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Binge Eating in

Parkinsons Disease:
Prevalence, Correlates
and the Contribution of
Deep Brain Stimulation
Laura B. Zahodne, M.S.
Frandy Susatia, M.D.
Dawn Bowers, Ph.D.
Tiara L. Ong, B.A.
Charles E. Jacobson IV, B.S.
Michael S. Okun, M.D.
Ramon L. Rodriguez, M.D.
Irene A. Malaty, M.D.
Kelly D. Foote, M.D.
Hubert H. Fernandez, M.D.

Of 96 Parkinsons disease patients surveyed at


the University of Florida Movement Disorders P arkinsons disease (PD) is a neurodegenerative dis-
order characterized by the prominent loss of dopa-
mine neurons in the substantia nigra pars compacta.
Center, one (1%) met diagnostic criteria for
binge-eating disorder. Eight (8.3%) exhibited Although first recognized as a purely motor disorder
subthreshold binge eating. Psychometric criteria featuring resting tremor, rigidity, bradykinesia, and
postural instability, PD is increasingly being conceptu-
classified problem gambling in 17.8%, hoarding
alized as a neuropsychiatric disorder because of the
in 8.3%, compulsive buying in 11.5%, hypersex-
high prevalence of nonmotor symptoms.1 Psychiatric
uality in 1.0%, and mania in 1.0% of patients. features include depression, apathy, anxiety, psychosis,
More overeaters met psychometric criteria for at and sleep disturbance.
least one additional impulse-control disorder Recent studies have identified a subpopulation of
(67% versus 29%). No more overeaters than PD patients who exhibit impulsive and compulsive
non-overeaters were taking a dopamine agonist behaviors, such as pathological gambling, hypersex-
(44% versus 41%). More overeaters had a his- uality, compulsive shopping, punding, and binge-
tory of subthalamic deep brain stimulation (DBS; eating.2 Many consider impulse-control disorders
44% versus 14%). History of DBS was the only
independent predictor of overeating. Received November 23, 2009; revised January 28, 2010; accepted Feb-
(The Journal of Neuropsychiatry and Clinical ruary 12, 2010. Ms. Zahodne and Dr. Bowers are affiliated with the
Neurosciences 2011; 23:56 62) Dept. of Clinical & Health Psychology, Drs. Susatia, Okun, Rodri-
guez, and Malaty and Ms. Ong and Mr. Jacobson are in the Dept. of
Neurology, Drs. Foote and Okun are in the Dept. of Neurosurgery, all
at the University of Florida in Gainesville, FL; Dr. Fernandez is affil-
iated with the Center for Neurological Restoration at the Cleveland
Clinic. Address correspondence to Hubert H. Fernandez, M.D., Cen-
ter for Neurological Restoration, Cleveland Clinic,9500 Euclid Ave.,
S-31, Cleveland, OH 44195. e-mail: fernanh@ccf.org
Copyright 2011 American Psychiatric Association

56 http://neuro.psychiatryonline.org J Neuropsychiatry Clin Neurosci 23:1, Winter 2011


ZAHODNE et al.

