The Effects of a Socially Evaluated Cold Press Stressor on Inhibitory Gating in Persons With Parkinson’s Disease

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The Effects of a Socially Evaluated Cold Press Stressor on Inhibitory Gating in Persons With Parkinson’s Disease

https://doi.org/10.21203/rs.3.rs-4965100/v1

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Impaired inhibitory gating is a sensory processing symptom of Parkinson’s disease (PD) associated with common motor symptoms, such as bradykinesia and motor inhibition. Acute stress impairs inhibitory gating in healthy adults; however, it is unclear how stress impacts inhibitory gating in people with PD. Using a Socially Evaluated Cold Pressor (SECP) to induce acute stress, inhibitory gating was assessed through electroencephalography (EEG) in fifteen individuals diagnosed with PD in the mild to moderate range of symptom severity by measuring the p50 ratio (S1/S2) during an auditory paired click paradigm, relative to age- and gender-matched healthy older adults (HOAs). Results confirmed decreased inhibitory gating in both persons with PD and HOAs following the induction of an acute stressor. Persons with PD experienced greater, though insignificant, S1 and S2 amplitudes than HOAs with a medium-to-large effect size in the condition by group interaction (ηp² = 0.104). These findings provide evidence to suggest that PD may also affect early auditory processing, possibly through over-compensation of the reticular activating system. However, interpretations are limited to eight individuals with PD and fifteen HOAs. Future research should examine the relationship between stress and sensory functioning on motor symptoms and cognition in persons with PD to unlock potential clinical targets for therapeutics.

Biological sciences/Neuroscience/Cognitive neuroscience

Biological sciences/Neuroscience/Sensory processing

Biological sciences/Physiology

Biological sciences/Physiology/Ageing

Biological sciences/Neuroscience

Biological sciences/Neuroscience/Diseases of the nervous system/Parkinsons disease

Parkinson’s disease

Stress

Inhibitory Gating

p50

paired click

Motor impairments such as tremor, bradykinesia, rigidity are hallmark symptoms of Parkinson’s disease (PD). However, in addition to motor symptoms, persons with PD also have a number of secondary non-motor symptoms, including sensory processing impairments (Boecker et al., 1999, Gulberti, et al., 2015; Kaji, 2001; Patel, Jankovic, & Hallett, 2014; Teo et al., 1997). One sensory processing impairment seen in persons with PD is reduced inhibitory gating (Gulberti, et al., 2015; Lukhanina, et al., 2009; Lukhanina, Berezetskaya, & Karaban, 2011; Teo et al., 1997), which has been associated with motor symptoms such as bradykinesia (Lukhanina, et al., 2011). Inhibitory gating is a natural pre-attentional sensory process that filters out repetitive information (Buotros & Belger, 1999; Gjini, Arfken, & Boutros, 2010). Acute stress has been shown to negatively impact inhibitory gating in heathy adults (Ermutlu, Karamürsel, Ugur, Senturk, & Gokhan, 2005; Johnson & Adler, 1993; White & Yee, 1997). However, it is unknown how stress impacts inhibitory gating in persons with PD.

While there is no consensus about the brain regions involved in inhibitory gating, most studies find that the prefrontal, somatosensory, supplementary motor, anterior cingulate, parietal, and thalamic areas are involved (Boutros, Gjini, Eickhoff, Urbach, & Pflieger, 2013; Garcia-Rill, et al., 2008; Grunwald, et al., 2003; Korzyukov et al., 2007; Tregellas et al., 2007; Williams, Nuechterlein, Subotnik, & Yee, 2011). Although the basal ganglia has not been directly implicated in inhibitory gating, evidence suggests it is also involved. For example, the basal ganglia modulates sensory information (Juri, Rodriquez-Oroz, & Obeso, 2011) and is functionally connected to prefrontal and parietal regions via subcortical loops (McHaffie, Stanford, Stein, Coizet, & Redgrave, 2005). Furthermore, impaired gating is seen in disorders of the basal ganglia such as PD, Huntington’s disease, and focal dystonia (Gulberti, et al., 2015; Teo et al., 1997; Lim, Bradshaw, Nicholls, & Altenmueller, 2005; Uc, Skinner, Rodnitzsky, & Garcia-Rill, 2003). Additionally, involvement of the basal ganglia is also demonstrated by studies where subthalamic nucleus deep brain stimulation, and ablative pallidal surgery restore normal inhibitory gating in persons with PD (Gulberti, et al., 2015; Mohamed, Lacono, & Yamada, 1996, Teo, Rasco, Skinner, & Garcia-Rill, 1998). Overall, this evidence suggests the basal ganglia and sensorimotor loop are involved in inhibitory gating, and that inhibitory gating is associated with the proper functioning of sensory and motor processes.

