 64 participants who did not
were diagnosed with paratonia over the course of develop paratonia and completed the study are
one year, of which 39 completed the study, and outlined in Table 3. The baseline scores were lower
12 were lost to follow-up. Of the remaining 82 and the one-year rates of decline in both the MMSE
participants who were not diagnosed with paratonia, and the TUG were higher in the patients who
64 completed the study, and 18 were lost to follow- developed paratonia compared with those who did
up. The patients without a complete follow-up did not (MMSE: a mean decline of 3.5 points in the
not differ from those who completed the study with paratonia group and 1.3 in the non-paratonia group,
regard to age, gender or severity of dementia. p<0.01).
For the different types of dementia, VaD The logistic regression on the longitudinal data
participants had the highest hazard ratio for indicates that a decrease in the MMSE score was
developing paratonia (HR = 3.07, 95% CI 0.7– a significant risk factor for developing paratonia
14.1, NS), with DLB as a reference. The hazard in one year (OR = 0.90, indicating that a one-
ratio between the different stages of dementia, point decrease on the MMSE increases the risk
with mild dementia as a reference, was significant, of paratonia by 10%; 95% CI = 0.83–0.98).
1056 J. S. M. Hobbelen et al.

Table 2. Cox regression with the PAI as dependent variable and the type and stage
of dementia as the independent variables (analyzed separately)
ß SD EXP ( ß) a 95% CI
..............................................................................................................................................................................................................................................

Type of dementia
DLB reference
AD 0.93 0.76 2.54 0.57–11.2
VaD 1.12 0.78 3.1 0.67–14.1
mixed 0.71 0.79 2.03 0.43–9.5
other 0.15 1.02 1.16 0.16–8.6
Stage of dementia
Mild (GDS 3+4) reference
Moderate (GDS 5) 0.45 0.29 1.57 0.88–2.79
Severe (GDS 6) 1.67 0.55 5.34 1.82–15.6b
a Exp (ß) = hazard ratio.
b p-value <0.05.
PAI = Paratonia Assessment Instrument; DLB = dementia with Lewy bodies; AD = Alzheimer’s disease;
VaD = vascular dementia; GDS = Global Deterioration Scale.

Table 3. Characteristics of participants who go on to develop paratonia after one year compared
with those who remain paratonia-free
CHARACTERISTICS
BASELINE CHARACTERISTICS AFTER 1 YEAR
......................................................................................................................................................................................................................................................................................