(ICDs) to result purely from iatrogenic factors, and tients carried a current diagnosis of idiopathic Par-
symptoms often subside when dopaminergic medi- kinsons disease, based on United Kingdom Parkin-
cations are reduced or replaced. However, several sons Disease Society Brain Bank Diagnostic Criteria
patient factors have been variably linked to ICD man- for Parkinsons Disease.8 We excluded all patients
ifestation, including male sex, younger age at PD with uncontrolled hypo/hyperthyroidism, brittle di-
onset, personal or family history of substance abuse abetes mellitus, or significant medical issues that
or other psychiatric disorders, and a personality style could affect normal dietary habits within the last 60
characterized by impulsiveness.3,4 True prevalence days before the survey.
rates for ICDs in Parkinsons disease are not well
established;4 however, preliminary evidence sup- Procedures
ports the idea that that ICDs are more common in Demographic and disease characteristics were ob-
Parkinsons disease than in the general population or tained directly from patients and their caregivers.
in healthy-control subjects. Prevalence estimates Motor severity was assessed by clinicians specializ-
range from 0.4% to 10%, depending on the specific ing in movement disorders using the Unified Parkin-
ICD.5 Although several authors have described the son Disease Rating Scale (UPDRS-III). All patients
phenomenon of binge-eating among PD patients, no were administered quality-of-life, cognitive, and be-
reliable point-prevalence estimates have been report- havioral assessments, including the Parkinson Dis-
ed.4 With regard to the general population, a recently ease Questionnaire (PDQ-39), the Beck Depression
completed, multi-national study identified binge-eat- Inventory-II (BDI-II), the StateTrait Anxiety Inven-
ing disorder in 1.12% of over 20,000 European par- tory, the Apathy Scale, and the Mini-Mental State
ticipants.6 Exam (MMSE).9 12 Next, all patients completed a bat-
DSM-IV defines binge-eating disorder as eating an tery of tests assessing impulsive and compulsive be-
amount of food that is definitely larger than most peo- haviors, as described below. All procedures were ap-
ple would eat during the same period of time under proved by the local Institutional Review Board at the
similar circumstances, coupled with a perceived lack of University of Florida.
control over ones eating (criterion A). Patients with
binge-eating disorder must exhibit marked distress re- Measures
garding binge-eating (criterion C), and three out of five Impulsive and compulsive behaviors were assessed
associated features (criterion B). Binge-eating episodes with a battery of well-validated self-report question-
must occur at least twice weekly for a 6-month period naires. The Barratt Impulsiveness Scale (BIS-11) con-
(criterion D), and individuals must not engage in inap- tains 30 Likert-type items, and higher scores indicate
propriate compensatory behaviors, such as purging or greater general impulsivity.13 The Yale-Brown Obses-
fasting (criterion E). Many researchers have recently sive-Compulsive Scale contains 19 items, and only
supported the consideration of subthreshold eating dis- the first 10 Likert-type items contribute to the total
orders in the case of individuals who fail to meet all of score.14 Scores of 0 to 7 indicate subclinical symp-
the above DSM-IV criteria.6,7 The purpose of the toms. The Young Mania Rating Scale contains 11 Lik-
present prospective study was to determine the preva- ert-type items, and scores above 20 indicate signifi-
lence of and factors associated with binge-eating disor- cant symptoms.15 The South Oak Gambling Screen
der and subthreshold binge-eating in Parkinsons dis- contains 16 items of varying formats.16 Total score is
ease. determined by the number of at-risk responses.
Scores of 1 to 4 indicate some problems with gam-
bling, and scores above 4 indicate probable patho-
METHOD logical gambling. The Sexual Compulsivity Scale
contains 10 Likert-type items.17 Suggested cut-scores
Participants for elevated sexual compulsivity are 2.1 for men and
One hundred consecutive PD patients were ap- 1.7 for women. The Saving InventoryRevised con-
proached during regularly scheduled follow-up visits tains 23 Likert-type items and yields a global score
at the University of Florida Movement Disorders and three subscale scores: Clutter, Acquisition, and
Clinic, from September to December 2008. All pa- Difficulty Discarding.18 A global score above 40 indi-

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BINGE EATING IN PARKINSONS DISEASE

