Neurochemical and functional imaging of movement disorders

Nicolaas I Bohnen MD PhD (Dr. Bohnen of the University of Michigan Medical Center has no relevant financial relationships to disclose.)
Kirk A Frey MD PhD (Dr. Frey of the University of Michigan Medical School received consultation fees from AVID Radiopharmaceuticals, MIM Software, and Siemens, grant support from General Electric, and owns stock in Bristol Meyers Squibb, General Electric, Medtronic, Merck, and Novo Nordisk.)
Joseph Jankovic MD, editor. (Dr. Jankovic, Director of the Parkinson's Disease Center and Movement Disorders Clinic at Baylor College of Medicine, received research funding from Allergan, Allon, Ceregene, Chelsea, EMD Serono, Impax, Ipsen, Lundbeck, Medtronic, Merz, and Teva, and compensation for his services as a consultant or an advisory committee member by Allergan, Auspex, EMD Serono, Lundbeck, Merz, Neurocrine Biosciences, and Teva.)
Originally released March 20, 2001; last updated July 15, 2015; expires July 15, 2018


PET or SPECT imaging provides the means to study the neurochemical, hemodynamic, or metabolic processes underlying movement disorders in vivo. The extent of presynaptic nigrostriatal dopaminergic denervation can be quantified in Parkinson disease even at an early or preclinical stage of the disease. Therefore, dopaminergic imaging may allow the selection of at-risk subjects for neuroprotective intervention trials. These techniques may also provide markers to follow progression of disease or evaluate the effects of neurorestorative interventions in patients with more advanced disease. Dopamine transporter SPECT imaging is now clinically approved to assist with the evaluation of adult patients with suspected Parkinsonian syndromes. In these patients, dopamine transporter imaging may be used to help differentiate essential tremor from tremor due to parkinsonian syndrome (idiopathic Parkinson disease, multiple system atrophy, and progressive supranuclear palsy). It may also have a limited role in the diagnosis of patients with symptoms suggestive of Parkinson disease yet who do not respond to typical dopaminergic drugs, such as patients with vascular parkinsonism or essential tremor with mild resting tremor who may have normal dopaminergic innervation. Patients with mixed tremor may reflect different etiologies, such as dystonic tremor. Subjects clinically diagnosed with Parkinson disease but with no evidence of dopaminergic denervation (SWEDD) may require further diagnostic assessment. Huntington chorea is characterized by more prominent striatal dopamine receptor loss, whereas nigrostriatal denervation is present to a lesser degree. Patients with Tourette syndrome may have enhanced synaptic dopamine release in the putamen. Studies have shown striatal dopamine receptor loss in selected subtypes of dystonic patients. Pharmacological radioligand displacement studies and the development of new nondopaminergic ligands, such as markers of microglial activation or phosphodiesterase activity, may further aid the unraveling of cerebral mechanisms underlying movement disorders.

In this article, the authors report on evidence of increased activated microglia-mediated neuroinflammation in bilateral caudate and bilateral lentiform nucleus in the PANDAS group and in bilateral caudate nuclei only in Tourette syndrome. These differences in the pattern and extent of neuroinflammation may signify a possible difference in pathophysiological etiology between PANDAS and Tourette syndrome patients.

Key points


• Nigrostriatal dopaminergic denervation is a key pathobiological event in Parkinson disease that can be quantified using brain SPECT or PET imaging and may allow for early diagnosis or monitoring of progression of disease. Dopamine transporter SPECT imaging is now available as a clinical diagnostic tool.


• Studies have shown that imaging findings of reduced dopamine D2 receptors are the most sensitive indicator of striatal changes in presymptomatic and symptomatic Huntington disease.


• Evidence of altered presynaptic dopaminergic regulation in Tourette syndrome is supported by exaggerated amphetamine response in striatal and extrastriatal subcortical and cortical regions, suggesting a mechanism for the hyperexcitability of basal ganglia thalamocortical circuits in Tourette syndrome.


• Imaging studies have shown that striatal serotonergic terminals may contribute to levodopa-induced dyskinesia pathophysiology via aberrant processing of exogenous levodopa and release of dopamine as a false neurotransmitter in the denervated striatum of dyskinetic Parkinson disease patients.


• The development of new tau protein binding PET ligands may allow more accurate distinction of progressive supranuclear palsy and corticobasal degeneration from idiopathic Parkinson disease.

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