Eckert T, Eidelberg DNeuroimaging and therapeutics in movement disorders. NeuroRx 2:361-371

Department of Neurology II and Psychiatry, University of Magdeburg, Germany.
NeuroRx 05/2005; 2(2):361-71. DOI: 10.1602/neurorx.2.2.361
Source: PubMed


In this review, we discuss the role of neuroimaging in assessing treatment options for movement disorders, particularly Parkinson's disease (PD). Imaging methods to assess dopaminergic function have recently been applied in trials of potential neuroprotective agents. Other imaging methods using regional metabolism and/or cerebral perfusion have been recently introduced to quantify the modulation of network activity as an objective marker of the treatment response. Both imaging strategies have provided novel insights into the mechanisms underlying a variety of pharmacological and stereotaxic surgical treatment strategies for PD and other movement disorders.

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Available from: Thomas Eckert, Nov 26, 2014
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    • "Several recent reviews describe the use of single-photon emission computed tomography (SPECT) alone or in combination with PET and/or functional magnetic resonance imaging (fMRI) in studies of human cognition, imaging of neuroreceptor systems, aiding diagnosis or assessment of progression or treatment response in various psychiatric and neurologic disorders, neuropharmacologic challenge studies and in the new field of molecular imaging, including imaging of transgene expression (Devous 2002; Catafau 2001; Mazziotta and Toga 2002; Lee and Newberg 2005; Bonte and Devous 2003; Devous Sr 1998; Brooks 2005; Heinz et al. 2000; Dickerson and Sperling 2005; Bammer et al. 2005; Eckert and Eidelberg 2005; Kuzniecky 2005). Brain SPECT is now commonly used in the diagnosis, prognosis assessment, evaluation of response to therapy, risk stratification, detection of benign or malignant viable tissue, and choice of medical or surgical therapy, especially in head injury, malignant brain tumors, cerebrovascular disease, movement disorders, dementia, and epilepsy (Lee and Newberg 2005; Bonte and Devous 2003; Devous Sr 1998; Brooks 2005; Heinz et al. 2000; Dickerson and Sperling 2005; Bammer et al. 2005; and Kuzniecky 2005). "
    01/2014; 5(1):23. DOI:10.1186/s40543-014-0023-4
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    • "In summary, the bulk of the evidence indicates that GABAergic inhibition of the thalamus lowers thalamic activity and blood flow. To be consistent with the mechanism proposed by Alexander et al. [1986], functional brain imaging results must reveal reduced blood flow in thalamus during DBS of the STN in patients with Parkinson's disease, if the DBS restores the normal resting striatal inhibition of the thalamocortical projections [Ceballos-Baumann et al., 1999, Payoux et al., 2004, Eckert and Eidelberg, 2005]. "
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    ABSTRACT: To test the hypothesis that deep brain stimulation of the subthalamic nucleus (STN) restores the inhibitory output to the striatothalamocortical loop in Parkinson's disease, we obtained functional brain images of blood flow in 10 STN-stimulated patients with Parkinson's disease. Patients were immobile and off antiparkinsonian medication for 12 h. They were scanned with and without bilateral STN-stimulation with a 4-h interval between the two conditions. The order of DBS stimulation (ON or OFF) was randomized. Stimulation significantly raised regional cerebral blood flow (rCBF) bilaterally in the STN and in the left nucleus lentiformis. Conversely, flow declined in the left supplementary motor area (BA 6), ventrolateral nucleus of the left thalamus, and right cerebellum. Activation of the basal ganglia and deactivation of supplementary motor area and thalamus were both correlated with the improvement of motor function. The result is consistent with the explanation that stimulation in resting patients raises output from the STN with activation of the inhibitory basal ganglia output nuclei and subsequent deactivation of the thalamic anteroventral and ventrolateral nuclei and the supplementary motor area.
    Human Brain Mapping 01/2009; 30(1):112-21. DOI:10.1002/hbm.20486 · 5.97 Impact Factor
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    • "Indeed, like the PDRP, these disease-related metabolic patterns may ultimately serve as objective descriptors of disease severity in clinical trials of new treatment strategies (e.g., Feigin et al., 2007a; cf. Eckert and Eidelberg, 2005). "
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    ABSTRACT: Normalization of regional measurements by the global mean is commonly employed to minimize inter-subject variability in functional imaging studies. This practice is based on the assumption that global values do not substantially differ between patient and control groups. In this issue of NeuroImage, Borghammer and colleagues challenge the validity of this assumption. They focus on Parkinson's disease (PD) and use computer simulations to show that lower global values can produce spurious increases in subcortical brain regions. The authors speculate that the increased signal observed in these areas in PD is artefactual and unrelated to localized changes in brain function. In this commentary, we summarize what is currently known of the relationship between regional and global metabolic activity in PD and experimental parkinsonism. We found that early stage PD patients exhibit global values that are virtually identical to those of age-matched healthy subjects. SPM analysis revealed increased normalized metabolic activity in a discrete set of biologically relevant subcortical brain regions. Because of their higher variability, the corresponding absolute regional measures did not differ across the two groups. Longitudinal imaging studies in this population showed that the subcortical elevations in normalized metabolism appeared earlier and progressed faster than did focal cortical or global metabolic reductions. The observed increases in subcortical activity, but not the global changes, correlated with independent clinical measures of disease progression. Multivariate analysis with SSM/PCA further confirmed that the abnormal spatial covariance structure of early PD is dominated by these subcortical increases as opposed to network-related reductions in cortical metabolic activity or global changes. Thus, increased subcortical activity in PD cannot be regarded as a simple artefact of global normalization. Moreover, stability of the normalized measurements, particularly at the network level, makes these metabolic indices suitable as imaging biomarkers of PD progression and the treatment response.
    NeuroImage 11/2008; 45(2):260-6. DOI:10.1016/j.neuroimage.2008.09.052 · 6.36 Impact Factor
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