cates significant hoarding. The Problematic Internet gone deep brain stimulation (DBS) surgery in either
Use Questionnaire contains 18 Likert-type items and the internal globus pallidus (6%) or the subthalamic
yields a global score and three subscale scores: Ob- nucleus (17%), whereas 74 (77.1%) were exclusively
session, Neglect, and Control Disorder.19 A global medically managed. Approximately 42% of patients
score above 42.4 indicates significant problems. The were taking a dopamine agonist when assessed. On
Valence Compulsive Buying Scale contains 13 Likert- average, patients did not have dementia or depres-
type items.20 Compulsive buyers tend to score 42.2 or sion. Only one patient scored below the cutoff for
higher. dementia (MMSE score 24). Seventeen patients ev-
Eating behaviors were assessed with the Eating idenced mild-to-moderate depression (BDI score
Disorder Examination Questionnaire (EDE-Q) and 14).
the Eating Disorder Diagnostic Scale (EDDS).21,22 The According to responses on the Eating Disorder Diag-
EDE-Q is a 36-item self-report measure adapted from nostic Scale, one patient met full diagnostic criteria for
the Eating Disorder Examination interview that fea- binge-eating disorder (1%). An additional 8 patients
tures a 7-point Likert-type scale. The EDDS is a 22- (8.3%) exhibited subthreshold binge-eating in that they
item self-report questionnaire containing both all met criteria A and E for binge-eating disorder. Five
Yes/No items and Likert-type scales. It assesses patients did not meet criterion B; 2 patients did not
DSM-IV criteria AE for binge-eating disorder. In the meet criterion C; and 1 patient did not meet criteria B,
present study, responses on the EDDS were used to C, or D. This latter individual reported weekly episodes
identify the presence of binge-eating disorder, based over the last 6 months.
on DSM-IV criteria: 1) yes to Items 5 and 6; 2) yes to at The severity of disordered eating habits was quanti-
least 3 of Items 9 13; 3) yes to Item 14; 4) a score of at fied using Eating Disorder Examination Questionnaire
least 2 on Item 7; and 5) scores of 0 on Items 1518. global scores. In the entire sample, disordered eating
Patients who met criteria 1 and 5 and reported at least correlated with general impulsiveness (r0.585;
weekly binge-eating episodes over the previous 6 p0.001) and mania (r0.366; p0.001). No significant
months but who failed to meet one or more of the correlations were noted between disordered eating and
additional criteria were identified as having sub- any of the demographic, disease, or psychological vari-
threshold binge-eating disorder.6,7 ables. Table 1 shows that overeaters (N9) did not differ
from non-overeaters (N87) on any demographic, motor,
Statistical Analyses or mood variables. However, overeaters endorsed greater
Descriptive statistics were used to characterize the sam- amounts of overall disordered eating, impulsivity, mania,
ple. Relationships between variables were initially ex- and clutter behaviors than non-overeaters.
plored using Pearson correlations. Nonparametric Using psychometric criteria described by the individ-
Mann-Whitney U tests were used to compare overeat- ual scales developers, the prevalence of impulse con-
ers and non-overeaters on a variety of demographic, trol behaviors other than binge eating was determined.
disease, and psychological characteristics. Categorical Note that DSM-IV clinical criteria were not used to
variables were analyzed with chi-square tests. The in- categorize individuals, as a complete diagnostic inter-
dependent influences of selected variables on overeat- view for these other impulse controls disorders was not
ing status were examined with hierarchical binary lo- part of the present protocol. Six patients (6.25%) were
gistic regression. identified as probable pathological gamblers; an addi-
tional 11 patients (11.5%) had problematic gambling.
Eight patients (8.3%) had compulsive hoarding; 11 pa-
RESULTS tients (11.5%) had compulsive buying; one patient
(1.0%) had hypersexuality; and one patient (1.0%) had
Of 100 consecutive patients approached, 96 patients clinically significant manic symptoms. No pathologic
completed the study. The four patients who declined Internet use, anorexia nervosa, or bulimia nervosa was
to participate all cited the number of questionnaires found.
as their reason for refusal. Demographic and disease Next, we examined whether overeaters were more
characteristics of the sample are shown in Table 1. Of likely than non-overeaters to demonstrate other im-
these 96 patients, 22 (22.9%) had previously under- pulse-control behaviors. Table 2 displays the number of

58 http://neuro.psychiatryonline.org J Neuropsychiatry Clin Neurosci 23:1, Winter 2011


ZAHODNE et al.

