Anhedonia in Japanese patients with Parkinson's disease: analysis using the Snaith-Hamilton Pleasure Scale

Background

Anhedonia, a lowered ability to experience physical or social pleasure, has recently been recognized as a non-motor symptom of Parkinson's disease.

Objective

To identify the frequency of anhedonia and the factors influencing hedonic tone in Japanese patients with Parkinson's disease.

Patients and methods

We recruited 86 consecutive outpatients with a clinical diagnosis of PD attending two Japanese hospitals (one university hospital and one community hospital) in February 2010. We used the self-rating Snaith–Hamilton Pleasure Scale (SHAPS) translated into Japanese language from the original English version to assess and quantify hedonic tone as a subjectively experienced phenomenon. We studied the association of anhedonia with the variables age, age at onset, gender, disease duration, disease severity and antiparkinsonian drugs.

Results

Thirty-nine patients (45%) were male and 47 (55%) were female. Mean age was 72.01 ± 9.07 (49–89) years, with mean age at onset of 64.93 ± 11.42 (31–88) years. Mean disease duration was 7.20 ± 5.54 (1–23) years. The mean Hoehn and Yahr scale was 2.76 ± 0.78. The mean SHAPS score of the total sample was 1.19 ± 1.86. The SHAPS score of 14 patients (16.3%) was 3 or more, indicating anhedonia. The mean SHAPS score was lower in patients taking pramipexole (0.58 ± 0.97) than in patients not taking pramipexole (1.57 ± 2.16). Multiple linear regression analysis identified pramipexole as a significant negative influencing factor on the SHAPS score, while disease severity and entacapone treatment were identified as positive influencing factors. The age, onset age, gender, disease duration, and use of pergolide, amantadine, zonisamide, selegiline, anticholinergic agents and droxidopa did not significantly affect the SHAPS score.

Conclusion

Anhedonia is not rare non-motor symptom in Japanese patients with Parkinson's disease. This study suggests an anti-anhedonic property of pramipexole.     

Social deprivation stress is a triggering factor for the emergence of anxiety- and depression-like behaviours and leads to reduced brain BDNF levels in C57BL/6J mice

Stress is a main risk factor that can trigger psychiatric disorders, including anxiety and major depression. Neurotrophins, such as Brain-Derived Neurotrophic Factor (BDNF), have been identified as neuroendocrine effectors involved in the response to stress and in the neurobehavioural changes associated with depression. Aim of this paper was to study the relationship between neuroendocrine activation (circulating corticosterone and brain BDNF levels) and a wide array of depression- and anxiety-like behaviours (anhedonia, behavioural despair, generalised and social anxiety) resulting from exposure to chronic stress. To this end, 3-month-old C57BL/6J male mice were exposed to either chronic disruption of the social structure (SS), to a stable social structure (SG) or to social deprivation (SD), a condition lacking social stimuli. Results show that, despite not developing anhedonia (decreased preference for a sucrose solution), SD mice were characterised by increased emotionality and hypothalamic-pituitary-adrenal axis reactivity in addition to reduced BDNF levels. By contrast, SG and SS mice showed increased anhedonia accompanied by no alterations in the behavioural and neuroendocrine profile. The results here reported indicate that mice exposed to different social housing conditions use different behavioural strategies to cope with external challenges. In addition they suggest that social deprivation might represent a stressful condition triggering the emergence of both anxiety- and depression-like behaviours and clearly indicate BDNF as a main neurobiological variable mediating these responses.     

Childhood trauma is associated with elevated anhedonia and altered core reward circuitry in major depression patients and controls

Childhood trauma (CT) is a well‐established risk factor for major depressive disorder (MDD). However, the underlying mechanism linking CT and MDD remains not fully understood. The present study tested the hypothesis that CT have effects on specific types of anhedonia in depression via reward system. To do so, we evaluated different aspects of anhedonia and resting‐state functional connectivity (FC) in reward system among 66 patients with MDD (44 with moderate‐to‐severe and 22 with no or low CT), and 57 healthy controls (HC; 23 with moderate‐to‐severe and 34 with no or low CT). Results showed that MDD patients with moderate‐to‐severe CT suffered more severe state anhedonic depression than patients with no or low level of CT. Individuals with moderate‐to‐severe CT, irrespective of MDD diagnosis, had elevated physical, social and anticipatory but not consummatory trait anhedonia, and demonstrated decreased left nucleus accumbens (NAcc)‐right orbital frontal cortex (OFC) and left ventral caudate‐left OFC connectivity compared to those with no or low exposure. Left NAcc‐right OFC connectivity mediated relationship between CT and state anhedonia in MDD. The total altered ventral striatum (VS)‐OFC connectivity mediated links between CT and physical trait anhedonia in HC. These findings highlight specific types of anhedonia and the core reward system as targets of CT. Blunted hedonic responses via decreased coupling within core reward system may be involved in the mechanism of depression following CT. Implications for clinical interventions are also discussed.     

首发精神病患者快感缺失水平与认知功能的关系

目的 探讨首发精神病患者快感缺失水平及其与认知功能的关系,分析其认知功能的影响因素.方法 选取2016年12月-2019年3月在广州医科大学附属脑科医院就诊的符合《精神障碍诊断与统计手册(第5版)》(DSM-5)诊断标准的首发精神病患者143例.采用阳性和阴性症状量表(PANSS)评定患者的精神症状,以其中N2情绪退缩...     

