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Salivary cortisol levels in Parkinson's disease and its correlation to risk behaviour.
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MedLine Citation:
PMID:  21478206     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
OBJECTIVE: To investigate salivary cortisol samples in patients with Parkinson's disease (PD) with and without impulsive compulsive behaviours (ICB) during a risk task.
METHODS: Salivary cortisol levels were measured in 13 PD patients without ICB (PD-ICB) and in 15 PD patients with ICB (PD+ICB) before, after medication and throughout the day, and were compared with results with 14 healthy controls. All participants also performed a gambling task to assess risk taking behaviour.
RESULTS: Significantly higher diurnal cortisol levels were found in the PD-ICB group compared with healthy controls but no differences were seen between the PD+ICB and the control group. Increased cortisol levels were significantly correlated with increased risk taking in PD+ICB patients but no interaction was found in the PD-ICB group.
CONCLUSIONS: The findings are in keeping with previous studies which have linked low cortisol levels with antisocial behaviour. The higher cortisol levels during the risk task in the PD+ICB group are consistent with reports in pathological gamblers during gambling and addicts during drug abuse. The results support the hypothesis that cortisol plays an important role in risk taking in ICBs.
Authors:
Atbin Djamshidian; Sean S O'Sullivan; Andrew Papadopoulos; Paul Bassett; Karen Shaw; Bruno B Averbeck; Andrew Lees
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Intramural     Date:  2011-04-08
Journal Detail:
Title:  Journal of neurology, neurosurgery, and psychiatry     Volume:  82     ISSN:  1468-330X     ISO Abbreviation:  J. Neurol. Neurosurg. Psychiatr.     Publication Date:  2011 Oct 
Date Detail:
Created Date:  2011-09-09     Completed Date:  2011-10-31     Revised Date:  2013-06-30    
Medline Journal Info:
Nlm Unique ID:  2985191R     Medline TA:  J Neurol Neurosurg Psychiatry     Country:  England    
Other Details:
Languages:  eng     Pagination:  1107-11     Citation Subset:  IM    
Affiliation:
Reta Lila Weston Institute of Neurological Studies and Queen Square Brain Bank for Neurological Diseases, University College London, London, UK.
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MeSH Terms
Descriptor/Qualifier:
Aged
Circadian Rhythm / physiology
Compulsive Behavior / blood,  psychology
Female
Gambling / blood,  psychology
Humans
Hydrocortisone / blood*
Impulsive Behavior / blood,  psychology
Male
Mental Status Schedule
Middle Aged
Neurologic Examination
Parkinson Disease / blood*,  psychology
Risk-Taking*
Saliva / chemistry
Statistics as Topic
Chemical
Reg. No./Substance:
50-23-7/Hydrocortisone
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Journal ID (nlm-ta): J Neurol Neurosurg Psychiatry
Journal ID (publisher-id): jnnp
Journal ID (hwp): jnnp
ISSN: 0022-3050
ISSN: 1468-330X
Publisher: BMJ Group, BMA House, Tavistock Square, London, WC1H 9JR
Article Information
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© 2011, Published by the BMJ Publishing Group Limited. For permission to use (where not already granted under a licence) please go to http://group.bmj.com/group/rights-licensing/permissions.
open-access:
Received Day: 11 Month: 11 Year: 2010
Accepted Day: 28 Month: 2 Year: 2011
Electronic publication date: Day: 8 Month: 4 Year: 2011
Print publication date: Month: 10 Year: 2011
pmc-release publication date: Day: 8 Month: 4 Year: 2011
Volume: 82 Issue: 10
First Page: 1107 Last Page: 1111
ID: 3171980
PubMed Id: 21478206
Publisher Id: jnnp245746
DOI: 10.1136/jnnp.2011.245746

Salivary cortisol levels in Parkinson's disease and its correlation to risk behaviour
Atbin Djamshidian1
Sean S O'Sullivan1
Andrew Papadopoulos2
Paul Bassett3
Karen Shaw1
Bruno B Averbeck45
Andrew Lees1
1Reta Lila Weston Institute of Neurological Studies and Queen Square Brain Bank for Neurological Diseases, University College London, London, UK
2The National Affective Disorders Unit, South London and Maudsley NHS Foundation Trust, Beckenham, Kent, UK
3UCL/UCLH/Royal Free, Biomedical Research Unit, London, UK
4Sobell Department of Motor Neuroscience and Movement Disorders, Institute of Neurology, UCL, London, UK
5Laboratory of Neuropsychology, National Institute of Mental Health, National Institutes of Health, Bethesda, Maryland, USA
Correspondence: Correspondence to Professor A Lees, Reta Lila Weston Institute of Neurological Studies, UCL Institute of Neurology, 1 Wakefield Street, London WC1N 1PJ, UK; alees@ion.ucl.ac.uk
[other] BBA and AL contributed equally to this study.