overeaters and non-overeaters who met psychometric port mania, hoarding, hypersexuality, and compulsive
criteria in one or more of these domains. As shown, buying. There was a trend for overeaters to be more
overeaters were more likely than non-overeaters to re- likely than non-overeaters to exhibit significant obses-

TABLE 1. Demographics, Disease Characteristics, and Group Comparisons


Overeaters Non-Overeaters
(n9) (n87)
Mann-Whitney U or
Mean SD Mean SD 2
Characteristics
Age 68.3 4.5 65.8 10.3 318
Sex 6 M/3 F 57 M/30 F 0.005
Education 14.4 3.0 14.7 2.8 324
Disease/Health
Age at Parkinsons disease onset 57.97 7.8 55.8 12.8 364.5
Months with symptoms 124.3 56.9 119.3 109.1 322.5
UPDRS-III 28.7 7.0 31.1 11.1 331.5
LEDD 563.1 250.9 680.8 490.4 274.5
Weight 176.8 36.3 179.7 44.6 386
BMI 29.2 7.1 29.3 7.9 391
Neuropsychological
MMSE 29.3 0.7 28.8 1.5 306
BDI-II 7.9 9.9 8.1 5.8 326.5
STAIState 36.0 16.1 38.0 10.6 318
STAITrait 38.1 17.0 36.0 9.9 390
Apathy Scale 14.8 9.2 13.6 12.1 352
Study Measures
EDE-Q Global 1.7 1.2 0.5 0.8 102**
EDE-Q Restraint 1.5 1.8 0.4 0.8 189.5**
EDE-Q Eating Concern 3.2 2.2 0.7 2.7 84**
EDE-Q Shape Concern 0.6 1.2 0.1 0.4 262**
EDE-Q Weight Concern 1.4 1.5 0.8 1.2 239.5*
BIS 19.4 10.1 4.6 6.8 68**
Y-BOCS 4.8 9.5 0.7 2.9 329.5
YMRS 4.7 6.6 1.4 3.0 204**
SOGS 1.4 3.1 0.7 2.1 364.5
SCS 1.2 0.4 1.1 0.2 365.5
SI-R 26.6 16.3 17.5 11.7 256***
SI-R Clutter subscale 8.8 6.1 4.7 5.0 210.5*
Compulsive buying 36.3 20.0 21.2 12.2 201*
PIUQ 20.7 5.5 20.9 6.9 376

UPDRS-III: Unified Parkinson Disease Rating Scale; LEDD: levodopa-equivalent daily dose; BMI: body mass index; MMSE: Mini-Mental State
Exam; BDI-II: Beck Depression Inventory-II; STAI: StateTrait Anxiety Inventory; EDE-Q: Eating Disorder Examination Questionnaire; BIS:
Barratt Impulsiveness Scale; Y-BOCS: Yale-Brown Obsessive-Compulsive Scale; YMRS: Young Mania Rating Scale; SOGS: South Oak Gambling
Scale; SCS: Sexual Compulsivity Scale; SI-R: Saving InventoryRevised; PIUQ: Problematic Internet Use Questionnaire.
*p0.05
**p0.01
***p0.1

TABLE 2. Proportions of Individuals Meeting Criteria for Other Impulse-Control Psychopathology


Overeaters Non-Overeaters
(N9) (N87) Analyses
Classification n % n % Pearson 2 p
Mania 1 11.1 0 0 9.77 0.002 0.32
Hoarding 3 33.3 5 5.7 8.13 0.004 0.29
Problem gambling 2 22.2 15 17.2 0.40 0.82 0.07
Compulsive buying 4 44.4 7 8.0 10.65 0.001 0.33
Obsessive-compulsive behavior 2 22.2 5 5.7 3.28 0.07 0.19
Sexual compulsivity 1 11.1 0 0 9.77 0.002 0.32
Pathological internet use 0 0 0 0
At least one of above 6 66.7 25 28.7 5.37 0.02 0.236

