Neuropsychiatric symptoms and striatal monoamine availability in early Parkinson’s disease without dementia

Oh, Yoon‐Sang; Kim, Jean Hee; Yoo, Sang‐Won; Hwang, Eo‐Jin; Lyoo, Chul Hyoung; Lee, Kwang Soo; Kim, Joong‐Seok

doi:10.1007/s10072-020-04859-8

Cited by 11 publications

(13 citation statements)

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“…Changes in neurotransmission may be another important cause of apathy [ 34 ]. In patients with WD, dopamine deficiency—most likely associated with copper deposition in the basal ganglia—may play a crucial role in inducing apathy [ 35 ].…”

Section: Discussionmentioning

confidence: 99%

Clinical significance of self-descriptive apathy assessment in patients with neurological form of Wilson’s disease

et al. 2021

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Background and aim Apathy is one of the neuropsychiatric symptoms of Wilson’s disease (WD) which typically affects the brain’s fronto-basal circuits. Lack of agreed diagnostic criteria and common use of self-description assessment tools lead to underestimation of this clinical phenomenon. The aim of this study was to investigate whether subjective and informant-based clinical features of apathy in patients with WD enable clinicians to make a valid diagnosis. Methods Multiple aspects of goal-oriented behavior were assessed in 30 patients with the neurological form of WD and 30 age-matched healthy participants using two questionnaires, the Lille Apathy Rating Scale (LARS) and the Dysexecutive Questionnaire (DEX). Both included a self-descriptive and a caregiver/proxy version. Cognitive functioning was estimated with the use of Addenbrooke’s Cognitive Examination-Revised. Results Patients obtained significantly worse scores on all clinical scales when more objective measures were considered. Features of apathy and executive dysfunction were revealed in patients’ caregiver versions of LARS and DEX, which may indicate poor self-awareness of patients with WD. Roughly 30% of participants were likely to present with clinically meaningful symptoms, independent of cognitive dysfunction. Conclusions Methods relying on self-description appear inferior to informant-based scales when diagnosing apathy. More objective criteria and measurement tools are needed to better understand this clinical syndrome.

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Section: Discussionmentioning

confidence: 99%

Clinical significance of self-descriptive apathy assessment in patients with neurological form of Wilson’s disease

et al. 2021

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“…VOI templates of four striatal subregions, the thalamus, and the cerebellum were normalized spatially to the MR template. Then subregional uptake values for each side of the caudate, putamen, globus pallidus, ventral striatum, thalamus, and cerebellum were calculated using the in-house MATLAB 2015a program (MathWorks, Natick, MA, USA) from our previous studies 26 – 28 . The mean standardized uptake value ratio (SUVR) was calculated as target SUV divided by cerebellar SUV.…”

Section: Methodsmentioning

confidence: 99%

Decreased thalamic monoamine availability in drug-induced parkinsonism

Yoo

Lyoo

et al. 2022

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Drug-induced parkinsonism (DIP) is caused by a dopamine receptor blockade and is a major cause of misleading diagnosis of Parkinson’s disease (PD). Striatal dopamine activity has been investigated widely in DIP; however, most studies with dopamine transporter imaging have focused on the clinical characteristics and prognosis. This study investigated differences in striatal subregional monoamine availability among patients with DIP, normal controls, and patients with early PD. Thirty-five DIP patients, the same number of age-matched PD patients, and 46 healthy controls were selected for this study. Parkinsonian motor status was examined. Brain magnetic resonance imaging and positron emission tomography with 18F-N-(3-fluoropropyl)-2beta-carbon ethoxy-3beta-(4-iodophenyl) nortropane were performed, and the regional standardized uptake values were analyzed with a volume-of-interest template and compared among the groups. The groups were evenly matched for age, but there were numerically more females in the DIP group. Parkinsonian motor symptoms were similar in the DIP and PD groups. Monoamine availability in the thalamus of the DIP group was lower than that of the normal controls and similar to that of the PD group. In other subregions (putamen, globus pallidus, and ventral striatum), monoamine availability in the DIP group and normal controls did not differ and was higher than that in the PD group. This difference compared to healthy subject suggests that low monoamine availability in the thalamus could be an imaging biomarker of DIP.

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“…Indeed, decreased binding of [11C]RTI-32, a PET ligand for the dopamine (DAT) and noradrenaline (NERT) transporters, was demonstrated in the (left) ventral striatum in patients with PD and more severe depression, next to noradrenergic dysfunction in other limbic structures [179]. In addition, decreased DAT correlating with depression severity was found in the left anterior putamen using (99m) Tc-TRODAT-1 [180], and in the bilateral striatum and putamen [181], thalamus [182,183], right caudate [184] and left cingulate cortex [185] using [123I]FP-CIT-SPECT. Interestingly, decreased DAT in the left caudate in PD and left putamen in primary dystonia correlated with greater depression [186].…”

Section: Dopamine Imagingmentioning

confidence: 99%

Depression in Patients with Parkinson’s Disease: Current Understanding of its Neurobiology and Implications for Treatment

et al. 2022

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Depression is one of the most frequent and burdensome non-motor symptoms in Parkinson's disease (PD), across all stages. Even when its severity is mild, PD depression has a great impact on quality of life for these patients and their caregivers. Accordingly, accurate diagnosis, supported by validated scales, identification of risk factors, and recognition of motor and non-motor symptoms comorbid to depression are critical to understanding the neurobiology of depression, which in turn determines the effectiveness of dopaminergic drugs, antidepressants and non-pharmacological interventions. Recent advances using in vivo functional and structural imaging demonstrate that PD depression is underpinned by dysfunction of limbic networks and monoaminergic systems, depending on the stage of PD and its associated symptoms, including apathy, anxiety, rapid eye movement sleep behavior disorder (RBD), cognitive impairment and dementia. In particular, the evolution of serotonergic, noradrenergic, and dopaminergic dysfunction and abnormalities of limbic circuits across time, involving the anterior cingulate and orbitofrontal cortices, amygdala, thalamus and ventral striatum, help to delineate the variable expression of depression in patients with prodromal, early and advanced PD. Evidence is accumulating to support the use of dual serotonin and noradrenaline reuptake inhibitors (desipramine, nortriptyline, venlafaxine) in patients with PD and moderate to severe depression, while selective serotonin reuptake inhibitors, repetitive transcranial magnetic stimulation and cognitive behavioral therapy may also be considered. In all patients, recent findings advocate that optimization of dopamine replacement therapy and evaluation of deep brain stimulation of the subthalamic nucleus to improve motor symptoms represents an important first step, in addition to physical activity. Overall, this review indicates that increasing understanding of neurobiological changes help to implement a roadmap of tailored interventions for patients with PD and depression, depending on the stage and comorbid symptoms underlying PD subtypes and their prognosis.

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Neuropsychiatric symptoms and striatal monoamine availability in early Parkinson’s disease without dementia

Cited by 11 publications

References 35 publications

Clinical significance of self-descriptive apathy assessment in patients with neurological form of Wilson’s disease

Clinical significance of self-descriptive apathy assessment in patients with neurological form of Wilson’s disease

Decreased thalamic monoamine availability in drug-induced parkinsonism

Depression in Patients with Parkinson’s Disease: Current Understanding of its Neurobiology and Implications for Treatment

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