PET Imaging in Movement Disorders

Abstract

Positron emission tomography (PET) has revealed key insights into the pathophysiology of movement disorders. This paper will focus on how PET investigations of pathophysiology are particularly relevant to Parkinson disease, a neurodegenerative condition usually starting later in life marked by a varying combination of motor and nonmotor deficits. Various molecular imaging modalities help to determine what changes in brain herald the onset of pathology; can these changes be used to identify presymptomatic individuals who may be appropriate for to-be-developed treatments that may forestall onset of symptoms or slow disease progression; can PET act as a biomarker of disease progression; can molecular imaging help enrich homogenous cohorts for clinical studies; and what other pathophysiologic mechanisms relate to nonmotor manifestations. PET methods include measurements of regional cerebral glucose metabolism and blood flow, selected receptors, specific neurotransmitter systems, postsynaptic signal transducers, and abnormal protein deposition. We will review each of these methodologies and how they are relevant to important clinical issues pertaining to Parkinson disease.

Figure 1

6-[¹⁸F]fluorodopa (FD) PET in a normal individual (A) and two PD patients with mild (B) and moderate (B) motor impairments showing asymmetric, gradient loss of putaminal FD uptake in PD patients compared to controls.

Figure 2

[¹¹C]-PiB PET images from three PD patients with dementia (Case 1–3) and a normal individual. Case 1 and Case 2 both have increased PiB signal in multiple cortical areas signifying diffuse amyloid burden, while Case 3 had only minimal cortical PiB signal like the normal individual. The signal in the white matter areas is likely secondary to non-specific PiB binding. (Image adapted from Burack et al.)