Taste responses in patients with Parkinson’s disease
01 Jan 2005-Journal of Neurology, Neurosurgery, and Psychiatry (J Neurol Neurosurg Psychiatry)-Vol. 76, Iss: 1, pp 40-46
TL;DR: Perceived intensity, pleasantness, and identification of the sucrose, quinine, citric acid, or sodium chloride samples did not differ between the PD patients and controls, and patients with PD may present enhanced taste acuity in terms of electrogustometric threshold.
Abstract: Objective: Preclinical studies indicate that dopaminergic transmission in the basal ganglia may be involved in processing of both pleasant and unpleasant stimuli. Given this, the aim of the present study was to assess taste responses to sweet, bitter, sour, and salty substances in patients with Parkinson's disease (PD).
Methods: Rated intensity and pleasantness of filter paper discs soaked in sucrose (10–60%), quinine (0.025–0.5%), citric acid (0.25–4.0%), or sodium chloride (1.25–20%) solutions was evaluated in 30 patients with PD and in 33 healthy controls. Paper discs soaked in deionised water served as control stimuli. In addition, reactivity to 100 ml samples of chocolate and vanilla milk was assessed in both groups. Taste detection thresholds were assessed by means of electrogustometry. Sociodemographic and neuropsychiatric data, including cigarette smoking, alcohol consumption, tea and coffee drinking, depressive symptoms, and cognitive functioning were collected.
Results: In general, perceived intensity, pleasantness, and identification of the sucrose, quinine, citric acid, or sodium chloride samples did not differ between the PD patients and controls. Intensity ratings of the filter papers soaked in 0.025% quinine were significantly higher in the PD patients compared with the control group. No inter-group differences were found in taste responses to chocolate and vanilla milk. Electrogustometric thresholds were significantly (p = 0.001) more sensitive in the PD patients.
Conclusions: PD is not associated with any major alterations in responses to pleasant or unpleasant taste stimuli. Patients with PD may present enhanced taste acuity in terms of electrogustometric threshold.
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TL;DR: Dopamine’s contribution appears to be chiefly to cause ‘wanting’ for hedonic rewards, more than ‘liking’ or learning for those rewards.
Abstract: Introduction
Debate continues over the precise causal contribution made by mesolimbic dopamine systems to reward. There are three competing explanatory categories: ‘liking’, learning, and ‘wanting’. Does dopamine mostly mediate the hedonic impact of reward (‘liking’)? Does it instead mediate learned predictions of future reward, prediction error teaching signals and stamp in associative links (learning)? Or does dopamine motivate the pursuit of rewards by attributing incentive salience to reward-related stimuli (‘wanting’)? Each hypothesis is evaluated here, and it is suggested that the incentive salience or ‘wanting’ hypothesis of dopamine function may be consistent with more evidence than either learning or ‘liking’. In brief, recent evidence indicates that dopamine is neither necessary nor sufficient to mediate changes in hedonic ‘liking’ for sensory pleasures. Other recent evidence indicates that dopamine is not needed for new learning, and not sufficient to directly mediate learning by causing teaching or prediction signals. By contrast, growing evidence indicates that dopamine does contribute causally to incentive salience. Dopamine appears necessary for normal ‘wanting’, and dopamine activation can be sufficient to enhance cue-triggered incentive salience. Drugs of abuse that promote dopamine signals short circuit and sensitize dynamic mesolimbic mechanisms that evolved to attribute incentive salience to rewards. Such drugs interact with incentive salience integrations of Pavlovian associative information with physiological state signals. That interaction sets the stage to cause compulsive ‘wanting’ in addiction, but also provides opportunities for experiments to disentangle ‘wanting’, ‘liking’, and learning hypotheses. Results from studies that exploited those opportunities are described here.
2,161 citations
Cites background from "Taste responses in patients with Pa..."
...…have been reported to have normal subjective pleasure ratings for sweet food rewards: the “perceived pleasantness of the sweet samples (sucrose, chocolate milk, and vanilla milk) did not differ between the PD (Parkinson’s disease patients) and control group” (Sienkiewicz-Jarosz et al. 2005, p. 44)....
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...For example, patients with the dopamine deterioration of Parkinson’s disease have been reported to have normal subjective pleasure ratings for sweet food rewards: the “perceived pleasantness of the sweet samples (sucrose, chocolate milk, and vanilla milk) did not differ between the PD (Parkinson’s disease patients) and control group” (Sienkiewicz-Jarosz et al. 2005) p....