The cause of Parkinson's disease (PD) remains unknown but acute severe stress has been suggested as a possible precipitant.1 Elevated cortisol levels in animal models of PD have been associated with dopaminergic cell loss and motor handicap.2 Higher cortisol levels have been described in depression,3 anxiety4 and also in Alzheimer's disease and PD.5 An acute increase in cortisol levels has been reported during intake of illicit drugs.6 Although a large proportion of addiction related research has highlighted the importance of dopaminergic pathways,7 there is also a line of evidence supporting the role of cortisol in the development of addictive or impulsive behaviours.8, 9

A subgroup of PD patients develop impulsive compulsive behaviours (ICB) which are associated with antisocial behaviour.10 ICBs are usually triggered by dopamine agonist therapy and there is growing evidence linking the aetiology of these ICBs to the development of drug addictions.11, 12 Previous studies have found lower cortisol levels in impulsive non-PD participants.13, 14 Given the link between cortisol and addiction in healthy subjects, and between addiction and the development of ICBs in PD patients, we hypothesised that cortisol levels might be reduced in PD patients with ICBs, relative to PD patients without ICBs.

For this study, we measured salivary cortisol levels from PD patients with (PD+ICB) and without (PD−ICB) ICBs, and healthy controls, and correlated these results with their performance on a risk task.15 Increased salivary cortisol levels have also been positively correlated with risk taking in non-PD pathological gamblers.16 Therefore, we sought to correlate cortisol with risk taking behaviour, having previously shown increased risk taking in gambling tasks in all PD patients on medication compared with controls, with highest risk taking behaviour in PD patients with pathological gambling.17


Methods
Participants

Cortisol samples from 13 PD−ICB, 15 PD+ICB patients and 14 healthy controls were collected. All patients were recruited from the National Hospital for Neurology and Neurosurgery, Queen Square, London, fulfilling the Queen Square Brain Bank criteria for PD18 and were taking L-dopa. PD+ICB patients were diagnosed using proposed criteria.19–21 Most PD+ICB patients had more than one ICB. Healthy controls were usually recruited from among the patient's partners and were not taking any medication that could influence cortisol measurement. None of the participants was taking steroids. Written informed consent was obtained from all subjects according to approved ethical protocols from the regional and local research ethics committee.

We excluded participants who scored under 27/30 points on the Mini-Mental State Examination and who had a current or past medical history of an anxiety disorder, and patients with current depression. Patients without a known previous diagnosis of anxiety or depression were screened for these conditions in a semi-structured clinical assessment. Furthermore, all participants were asked to complete the positive and negative affect schedule which has been recommended as a supplement to measure anxiety and depression.22 Samples were obtained in a quiet environment, usually at the patient's home, to control for and reduce the amount of stress.

To control for the potential effects of food23 and L-dopa24 on cortisol levels, PD patients were asked not to take their usual anti-Parkinson medication for at least 12 h and not to have breakfast on the day of testing. All participants woke up between 6:00 and 7:00. The morning samples were obtained together with the researcher and the other samples were collected by the participants themselves.

Cortisol

Participants were instructed to collect saliva samples by turning the cotton roll for 2–3 min in their mouth. In total, five saliva samples were collected from controls and 10 samples from patients. Samples from all participants were obtained between 8:15 and 8:45—baseline level. All patients were tested in their ‘off condition’ in the morning, which was assessed by the Unified Parkinson's Disease Rating Scale (UPDRS) part 3 motor score. Furthermore, we collected five more saliva samples from the patient group. One was obtained immediately prior to the risk task, one just after the risk test and prior to medication, the next 5 min after medication, then 15 min after medication, 30 min after medication and 45 min after medication. Sixty minutes after medication, between 9:15 and 9:45 and after the second test (‘on condition’ in patients), another sample was taken, this time from both controls and patients (figure 1).

