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BRIEF REPORTS

Prevalence and Impact of P aratonia is an alteration of tone to passive move-


ment. It can be divided into oppositional para-
Paratonia in Alzheimer tonia (also called “gegenhalten”) and facilitatory
paratonia.1 In oppositional paratonia, the patient re-
Disease in a Multiracial sists passive movement; in facilitatory paratonia, the
Sample patients acts in the same direction as passive move-
ment. Our research focused only on oppositional
paratonia, and the term paratonia is used to refer to
Ipsit Vahia, M.D. the oppositional form in this article. It is clinically
Carl I. Cohen, M.D. distinguishable from parkinsonian rigidity. Parato-
Alla Prehogan, M.D. nia has been shown to correlate with cognitive de-
cline in patients with dementia in general.1 Although
Zaitoon Memon, M.D.
it may be the most commonly occurring motor dys-
function in Alzheimer disease (AD),2 it has not been
well studied in this disorder. Moreover, none of
Objective: Paratonia is an external stimulus depen- the earlier studies have examined to what extent
dent increase in muscle tone that is absent at rest. It various demographic and clinical variables may im-
is thought to occur commonly in Alzheimer disease pact on the prevalence of paratonia. Therefore, the
(AD) but is understudied. This study examines para- aims of this study will be: 1) to determine if the
presence of paratonia increases with the worsening
tonia in a multiracial sample. Methods: The sample
of AD; and 2) to examine whether any demographic
consisted of 80 patients who met Diagnostic and
and clinical variables are associated with paratonia
Statistical Manual of Mental Disorders, Fourth Edi-
in AD.
tion (DSM-IV) criteria for AD. They received a battery
of neuropsychiatric assessments. The authors exam-
ined the relationship between paratonia and multi-
ple variables. Results: Bivariate and logistic regres-
sion analyses revealed that paratonia correlated METHODS
significantly with disease stage (based on the Geriat-
ric Depression Scale) and number of frontal release The sample consisted of 80 consecutive DSM-IV–
symptoms. There were no significant correlations of diagnosed AD patients evaluated at the Brooklyn
paratonia with age, race, sex, depression, physical Alzheimer’s Disease Assistance at the State Univer-
health, neuroimaging findings, functioning, or neu- sity of New York Downstate Medical Center who
ropsychiatric symptoms. The authors found signifi- were able to complete a comprehensive exami-
cant association with frontal symptoms. Conclu- nation. Persons scoring 4 or more on the Modified
sions: The potential utility of paratonia as an Ischemia Scale3 were excluded from the study even
independent marker of disease stage in AD and its if they met the DSM-IV criteria for AD. Neurological
role in signifying frontal lobe dysfunction suggests examinations were conducted a by a board-certified
that closer attention should be paid to its assessment. neurologist who was trained in the identification of
(Am J Geriatr Psychiatry 2007; 15:351–353) paratonia and frontal release signs according to the
criteria of Franssen and associates.4 The final sam-
Key Words: Paratonia, Alzheimer disease, frontal lobe ple represented 39% of all AD patients seen at our
degeneration center. Their mean age was 76 years, 79% of the
sample population was women, 76% were black,

Received February 18, 2006; revised July 7, 2006; accepted July 10, 2006. From the Department of Psychiatry, Division of Geriatric Psychiatry
(IV, CIC, AP), and the Department of Neurology (ZM), State University of New York Downstate Medical Center, Brooklyn, NY. Send
correspondence and reprint requests to Ipsit Vahia, 49 Willow St. #1F, Brooklyn, NY 11201. e-mail: ipsit@hotmail.com.
© 2007 American Association for Geriatric Psychiatry