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BINGE EATING IN PARKINSONS DISEASE

sive-compulsive features. Six of the nine overeaters in only 1% of our unselected sample of 96 consecutive
(67%) met psychometric criteria for at least one other PD patients, which is comparable to the 1.12% prev-
ICD, versus 25 out of 87 non-overeaters (29%). This alence estimate reported in a recent multinational
difference was significant (25.367; df1; 0.236; study.6 In the future, a larger sample size should be
p0.02). used to confirm this prevalence value. The current
Four of the nine overeaters (44%) were currently on estimate of binge-eating disorder prevalence is lower than
an agonist, versus 41% of control subjects, and this those reported for pathological gambling and hypersexu-
difference was not statistically significant. Four out of ality and higher than that reported for compulsive buying
nine overeaters (44%) had undergone subthalamic in PD.2 Despite the lack of higher prevalence of binge-
nucleus DBS surgery, and 0 had undergone internal eating disorder in this sample of PD patients, we identi-
globus pallidus DBS. Twelve (14%) and six (7%) non- fied subclinical binge-eating disorder in 8% of the sample,
overeaters had undergone DBS in the subthalamic which is similar to or higher than rates of other ICDs.2
nucleus and internal globus pallidus, respectively. Using psychometric criteria, we also identified relatively
The association between overeating and DBS history high levels of problem gambling (11.5%), compulsive buy-
(subthalamic nucleus, internal globus pallidus or no ing (11.5%), and hoarding (8.3%) within our sample.
DBS) was at trend level (25.82; df2; Cramers We found substantial support for the co-occurrence
V0.246; p0.055). of ICD behaviors among individuals with Parkinsons
In order to determine the relative contributions of disease. Binge-eating severity correlated with measures
demographic, disease, and iatrogenic variables to over- of impulsivity and mania. More overeaters met psycho-
eating, a hierarchical logistic regression was conducted, metric criteria for at least one other ICD than did non-
in which the dependent variable was eating status overeaters. This overlap is consistent with the current
(Overeater versus Non-overeater). Based on previous view of a common pathophysiological mechanism un-
research, the first block comprised iatrogenic variables
(DBS, dopamine-agonist therapy, l-dopa equivalent TABLE 3. Hierarchical Logistic-Regression Results
daily dose [LEDD]). The second block comprised dis- SE Exp p
ease characteristics (age at PD onset, UPDRS-III total
Step 1
score), and the third block comprised demographic Constant 0.019 1.202 1.019 0.988
characteristics (age, sex, education). Results are shown DBS 2.109 0.927 0.121 0.023*
Dopamine agonist 0.130 0.841 0.878 0.878
in Table 3. Although the model did not reach signifi- LEDD 0.002 0.001 0.998 0.192
cance at any of the three steps, DBS emerged as the only Step 2
Constant 1.908 2.706 0.148 0.481
independent predictor of being Overeater status at all DBS 2.679 1.163 0.069 0.021*
three steps (p0.023 after Step 1; p0.021 after Step 2; Dopamine agonist 0.052 0.876 1.053 0.953
LEDD 0.002 0.001 0.998 0.182
and p0.019 after Step 3). UPDRSIII 0.021 0.048 0.980 0.668
Age at PD onset 0.050 0.054 1.052 0.354
Step 3
Constant 3.722 4.448 0.024 0.024
DISCUSSION DBS 2.688 1.142 0.068 0.019*
DA agonist 0.234 0.908 1.264 0.796
LEDD 0.002 0.001 0.998 0.147
Our study is cross-sectional, with all of its inherent UPDRSIII 0.029 0.050 0.971 0.562
weaknesses. Nonetheless, the present report de- Age at PD onset 0.005 0.051 0.995 0.917
Age 0.080 0.070 1.083 0.257
scribes results from the first prospective study on the Sex 0.046 0.958 1.047 0.961
point prevalence of binge-eating disorder in Parkin- Education 0.002 0.173 0.998 0.989
sons disease patients in the United States. It provides PD: Parkinsons disease; DBS: deep brain stimulation; LEDD: levo-
further support for a relationship between binge-eat- dopa-equivalent daily dose; UPDRS-III: Unified Parkinson Disease
Rating Scale.
ing and other behaviors on the impulsive-compulsive R20.069 (Cox & Snell), 0.155 (Nagelkerke). Model 25.777, df3,
spectrum. Results also suggest that future research p0.123 for Step 1.
should explicitly examine the contribution of deep R20.011 (Cox & Snell), 0.025 (Nagelkerke). Model 210.463,
df5, p0.234 for Step 2.
brain stimulation in the subthalamic nucleus to R20.012 (Cox & Snell), 0.026 (Nagelkerke). Model 210.979,
binge-eating behaviors. df8, p0.203 for Step 3.
*p0.05.
We identified the presence of binge-eating disorder