Paratonia after 1 year No paratonia Paratonia No paratonia

Participants, n (%) 39 (37.9%) 64 (62.1%) 39 (37.9%) 64 (62.1%)
Male, n (%) 17 (43.6%) 28 (43.8%)
Female, n (%) 22 (56.4%) 36 (56.2%)
Age, mean (sd) 82.4 (7.2) 78 (8.2)
Diagnosis by type of dementia, n
AD 15 (38.5%) 31 (48.4%)
VaD 11 (28.2%) 13 (20.3%)
Mixed AD + VaD 9 (23.1%) 8 (12.5%)
DLB 2 (5.1%) 5 (7.8%)
Different etiologies 2 (5.1%) 7 (10.9%)
Comorbidities, median (range) 4 (0–9) 3 (0–9) 5 (0–11) 3 (0–9)
Diabetes mellitus n (%)a 11 (28.2%) 5 (7.8%)∗ 11 (28.2%) 5 (7.8%)∗
Stroke-TIA n (%)a 14 (35.9%) 20 (31.3%) 14 (35.9%) 20 (31.3%)
Use of medicines, median (range) 5 (0–14) 5 (0–10) 5 (2–15) 5 (0–9)
Antipsychotic drugs, n (%)a 8 (20.5%) 9 (14.1%) 15 (38.5%) 13 (20.3%)
NSAIDS, n (%)a 1 (2.6%) 1 (1.6%) 2 (5.1%) 1 (1.6%)
TUG > 20 sec, n (%)a 9 (23.1%) 7 (10.9%) 22 (56.4%) 8 (12.5%)∗
Qualidem, mean (sd)b 93.4 (12.7) 96.7 (15.2) 87 (14.3) 90.9 (16.6)
MMSE, mean (sd)c 17 (7.4) 20 (5)∗ 13.5 (7.6) 18.7 (6.1)∗
GDS, median (range)d 4 (3–6) 5 (3–6) 5 (3–6) 5 (3–6)
GDS 3 + 4 20 (51.3%) 45 (70.3%) 6 (15.4%) 28 (43.8%)
GDS 5 18 (46.2%) 19 (29.7%) 18 (46.2%) 26 (40.6%)
GDS 6 1 (2.5%) 0 (0%) 13 (33.3%) 8 (12.5%)
∗ p-value <0.01.
mellitus, stroke/TIA, antipsychotic drugs, NSAIDS and Timed Up and Go (TUG) >20 seconds
a The variables diabetes
are dichotomous.
b Qualidem score range 0–120; higher score indicates a higher quality of life.
c MMSE cognitive decline score range 0–30:, score 24–28 indicates very mild; 19–23: mild; 14–18 moderately severe; <14
severe.
d GDS stages range from 1 (normal cognition) to 7 (very severe cognitive decline).
AD = Alzheimer’s disease; VaD = vascular dementia; DLB = dementia with Lewy bodies; TIA = transient ischemic
attack; NSAIDs = non-steroidal anti-inflammatory drugs; TUG = Timed Up and Go; MMSE = Mini-mental State
Examination; GDS = Global Deterioration Scale.
 Paratonia in patients with dementia 1057

Table 4. logistic regression with baseline data of those participants

with no paratonia at baseline
VA R I A B L E a ß SD EXP ( ß) 95% CI
.......................................................................................................................................................................................................

Age 0.072 0.04 1.08 0.99–1.16

Gender −1.0 0.58 0.37 0.12–1.13
MMSEb −0.10 0.04 0.90 0.83–0.98
TUG 0.64 0.69 1.9 0.49–7.32
Comorbidities −0.07 0.14 0.93 0.71–1.21
Diabetesc 2.37 0.81 10.66 2.2–51.7
Stroke-TIA 0.01 0.47 1.01 0.4–2.52
Total medication 0.07 0.1 1.08 0.89–1.3
Antipsychotics 0.28 0.71 1.32 0.33–5.32
Type of dementia −0.23 0.7 0.8 0.2–3.2
AD
DLB −0.81 1.2 0.45 0.04–4.7
VaD 0.38 0.79 1.5 0.31–6.9
Other −0.54 1.2 0.58 0.06–5.7
Intercept −3.34 3.4 0.04
a Dependent variable: Paratonia Assessment Instrument (PAI); the presence of paratonia
"No/Yes" after one year.
Model: (Intercept), Age, Gender, Mini-mental State Examination (MMSE), Timed Up
and Go (TUG), total amount of co-morbidities, Diabetes Mellitus, Stroke-TIA, total
amount of medication, antipsychotics, Type of dementia (AD+VaD reference group).
b p-value <0.05.
c p-value <0.01.
MMSE = Mini-mental State Examination; TIA = transient ischemic attack; AD =
Alzheimer’s disease; DLB = dementia with Lewy bodies; VaD = vascular dementia.