All participants then collected samples between 13:00 and 14:00, between 19:00 and 20:00 and between 22:00 and 23:00 on their own. These times were deliberately flexible for patients to ensure that the cortisol sampling was undertaken approximately 1 h after taking their usual dopamine replacement therapy. Controls were tested in the same way without taking any medication in between.

Subjects were asked to avoid excessive physical activity, stress and heavy meals on the study day, and were provided with a collection diary where they entered the time of saliva collection and their activity during the hour prior to each cortisol sample. In addition, participants were instructed not to eat anything at least 30 min prior to collecting a sample.

The therapeutic motor response to L-dopa was assessed by UPDRS scores (part 3) during ‘off’ and ‘on’ states. All patients had an excellent L-dopa response and had a similar improvement in UPDRS scores. All patients were ‘on’ at the time of the second risk task. Levodopa equivalent units (LEU) was calculated as described previously21 (see table 1 for demographic information).

Risk task

All patients were tested on a validated computerised gambling task to assess risk behaviour15 once in their ‘off medication’ state after their first salivary cortisol sampling, and once in their ‘on medication’ state approximately 50 min after receiving their usual morning anti-Parkinson medications. Controls were tested in the same way but did not take dopaminergic medication between the tests. Participants had to choose between two gambles with varying levels of risks—either a low risk or a high risk gamble, where participants could win real money. Feedback was given immediately. Details about this task are published elsewhere.17 Risk aversion was assessed parametrically by fitting a model to each participant's behaviour, separately for each test session.17

Biochemical measurements

Saliva samples for the determination of cortisol concentration were collected in Salivettes (Sarstedt, Leicester, UK) and stored at −20°C until analysed. Details on the analysis were published recently elsewhere.25

Statistical analysis
Demographic and clinical features

Data analyses were performed using SPSS V.18. Age, gender, age of onset, UPDRS scores, L-dopa and LEU dose were used as dependent variables and group (PD−ICB, PD+ICB and control) was modelled as a between subject factor. We used ANOVA, the Student's t test or the χ2 test where appropriate.

Cortisol salivary samples

The data were positively skewed as cortisol levels show a diurnal variation with a peak during the morning (figure 2). As a result, we log transformed the data and residuals were checked and found to be normally distributed. We performed a linear mixed model ANOVA with the log transformed scores as the dependent variable and group (PD−ICB, PD+ICB and control) was modelled as a between subject factor. The model also included subject as a random factor, and the interactions between the two fixed factors (time and group). All post hoc comparisons were corrected by the Bonferroni method; the level of significance was p<0.05. For the diurnal cortisol measurement we excluded those extra samples that were obtained from the patients between the tests.

We correlated the change in risk aversion with the change in cortisol levels. This is a within subjects analysis. Specifically, we calculated the correlation coefficient between: ΔR and ΔC, where ΔR=R1–R2 is the difference in risk aversion in the first and second test session; ΔC was defined accordingly for cortisol levels. One value for ΔR and one for ΔC was derived for each subject, and these values were then correlated using Pearson's correlation test.


Results
Demographic characteristics

The groups were generally well matched. There was no significant age difference between the groups (F(2,38)=2.5, p=0.091). However, PD+ICB patients had an earlier disease onset (t24=2.6, p=0.014). There was no difference in the daily L-dopa doses or the dose given in the morning, LEU dose, UPDRS (part 3 motor) scores or disease duration (see table 1 for further details).

Cortisol levels

We found a main effect of group (F(2,37)=4.6, p=0.016) and a main effect of time (F(4,144)=51.0, p<0.001), with the highest cortisol level being in the morning. There was no interaction between time and group (F(8,144)=0.9, p=0.48). Post hoc analysis revealed that the PD−ICB group had significantly higher cortisol levels than the control group (p=0.019) (figure 3). There was no difference between the control and PD+ICB group (p=0.1) and no difference between the patient groups (p=1.0). We next looked at just the morning cortisol levels between the patient groups by excluding the control group but found no significant difference (t24=2.4, p=0.2). There was no correlation between UPDRS off score and baseline cortisol levels (all p values >0.4).