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ZAHODNE et al.

derlying these behaviors in PD that involve mesocorti- whether they demonstrated subclinical symptoms. Of
colimbic sensitization. Recent neurobiological experi- note, two of these four overeaters described an in-
ments show enhanced dopaminergic activity within the crease in their desire for sweets (i.e., candies and ice
ventral striatum of PD patients displaying pathological cream) after DBS.
gambling or dopamine dysregulation syndrome Reports of the effects of DBS on impulsive and
(DDS).23 compulsive behaviors have been somewhat conflict-
Previous studies have variably identified male sex, ing and have included descriptions of worsened, im-
younger age at PD onset, and depression as risk fac- proved, and newly-developed ICDs after sur-
tors for ICDs.2 In our sample, overeaters and non- gery.28 31 All four overeaters with a history of DBS in
overeaters did not differ on any of these variables. the present study were implanted in the subthalamic
However, most previous studies focused on patho- nucleus, and it has been suggested that subthalamic
logical gambling. Many have failed to identify these nucleus DBS results in more nonmotor complications
variables as independent risk factors when using than DBS in other targets.32,33 Further controlled
multivariate analyses.4,5 No study has yet examined studies are needed to determine the specificity of our
the contributions of these variables exclusively to findings to DBS in the subthalamic nucleus. Interestingly,
binge-eating in Parkinsons disease. Of note, a recent recent experimental evidence has shown that high-fre-
mail-survey study involving 312 PD patients simi- quency stimulation of the subthalamic nucleus modulates
larly failed to identify male sex, mean daily l-dopa neurotransmission in limbic regions such as the nucleus
dose, or age at Parkinsons disease onset as statisti- accumbens shell, which has been implicated in the patho-
cally significant predictors of ICD behaviors.24 These physiology of ICDs.34
results suggest that additional risk factors for these Weight-gain after DBS has been documented by nu-
symptoms must be explored. merous groups.35 Bilateral and unilateral subthalamic
Surprisingly, we did not find any association be- nucleus stimulation have been associated with weight-
tween the use of dopamine agonists and the presence of gains of approximately 10 kg and 4 kg after 1 year,
binge-eating. Multiple studies have implicated dopa- respectively.35 Postsurgical weight-gain has been attrib-
mine agonists acting on D3 receptors in the pathophys- uted to medication reduction, improved ability to eat,
iology of ICDs and repetitive behavior in Parkinsons and/or decreased basal energy expenditure.36 Despite
disease.4,5,24,25 However, confounding variables such as reports of uncontrolled appetitive behaviors after DBS,
differing prescribing practices may have contributed to the potential effect of increased frequency of binge-
initial findings.26 A recent meta-analysis failed to dem- eating episodes has not yet been systematically evalu-
onstrate a significant relationship between ICDs and ated.
individual dopamine agonists.27 A significant percent- The relatively high prevalence of clinical and sub-
age of our cohort underwent deep brain stimulation clinical symptomatology reported here suggests that
surgery, which could have altered the patients medi- physicians should be aware of binge-eating in their
cation regimen postsurgery. PD patients, especially considering the potential ad-
This study identified a history of subthalamic nu- verse consequences of prolonged occurrences. The
cleus DBS surgery as the only significant predictor of relationship between binge-eating and weight-gain
binge-eating in a nonselected sample of consecutive after DBS surgery should also be elucidated, as it is
PD patients. Furthermore, there was a trend for an important for physicians and patients to be cognizant
association between subthalamic nucleus DBS and of potential surgical side effects during treatment
being an overeater. However, because the present planning.
study did not systematically measure and compare
ICD symptomatology before and after surgery, it can-
not be concluded that DBS induced binge-eating in National Parkinson Center of Excellence, National Insti-
these patients. Identification of such a relationship tute on Aging (T32-AG020499 [UF-LBZ]). The authors
requires future prospective studies with matched gratefully acknowledge the work of Janet Romrell, PA-C, for
controls. None of the four overeaters with a history of her invaluable assistance with patient recruitment and as-
subthalamic nucleus DBS carried a psychiatric diag- sessment. This work has already been presented as a poster
nosis before surgery. However, it is not known under this title at the annual meeting of the ANPA.

