Imaging Neurodegeneration in Parkinson's Disease

Table 1.

Differential Imaging Findings in Parkinsonian Syndromes

Table 2.

Differential Imaging Findings in Dementias

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Catafau AM and Tolosa E (2004) Impact of dopamine transporter SPECT using ¹²³I-ioflupane on diagnosis and management of patients with clinically uncertain Parkinsonian syndromes. Mov Disord 19: 1175-1182
Jennings DL et al. (2004) (¹²³I) β-CIT and singlephoton emission computed tomographic imaging vs clinical evaluation in Parkinsonian syndrome: unmasking an early diagnosis. Arch Neurol 61: 1224-1229
Booij J et al. (2001) The clinical benefit of imaging striatal dopamine transporters with [¹²³I]FP-CIT SPET in differentiating patients with presynaptic parkinsonism from those with other forms of parkinsonism. Eur J Nucl Med 28: 266-272
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Brooks DJ (1993) Functional imaging in relation to parkinsonian syndromes. J Neurol Sci 115: 1-17
Eidelberg D et al. (1994) The metabolic topography of parkinsonism. J Cereb Blood Flow Metab 14: 783-801
Su PC et al. (2001) Metabolic changes following subthalamotomy for advanced Parkinson’s disease. Ann Neurol 50: 514-520
Feigin A et al. (2001) Metabolic correlates of levodopa response in Parkinson’s disease. Neurology 57: 2083-2088
Eckert T et al. (2007) Regional metabolic changes in parkinsonian patients with normal dopaminergic imaging. Mov Disord 22: 167-173
Burn DJ et al. (1994) Differential diagnosis of Parkinson’s disease, multiple system atrophy, and Steele-Richardson-Olszewski syndrome: discriminant analysis of striatal ¹⁸F-dopa PET data. J Neurol Neurosurg Psychiatry 57: 278-284
Pirker W et al. (2000) [¹²³I]β-CIT SPECT in multiple system atrophy, progressive supranuclear palsy, and corticobasal degeneration. Mov Disord 15: 1158-1167
Eckert T et al. (2005) FDG PET in the differential diagnosis of parkinsonian disorders. Neuroimage 26: 912-921
Moore RY et al. (2007) Extrastriatal monoamine neuron function in Parkinson’s disease: an ¹⁸F-dopa PET study. Neurobiol Dis [doi:10.1016/j.nbd.2007.09.004]
Doder M et al. (2003) Tremor in Parkinson’s disease and serotonergic dysfunction: an ¹¹C-WAY 100635 PET study. Neurology 60: 601-605
Kim SE et al. (2003) Serotonin transporters in the midbrain of Parkinson’s disease patients: a study with ¹²³I-β-CIT SPECT. J Nucl Med 44: 870-876
Remy P et al. (2005) Depression in Parkinson’s disease: loss of dopamine and noradrenaline innervation in the limbic system. Brain 128: 1314-1322
Kuhl DE et al. (1996) in vivo mapping of cholinergic terminals in normal aging, Alzheimer’s disease, and Parkinson’s disease. Ann Neurol 40: 399-410
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Bohnen NI et al. (2005) Cognitive correlates of alterations in acetylcholinesterase in Alzheimer’s disease. Neurosci Lett 380: 127-132
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Berg D et al. (2001) Relationship of substantia nigra echogenicity and motor function in elderly subjects. Neurology 56: 13-17
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Sommer U et al. (2004) Detection of presymptomatic Parkinson’s disease: combining smell tests, transcranial sonography, and SPECT. Mov Disord 19: 1196-1202
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Summerfield C et al. (2005) Structural brain changes in Parkinson disease with dementia: a voxel-based morphometry study. Arch Neurol 62: 281-285
Ramirez-Ruiz B et al. (2005) Longitudinal evaluation of cerebral morphological changes in Parkinson’s disease with and without dementia. J Neurol 252: 1345-1352
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Hu MT et al. (2000) Cortical dysfunction in nondemented Parkinson’s disease patients: a combined 31P-MRS and ¹⁸FDG-PET study. Brain 123: 340-352
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Summary and Introduction

Summary

Currently, the clinical diagnosis of Parkinson’s disease (PD) can be problematic, particularly at the early stages of the disease when the full spectrum of symptoms and signs might not yet be manifest. In addition, the mechanisms that underlie the nonmotor complications of PD, such as dementia and depression, are poorly understood, despite the fact that these symptoms largely determine the patient’s quality of life at the end stage of the disease. This article reviews the latest advances in structural and functional imaging that have provided important insights into the structural, pathophysiological and pharmacological changes associated with PD. The contribution of inflammatory processes to the pathology of PD is discussed, as are the various possible mechanisms that lead to coexistent dementia and depression.

Introduction

The definitive diagnosis of idiopathic Parkinson’s disease (PD) requires the demonstration of intracellular Lewy body inclusions via histological examination of brain tissue, which is not a viable approach in living individuals. Retrospective clinico pathological studies have shown that a clinical diagnosis of PD during life correlates with a postmortem finding of brainstem Lewy body disease in, at best, 85% of patients.^[1] Atypical parkinsonian disorders, such as multiple system atrophy (MSA) and progressive supra nuclear palsy (PSP), can mimic PD, as can severe essential and dystonic tremors. Patients with early-stage disease, in which the full constellation of parkinsonian symptoms and signs are not yet manifest, can be the most difficult to diagnose. Consequently, the ability to detect or exclude loss of nigral dopaminergic neurons or striatal dopamine terminal function by use of non invasive imaging approaches would be a valuable tool that could not only help physicians to increase diagnostic specificity, but could also enable the appropriate management decisions to be made at the initial stages of the disease.

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Lewy Body Pathology in Parkinson's Disease

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Table 1.

Table 2.

Technology Insight: Imaging Neurodegeneration in Parkinson's Disease

Summary and Introduction

Summary

Introduction

Table of Contents

Table 1.

Table 2.

References

Faculty and Disclosures

Author(s)

David J Brooks, MD, DSc, FRCP, FMedSci

Editor(s)

Heather Wood

Technology Insight: Imaging Neurodegeneration in Parkinson's Disease

Summary and Introduction

Summary

Introduction

Table of Contents