Inhibitory gating is modulated by key neurotransmitters such as norepinephrine. For example, inhibitory gating has an inverted-U shaped relationship with norepinephrine, where both agonists and antagonists have been shown to disrupt normal gating (Adler, et al., 1991; Stevens, Meltzer, & Rose, 1993). Additionally, acute stressors impair inhibitory gating, proposedly by increasing the release of norepinephrine (Ermutlu et al., 2005; Johnson & Adler, 1993). Persons with PD suffer cellular loss in the locus coeruleus, a region that produces and projects norepinephrine (Vermeiren & De Deyn, 2017), and thus impaired gating in persons with PD might be mediated by low levels of norepinephrine. However, it remains unknown how acute stress will impact inhibitory gating in persons with PD. Thus, the main purpose of this study is to examine how an acute stressor [Socially Evaluated Cold Pressor (SECP)] impacts inhibitory gating (p50 ratio) in persons with PD. Given the aforementioned gaps in knowledge, we hypothesize that the SECP task will impair inhibitory gating in both persons with PD and healthy older adults (HOAs).

Participants

Fifteen participants diagnosed with idiopathic PD (mean age 67.8 ± 4.7 years; 5 males and 10 females), and fifteen age- and gender-matched HOAs (mean age 68.7 ± 5.0 years) completed this study (Table 1). Participants with PD were recruited via the Iowa State University Alternative Medicine and Music for PD Lab Database, which consists of a list of individuals diagnosed with PD who have indicated interest in research opportunities. HOAs were recruited via word of mouth. The primary inclusion criterion for this group was being between the ages of 50 and 80 (the average age range of a person with PD) (Wirdefeldt et al., 2011). Participants with PD needed to have been diagnosed with PD by a neurologist. Participants were excluded if they demonstrated any cognitive impairment (Mini-Mental Status Exam < 25). Participants were further excluded if they had: 1) severe hearing loss; 2) any metallic objects in the head (outside the mouth); 3) any implanted objects such as a pacemaker; 4) brain surgery; 5) been diagnosed with a mental disorder besides anxiety or depression; 6) any musculoskeletal disorders; 7) any other brain-related conditions; 8) were pregnant or taking birth control; 9) used tobacco, illicit drugs, or excessive amounts of alcohol; 10) had either a systolic blood pressure (SBP) above 140 mmHg or a diastolic blood pressure above 90 mmHg during the initial screening. One HOA was excluded during the initial blood pressure screening to avoid any potential cardiac events during the SECP. All participants provided written informed consent. All procedures were approved by the Iowa State University Institutional Review Board (approval #: 15–499) and were performed in accordance with relevant guidelines and regulations.

Procedure

Participants were scheduled for two lab visits within a one-week timespan. During the initial visit, participants were screened for cognitive impairment with the Mini-Mental Status Exam (MMSE) and high blood pressure using an automated Omron blood pressure cuff. Of note no participants scored less than 28 (out of 30) on the MMSE, however the ability of the MMSE to distinguish individuals with mild cognitive impairment (MCI) is poor and some participants might have been in the early stages of cognitive decline. Participants then provided demographic information and completed a battery of questionnaires that have been found to be reliable and valid measures for persons with PD including the Geriatric Depression Scale (GDS) (Ertan, Ertan, Kızıltan, & Uygucgil, 2005), and the State and Trait Anxiety Inventory (STAI) (Yang, et al., 2019). The Perceived Stress Scale (PSS) was also collected. While this scale has not been tested for its psychometric properties in persons with PD, it has been shown to be reliable and valid in older adults (Lee, 2012; Jiang, et al., 2017). Participants with PD also completed the Movement Disorders Society-Unified Parkinson’s Disease Rating Scale (MDS-UPDRS). Table 1 shows the means and standard deviations of demographic and questionnaire data.