Risk task

Participants were tested twice on a behavioural task that assessed risk taking behaviour15 once off medication and once on medication. Cortisol samples were taken just before each administration of the task. The task assessed the extent to which participants preferred large, low probability rewards to smaller more probable rewards. We have reported detailed analyses of the behavioural results previously, the main finding being that patients became more risk prone on medication, relative to controls.17 Here we focus on the relationship between cortisol and behaviour in the task. In the PD+ICB group, there was a significant correlation between change in risk from the first to the second test session (from the off medication state to the on medication state) and change in cortisol levels measured just before each test session (r=−0.617, p=0.0144, n=15). Specifically, increased risk preference was associated with increased cortisol levels. In the PD−ICB group, the correlation was not significant (r=0.166, p=0.669, n=11). Furthermore, the correlation coefficients were significantly different between the PD−ICB and the PD+ICB groups (Z=1.99, p=0.047) such that there was a significantly stronger correlation in the PD+ICB group than in the PD−ICB group.


Discussion

As expected, cortisol levels were found to be highest in the morning in all participants and decreased over the day (figure 2). Furthermore, we found significantly higher daily salivary cortisol levels in PD−ICB patients compared with healthy controls but no difference between PD+ICB patients and controls.

Increased irritability and lability, higher scores of disinhibition and novelty seeking and a previous history of addictive behaviours have been reported in PD+ICB patients.12, 26 Furthermore, all PD+ICB patients had higher schizotypy scores, which is a personality trait related to the risk for psychosis, than controls.27 In this study, it is not possible to determine whether changes in cortisol are a cause or effect of the impulsive compulsive behaviours. However, impulsiveness, carelessness and aggressive behaviour have been associated with attenuated cortisol levels in adolescents and adults.13, 28–30 Impulsive adults with illicit drugs abuse,14 patients with antisocial behaviour31, 32 and controls with reduced negative feedback learning33 also had lower cortisol levels. Increased temporal discounting, the tendency to choose earlier, smaller over delayed, larger rewards has been found only in PD+ICB patients27 and has been associated with attenuated cortisol levels in healthy volunteers.34 Various studies have also shown impairment in feedback learning in PD+ICB patients.17, 35, 36

However, we did not find any difference between the two patient groups and between the control and PD+ICB groups. Previous studies found sustained elevated cortisol levels in Aborigines after receiving their wages which they planned to gamble with.37 Therefore, the expectance of being tested and the subsequent modest monetary reward for completing the study could have led to an increase in baseline cortisol levels in PD+ICB patients. Another possible explanation is that PD itself is associated with increased cortisol levels5 while personality traits typical of PD+ICB patients are linked with lower cortisol levels. This might explain why we did not find any difference between PD+ICB patients and the two other groups. Critically, we observed a change of direction of cortisol levels only in the PD+ICB group during gambling. This change of direction in cortisol levels following a stressor has been linked with antisocial behaviour.30

We have reported previously that all PD patients were more risk prone on medication compared with controls, with a subgroup of PD+ICB with pathological gambling taking the most risky decisions.17 When correlating changes in cortisol levels with risk taking behaviour, we found a significant interaction in the PD+ICB group but not in the PD−ICB group, despite both groups showing similar performance on the risk task. Our findings are consistent with previous studies in male non-PD gamblers showing a rise in salivary cortisol levels16, 38 and blood cortisol levels39 during gambling. Acutely raised cortisol has been linked with anticipation of increased chances of making money and can be euphorogenic.40, 41 Alcohol and nicotine induce an increase in cortisol levels8, 42 and addicts have an increased activation of the hypothalamic–pituitary–axis during drug intake.8 Several preclinical studies have also shown that cortisol acts as a positive reinforcer and causes addiction.43 Self-administration of cocaine leads to elevated cortisol levels in rodents,9 non-human primates44 and humans.45

Our findings, with a relative increase in cortisol in PD+ICB during a risk task, further strengthen the links between biological and drug addictions. This finding in a PD population is especially interesting since L-dopa has a dual effect on cortisol and behaviour. It increases risk behaviour in all PD patients17 and high doses of L-dopa can reduce cortisol levels.24 The latter finding contrasts with our results but in this study by Muller et al, a control group was not included, morning samples were obtained at a time of the day when cortisol levels decrease fastest and no information on circadian cortisol levels was provided.