Furthermore, we found that the participants with paratonia in the data, masking the importance of
DM (n = 39) had an almost eleven-fold higher this particular factor. The 95% CI was very broad,
risk of developing paratonia in one year than those indicating that the uncertainty of the true OR was
without DM (OR = 10.7; 95% CI = 2.2–51.7). high, which was probably caused by the relatively
Other comorbidities and the use of antipsychotics or small group of 39 participants with paratonia in this
other medications were not related to an increased analysis.
prevalence or incidence of paratonia (Table 4). DM appeared to be a factor of importance
in the development of paratonia. It has already
been shown that DM is associated with a
Discussion variety of complications and an increased risk of
dementia (Araki and Ito, 2009). Recent findings
The profile of a typical participant with paratonia have suggested that different patterns of cerebral
includes having a higher GDS rating, a lower injury in dementia exist with or without DM,
MMSE score and lower functional mobility. including microvascular infarcts and the activation
The present study confirmed that the risk of of neuroinflammation in individuals with dementia
developing paratonia increases with the progression and DM (Sonnen et al., 2009). Moreover, research
of dementia and a decrease in cognitive abilities by Arvanitakis et al. (2007) has shown that
(Souren et al., 1997). DM causes rigidity and gait disturbances in
In general, the prevalence (34.8%) and incidence older persons without dementia. These authors
(38.3%) of paratonia in this cohort was higher than suggested that, aside from possible damage to the
we expected at the start of the study; however, nigrostriatal system and/or white matter changes,
these higher rates enhanced the power of the present DM also causes damage to the peripheral nervous
study. system. Furthermore, it is known that high levels
Our most striking result was the finding that of glucose cause nonenzymatic glycation with
participants with DM had an almost eleven-fold advanced glycation endproducts (AGE), forming
higher risk of developing paratonia. DM was not cross-links in collagen. This process causes a
a significant variable in our cross-sectional analyses stiffening of all tissues, a process normally seen
at baseline. This difference can be explained by the in aging that is accelerated by DM (Ulrich
obvious disadvantage of the cross-sectional analyses and Cerami, 2001). We must acknowledge the
that included patients who are likely to develop possibility that the PAI was not able to distinguish
1058 J. S. M. Hobbelen et al.
between this stiffness and mild paratonia, resulting
in an overestimation of the importance of DM
as a risk factor. Further longitudinal research
with a longer follow-up period is necessary to
identify the contribution of DM to the development
of paratonia. This topic is especially interesting
because it is clear that the negative long-term effects
of DM can be influenced by various preventive
interventions; in particular, an increase in physical
activity has been shown to be very effective (Sigal
et al., 2006; Chodzko-Zajko et al., 2009).
Paratonia is seen in all types of dementia patients.
The higher prevalence of paratonia and the higher
hazard ratio in the VaD and mixed group of AD
and VaD are an indication that vascular damage,
in conjunction with dementia, most likely plays an
important role in the development of paratonia. It
is interesting to note that DM is a known cause
of vascular damage and that both VaD and DM
are likely important factors in the development of
paratonia. We may be observing a common pathway
in both conditions that enhances the development of
paratonia. However, the risk of paratonia associated
with DM did not appear to be more pronounced
in participants with VaD compared to other
dementias. It should be noted that our analysis
did not indicate collinearity between VaD and
DM and stroke. Further fundamental research is
recommended to reveal the pathways through which
vascular damage may contribute to the development
of paratonia.
A decline in functional mobility appears to be
a good indicator of the presence of paratonia in
patients with dementia. However, the results of
the present study do not indicate that a decline
in functional mobility can predict the development
of paratonia in one year. Therefore, the hypothesis
that paratonia is enhanced by changes in the
biomechanical properties that are equivalent to
those seen in stroke and cerebral palsy patients
is therefore not supported. Paratonia may be a
cause of the decline in functional mobility. However,
because this finding is the result of a cross-sectional
analysis, it should be interpreted with caution.
Limitations
A limitation of the present study is that we
included fewer early-stage dementia patients than
we expected, influencing the expected prevalence
and incidence of paratonia in this cohort. In
addition, the participants in the selected day-care
centers were generally at a more advanced stage
of deterioration than we anticipated. This level
of deterioration is one possible explanation for
the relatively high attrition rate of 28% of the
participants (n = 57).
A further limitation of this study was the
difficulty we encountered in retrieving the patients’
medical records from their GPs. Although all of
the participants provided written (proxy) consent,
the GPs were very reluctant to share information,
and in some cases (46%, n = 94), we only received
information from the records that were available at
the DCUs. It is possible that this difficulty caused
some bias in the analysis of the comorbidities and
medication.
Although the ad hoc power calculation indicated
that we attained enough power for our analyses, the
level of power was not enough for a proper analysis
of the effect of medication on paratonia. Our study
sample used such a wide variety of medication that
the clustering of medication types was not sufficient
for the analysis of 204 participants. We therefore
only separated the use of antipsychotics as a variable
in the analysis, as use of this type of medication can
induce paratonia-like rigidity. As shown in Tables 1
and 3, the use of antipsychotic medication was not a
factor that influenced the development of paratonia.
Another limitation was that behavioral symptoms
were not quantifiably measured in this study. This
type of analysis could have been relevant, as
anxiety and other behavioral disorders have been
associated with an increased prevalence of paratonia
(Hobbelen et al., 2006). The measurement of
behavioral symptoms is a subject for further study
with a larger patient sample.
The cohort in the present study was hetero-
geneous, with participants ranging from mild to
severe dementia and having different types of
dementia. Some selection bias may have also
occurred, especially in the mild dementia cases,
because we recruited participants for this study
in DCUs. It can be hypothesized that only mild
dementia patients who have a more problematic
disease course are offered DCU treatment. In
addition, we realize that the MMSE is more of a
cognitive screening tool than a reliable measure of
cognitive function; nevertheless, this scale is now
used worldwide to determine the degree of overall
cognitive impairment.
Finally, a follow-up time of one year is brief, as
most types of dementia progress over 5 to 10 years.
Further longitudinal research over a longer period of
time with larger cohorts is therefore recommended
to verify our conclusions.
Clinical implications
For daily clinical practice, the early detection of
patients with dementia who are at risk of developing
paratonia is important. Our findings suggest
that patients with DM and vascular risk factors
experience higher risks of developing paratonia.