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BINGE EATING IN PARKINSONS DISEASE

References
1. Simuni T, Sethi K: Nonmotor manifestations of Parkinsons Disorder Examination Questionnaire (EDE-Q) in screening for
disease. Ann Neurol 2008; 64:S65S80 eating disorders in community samples. Behav Res Ther 2004;
2. Wolters E, van der Werf YD, van den Heuvel OA: Parkinsons 42:551567
disease-related disorders in the impulsive-compulsive spec- 22. Stice E, Telch CF, Rizvi SL: Development and validation of the
trum. J Neurol 2008; 255:48 56 eating disorder diagnostic scale: a brief self-report measure of
3. Evans AH, Lees AJ: Dopamine dysregulation syndrome in anorexia, bulimia, and binge-eating disorder. Psychol Assess
Parkinsons disease. Curr Opin Neurol 2004; 17:393398 2000; 12:123131
4. Weintraub D: Dopamine and impulse control disorders in 23. Evans AH, Pavese N, Lawrence AD, et al: Compulsive drug
Parkinsons disease. Ann Neurol 2008; 64:S93100 use linked to sensitized ventral striatal dopamine transmis-
5. Weintraub D, Siderowf AD, Potenza MN, et al: Association of sion. Ann Neurol 2006; 59:852 858
dopamine agonist use with impulse control disorders in Par- 24. Fan W, Ding H, Ma J, et al: Impulse control disorders in
kinson disease. Arch Neurol 2006; 63:969 973 Parkinsons disease in a Chinese population. Neurosci Lett
6. Preti A, de Girolamo G, Vilagut G, et al. The epidemiology of 2009; 465:6 9
eating disorders in six European countries: results of the 25. Evans AH, Katzenschlager R, Pavious D, et al: Punding in
ESEMeD-WMH project. J Psychiatr Res 2009; 43:11251132 Parkinsons disease: its relation to the dopamine dysregula-
7. Striegel-Moore RH, Dohm FA, Solomon EE, et al: Subthresh- tion syndrome. Mov Disord 2004; 19:397 405
old binge eating disorder. Int J Eat Disord 2000; 27:270 278 26. Voon V, Hassan K, Zurowski M, et al: Prevalence of repetitive
8. Hughes AJ, Daniel SE, Kilford L, et al: Accuracy of clinical and reward-seeking behaviors in Parkinson disease. Neurol-
diagnosis of idiopathic Parkinsons disease: a clinico-patho- ogy 2006; 67:1254 1257
logical study of 100 cases. J Neurol Neurosurg Psychiatry 27. Gallagher DA, OSullivan SS, Evans AH, et al: Pathological
2002; 55:181184 gambling in Parkinsons disease: risk factors and differences
9. Peto V, Jenkinson C, Fitzpatrick R, et al: The development and from dopamine dysregulation: an analysis of published case
validation of a short measure of functioning and well being
series. Mov Disord 2007; 22:17571763
for individuals with Parkinsons disease. Qual Life Res 1995;
28. Ardouin C, Voon V, Worbe Y, et al: Pathological gambling in
4:241248
Parkinsons disease improves on chronic subthalamic nucleus
10. Beck AT, Steer R, Brown G: The Beck Depression Inventory-II.
stimulation. Mov Disord 2006; 21:19411946
San Antonio, Tex, Psychological Corporation, 1996
29. Frank MJ, Samanta J, Moustafa AA, et al: Hold your horses:
11. Spielberger CD: Manual for the State-Trait Anxiety Inventory.