Am J Geriatr Psychiatry 15:4, April 2007 351


Paratonia in Alzheimer Disease

and 24% were white. Their evaluation included psy-


chiatric, neurological, and physical assessments, a RESULTS
laboratory panel, and neuroimaging.
Paratonia was present in 48%, 70%, and 83% of per-
Each patient also received a battery of tests that
sons in GDS stages 4, 5, and 6, respectively. As seen
included Hamilton Depression Rating Scale (HAM-D),5 in Table 1, there were significant correlations (p
Mini-Mental State Exam (MMSE),6 Global Deteriora- ⬍0.01) between the presence of paratonia and cogni-
tion Scale (GDS),7 Behavioral Pathology in Alzheimer’s tion (MMSE), illness stage (GDS), HAM-D, BCRS
Disease Scale (BEHAVE-AD), 8 Brief Cognitive Rating Functioning and Self-Care, and the number of frontal
Scale Functioning and Self-Care,9 the presence of cog- release signs. The GDS remained significantly asso-
wheel rigidity, and a summed score of the number of ciated with paratonia even after controlling for the
physical illnesses. We combined the delusions and potential confounding effects of age, race, sex, and
hallucinations subscales of the BEHAVE-AD to create a education (Wald ␹2: 4.36, degrees of freedom: 1, p⫽
Psychoses scale and we combined the activity and ag- 0.04). There were no significant correlations with age,
gressiveness subscales of the BEHAVE-AD to create race, sex, physical health, neuroimaging findings,
an Agitation scale. We created a summed score for ischemia score, tremors, psychoses, or agitation
evidence of nine frontal release signs (maximum scores. Of the three significant noncognitive vari-
score of 14) to allow for bilateral findings based on ables, after we controlled for the effect of illness
the criteria of Franssen and colleagues.4 The signs severity using the MMSE, only the number of frontal
consisted of the glabellar blink, snout, sucking, visual release symptoms retained a significant association
sucking, rooting, forced biting, hand grasp, foot grasp, with paratonia (Table 2).
and palmomental reflexes. The criteria of Franssen
and colleagues4 were also used to rate paratonia on
a scale of 1 (none) to 7 (severe). Because scores of 2
were often equivocal, we used a cutoff score of 3 or DISCUSSION
more (i.e., mild severity or greater) as an indicator
This study aimed at clarifying the relationship of
of paratonia. Because the paratonia scores were not
paratonia to the clinical spectrum of AD as well as
normally distributed, we used only the dichotomized
indicator of paratonia in our analyses. The internal
reliability (alpha) for the MMSE, HAM-D, Psychoses, TABLE 1. Bivariate Correlations of Selected Variables With
and Agitation were 0.76, 0.60, 0.67, and 0.64, respec- Paratonia
tively. Scores of 0.60 and above were considered ac- Correlation p
Data Coefficient Value
ceptable.10
With respect to data analysis, we initially con- Women (%) 79 0.09a 0.42
White (%) 24 ⫺0.19a 0.09
ducted bivariate correlations using Spearman rho for Age 75.5 (7.0) 0.23b 0.04
continuous and nominal variables and phi for di- Education 9.9 ⫺0.14b 0.21
Mean Brief Cognitive Rating Scale
chotomous variables. We next used separate logistic Function and Self-Care 5.8 (1.9) 0.30b 0.007
regression analyses to examine the relationship be- Mean Ischemia Score 0.7 (0.8) ⫺0.07b 0.53
tween paratonia and variables that were significant Presence of vascular infarcts on
CT/MRI (%) 8 0.09a 0.42
in bivariate analyses after controlling for the severity Mini-Mental State Exam 16.1 (6.7) ⫺0.31b 0.006
of illness with the MMSE. We used the MMSE as an Global Deterioration Scale 5.1 (0.8) 0.29b 0.009
Psychoses scale 3.5 (3.6) 0.08b 0.50
indicator of illness severity instead of the GDS. This Agitation scale 3.1 (2.6) 0.03b 0.78
was because the latter incorporated the measure of Hamilton Depression Scale 7.5 (4.3) 0.28b 0.01
daily functioning (Brief Cognitive Rating Scale) into Frontal release signs 2.6 (2.3) 0.38b 0.001
Physical illnesses 1.3 (1.1) ⫺0.07b 0.55
its stage criteria, thereby making them more highly Cogwheel rigidity (%) 13 0.02a 0.86
correlated. To allow for the exploratory nature of this
Notes: Data are means (SD) unless noted; N ⫽ 80.
study, but also to take into account the multiple a
Phi.
b
comparisons, we used a conservative statistical cut- Spearman rho.
CT, cat scan; MRI, magnetic resonance imaging.
off of p ⬍0.01.

352 Am J Geriatr Psychiatry 15:4, April 2007


Vahia et al.

lated with functional decline in bivariate analysis, it


TABLE 2. Logistic Regression Analyses of Variables
Associated With Paratonia Controlling for did not have an independent effect on functioning
Cognitive Severitya when cognitive decline was controlled. Thus, the
Degrees of p presence of paratonia does not appear to worsen
Wald ␹2 Freedom Value functioning.
Brief Cognitive Rating Scale Finally, the reader should exercise appropriate
Function and Self-Care 0.71 1 0.40
Hamilton Depression Scale 3.68 1 0.06
caution in interpreting the results because of our
Number of frontal signs 8.57 1 0.003 modest sample size, reliance on one urban clinic with
Notes: N ⫽ 80.
a high proportion of African Americans, use of cross-
a
Controlling for Mini-Mental State Exam score. sectional data, and the possibility of Type 1 errors
because of multiple comparisons.
determining whether paratonia is associated with Anecdotal evidence suggests that paratonia is fre-
other factors that accompany the disorder. We found quently confused with other motor dysfunctions, es-
that the only reliable predictors of paratonia in AD pecially parkinsonian rigidity.11 However, clinicians
were the stage of the illness and the number of can easily learn to distinguish paratonia and parkin-
frontal symptoms. Thus, the fact that paratonia was sonian rigidity. Our finding that paratonia is signif-
not associated with any demographic (i.e., age, race, icantly associated with the GDS suggests that para-
education, sex) and clinical variables (i.e., physical tonia may have convergent validity as a marker for
health, neuropsychiatric symptoms) suggests that illness stage in AD. Thus, future studies need to
paratonia may be independently related to the dis- more fully validate paratonia’s role as a marker of
ease process. Our finding is consistent with earlier disease stage as well as it role in signifying frontal
reports that suggested paratonia correlates with the lobe dysfunction. Such studies should be directed to
severity of dementia.1 assessing paratonia’s concurrent validity—i.e., its
Another important finding was the strong associ- sensitivity and specificity as a marker of disease
ation that we found between paratonia and the num- stage—and its predictive validity as a prognostic
ber of frontal release signs, which was independent measure of the course and outcome of AD.
of illness severity as measured by the MMSE. Be-
cause paratonia is thought to be a movement dis- This work was supported in part by NIA Grant
order of frontal lobe origin,1 when it is detected, it P30AG08051.
may be a marker for frontal lobe degeneration in AD. This was presented in part at the annual meetings of
An examination of paratonia in frontal dementia the American Psychiatric Association, May 2005; and the
would provide further confirmation of this hypoth- American Association of Geriatric Psychiatry, March 12,
esis. Although we also found that paratonia corre- 2006.

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