Serotonin transporter binding and anxiety symptoms in Parkinson’s disease

2017 ◽  
Vol 89 (1) ◽  
pp. 89-94 ◽  
Author(s):  
Merijn Joling ◽  
Odile A van den Heuvel ◽  
Henk W Berendse ◽  
Jan Booij ◽  
Chris Vriend

BackgroundAnxiety is a common neuropsychiatric symptom in Parkinson’s disease (PD), yet the neural mechanisms have been scarcely investigated. Disturbances in dopaminergic and serotonergic signalling may play a role in its pathophysiology. 123I-N-ω-fluoropropyl-2β-carbomethoxy-3β-(4-iodophenyl)nortropane (123I-FP-CIT) is a single-photon emission CT radiotracer, and its binding in striatal and extrastriatal subcortical brain areas represents predominant binding to the presynaptic dopamine transporter (DAT) and the serotonin transporter (SERT), respectively. Availability of DAT and SERT may thus provide an in vivo measure for the integrity of both dopamine and serotonin neurons.MethodsWe studied the association between anxiety symptoms, measured with an affective subscale of the Beck Anxiety Inventory, and (extra)striatal 123I-FP-CIT binding in 127 non-demented patients with PD with a median disease duration of 2.55 (IQR 2.90) years. We conducted the analyses on patients currently on or not on dopamine replacement therapy (DRT).ResultsSeverity of anxiety symptoms showed a significant negative association with 123I-FP-CIT binding ratios in the right thalamus (β=−0.203, p=0.019; ΔR2=0.040) (multiple testing pcorr <0.020). In the subgroup of patients not on DRT (n=81), we found a significant negative association between anxiety and thalamic 123I-FP-CIT binding ratios bilaterally (right: β=−0.349, p=0.001, ΔR2=0.119; left: β=−0.269, p=0.017, ΔR2=0.071) (pcorr <0.020).ConclusionThis study shows that higher levels of anxiety in patients with PD are associated with lower thalamic 123I-FP-CIT binding, pointing towards a contribution of serotonergic degeneration to anxiety symptoms in PD.

Author(s):  
Fulvio Lauretani ◽  
Yari Longobucco ◽  
Giulia Ravazzoni ◽  
Elena Gallini ◽  
Marco Salvi ◽  
...  

The neurobiology of Parkinson’s disease and its progression has been investigated during the last few decades. Braak et al. proposed neuropathological stages of this disease based on the recognizable topographical extent of Lewy body lesions. This pathological process involves specific brain areas with an ascending course from the brain stem to the cortex. Post-mortem studies are of importance to better understand not only the progression of motor symptoms, but also the involvement of other domains, including cognition and behavior. The correlation between the neuropathological expansion of the disease and the clinical phases remains demanding. Neuroimaging, including magnetic resonance imaging (MRI), positron emission tomography (PET), and single photon emission computed tomography (SPECT), could help to bridge this existing gap by providing in vivo evidence of the extension of the disorders. In the last decade, we observed an overabundance of reports regarding the sensitivity of neuroimaging techniques. All these studies were aimed at improving the accuracy of Parkinson’s disease (PD) diagnosis and discriminating it from other causes of parkinsonism. In this review, we look at the recent literature concerning PD and address the new frontier of diagnostic accuracy in terms of identification of early stages of the disease and conventional neuroimaging techniques that, in vivo, are capable of photographing the basal ganglia network and its cerebral connections.


2011 ◽  
Vol 6 (3) ◽  
pp. 161
Author(s):  
Pankaj A Agarwal ◽  
A Jon Stoessl ◽  
◽  

Since structural imaging has generally failed to demonstrate consistent abnormalities in Parkinson’s disease (PD), from an imaging perspective, the diagnosis has typically been based upon the demonstration of impaired striatal dopamine (DA) function. Radiotracer imaging techniques such as positron emission tomography (PET) and single photon emission computerised tomography (SPECT) allow thein vivoassessment of nigrostriatal DA function as well as regional cerebral blood flow, glucose metabolism, and functional connectivity, and changes in these measures have been used to infer disease progression. Pre-synaptic radiotracer imaging (RTI) has shown that striatal dopaminergic hypofunction follows a negative exponential pattern with the fastest rate of decline in early disease. Moreover, while striatal subregions remain differentially affected throughout the course of disease, with the posterior putamen affected more than anterior structures, the rate of deterioration is similar in all subregions. However, although functional imaging is undoubtedly a very useful tool in the assessment of PD progression, various studies have shown discordance between clinical progression of PD and nigrostriatal degeneration estimated by PET or SPECT. Therefore, considerable caution is warranted in the interpretation of imaging findings. While a potentially invaluable complement in assessing the severity of dopaminergic dysfunction, functional imaging is not a substitute for clinical assessment and other objective measures of PD severity, and cannot be currently considered a biomarker for progression of PD.