Participants were reminded to adhere to dietary and medical restrictions prior to their second lab visit which included limiting their caffeine intake to one cup (8 oz.) of a caffeinated beverage finished at least 3 hours prior to the start of the second visit and refraining from alcoholic beverages during the 24 hours prior to the start of the second visit. If they were non-compliant with any of these restrictions, participants were asked to reschedule. All participants were also asked to eat 1–2 hours before the second visit. Participants with PD were asked to take their Parkinson’s medication 1 hour prior to the beginning of the second visit. The second visit was scheduled to align with their normal medication times. The second visit starting times were scheduled between 12PM and 3PM.

During the second visit, adherence to the dietary and medical restrictions and recommendations were reviewed to ensure compliance. Electroencephalogram (EEG) was then fitted on the participant (see methods below). Next, a salivary cortisol sample was collected and then the participants completed either the stress intervention (SECP) or the control intervention (warm water hand bath). The order was counter balanced. After completing either the stress task or the control task, blood pressure was obtained with an automated Omron blood pressure cuff. Then, they verbally reported how stressful they thought the task was on a Likert scale from 1 to 10, with respective response anchors of “not stressful at all”, and the “most stressful thing I can imagine”. Cortisol, blood pressure, and perceived stress were measured to assess the effectiveness of the stress and control interventions.

Participants then completed 80 trials of the paired click paradigm to examine inhibitory gating. Inhibitory gating is typically evaluated using a paired click paradigm where pairs of simple auditory stimuli elicit the EEG p50 auditory components (Lijffijt et al., 2009). During the paired-click paradigm, the first click is referred to as the S1 and is followed shortly thereafter by the second click or S2. The most common inhibitory gating measure is the S2/S1 ratio of the p50 component (p50 ratio) (Boutros & Belger, 1999; Guterman, Josiassen, & Bashore, 1992; Jones et al., 2016). The normal gating response is indicated by a low S2/S1 ratio, with a large amplitude response to S1 and a reduced amplitude response to S2.

Twenty-five minutes after completing the paired click paradigm, a salivary cortisol sample was collected from each participant. Following this, participants rested or read a magazine/book for half an hour. After the rest period, participants completed the same series of steps and tasks again with the uncompleted intervention (i.e., warm water bath or SECP). See Fig. 1 for the order of first and second visit procedures.

Stress and Control Tasks

The stress intervention was a SECP task where the participants placed their hand up to the wrist in an ice water bath (2–4° C) for 90 seconds. Participants were also made aware that this task was being video recorded and that their facial expressions were to be judged by trained experimenters at a later time. During the control condition, participants placed their hand in warm water (36–38°C) for 90 seconds. During the control condition participants were reminded that they were not being videotaped and the camera was moved out of sight.

EEG Data Acquisition and Analysis

The subjects were sitting comfortably in a semi-reclined armchair in a quiet well lit room. Participants were instructed to keep their movement to a minimum and their eyes open and focused on a piece of tape stuck to a desk 5 feet in front of them. Participants were also instructed to refrain from falling asleep.

