Review
Copyright ©The Author(s) 2016. Published by Baishideng Publishing Group Inc. All rights reserved.
World J Radiol. Mar 28, 2016; 8(3): 226-239
Published online Mar 28, 2016. doi: 10.4329/wjr.v8.i3.226
Molecular imaging of movement disorders
Karlo J Lizarraga, Alessandra Gorgulho, Wei Chen, Antonio A De Salles
Karlo J Lizarraga, Department of Neurology, Jackson Memorial Hospital, University of Miami Miller School of Medicine, Miami, FL 33136, United States
Alessandra Gorgulho, Antonio A De Salles, Department of Neurosurgery, David Geffen School of Medicine, University of California Los Angeles, Los Angeles, CA 90095, United States
Wei Chen, Department of Molecular and Medical Pharmacology, David Geffen School of Medicine, University of California Los Angeles, Los Angeles, CA 90095, United States
Author contributions: Lizarraga KJ conceptualized and designed the manuscript, reviewed the literature and drafted all article versions; Gorgulho A, Chen W and De Salles AA interpreted data and critically revised all manuscript versions; all authors approved the final version of the article to be published.
Conflict-of-interest statement: The authors declare no potential conflict of interest for this review.
Open-Access: This article is an open-access article which was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/
Correspondence to: Karlo J Lizarraga, MD, MS, Department of Neurology, Jackson Memorial Hospital, University of Miami Miller School of Medicine, 1120 N.W. 14th Street, Suite 1383, Miami, FL 33136, United States. klizarraga@med.miami.edu
Telephone: +1-305-2432742 Fax: +1-305-2438108
Received: September 30, 2015
Peer-review started: October 3, 2015
First decision: November 4, 2015
Revised: November 19, 2015
Accepted: January 5, 2016
Article in press: January 7, 2016
Published online: March 28, 2016
Processing time: 173 Days and 17 Hours
Abstract

Positron emission tomography measures the activity of radioactively labeled compounds which distribute and accumulate in central nervous system regions in proportion to their metabolic rate or blood flow. Specific circuits such as the dopaminergic nigrostriatal projection can be studied with ligands that bind to the pre-synaptic dopamine transporter or post-synaptic dopamine receptors (D1 and D2). Single photon emission computerized tomography (SPECT) measures the activity of similar tracers labeled with heavy radioactive species such as technetium and iodine. In essential tremor, there is cerebellar hypermetabolism and abnormal GABAergic function in premotor cortices, dentate nuclei and ventral thalami, without significant abnormalities in dopaminergic transmission. In Huntington’s disease, there is hypometabolism in the striatum, frontal and temporal cortices. Disease progression is accompanied by reduction in striatal D1 and D2 binding that correlate with trinucleotide repeat length, disease duration and severity. In dystonia, there is hypermetabolism in the basal ganglia, supplementary motor areas and cerebellum at rest. Thalamic and cerebellar hypermetabolism is seen during dystonic movements, which can be modulated by globus pallidus deep brain stimulation (DBS). Additionally, GABA-A receptor activity is reduced in motor, premotor and somatosensory cortices. In Tourette’s syndrome, there is hypermetabolism in premotor and sensorimotor cortices, as well as hypometabolism in the striatum, thalamus and limbic regions at rest. During tics, multiple areas related to cognitive, sensory and motor functions become hypermetabolic. Also, there is abnormal serotoninergic transmission in prefrontal cortices and bilateral thalami, as well as hyperactivity in the striatal dopaminergic system which can be modulated with thalamic DBS. In Parkinson’s disease (PD), there is asymmetric progressive decline in striatal dopaminergic tracer accumulation, which follows a caudal-to-rostral direction. Uptake declines prior to symptom presentation and progresses from contralateral to the most symptomatic side to bilateral, correlating with symptom severity. In progressive supranuclear palsy (PSP) and multiple system atrophy (MSA), striatal activity is symmetrically and diffusely decreased. The caudal-to-rostral pattern is lost in PSP, but could be present in MSA. In corticobasal degeneration (CBD), there is asymmetric, diffuse reduction of striatal activity, contralateral to the most symptomatic side. Additionally, there is hypometabolism in contralateral parieto-occipital and frontal cortices in PD; bilateral putamen and cerebellum in MSA; caudate, thalamus, midbrain, mesial frontal and prefrontal cortices in PSP; and contralateral cortices in CBD. Finally, cardiac sympathetic SPECT signal is decreased in PD. The capacity of molecular imaging to provide in vivo time courses of gene expression, protein synthesis, receptor and transporter binding, could facilitate the development and evaluation of novel medical, surgical and genetic therapies in movement disorders.

Keywords: Positron emission tomography; Single photon emission computerized tomography; Movement disorders; Essential tremor; Huntington’s disease; Dystonia; Tourette’s syndrome; Parkinson’s disease; Parkinsonism

Core tip: By evaluating changes in regional brain perfusion, glucose metabolism and neurotransmitter systems, molecular imaging has shed light onto the etiology, pathophysiology, diagnosis, progression and therapeutic options of movement disorders, including the identification and individualization of potential neuromodulation targets. Continuing progress in the design of positron emission tomography and single photon emission computerized tomography systems, such as new detector materials and image reconstruction algorithms, higher performance technology, and improved availability will contribute to a wider range of applications. In particular, the combined use of genetic therapy and molecular imaging could provide opportunities for the design and evaluation of novel therapies at early stages of the disease.