To our knowledge, this is the first study that has tested salivary samples in PD+ICB patients. Our results suggest that in general, cortisol levels are elevated in PD−ICB patients compared with controls but not in the PD+ICB group. This is in keeping with the literature which links lower cortisol levels with antisocial behaviour, and further links ICBs with substance addiction. Additionally, we found a significant correlation between risk taking behaviour and cortisol levels in the PD+ICB group with higher cortisol levels being associated with risk prone behaviour but no significant interaction in the PD−ICB group.


Notes

Funding:This work was supported in part by the Intramural Program of the National Institutes of Health, National Institute of Mental Health.

Competing interests: AL serves as historical section editor for Movement Disorders; has served as a consultant to Genus; has served on advisory boards for and received honoraria from Novartis, Teva Pharmaceutical Industries Ltd, MEDA Pharmaceuticals Inc, Boehringer Ingelheim, GlaxoSmithKline, Ipsen, Lundbeck Inc, Allergan Inc, Orion Pharma UK Ltd and Eisai Inc; and has received research support from the PSP Association and the Reta Lila Weston Trust.

Ethics approval: This study was conducted with the approval of the the Joint UCL/UCLH Committees on the Ethics of Human Research.

Provenance and peer review: Not commissioned; externally peer reviewed.

The authors thank the patients and their families for participating. The authors also thank Irene Papadopoulos for technical assistance with the saliva cortisol assays and Professor Peter Brown for critically reading the manuscript.