To collect the potentials, a 64 electrode EEG cap was fitted according to the international 10–20 system (Biosemi, Amsterdam, Netherlands). Eye movements were monitored with electrodes placed above and below the right eye for filtering purposes. A single common reference electrode was placed over the mastoid process ipsilateral to the participants most affected side (HOAs were matched) and the ground electrode was placed on the forehead just above the nose and between the eyebrows. The electrode of interest was Cz, which is located in the midline at the ‘vertex’ or top of the head. Impedances were checked to make sure they are below 5k ohms prior to beginning the data collection. Signals were recorded at 2kHz and amplified. During the task, auditory clicks were presented through speakers at 80dB hearing level. The auditory stimuli were pairs of identical auditory clicks (1000-Hz tone) with a duration of 20ms and an interval of 500ms between clicks. 80 trials were presented with a 7 second interval between trials. The time for each recording epoch was 300ms before the first pair of clicks until 1s following the second click. The auditory tones were collected simultaneously by the EEG data collection system to ensure synchronization. Overall, these are the recommended methods for collecting the p50 response (Dalecki, Croft, & Johnstone, 2011).

EEG data were processed using standard methods from the Krigolson Laboratory (https://www.krigolsonlab.com/data-analysis.html). Signals were re-referenced offline using a bipolar montage (Cz-Iz) and filtered using a 0.5-45Hz 4th order dual-pass Butterworth band-pass and ^a 60Hz notch filter. Next, data was divided into smaller epochs (-200ms to 300ms) around each auditory tone. Finally, a trial was discarded if the voltage on any channel exceeded 10 µV/ms gradient and an absolute voltage difference > 100 µV.

The P50 ratio (S2/S1) was the measure of habituation (Dalecki et al., 2011). S1 (peak-to-peak method) was the difference in amplitudes in the positive deflection between 35–65ms and the most negative deflection between 15–45 ms of the first stimulus. S2 was the difference of those amplitudes for the second stimulus. In addition, latency measures were also calculated for S2 and S1where the latency value reflected the timing difference between the maximum positive deflection and the auditory stimulus. Due to technical difficulties, EEG was not collected for 4 of the participants with PD. A clear p50 component was interpretable in both the S1 and S2 in both conditions (SECP and control) for 19 participants (8 PD and 11 HOAs). These were entered for statistical analysis.

Cortisol Analysis

On the day of collection, salivary cortisol samples were stored in -20°C freezer within 30 minutes. Cortisol was analyzed with the Salimetrics® Cortisol Enzyme Immunoassy Kit (RRID AB_2801306). The kit uses a competitive immunoassay in which cortisol competes with cortisol conjugated to horseradish peroxidase for the antibody binding sites. To determine the cortisol reactivity, the area under the curve was calculated using the baseline and the 25 min post intervention samples for each condition.

Statistical Analysis

An independent samples t-test was used to examine any group differences on demographic and questionnaire outcome measures. A 2 condition (stress, control) x 2 group (PD, HOA) repeated measures ANOVA was completed for measures of stress (perceived stress, blood pressure, and cortisol) to confirm that the SECP initiated an increase in stress for participants. To test the hypothesis that the SECP task will impair inhibitory gating (higher p50 ratios) in both persons with PD and HOAs, a 2 condition (stress, control) x 2 group (PD, HOA) repeated measures ANOVA was used to determine differences on inhibitory gating (p50 ratio) and measures of early auditory processing (amplitude and latency of S1 and S2). For all repeated measures ANOVAs, partial eta squared (η_p²) effect sizes were calculated. Significance was set at α = 0.05. For all post hoc analyses, a Bonferroni correction was used to interpret statistical significance.

Table 2 shows the means and standard deviations for all stress related measures (perceived stress, blood pressure, and cortisol). Table 3 shows the means and standard deviations for all auditory processing measures.

Participants

Participants with PD had higher trait anxiety than the HOAs (t₍₂₈₎ = 3.086, p = 0.005, Mean Difference (MD) = + 9.2, d = 1.126). No other demographic variables were significantly different (Table 1).

Perceived Stress

There was a main effect of condition (F_(1,28) = 147.393, p < 0.001, η_p² = 0.840). The participants found that the SECP was more stressful than the control condition (MD = + 5.2, d = 2.256). There was no main effect of group (F_(1,28) = 0.267, p = 0.609, η_p² = 0.009), or an interaction effects for group x condition (F_(1,28) = 0.006, p = 0.938, η_p² = 0.000).