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TL;DR: Human neuroimaging studies indicate that surprisingly similar circuitry is activated by quite diverse pleasures, suggesting a common neural currency shared by all.
996 citations
Cites background from "Taste responses in patients with Pa..."
...Closer inspection has suggested that many of these patients may not be anhedonic any more than Parkinson’s patients: at least sensory pleasures may persist virtually intact (Barch et al., 2014; Dowd and Barch, 2010; Sienkiewicz-Jarosz et al., 2005; Treadway and Zald, 2011)....
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TL;DR: Along with prefrontal cortex and the amygdala, nucleus accumbens is a component of the brain circuitry regulating effort-related functions and may have implications for understanding drug abuse, as well as energy-related disorders such as psychomotor slowing, fatigue, or anergia in depression.
Abstract: Background
Over the last several years, it has become apparent that there are critical problems with the hypothesis that brain dopamine (DA) systems, particularly in the nucleus accumbens, directly mediate the rewarding or primary motivational characteristics of natural stimuli such as food. Hypotheses related to DA function are undergoing a substantial restructuring, such that the classic emphasis on hedonia and primary reward is giving way to diverse lines of research that focus on aspects of instrumental learning, reward prediction, incentive motivation, and behavioral activation.
962 citations
Cites background from "Taste responses in patients with Pa..."
...Parkinson’s disease was not found to be associated with alterations in the perceived pleasantness of taste stimuli (Sienkiewicz-Jarosz et al. 2005)....
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TL;DR: This work discusses how mesocorticolimbic mechanisms generate the motivation component of incentive salience, and addresses the neurobiological state factors that participate to control generation of incentive Salience.
Abstract: Reward contains separable psychological components of learning, incentive motivation and pleasure. Most computational models have focused only on the learning component of reward, but the motivational component is equally important in reward circuitry, and even more directly controls behavior. Modeling the motivational component requires recognition of additional control factors besides learning. Here I discuss how mesocorticolimbic mechanisms generate the motivation component of incentive salience. Incentive salience takes Pavlovian learning and memory as one input and as an equally important input takes neurobiological state factors (e.g. drug states, appetite states, satiety states) that can vary independently of learning. Neurobiological state changes can produce unlearned fluctuations or even reversals in the ability of a previously learned reward cue to trigger motivation. Such fluctuations in cue-triggered motivation can dramatically depart from all previously learned values about the associated reward outcome. Thus, one consequence of the difference between incentive salience and learning can be to decouple cue-triggered motivation of the moment from previously learned values of how good the associated reward has been in the past. Another consequence can be to produce irrationally strong motivation urges that are not justified by any memories of previous reward values (and without distorting associative predictions of future reward value). Such irrationally strong motivation may be especially problematic in addiction. To understand these phenomena, future models of mesocorticolimbic reward function should address the neurobiological state factors that participate to control generation of incentive salience.
599 citations
Cites background from "Taste responses in patients with Pa..."
...(ii) Likewise, normal pleasure ratings are given to sweet tastes by Parkinson’s patients who have extensive dopamine depletion (Sienkiewicz-Jarosz et al., 2005), and normal pleasure ratings are given to cocaine by normal people who are in a drug-induced state of dopamine depletion or blockade…...
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TL;DR: Current knowledge and future prospects of weight loss and malnutrition in the context of PD are presented to appeal clinicians and researchers to pay a closer attention to this phenomena and enable better management and therapeutic strategies in future clinical practice.
Abstract: Parkinson's Disease (PD) is currently considered a systemic neurodegenerative disease manifested with not only motor but also non-motor symptoms. In particular, weight loss and malnutrition, a set of frequently neglected non-motor symptoms, are indeed negatively associated with the life quality of PD patients. Moreover, comorbidity of weight loss and malnutrition may impact disease progression, giving rise to dyskinesia, cognitive decline and orthostatic hypotension, and even resulting in disability and mortality. Nevertheless, the underlying mechanism of weight loss and malnutrition in PD remains obscure and possibly involving multitudinous, exogenous or endogenous, factors. What is more, there still does not exist any weight loss and malnutrition appraision standards and management strategies. Given this, here in this review, we elaborate the weight loss and malnutrition study status in PD and summarize potential determinants and mechanisms as well. In conclusion, we present current knowledge and future prospects of weight loss and malnutrition in the context of PD, aiming to appeal clinicians and researchers to pay a closer attention to this phenomena and enable better management and therapeutic strategies in future clinical practice.
328 citations
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