MR imaging of the superior profile of the midbrain: differential diagnosis between progressive supranuclear palsy and Parkinson disease.

BACKGROUND AND PURPOSE: Quantitative evaluation of midbrain atrophy may be useful in differentiating progressive supranulear palsy (PSP) from Parkinson disease (PD); however, this finding is not specific of PSP, and quantitative measurements are not always practical. We determined whether an abnormal superior midbrain profile (flat or concave aspect) is a more practical diagnostic parameter for PSP. METHODS: MR imaging studies of 25 patients with PSP and 27 with PD were reviewed by means of five parameters: midbrain superior profile on midsagittal T1-weighted images, midbrain atrophy, tegmental abnormal T2 hyperintensity, abnormal T2 putaminal hypointensity or hyperintensity on axial proton density-weighted images. We also measured the anteroposterior diameter of the midbrain on axial T2-weighted sections at the level of the superior colliculus. RESULTS: The finding of an abnormal superior profile of the midbrain had 68% sensitivity and 88.8% specificity. Midbrain atrophy had 68% sensitivity and 77.7% specificity. Tegmental T2 hyperintensity had 100% specificity but poor sensitivity (28%). Only 14.8% of patients with PD and 24% of those with PSP had abnormal putaminal T2 hypointensity; none had proton-density hyperintensity. With PSP, the average midbrain diameter was smaller than that with PD, but an important overlap was observed. Reader discordance was lower for the midbrain superior profile sign (eight of 52 cases); this was similar for tegmental hyperintensity (nine of 52 cases) and higher for midbrain atrophy (16 of 52 cases). CONCLUSION: An abnormal superior profile of the midbrain facilitates the distinction of PSP from PD and may support the clinical differential diagnosis of parkinsonism.

Protein intake in Parkinsonian patients using the EPIC food frequency questionnaire.

The dietary habits of 45 Italian patients with Parkinson's disease (PD) and their spouses were investigated using the EPIC food frequency questionnaire. Average daily energy intake was similar, but PD patients consumed significantly more vegetable proteins and carbohydrates (both +18%; P = 0.01 and P = 0.001, respectively). Daily protein intake, which interferes with levodopa absorption, was 50% higher than the recommended daily allowance (1.2 vs. 0.8 g/kg) in both PD patients and spouses and was significantly higher in patients with moderate/severe symptoms (1.27 +/- 0.29 vs. 1.07 +/- 0.28 g/kg; P < 0.001). In patients taking levodopa, there was a correlation between daily levodopa dosage and protein intake (P = 0.027). Dietary habits of patients with advanced and/or fluctuating PD should always be checked, with particular reference to protein intake.

Special low-protein foods ameliorate postprandial off in patients with advanced Parkinson's disease.

Protein intake interferes with levodopa therapy. Patients with advanced Parkinson's disease (PD) should restrict daily protein intake and shift protein intake to the evening. For further reduction of protein intake in the first part of the day, special low-protein products (LPP) should be used instead of normal food products at breakfast and lunch. We studied the efficacy of LPP on postprandial off periods, in PD patients on levodopa therapy. The methods included a randomized, cross-over, single-blind, pilot clinical trial comparing a 2-month balanced diet with a 2-month LPP diet in 18 PD patients with motor fluctuations. The off phases were significantly shorter after LPP diet than after balanced diet (postprandial off, 49 +/- 73 min vs. 79 +/- 72 min and total off, 164 +/- 148 min vs. 271 +/- 174 min, both P < 0.0001). Moreover, a reduction in total off time during LPP diet (3.3 +/- 2.7 hr vs. 4.7 +/- 3.3 hr, P < 0.0001), occurred also in the 9 patients who did not experience subjective benefit. No significant changes in hematological and biochemical variables or body composition were recorded; a slight reduction in body weight (mean, -1.8%) was observed. Consumption of LPP in the first part of the day ameliorates off periods in PD patients, but additional studies including pharmacokinetics are needed.

Thin section MR study of the basal ganglia in the differential diagnosis between striatonigral degeneration and Parkinson disease.

PURPOSE: Signal abnormalities within the putamen in MRI have been related to tissue degeneration in the striatonigral variant of multiple system atrophy (MSA-P). While previous work demonstrated the high specificity of these MR findings, sensitivity rates were unsatisfactory. We evaluated the specificity and sensitivity of an acquisition protocol using thin section MRI to differentiate MSA-P from Parkinson disease (PD). METHOD: Axial 3-mm-thick conventional T2 and proton density spin echo images at the level of basal ganglia were acquired at 1.5 T in 24 patients with MSA-P and 27 patients with PD. RESULTS: We found an abnormal putaminal T2 hypointensity in 21 of 24 MSA-P patients (87.5% sensitivity) and a proton density hyperintensity in 20 of 24 MSA-P patients (83.3% sensitivity). Three among 27 PD patients had an abnormal putaminal T2 hypointensity (88.8% specificity) and there were no proton density abnormalities (100% specificity). CONCLUSION: Our thin section conventional spin echo protocol showed a substantial increase in MR sensitivity compared with previous reports. We believe that a better depiction of even mild signs of degeneration in the putamen may allow a more widespread use of this technique in the differential diagnosis of parkinsonisms.

Tc-99m ethylene cysteinate dimer SPECT in the differential diagnosis of parkinsonism.

Positron emission tomography (PET) and network analysis have been used to identify a reproducible pattern of regional metabolic covariation that is associated with idiopathic Parkinson's disease (PD). The activity of this PD-related pattern can be quantified in individual subjects and used to discriminate PD patients from atypical parkinsonians. Because PET is not commonly available, we sought to determine whether similar discrimination could be achieved using more routine single photon emission computed tomography (SPECT) perfusion methods. Twenty-three subjects with PD (age, 63 +/- 9 years), 22 subjects with multiple system atrophy (MSA; age, 64 +/- 7 years), and 20 age-matched healthy controls (age, 62 +/- 13 years) underwent SPECT imaging of regional cerebral perfusion with Tc-99m ethylene cysteinate dimer (ECD). Using network analysis, we determined whether a PD-related pattern existed in the SPECT data, and whether its expression discriminated PD from MSA patients. Additionally, we compared the accuracy of group discrimination achieved by this pattern with that of the PET-derived PD-related pattern applied to the SPECT data. Network analysis of the SPECT data identified a significant pattern characterized by relative increases in cerebellar, lentiform, and thalamic perfusion covarying with decrements in the frontal operculum and in the medial temporal cortex. Subject scores for this pattern discriminated PD patients from controls (P < 0.01) and from MSA patients (P < 0.03). Subject scores for the PET-derived PD-related pattern computed in the individual SPECT scans more accurately distinguished PD patients from controls (P < 0.005) and from MSA patients (P = 0.0002). A significant PD-related covariance pattern can be identified in SPECT perfusion data. Moreover, the disease related pattern identified previously with PET can be applied to individual SPECT perfusion scans to provide group discrimination between PD patients, healthy controls, and individuals with MSA. Because of significant individual subject overlap between groups, however, the clinical utility of this method in the differential diagnosis of Parkinsonism remains uncertain.