Blood Pressure

There was a main effect of condition for both systolic (F_(1,28) = 8.003, p = 0.009, η_p² = 0.222) and diastolic blood pressure (F_(1,28) = 5.543, p = 0.026, η_p² = 0.165). The participants had higher systolic blood pressure after the SECP compared to the control condition (MD = + 6.4 mmHg, d = 0.518). Participants also had higher diastolic blood pressure after the SECP compared to the control condition (MD = + 2.8 mmHg, d = 0.430). There was no main effect of group for systolic blood pressure (F_(1,28) = 2.138, p = 0.155, η_p² = 0.071) or diastolic blood pressure (F_(1,28) = 0.360, p = 0.553, η_p² = 0.013). There were no interaction effects of group x condition for systolic blood pressure (F_(1,28) = 0.889, p = 0.354; η_p² = 0.031) or diastolic blood pressure (F_(1,28) = 0.767, p = 0.388; η_p² = 0.027)).

Cortisol

There was a main effect of condition for cortisol (F_(1,28) = 6.780, p = 0.015 η_p² = 0.195). Participants had a higher cortisol area under the curve (AUC) values during the SECP compared to the control condition (MD = + 13.4 ng/dl/hr, d = 0.479). There was no main effect of group (F_(1,28) = 0.187, p = 0.699, η_p² = 0.007) and no interaction effects for group x condition (F_(1,28) = 0.596, p = 0.447, η_p² = 0.021).

Inhibitory Gating

Figure 2A shows the results for inhibitory gating (see Fig. 2B for EEG waveform from one person with PD in both conditions). Results revealed a main effect of condition (F_(1,17) = 12.813, p = 0.002, η_p² = 0.430). In general, there was less inhibitory gating following the SECP compared to the control condition (MD = + 0.20, d = 0.760). No main effect of group (F_(1,17) = 0.736, p = 0.403, η_p² = 0.042) or interaction effects for condition x group (F_(1,17) = 1.971, p = 0.178, η_p² = 0.104) were found.

Early Auditory Components

Figure 2C and 2D show the results for S1 amplitude and S2 amplitude. No main effects of condition were found [S1 amplitude (F_(1,17) = 0.261, p = 0.616, η_p² = 0.015 ); S2 amplitude (F_(1,17) = 1.527, p = 0.233, η_p² = 0.082))]. However, there was a group trend for S1 amplitude (F_(1,17) = 3.560, p = 0.076, η_p² = 0.173), and S2 amplitude (F_(1,17) = 4.109, p = 0.059, η_p² = 0.195). Persons with PD had a greater S1 amplitude (MD = + 4.1 µV, d = 0.672) and S2 amplitude (MD = + 3.0 µV, d = 0.675) than HOAs. No condition x group interactions were found [S1 amplitude (F_(1,17) = 0.206, p = 0.656, η_p² = 0.012 ); S2 amplitude (F_(1,17) = 0.376, p = 0.548, η_p² = 0.022)].

This present study aimed to test the effects of SECP on inhibitory gating in persons with PD. The results revealed that the SECP was successful in increasing stress related measures (perceived stress, blood pressure, and cortisol) and decreasing inhibitory gating in both HOAs and persons with PD. While not significant, the SECP decreased inhibitory gating to a greater degree in persons with PD (MD = + 0.293) compared to HOAs (MD = + 0.127), with the condition by group interaction showing a medium to large effect size (η_p² = 0.104). Similar to previous research (Teo et al., 1997), the results also showed that persons with PD had larger (albeit not significantly different), S1 and S2 amplitudes, suggesting that PD may also affect early auditory processing.

During the control condition, persons with PD and HOAs had similar inhibitory gating ratios, and stress decreased inhibitory gating in both groups. While not statistically significant, there was a medium to large condition by group interaction effect size (η_p² = 0.104), where the stress condition resulted in a decrease in inhibitory gating in persons with PD that was more than double what was observed in the HOAs. This suggests that in persons with PD, stress may impair inhibitory gating to a greater degree.

The negative impact stress has on inhibitory gating in persons with PD has several clinical implications including deleterious effects on motor, cognitive, and sensory functioning.