References
1. Charcot JM. Lectures on the diseases of the nervous system, vol 1, English translation by Sigerson G. London: The New Sydenham Society, Year: 1878
2. Smith LK,Jadavji NM,Colwell KL,et al. Stress accelerates neural degeneration and exaggerates motor symptoms in a rat model of Parkinson's disease. Eur J NeurosciYear: 2008;27:2133–4618412632
3. Bhagwagar Z,Hafizi S,Cowen PJ. Increased salivary cortisol after waking in depression. Psychopharmacology (Berl)Year: 2005;182:54–715991000
4. Vreeburg SA,Zitman FG,van Pelt J,et al. Salivary cortisol levels in persons with and without different anxiety disorders. Psychosom MedYear: 2010;72:340–720190128
5. Hartmann A,Veldhuis JD,Deuschle M,et al. Twenty-four hour cortisol release profiles in patients with Alzheimer's and Parkinson's disease compared to normal controls: ultradian secretory pulsatility and diurnal variation. Neurobiol AgingYear: 1997;18:285–99263193
6. Goeders NE. Stress and cocaine addiction. J Pharmacol Exp TherYear: 2002;301:785–912023504
7. Koob GF,Volkow ND. Neurocircuitry of addiction. NeuropsychopharmacologyYear: 2010;35:217–3819710631
8. Lovallo WR. Cortisol secretion patterns in addiction and addiction risk. Int J PsychophysiolYear: 2006;59:195–20216434116
9. Koob G,Kreek MJ. Stress, dysregulation of drug reward pathways, and the transition to drug dependence. Am J PsychiatryYear: 2007;164:1149–5917671276
10. Slutske WS,Eisen S,Xian H,et al. A twin study of the association between pathological gambling and antisocial personality disorder. J Abnorm PsycholYear: 2001;110:297–30811358024
11. Evans AH,Pavese N,Lawrence AD,et al. Compulsive drug use linked to sensitized ventral striatal dopamine transmission. Ann NeurolYear: 2006;59:852–816557571
12. Voon V,Thomsen T,Miyasaki JM,et al. Factors associated with dopaminergic drug-related pathological gambling in Parkinson disease. Arch NeurolYear: 2007;64:212–1617296836
13. McBurnett K,Lahey BB,Rathouz PJ,et al. Low salivary cortisol and persistent aggression in boys referred for disruptive behavior. Arch Gen PsychiatryYear: 2000;57:38–4310632231
14. King RJ,Jones J,Scheuer JW,et al. Plasma cortisol correlates of impulsivity and substance abuse. Pers Indiv DifferYear: 1990;11:287–91
15. Huettel SA,Stowe CJ,Gordon EM,et al. Neural signatures of economic preferences for risk and ambiguity. NeuronYear: 2006;49:765–7516504951
16. Meyer G,Hauffa BP,Schedlowski M,et al. Casino gambling increases heart rate and salivary cortisol in regular gamblers. Biol PsychiatryYear: 2000;48:948–5311074233
17. Djamshidian A,Jha A,O'Sullivan S,et al. Risk and learning in impulsive and non impulsive patients with Parkinson's disease. Mov DisordYear: 2010;25:2203–1020721918
18. Gibb WR,Lees AJ. The relevance of the Lewy body to the pathogenesis of idiopathic Parkinson's disease. J Neurol Neurosurg PsychiatryYear: 1988;51:745–522841426
19. Voon V,Potenza MN,Thomsen T. Medication-related impulse control and repetitive behaviors in Parkinson's disease. Curr Opin NeurolYear: 2007;20:484–9217620886
20. Lawrence AD,Evans AH,Lees AJ. Compulsive use of dopamine replacement therapy in Parkinson's disease: reward systems gone awry?Lancet NeurolYear: 2003;2:595–60414505581
21. Evans AH,Katzenschlager R,Paviour D,et al. Punding in Parkinson's disease: its relation to the dopamine dysregulation syndrome. Mov DisordYear: 2004;19:397–40515077237
22. Crawford JR,Henry JD. The positive and negative affect schedule (PANAS): construct validity, measurement properties and normative data in a large non-clinical sample. Br J Clin PsycholYear: 2004;43:245–6515333231
23. Van Cauter E,Kerkhofs M,Caufriez A,et al. A quantitative estimation of growth hormone secretion in normal man: reproducibility and relation to sleep and time of day. J Clin Endocrinol MetabYear: 1992;74:1441–501592892
24. Muller T,Muhlack S. Acute levodopa intake and associated cortisol decrease in patients with Parkinson disease. Clin NeuropharmacolYear: 2007;30:101–617414942
25. Mondelli V,Dazzan P,Hepgul N,et al. Abnormal cortisol levels during the day and cortisol awakening response in first-episode psychosis: the role of stress and of antipsychotic treatment. Schizophr ResYear: 2010;116:234–4219751968
26. Siri C,Cilia R,De Gaspari D,et al. Cognitive status of patients with Parkinson's disease and pathological gambling. J NeurolYear: 2010;257:247–5219727901
27. Housden CR,O'Sullivan SS,Joyce EM,et al. Intact reward learning but elevated delay discounting in Parkinson's disease patients with impulsive-compulsive spectrum behaviors. NeuropsychopharmacologyYear: 2010;35:2155–6420631686
28. Ramirez J. Hormones and aggression in childhood and adolescence. Aggress Violent BehavYear: 2003;8:621–44
29. Bergman B,Brismar B. Hormone levels and personality traits in abusive and suicidal male alcoholics. Alcohol Clin Exp ResYear: 1994;18:311–168048732
30. Susmann E. Psychobiology of persistent antisocial behavior: Stress, early vulnerabilities and the attenuation hypothesis. Neurosci Biobehav RevYear: 2006;30:376–8916239030
31. Pajer K,Gardner W,Rubin RT,et al. Decreased cortisol levels in adolescent girls with conduct disorder. Arch Gen PsychiatryYear: 2001;58:297–30211231837
32. Susmann E. Cortisol and alpha amylase reactivity and timing of puberty: Vulnerabilities for antisocial behaviour in young adolescents. PsychoneuroendocrinologyYear: 2010;35:557–6919819639
33. van Honk J,Schutter DJ,Hermans EJ,et al. Low cortisol levels and the balance between punishment sensitivity and reward dependency. NeuroreportYear: 2003;14:1993–614561936
34. Takahashi T. Cortisol levels and time-discounting of monetary gain in humans. NeuroreportYear: 2004;15:2145–715486498
35. Voon V,Pessiglione M,Brezing C,et al. Mechanisms underlying dopamine-mediated reward bias in compulsive behaviors. NeuronYear: 2010;65:135–4220152119
36. Rossi M,Gerschcovich ER,de Achaval D,et al. Decision-making in Parkinson's disease patients with and without pathological gambling. Eur J NeurolYear: 2010;17:97–10219780806
37. Schmitt LH,Harrison GA,Spargo RM. Variation in epinephrine and cortisol excretion rates associated with behavior in an Australian Aboriginal community. Am J Phys AnthropolYear: 1998;106:249–539637187
38. Franco C,Paris JJ,Wulfert E,et al. Male gamblers have significantly greater salivary cortisol before and after betting on a horse race, than do female gamblers. Physiol BehavYear: 2010;99:225–919683542
39. Meyer G,Schwertfeger J,Exton MS,et al. Neuroendocrine response to casino gambling in problem gamblers. PsychoneuroendocrinologyYear: 2004;29:1272–8015288706
40. Coates JM,Herbert J. Endogenous steroids and financial risk taking on a London trading floor. Proc Natl Acad Sci U S AYear: 2008;105:6167–7218413617
41. Erickson K,Drevets W,Schulkin J. Glucocorticoid regulation of diverse cognitive functions in normal and pathological emotional states. Neurosci Biobehav RevYear: 2003;27:233–4612788335
42. Kirschbaum C,Wust S,Strasburger CJ. 'Normal' cigarette smoking increases free cortisol in habitual smokers. Life SciYear: 1992;50:435–421734161
43. Deroche V,Piazza PV,Deminiere JM,et al. Rats orally self-administer corticosterone. Brain ResYear: 1993;622:315–208242374
44. Sarnyai Z,Mello NK,Mendelson JH,et al. Effects of cocaine on pulsatile activity of hypothalamic-pituitary-adrenal axis in male rhesus monkeys: neuroendocrine and behavioral correlates. J Pharmacol Exp TherYear: 1996;277:225–348613924
45. Heesch CM,Negus BH,Keffer JH,et al. Effects of cocaine on cortisol secretion in humans. Am J Med SciYear: 1995;310:61–47631644

