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: [email protected] and results in a loss of mobility and the development
and [email protected]. 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
 Paratonia in patients with dementia 1053

present: (1) an involuntary variable resistance; (2) baseline and every three months after baseline. All
a degree of resistance that varies depending on the other variables were assessed at baseline and
the speed of the movement (e.g. a low resistance after 12 months.
to slow movements and a high resistance to fast
movement); (3) resistance to passive movement in Statistical analysis
any direction; (4) no clasp-knife phenomenon; and The data were analyzed using SPSS 16.0 for
(5) resistance in two movement directions in one Macintosh. With an expected paratonia prevalence
limb or in two different limbs. of 25% in this population, an estimated one-
year incidence of 25% and the presence of six
Baseline variables factors that may influence the development of
paratonia (e.g. age, medication type, severity of
Each patient’s functional mobility was assessed using dementia, type of dementia, functional mobility
the Timed Up and Go (TUG) test (Podsiadlo and and comorbidities), the sample size calculations
Richardson, 1991; Ries et al., 2009). The TUG indicated that 240 participants would be needed
measures the time in seconds that it takes a patient to study the development of paratonia (with 10
to stand up from a chair (with an approximate height participants per factor). These prevalence estimates
of 46 cm), walk 3 meters, turn around a cone, walk were derived from our development of the PAI
back to the chair and sit down. A score of 20 seconds combined with the estimates of Souren et al.,
or more is associated with a higher risk of falling. who used an equivalent definition of paratonia
Each patient’s quality of life was assessed with the (Hobbelen et al., 2006; Souren et al., 1997).
Qualidem (Ettema et al., 2007). The Qualidem is a We first analyzed the baseline characteristics
40-item, caregiver-rated assessment scale that was and the different determinants of paratonia in the
developed for dementia patients in residential care. baseline cohort with independent sample t-tests
The maximum score is 120, which indicates a high or cross-tabulation chi-squared tests. Second, the,
quality of life. at baseline paratonia-free cohort, was studied to
Each patient’s severity of dementia was classified establish the hazard ratio between the different
using the 7-point Global Deterioration Scale (GDS; GDS stages and the different types of dementia.
Reisberg et al., 1982). The GDS rates cognitive For these analyses, we performed a Cox regression
deterioration in dementia patients, from normal with the PAI as dependent variable in time intervals
cognition (stage 1) to a very severe cognitive decline of three months, the total number of days in the
(stage 7). We considered GDS 3 and 4 as mild study as the time variable, and the GDS and the
dementia, GDS 5 as moderate dementia and GDS type of dementia as independent variables, in two
6 as severe dementia. separate analyses. Furthermore, we analyzed the
Each patient’s cognitive function was tested characteristics of those participants who developed
using the Mini-mental State Examination (MMSE) paratonia in one year’s time at baseline and after
(Folstein et al., 1975). The MMSE is an 11-item one year. Lastly, we analyzed the risk factors for
questionnaire with a maximum score of 30, which paratonia using a logistic regression with the PAI
indicates no cognitive decline, and a minimum score after 12 months as dependent variable and with
of 0, which indicates a very severe cognitive decline. age, gender, MMSE score, TUG score, number
The diagnosis of dementia and its subtypes of co-morbidities, diabetes mellitus, stroke/TIA
(AD, VaD and DLB) was made using regular score, type of medication, use of antipsychotic
guidelines (McKhann et al., 1984; Román et al., medications and the type and severity of dementia
1993; McKeith et al., 1996). The presence of as the independent variables. In this logistic
comorbidities and the use of medication were regression analysis, we also discarded data from
retrieved from the participants’ medical records those participants who exhibited paratonia at
and the GP files. The comorbidities were classified baseline.
according to the Dutch classification of diseases For all analyses, we considered p-values <0.05
in nursing home care. The medications were to be statistically significant.