Furthermore, it is important to diagnose paratonia
in early-stage dementia patients when investigating
risk factors that enhance the development of
paratonia. Our findings may be helpful in the
development of a more focused care program.
Conclusion
A decline of functional mobility is a good indicator
of the presence of paratonia in patients with
dementia. DM and likely vascular damage are risk
factors for the development of paratonia. This
finding enables us to look further into the possible
pathogenesis of paratonia. Furthermore, it is a
pretext for preventive intervention.
Conflict of interest declaration
The first author, J. Hobbelen, was a part-time
employee at the Vitalis WoonZorg Groep (a non-
profit foundation) in Eindhoven, which supported
this study with a grant. The sponsor had no
role in the design, methods, subject recruitment,
data collection, analysis, or preparation of the
manuscript.
Description of authors’ roles
J. Hobbelen designed the study, coordinated the
study, analyzed and interpreted the data and
prepared the paper. F. Tan performed the statistical
analyses and helped write the paper. F. Verhey, R.
Koopmans and R. de Bie supervised the design of
the study and the data collection, interpreted the
results of the analysis and helped write the paper.
Acknowledgments
This study was supported by a grant from the Vitalis
WoonZorg Groep, Eindhoven.
We thank all the participants and their relatives
for their cooperation in this study, as well as the
participating DCUs and day-care centers from
“de Zorgboog” Helmond, “SVVE” Eindhoven, “de
Wever” Tilburg and “Vitalis WoonZorg Groep”
Eindhoven.
We are grateful for the help of the GPs
and personnel who actively contributed to this
study. We thank Sytse Zuidema, a senior scientist
in the Department of Primary and Community
Care, Center for Family Medicine, Geriatric Care
and Public Health, Radboud University Nijmegen
Medical Center, Nijmegen, the Netherlands, for
his enthusiastic and insightful contribution to
the analyses of this study. Lastly, we thank
Paratonia in patients with dementia 1059
Bob Wilkinson from the Maastricht University
Translation and Editing Department.
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