Inhibitory gating is associated with PD motor symptoms such as motor inhibition as well as bradykinesia (Cheng, et al., 2016; Liu, Xiao, Shi, & Zhao, 2011; Lukhanina et al., 2011; Yadon, et al., 2009). Two likely mechanisms associated with this motor impairment due to reduced inhibitory gating include 1) increased sensory overload, which may impair cognitive functioning by competing for limited cognitive resources (Croft, Lee, Bertolot, & Gruzelier, 2001; Desimone & Duncan, 1995; Yadon, et al., 2009); and 2) disrupting sensory processes that might contribute to motor impairments (Chudler & Dong, 1995; Conte, Khan, Defazio, Rothwell, & Berardelli, 2013; Konczak et al., 2009; Müller, et al., 2013; Nieuwboer & Giladi, 2013). Thus, stress has the potential to negatively impact PD motor symptoms via its negative impact on cognitive and sensory functions.

One important consideration in interpreting the results of this study is the stage of PD progression. As previously stated, persons with PD and HOAs had similar inhibitory gating ratios during the control condition. This was not completely unexpected as our sample of persons with PD were in the mild to moderate stages of disease severity (Hoehn and Yahr (H&Y) = 2.3). While, previous research demonstrated that compared to HOAs persons with PD have greater impairment in inhibitory gating (Teo et al., 1997), those differences were driven by individuals with PD who were in the later stages of the disease (H&Y = 4 & 5). It may be the stage of the PD modulates how stress impacts inhibitory gating due to greater degeneration in various parts of the brain (e.g. locus coeruleus, prefrontal cortex, basal ganglia, etc.). For example, individuals in the later stages of PD are likely to have impaired inhibitory gating in non-stressful conditions, while their inhibitory gating under stress might be differentially impacted.

Consistent with other studies that observed larger auditory event-related potentials in persons with PD (Gulberti et al., 2015; Tanaka et al., 2000; Teo et al. 1997), there was a trend (p < 0.1) for p50 amplitudes to be greater in persons with PD. This may suggest an over-activation of the ascending cholinergic reticular activating system within persons with PD (Skinner, Miyazato, & Garcia-Rill, 2002; Teo, et al., 1997). This over-activation is thought to be a compensatory mechanism to attenuate cognitive and motor deficits due to nigrostriatal dopamine loss (Bohnen et al., 2015; Kucinski, de Jong, & Sarter, 2017). Thus, the auditory p50 amplitude may be a useful biomarker to examine the interaction between dopaminergic and cholinergic systems in persons with PD. However, it is important to note that the effect of the stress on p50 amplitudes was not statistically significant, suggesting that the SECP had a greater impact on the gating of S2, and less of an impact the auditory event-related potentials mediated by the ascending reticular activating system.

Limitations

While our sample size was large enough to support our initial hypothesis that the SECP reduced inhibitory gating in both HOAs and persons with PD, we were likely underpowered to find a group by condition interaction. However, the effect sizes suggested that stress reduces inhibitory gating in individuals with PD to a greater degree. Another limitation is that our participants with PD had greater trait anxiety levels than our HOAs (as measured by the STAI2), while unknown this could potentially impact their inhibitory gating responses to an acute stressor. Finally, the potential mechanisms, mediating neurotransmitters, and motor symptoms discussed as having been associated with inhibitory gating were not assessed and future studies are needed to clarify how stress might impact these in persons with PD.

The acute SECP stressor decreased inhibitory gating in persons with PD and HOAs, and the decrease appeared to be larger in persons with PD. Moreover, a statistical trend (p < 0.1) for persons with PD to have larger S1 and S2 amplitudes was revealed, possibly suggesting an over-activation /compensation by the reticular activating system. Understanding the impact of stress and inhibitory gating in persons with PD has the potential to unlock important mechanisms and neuropharmacological targets for treatment. In the future, work will be expanded to assess the relationship between stress and inhibitory gating on motor symptoms as well as cognition in persons with PD.

