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With the advent of high-field magnetic resonance imaging (MRI), volumetric acquisitions, and more sophisticated sequences, the role of structural imaging in the diagnosis of parkinsonian disorders is becoming more important. MRI can help exclude structural lesions such as basal ganglia tumors, hemorrhages, small vessel disease, and calcification, which have all been associated with parkinsonism, as has hydrocephalus. There is still debate concerning whether vascular parkinsonism is a distinct entity, although 5% of parkinsonian cases have no other evident pathology1 (see Chapter 24). High-field MRI utilizing gray and white matter signal-suppressing inversion recovery sequences can show abnormal signal from the substantia nigra compacta in idiopathic Parkinson's disease (PD) patients.2,3 Volumetric MRI has so far failed to detect a reduction in nigral volume in PD, possibly because of difficulties in accurately defining the border of the nigra compacta.4 Interestingly, however, a reduction in putamen volume was noted by these workers, even in early cases. T2-weighted MRI sequences directly reflect the iron content of brain areas. Michaeli and colleagues5 have been able to detect increased nigral magnetic susceptibility in PD, although midbrain relaxation times overlapped considerably with those of healthy normals.
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The striatum appears normal on T2-weighted MRI in PD, but in striatonigral degeneration (SND) and multisystem atrophy (MSA), the putamen characteristically shows reduced signal running up the lateral extent due to iron deposition, and this may be covered by a rim of increased signal due to gliosis.6–8 If concomitant pontocerebellar degeneration is also present, the lateral as well as longitudinal pontine fibers become evident as high signal on T2 MRI, manifesting as the “hot cross bun” sign. Cerebellar and pontine atrophy may be visually obvious with increased signal evident in the cerebellar peduncles. Formal MR volumetry detects putamen and brain stem atrophy in most established cases.9 Patients with progressive supranuclear palsy (PSP) do not show the putamen signal changes characteristic of MSA but may show third ventricular widening and midbrain atrophy. Recently, visual assessment of superior cerebellar peduncle atrophy has been shown to differentiate PSP patients from control, PD, and MSA patients with a sensitivity of 74% and a specificity of 94%.10 In corticobasal degeneration (CBD), asymmetric hemispheric atrophy may be present, and MRI can usefully exclude multi-infarct disease and multifocal leukoencephalopathy. Putaminal hypointensity and hyperintense signal changes in the motor cortex or subcortical white matter on T2-weighted images have also been reported.11,12
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Diffusion-weighted imaging (DWI) and tensor MRI provide more sensitive modalities for discriminating atypical from typical parkinsonian disorders. Diffusion tensor imaging (DTI) detects altered water diffusibility as a raised apparent diffusion coefficient (ADC) and loss of directionality of diffusion as reduced fractional anisotropy (FA). To date only minor reductions in nigral FA have been reported in PD.13 However, 90–100% of cases with clinically probable MSA and PSP have shown a raised putamen ADC across different series, whereas putamen ...