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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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
Burton EJ et al. (2005) Brain atrophy rates in Parkinson’s disease with and without dementia using serial magnetic resonance imaging. Mov Disord 20: 1571-1576
Bohnen NI et al. (1999) Motor correlates of occipital glucose hypometabolism in Parkinson’s disease without dementia. Neurology 52: 541-546
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
Klunk WE et al. (2004) Imaging brain amyloid in Alzheimer’s disease with Pittsburgh Compound-B. Ann Neurol 55: 306-319
Edison P et al. (2007) Amyloid load in Lewy body dementia (LBD), Parkinson’s disease dementia (PDD) and Parkinson’s disease (PD) measured with C-11-PIB PET. Neurology 68: A98
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Walker Z et al. (2004) Striatal dopamine transporter in dementia with Lewy bodies and Parkinson disease: a comparison. Neurology 62: 1568-1572
Ito K et al. (2002) Striatal and extrastriatal dysfunction in Parkinson’s disease with dementia: a 6-[¹⁸F]fluoro-L-dopa PET study. Brain 125: 1358-1365
Rinne JO et al. (2000) Cognitive impairment and the brain dopaminergic system in Parkinson disease: [¹⁸F]fluorodopa positron emission tomographic study. Arch Neurol 57: 470-475

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Conclusions

Table 1 and Table 2 summarize the differential imaging findings in parkinsonian syndromes and dementias, respectively.

TCS and MRI can both be used to image structural changes in the substantia nigra of patients with PD. Although the altered signals that are observed do not correlate well with either clinical status or loss of dopamine terminal function in the striatum, they might prove to be valuable for revealing a susceptibility to PD. By contrast, PET and SPECT measurements of dopamine terminal function do correlate significantly with clinical disability. In patients who are suspected of having PD, a finding of normal presynaptic dopaminergic function on a PET or SPECT scan implies a good prognosis.

The severity of a parkinsonian tremor correlates better with loss of 5-HT_1A receptor binding potential in the median raphe than with nigro striatal dysfunction, which indicates that midbrain tegmentum pathology is involved in the generation of the tremor. Surprisingly, depression in PD seems to reflect a loss of noradrenergic and limbic monoaminergic function, rather than a serotonergic etiology.

DLB can be reliably discriminated from AD by the detection of a loss of striatal DAT binding in the former. Amyloid pathology contributes notably to DLB in the majority of cases, whereas only 20% of patients who have PDD show a raised plaque load.

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Table 1.

Table 2.

Technology Insight: Imaging Neurodegeneration in Parkinson's Disease: Conclusions

Conclusions

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: Conclusions

Conclusions

Table of Contents