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Neurology

Volume 54 . Number 3 . February 8, 2000

Copyright © 2000 American Academy of Neurology

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Articles

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Differentiation of atypical parkinsonian syndromes with routine MRI

A. Schrag MD, C. D. Good FRCR, K. Miszkiel FRCR, H. R. MRCP, C. J.

Mathias MD, A. J. Lees MD, N. P. Quinn MD

From the Departments of Clinical Neurology (Drs. Schrag, Mathias, Lees, and

Quinn), Neuroradiology (Drs. Good, Miszkiel, and ), and the Autonomic

Unit (Dr. Mathias), Institute of Neurology, London, UK.

Received May 18, 1999.

Accepted in final form September 16, 1999.

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Address correspondence and reprint requests to Dr. N.P. Quinn, Department of

Clinical Neurology, Institute of Neurology, Queen Square, London WC1 3BG,

UK.

Objective: To evaluate the use of routine MRI in differentiating between

patients with progressive supranuclear palsy (PSP), multiple system atrophy

(MSA), corticobasal degeneration (CBD) and control subjects.

Methods: Two neuroradiologists rated blindly and independently axial

T2-weighted and proton density MR images of 54 patients with MSA, 35

patients with PSP, 5 patients with CBD, and 44 control subjects.

Results: More than 70% of patients with PSP and more than 80% of patients

with cerebellar predominant MSA could be classified correctly with 0.5-T or

1.5-T scans, and no patient in these groups was misclassified. In the

remaining patients an unequivocal differentiation could not be made.

However, only approximately 50% of patients with parkinsonism-predominant

MSA could be classified correctly, and 19% of them (all of whom had had

0.5-T scans) were misclassified.

Conclusions: Characteristic findings on routine MRI, either 1.5 T or 0.5 T,

can contribute to the identification of MSA and PSP. However, in a minority

of patients no unequivocal diagnosis can be made using MRI findings alone.

Key words: Progressive supranuclear palsy; Multiple system atrophy;

Corticobasal degeneration; MRI; Diagnosis

Introduction

The clinical differentiation of atypical parkinsonian syndromes--such as

multiple system atrophy (MSA), progressive supranuclear palsy (PSP), and

corticobasal degeneration (CBD)--from idiopathic Parkinson's disease (IPD)

and between each other is often difficult, leading to misdiagnosis even up

to the time of death. [1] [2]

We examined the value of routine MRI in differentiating patients with MSA

from patients with IPD and from control subjects. [3] The findings

characteristically differentiating MSA from IPD patients and control

subjects were: supratentorially, a hyperintense rim at the putaminal edge,

putaminal hyperintensity (on 0.5-T scans only), and putaminal atrophy; and

infratentorially, atrophy and signal change, corresponding to degeneration

of pontine nuclei, transverse pontine fibers, Purkinje cells, and cell loss

in the inferior olives. The majority of MSA patients showed these

abnormalities. However, in a minority of patients with predominantly

parkinsonian features (MSA-P) with none of these specific findings, MRI

alone was not helpful diagnostically, even though a clinical diagnosis of

probable MSA could be made. MR images in IPD patients did not differ in any

of the investigated findings from those in control subjects. In PSP, MRI has

often been considered to be of little help in making a diagnosis. [4]

Nevertheless, a number of findings suggestive of PSP--such as midbrain

atrophy with enlargement of the third ventricle [4] and pontine tegmental

atrophy, signal increase in the midbrain, as well as frontal and temporal

lobe atrophy later on [5] --have all been described. Occasionally, signal

increase in the inferior olives was also seen. [6] On the other hand, MRI in

CBD can show cortical atrophy and hypointensity of putamen and globus

pallidus, and asymmetry of global atrophy, when sought specifically. [7] In

a recent study comparing MR images of PSP and CBD patients, midbrain atrophy

was found to be highly specific for PSP, and asymmetric frontoparietal

atrophy for CBD. [8] We studied the specificity and sensitivity of these

findings in a direct and blinded evaluation of MR images in MSA compared

with PSP and CBD patients.

Methods.

Patients.

We examined MR images of 35 patients with PSP, in four of whom the diagnosis

was confirmed subsequently at autopsy. Twenty-three of these patients

fulfilled the National Institute of Neurological Disorders and Stroke

criteria [9] for probable PSP, and eight patients met the criteria for

possible PSP because they did not have falls within the first year of

symptom onset. However, all of these patients fulfilled other proposed

criteria for PSP. [10] [11] A total of 54 patients had clinically probable

MSA, [12] two cases of which were proved subsequently pathologically, and 30

of whom had MSA-P and 24 MSA-C (with predominantly cerebellar features).

Five patients had CBD (autopsy confirmed in four patients) according to

criteria derived from clinicopathologic correlation. [13] A total of 44

control subjects had no clinical suspicion of parkinsonism. None of the

diagnostic criteria for PSP, MSA, or CBD incorporate or are influenced by

MRI findings, except when they point to an alternative diagnosis. Mean age

was not different between the groups, but disease duration was shorter in

the PSP group than in the MSA and CBD groups (both, p < 0.05). Table 1

provides the demographic data. In addition, we evaluated the MR images of

nine patients with atypical parkinsonism in whom a probable clinical

diagnosis could not be made according to the previously mentioned criteria.