Competing Interests:

None.

Data Availability

Data is available upon request from the corresponding author.

Funding Source:

None

Author Contribution

Lab: Alternative Medicine and Music for Parkinson’s Disease Lab, Department of Kinesiology, Iowa State UniversityAZ: Conception and design of the work, acquisition, analysis, and interpretation of data, drafting of manuscriptCJ: Drafting of manuscriptPI: Critical revision of workELS: Conception and design of the work, interpretation of data, critical revision of work

Data Availability

Data Availability: Data is available upon request from the corresponding author.

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Additional & Information.

Table 1

Demographic and Questionnaire Information Means and standard deviations for all demographic measures, and cognitive questionnaires. For between subjects comparisons **p < 0.01. HOA; healthy older adult; PD: Parkinson’s disease; Movement Disorder Society - Unified Parkinson’s Disease Rating Scale: MDS - UPDRS; H&Y: Hoehn and Yahr; MMSE: Mini-Mental Status Exam; MOCA: Montreal Cognitive Assessment; GDS: Geriatric Depression Scale; PSS: Perceived Stress Scale; STAI1: State and Trait Anxiety Inventory (State); STAI2: State and Trait Anxiety Inventory (Trait).
	PD	HOA
Age (Years)	67.8 ± 4.7	68.7 ± 5.0
Gender (% Male)	33.3 ± 50.0	33.3 ± 50.0
MDS - UPDRS	66.9 ± 5.8	N/A
H&Y	2.3 ± 0.1	N/A
Years Diagnosed	9.9 ± 1.7	N/A
MMSE	29.3 ± 0.7	29.7 ± 0.6
GDS	6.5 ± 4.5	3.8 ± 3.7
PSS	13.5 ± 5.6	9.2 ± 6.6
STAI1	33.3 ± 8.5	28 ± 10.9
STAI2**	38.3 ± 8.7	29.1 ± 7.6

Table 2

Stress Measures Means and standard deviations for all measures of stress for both groups and both conditions. For a main effect of condition *p < 0.05, **p < 0.01, ***p < 0.001. DBP: Diastolic blood pressure; HOA: healthy older adult; PD: persons with Parkinson’s disease; SBP: Systolic blood pressure.
Table 2
	PD Control	HOA Control	PD SECP	HOA SECP
Perceived Stress***	1.20 ± 0.56	1.00 ± 0.00	6.40 ± 2.53	6.13 ± 2.27
SBP (mmHg)**	121.3 ± 13.0	130.5 ± 16.2	129.7 ± 15.4	134.7 ± 13.8
DBP (mmHg)*	75.6 ± 9.3	74.9 ± 8.0	79.5 ± 8.7	76.7 ± 8.3
Cortisol (ng/dl/hr)*	66.7 ± 26.4	58.8 ± 23.2	76.1 ± 27.0	76.3 ± 34.2

Table 3

p50 Measures Means and standard deviations for all p50 measures for both groups and both conditions. For a main effect of condition, **p < 0.01. HOA: healthy older adult; PD: Parkinson’s disease; S1: stimulus 1; S2: stimulus 2.
Table 3
	PD Control	HOA Control	PD SECP	HOA SECP
p50 Ratio**	0.61 ± 0.28	0.60 ± 0.12	0.90 ± 0.47	0.72 ± 0.16
S1Amplitude (µV)	10.42 ± 5.73	6.04 ± 2.86	9.82 ± 7.56	6.01 ± 3.00
S2 Amplitude (µV)	6.31 ± 4.27	3.71 ± 2.16	7.59 ± 5.50	4.14 ± 2.00

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The Effects of a Socially Evaluated Cold Press Stressor on Inhibitory Gating in Persons With Parkinson’s Disease

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Introduction

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Participants

Procedure

Stress and Control Tasks

EEG Data Acquisition and Analysis

Cortisol Analysis

Statistical Analysis

Results

Participants

Perceived Stress

Blood Pressure

Cortisol

Inhibitory Gating

Early Auditory Components

Discussion

Limitations

Conclusion

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