impulsivity, deep brain stimulation, and medication in par-
Palo Alto, Calif, Consulting Psychologists Press, 1983
kinsonism. Science 2007; 318:1309 1312
12. Starkstein SE, Mayberg HS, Preziosi TJ, et al: Reliability, va-
30. Halbig TD, Tse W, Frisina PG, et al: Subthalamic deep brain
lidity, and clinical correlates of apathy in Parkinsons disease.
stimulation and impulse control in Parkinsons disease. Eur
J Neuropsychiatry Clin Neurosci 1992; 4:134 139
13. Patton JH, Stanford MS, Barratt ES: Factor structure of the J Neurol 2009; 16:493 497
Barratt Impulsiveness Scale. J Clin Psychol 1995; 51:768 774 31. Smending HM, Goudriaan AE, Foncke EM, et al: Pathological
14. Goodman WK, Price LH, Rasmussen SA, et al: The Yale- gambling after bilateral subthalamic nucleus stimulation in
Brown Obsessive Compulsive Scale. I: development, use, and Parkinsons disease. J Neurol Neurosurg Psychiatry 2007; 78:
reliability. Arch Gen Psychiatry 1989; 46:1006 1011 517519
15. Young RC, Biggs JT, Ziegler VE, et al: A rating scale for mania: 32. Okun MS, Fernandez HH, Wu SS, et al: Cognition and mood
reliability, validity and sensitivity. Br J Psychiatry 1978; 133: in Parkinsons disease in subthalamic nucleus versus globus
429 435 pallidus internal deep brain stimulation: the compare trial.
16. Lesieur HR, Blume SB: The South Oaks Gambling Screen Ann Neurol 2009; 65:586 595
(SOGS): a new instrument for the identification of pathological 33. Zahodne LB, Okun MS, Foote KD, et al: Greater improvement
gamblers. Am J Psychiatry 1987; 144:1184 1188 in quality of life following unilateral deep brain stimulation
17. Kalichman SC, Rompa D: The sexual compulsivity scale: fur- surgery in the globus pallidus as compared to the subthalamic
ther development and use with HIV-positive persons. J Pers nucleus. J Neurol 2009; 256:13211329
Assess 2001; 76:379 395 34. Winter C, Lemke C, Sohr R, et al: High frequency stimulation
18. Frost RO, Steketee G, Grisham J: Measurement of compulsive of the subthalamic nucleus modulates neurotransmission in
hoarding: saving inventory-revised. Behav Res Ther 2004; 42: limbic brain regions of the rat. Exp Brain Res 2008; 185:497
11631182 507
19. Demetrovics Z, Szeredi B, Rozsa S: The three-factor model of 35. Walker HC, Lyerly M, Cutter G, et al: Weight changes asso-
internet addiction: the development of the Problematic Inter- ciated with unilateral STN DBS and advanced PD. Parkinson-
net Use Questionnaire. Behav Res Methods 2008; 40:563574 ism Relat Disord 2009; 15:709 711
20. Valence G, dAstous A, Fortier L: Compulsive buying: concept 36. Montaurier C, Morio B, Bannier S, et al: Mechanisms of body
and measurement. J Consum Policy 1988; 11:419 433 weight gain in patients with Parkinsons disease after subtha-
21. Mond JM, Hay PJ, Rodgers B, et al: Validity of the Eating lamic stimulation. Brain 2007; 130:1808 1018

62 http://neuro.psychiatryonline.org J Neuropsychiatry Clin Neurosci 23:1, Winter 2011

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