classified according to the international Anatomic
Therapeutic Chemical (ATC) classification system
(Skrbo et al., 2004). Results
One experienced and well-trained assessor
administered the PAI, TUG and MMSE and Of the 366 eligible participants, 210 (57.4%) agreed
assessed all of the patients at every time point. to participate. Four participants were excluded due
Trained personnel at the participating day- to severe illness, resulting in 206 participants in
care centers assessed the participants using the the present study. Over one year, 59 participants
Qualidem and the GDS. The PAI was assessed at 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 in the patients with mixed dementia (44.4%, 16
(cause of death not noted), and 16 were transferred out of 36) and in the VaD group (42%, 21 out of
to unknown addresses or became severely ill 50). However, when compared to the prevalence
(Figure 1). of paratonia in the AD group (29.7%, 27 out of
Baseline measures were assessed in 204 91), the prevalence in the VaD group was not
participants – 111 (54.4%) females and 93 (45.6%) significantly different. The prevalence of paratonia
males, with a mean age of 79.8 years (range 56– increased significantly as the severity of dementia
97) (Table 1). We obtained medical files for all increased: 25.2% (28 out of 111) of patients with
participants and received GP files for 54% of the mild dementia (GDS 3 and 4), 44.4% (36 out of
participants (n = 110). Most participants had AD 81) of patients with moderate dementia (GDS 5)
(44.6%, n = 91), VaD (24.5%, n = 50) or mixed and 58.3% (7 out of 12) of patients with severe
dementia (VaD and AD) (17.6%, n = 36). 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
Baseline characteristics (scores: 15.4 versus 18.2; independent sample t-
Paratonia was diagnosed in 71 patients (34.8%) at test, p <0.01) and a longer time on the TUG (cross-
baseline. The prevalence of paratonia was highest 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 A further limitation of this study was the
in an overestimation of the importance of DM difficulty we encountered in retrieving the patients’
as a risk factor. Further longitudinal research medical records from their GPs. Although all of
with a longer follow-up period is necessary to the participants provided written (proxy) consent,
identify the contribution of DM to the development the GPs were very reluctant to share information,
of paratonia. This topic is especially interesting and in some cases (46%, n = 94), we only received
because it is clear that the negative long-term effects information from the records that were available at
of DM can be influenced by various preventive the DCUs. It is possible that this difficulty caused
interventions; in particular, an increase in physical some bias in the analysis of the comorbidities and
activity has been shown to be very effective (Sigal medication.
et al., 2006; Chodzko-Zajko et al., 2009). Although the ad hoc power calculation indicated
Paratonia is seen in all types of dementia patients. that we attained enough power for our analyses, the
The higher prevalence of paratonia and the higher level of power was not enough for a proper analysis
hazard ratio in the VaD and mixed group of AD of the effect of medication on paratonia. Our study
and VaD are an indication that vascular damage, sample used such a wide variety of medication that
in conjunction with dementia, most likely plays an the clustering of medication types was not sufficient
important role in the development of paratonia. It for the analysis of 204 participants. We therefore
is interesting to note that DM is a known cause only separated the use of antipsychotics as a variable
of vascular damage and that both VaD and DM in the analysis, as use of this type of medication can
are likely important factors in the development of induce paratonia-like rigidity. As shown in Tables 1
paratonia. We may be observing a common pathway and 3, the use of antipsychotic medication was not a
in both conditions that enhances the development of factor that influenced the development of paratonia.
paratonia. However, the risk of paratonia associated Another limitation was that behavioral symptoms
with DM did not appear to be more pronounced were not quantifiably measured in this study. This
in participants with VaD compared to other type of analysis could have been relevant, as
dementias. It should be noted that our analysis anxiety and other behavioral disorders have been
did not indicate collinearity between VaD and associated with an increased prevalence of paratonia
DM and stroke. Further fundamental research is (Hobbelen et al., 2006). The measurement of
recommended to reveal the pathways through which behavioral symptoms is a subject for further study
vascular damage may contribute to the development with a larger patient sample.
of paratonia. The cohort in the present study was hetero-
A decline in functional mobility appears to be geneous, with participants ranging from mild to
a good indicator of the presence of paratonia in severe dementia and having different types of
patients with dementia. However, the results of dementia. Some selection bias may have also
the present study do not indicate that a decline occurred, especially in the mild dementia cases,
in functional mobility can predict the development because we recruited participants for this study
of paratonia in one year. Therefore, the hypothesis in DCUs. It can be hypothesized that only mild
that paratonia is enhanced by changes in the dementia patients who have a more problematic
biomechanical properties that are equivalent to disease course are offered DCU treatment. In
those seen in stroke and cerebral palsy patients addition, we realize that the MMSE is more of a
is therefore not supported. Paratonia may be a cognitive screening tool than a reliable measure of
cause of the decline in functional mobility. However, cognitive function; nevertheless, this scale is now
because this finding is the result of a cross-sectional used worldwide to determine the degree of overall
analysis, it should be interpreted with caution. cognitive impairment.
Finally, a follow-up time of one year is brief, as
most types of dementia progress over 5 to 10 years.
Limitations Further longitudinal research over a longer period of
A limitation of the present study is that we time with larger cohorts is therefore recommended
included fewer early-stage dementia patients than to verify our conclusions.
we expected, influencing the expected prevalence
and incidence of paratonia in this cohort. In
addition, the participants in the selected day-care Clinical implications
centers were generally at a more advanced stage For daily clinical practice, the early detection of
of deterioration than we anticipated. This level patients with dementia who are at risk of developing
of deterioration is one possible explanation for paratonia is important. Our findings suggest
the relatively high attrition rate of 28% of the that patients with DM and vascular risk factors
participants (n = 57). experience higher risks of developing paratonia.
 Paratonia in patients with dementia 1059

Furthermore, it is important to diagnose paratonia Bob Wilkinson from the Maastricht University
in early-stage dementia patients when investigating Translation and Editing Department.
risk factors that enhance the development of
paratonia. Our findings may be helpful in the
development of a more focused care program.
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