Doctor Ru ◽  
2020 ◽  
Vol 19 (9) ◽  
pp. 6-12
Author(s):  
M.R. Sapronova ◽  
◽  
D.V. Dmitrenko ◽  
N.A. Schnaider ◽  
A.A. Molgachev ◽  
...  

Objective of the Review: To describe available functional neuroimaging techniques for use in patients with Parkinson’s disease (PD). Key Points: Parkinson’s disease is a neurodegenerative disorder which affects 2-3% of people older than 65 years. The main neuropathological hallmarks of PD are an accumulation of alpha-synuclein aggregates in the cellular cytoplasm and a loss of neurons in the pars compacta of the substantia nigra, leading to dopamine deficiency. Clinical symptoms of the disease appear when the underlying neural impairment is already advanced, which significantly reduces treatment options. Over the two last decades, functional neuroimaging techniques such as positron emission tomography, single-photon emission computed tomography, proton magnetic resonance spectroscopy, and transcranial sonography have increasingly been used for diagnosing PD during patients’ lifetime and understanding the neuropathological mechanisms and compensatory reactions underlying its symptoms, as well as for monitoring the progression of PD. Conclusion: Modern functional neuroimaging techniques not only facilitate differential diagnosis of PD, but also make it possible to detect the disease at its early/preclinical stage. Keywords: Parkinson’s disease, neuroimaging, positron emission tomography, single-photon emission computed tomography, proton magnetic resonance spectroscopy, transcranial sonography.


2013 ◽  
Vol 6 ◽  
pp. CCRep.S11903 ◽  
Author(s):  
Robert Fekete ◽  
Jin Li

We present clinical features and tremor characterization in a patient with Parkinson's disease (PD) as well as in two cases of essential tremor (ET) with some parkinsonian features but no evidence of dopaminergic terminal loss on 123I-FP-CIT Single Photon Emission Computed Tomography (SPECT). Relatively slow frequency rest tremor and bilateral upper extremity bradykinesia without decrementing amplitude were observed in the ET cases, with unilaterally decreased arm swing in case 3. Alternating rest tremor and re-emergent tremor with 13 second latency was confirmed in the PD case. Re-emergent tremor had alternating characteristics, which to our knowledge has not been previously reported. The ET cases had synchronous postural tremor. Alternating re-emergent tremor in PD provides further evidence for re-emergent tremor as an analogue of rest tremor in PD. Two cases of ET with synchronous postural tremor and one to two year history of parkinsonian features had no evidence of dopaminergic terminal loss up to 40 years after the initial onset of ET. Tremor synchronicity characterization can assist in differential diagnosis between the two disorders.


1999 ◽  
Vol 175 (1) ◽  
pp. 63-69 ◽  
Author(s):  
David M. Semple ◽  
Klaus P. Ebmeier ◽  
Michael F. Glabus ◽  
Ronan E. O'Carroll ◽  
Eve C. Johnstone

BackgroundThe use of MDMA (‘ecstasy’) is common among young people in Western countries. Animal models of MDMA toxicity suggest a loss of serotonergic neurons, and potentially implicate it in the development of significant psychiatric morbidity in humans.AimsTo test whether long-term use of MDMA can produce abnormalities in cerebral serotonin, but not dopamine, transporter binding measured by single photon emission computed tomography (SPECT)MethodTen male regular ecstasy users and 10 well-matched controls recruited from the same community sources participated in SPECT with the serotonin transporter (SEPT) ligand [123I]-CIT. Dopamine transporter binding was determined from scans acquired 23 hours after injection of the tracer.ResultsEcstasy users showed a cortical reduction of SERT binding, particularly prominent in primary sensory-motor cortex, with normal dopamine transporter binding in lenticular nuclei.ConclusionsThis cross-sectional association study provides suggestive evidence for specific, at least temporary, serotonergic neurotoxicity of MDMA in humans.


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