首发精神分裂症患者快感缺乏的成分特征与相关因素

目的探索首发精神分裂症患者快感缺乏的成分特征及其与临床症状、认知功能和社会功能的相关性。方法纳入符合《国际疾病分类(第10版)》(ICD-10)诊断标准的31例首发精神分裂症患者和33例健康对照组。使用愉快情绪体验量表(TEPS)、阳性和阴性症状量表(PANSS)、重复性成套神经心理状态测验(RBANS)以及个人和社会功能量表(PSP)对患者的快感缺乏情况、精神症状、认知功能和社会功能进行评定。采用Pearson相关分析测查快感缺乏与临床症状、认知功能和社会功能的相关性。结果首发精神分裂症患者TEPS消费性快感评分低于健康对照组,差异有统计学意义[(27.71±5.48)分vs.(31.58±5.92)分,t=2.705,P=0.009]。相关分析显示,首发精神分裂症患者消费性快感缺乏与PANSS、RBANS和PSP评分的相关均无统计学意义(P均0.05)。结论首发精神分裂症患者存在消费性快感缺乏,其消费性快感缺乏可能独立于临床症状、认知功能损害和社会功能损害之外。     

Rats with congenital learned helplessness respond less to sucrose but show no deficits in activity or learning

Inbred rat strains for congenital learned helplessness (cLH) and for congenital resistance to learned helplessness (cNLH) were investigated as a model to study genetic predisposition to major depression. Congenitally helpless rats respond less to sucrose under a progressive ratio schedule. This is not confounded by locomotor hypoactivity: in contrast, cLH rats show a slight hyperactivity during the first 5 min of an open field test. cLH rats acquire operant responding to sucrose as readily as cNLH rats and exhibit normal memory acquisition and retrieval in the Morris water maze, thus ruling out general learning deficits as the cause of the decreased response to sucrose. Reduced total responses and reduced breaking points for sucrose in the cLH strain argue for anhedonia, which is an analogue to loss of pleasure essential for the diagnosis of major depressive episodes, and thus confirm the validity of congenitally learned helpless rats as a model of major depression.     

Amitifadine, a triple monoamine uptake inhibitor, reduces binge drinking and negative affect in an animal model of co-occurring alcoholism and depression symptomatology

The co-occurrence of alcoholism and depression is highly prevalent and difficult to treat. In an animal model of binge drinking that exhibits abstinence-induced behaviors reminiscent of negative affective states, the triple monoamine uptake inhibitor, amitifadine, produced a selective, dose dependent attenuation of binge drinking. Amitifadine also reversed abstinence-induced increases in the intracranial self-stimulation threshold, a model of anhedonia, and immobility in the forced swim test, reflecting behavioral despair. In view of the safety profile of amitifadine in humans, including low risk for weight gain, lack of sexual side effects, and low potential for abuse, we hypothesize that amitifadine will be effective in treating co-occurring alcoholism and depression.     

Anhedonia Following Early-Life Adversity Involves Aberrant Interaction of Reward and Anxiety Circuits and Is Reversed by Partial Silencing of Amygdala Corticotropin-Releasing Hormone Gene

Background

Anhedonia, the diminished ability to experience pleasure, is an important dimensional entity linked to depression, schizophrenia, and other emotional disorders, but its origins and mechanisms are poorly understood. We have previously identified anhedonia, manifest as decreased sucrose preference and social play, in adolescent male rats that experienced chronic early-life adversity/stress (CES). Here we probed the molecular, cellular, and circuit processes underlying CES-induced anhedonia and tested them mechanistically.

Neural activity and diurnal variation of cortisol: evidence from brain electrical tomography analysis and relevance to anhedonia

The medial prefrontal cortex (mPFC), hippocampus, and amygdala are implicated in the regulation of affect and physiological processes, including hypothalamic-pituitary-adrenal (HPA) axis function. Anhedonia is likely associated with dysregulation of these processes. Dense-array resting electroencephalographic and cortisol were obtained from healthy and anhedonic groups. Low-resolution electromagnetic tomography was used to compute intracerebral current density. For the control group, voxelwise analyses found a relationship between current density in beta and gamma bands and steeper cortisol slope (indicative of more adaptive HPA axis functioning) in regions of the hippocampus, parahippocampal gyrus, and mPFC. For the anhedonic group, the mPFC finding was absent. Anhedonia may be characterized by disruptions of mPFC-mediated neuroendocrine regulation, which could constitute a vulnerability to the development of stress-related disorders.     

Poor savouring and low self-efficacy are predictors of anhedonia in patients with schizophrenia spectrum disorders

Previous research suggests that negative schizotypes may be impaired in their ability to savour pleasant events (Applegate et al., 2009) and that schizophrenia patients believe that everyday tasks are excessively difficult to complete so that they attempt these tasks less frequently (32 and 10). It is possible that these beliefs and behaviours underpin negative symptoms such as anhedonia, avolition, apathy and associality. In the present study, 50 schizophrenia patients and 100 matched controls (half employed and half unemployed) completed self-report measures of self-efficacy and savouring. Patients reported savouring past, present and future events less than employed and unemployed groups, irrespective of mood state and I.Q. Patients also rated everyday tasks as more difficult to master. Inpatients compared to outpatients rated tasks more difficult but less important although they did not differ on the savouring measure. Abnormal judgements of difficulty and the reduced propensity to mentally rehearse past or future positive experiences to up-regulate mood could explain negative symptom patients' lack of engagement in everyday activities and eventual social withdrawal. These findings suggest the need to develop cognitive-behavioural savouring and self-efficacy interventions for patients experiencing the negative symptoms of schizophrenia.