Figures

[Figure ID: fig1]
Figure 1 

Schematic outline of the time course of saliva samples. Ten samples were taken from Parkinson's disease (PD) patients prior to medication (‘off’) and after medication (‘on’). Five samples were obtained from controls.



[Figure ID: fig2]
Figure 2 

(A) Diurnal cortisol levels of all three groups. (B) Cortisol levels between Parkinson's disease patients without (PD−ICB) and with (PD+ICB) impulsive compulsive behaviour. All values are mean (±1 SE). Although not significantly different, baseline morning cortisol levels were lower in the PD+ICB group.



[Figure ID: fig3]
Figure 3 

Log scores of diurnal salivary cortisol levels in controls and in patients with Parkinson's disease without (PD−ICB) and with (PD+ICB) impulsive compulsive behaviour. Box plot showing the median (horizontal line) within a box containing the central 50% of the observations (ie, the upper and lower limits of the box are the 75th and 25th percentiles). Outliners are shown as a circle symbol. *Significant difference.



Tables
[TableWrap ID: tbl1] Table 1 

Characteristics of patients and healthy controls


Control group PD−ICB group PD+ICB group t value, F value, χ2 p Value
Participants in total (n) 14 13 15
Gender (male) 6 11 10 χ2=5.2, df=2 0.075
Age (years)
 At time of testing 58±3 64±2 56±3 F=2.5, df=2 0.09
 At disease onset 52±2 43±3 t=2.6, df=24 0.014*
Disease duration (years) 11±2 12±2 t=0.4, df=24 0.7
Pathological gambling 9
Hypersexuality 6
Compulsive shopping 5
Binge eating 4
Punding 2
Morning L-dopa dose (mg) 170±22 185±25 t=0.4, df=24 0.6
Total L-dopa dose (mg) 580±74 625±100 t=0.3, df=24 0.7
LEU dose (mg) 722±85 797±100 t=0.5, df=24 0.6
DA (patients) 8 5 χ2=1.6, df=1 0.2
UPDRS off medication 25±1 32±4 t=1.9, df=24 >0.07
UPDRS on 14±2 19±3 t=1.8, df=24 0.08
Average improvement in UPDRS (%) 44 41

All values are mean±SEM.

*Significant difference.

DA, dopamine agonists; ICB, impulsive compulsive behaviour; LEU, L-dopa equivalent units; PD, Parkinson's disease; UPDRS, Unified Parkinson's Disease Rating Scale.



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