Table 1. Patient characteristics Characteristic Control subjects CBD

patients PSP patients MSA-P patients MSA-C patients

0.5 tesla

n 30 3 23 16 15

M:F 21:9 2:1 13:10 11:5 11:4

Mean age, y (range) 61.1 (40-75) 62 (43-72) 66.1 (43-79) 59.8 (45-75) 58.7

(50-66)

Mean disease duration, y (range) -- 5 (2-7) 2.9 (1-10) 4.8 (0.5-16) 4.1

(1-6)

1.5 tesla

n 14 2 12 14 9

M:F 9:5 1:1 8:4 8:6 8:1

Mean age, y (range) 60.2 (47-79) 66.5 (61-72) 64.8 (53-74) 64 (43-76) 59

(55-68)

Mean disease duration, y (range) -- 4 (2-6) 2.9 (1-5) 3.4 (1-8) 4.4 (1-8)

Total n 44 5 35 30 24

CBD = corticobasal degeneration; PSP = progressive supranuclear palsy; MSA-P

= multiple system atrophy parkinsonian features; MSA-C = MSA, cerebellar

features.

MRI evaluation.

All patients had axial and one midsagittal T2-weighted and proton-density

scans. A total of 23 PSP patients, 31 MSA patients, 3 CBD patients, 30

control subjects, and 3 patients with an unclear diagnosis were examined on

a 0.5-T Vectra scanner (General Electric Medical Systems, Milwaukee, WI),

and 12 PSP patients, 23 MSA patients, 2 CBD patients, 14 control subjects,

and 6 patients with an unclear diagnosis were examined on a 1.5-T Signa

scanner (General Electric Medical Systems, Milwaukee, WI). On the 0.5-T

scanner, repetition time (TR) was 2,400 to 3,800 msec, echo time (TE) was 23

to 35 msec and 90 to 92 msec, slice thickness was 6 mm, and the interslice

gap was 0.2 to 2 mm. On the 1.5-T scanner, TR was 2,400 to 4,000 msec, TE

was 20 to 39 msec and 90 to 100 msec, slice thickness was 5 mm, and the

interslice gap was 1.5 to 2 mm. Two experienced neuroradiologists rated all

the scans independently and were blind to the diagnosis or clinical features

except for age of the patient. The abnormal features evaluated were the

presence of global atrophy, frontal or temporal lobe atrophy exceeding the

global atrophy, a hyperintense lateral margination of the putamen (compared

with cortical signal), putaminal atrophy, putaminal hyper- or hypointense

signal relative to that of the globus pallidus, atrophy or abnormal signal

in the globus pallidus, thinning or smudging of the substantia nigra, and

abnormality of the red or subthalamic nucleus (STN). Other midbrain

abnormalities evaluated were atrophy and signal change of tectum or

tegmentum, and an anteroposterior midbrain diameter of less than 17 mm on

axial scan. The infratentorial items evaluated were the presence of atrophy

or signal change in the pons (diffuse or in the shape of a " hot-cross bun "

[3] ), middle cerebellar peduncles, cerebellum, medulla and inferior olives,

and the width of the third and fourth ventricles. All paired abnormalities

were evaluated for each side. Visual rating (other than measuring the

midbrain diameter) was preferred to volumetric measurements because these

were considered invalid in this retrospective study with varying slice

positions, and moreover are not in routine use.

Statistical comparison was performed with the chi-square test and Fisher's

exact test. Interrater reliability was calculated with Cohen's kappa (kappa

< 0.20 [slight agreement] to 0.81 to 1.00 [excellent agreement]. Comparison

of means was performed with the t -test for independent samples. Statistical

comparison of each item between all four groups was performed separately and

combined for 0.5-T and 1.5-T scans, and a finding was defined as abnormal if

at least one rater found an abnormality.

Results.

Interrater reliability was excellent (kappa = 0.81 to 1.0) for atrophy and

signal increase of middle cerebellar peduncles, pontine atrophy, and the

" hot-cross bun sign. " It was slight for diffuse signal changes in the pons

and medulla (both seen in two patients by only one rater), which were

therefore excluded from additional analysis. Signal increase in globus

pallidus (kappa = 0.56) and putamen (kappa = 0.66) were seen exclusively on

0.5-T scans , and signal decrease of globus pallidus and putamen was seen

almost exclusively on 1.5-T scans (kappa = 0.5 and kappa = 0.46).

Abnormalities of the STN were not seen, and hyperintensity of the red

nucleus was seen only on 0.5-T scans. For the remaining findings the

interrater reliability was good to fair (kappa = 0.41 to 0.8), and similar

for 0.5-T and 1.5-T scans.

Abnormal findings that occurred significantly more frequently in MSA and PSP

patients than control subjects are shown in table 2, table 3. The most

frequently seen abnormalities in PSP were signal increase and atrophy of the

midbrain, thinning or smudging of the substantia nigra, atrophy of the

putamen, atrophy and signal increase of globus pallidus (on 0.5-T scans),

and atrophy of the red nucleus. Supratentorial atrophy was seen in the

temporal and frontal lobes, and infratentorial atrophy was seen in the

cerebellum, pons, and middle cerebellar peduncles. Infratentorial signal

increase or atrophy of other infratentorial structures, hyperintense

putaminal rim, or putaminal hyperintensity were seen rarely, and were seen

only by one rater on scans otherwise showing the previously mentioned

findings typical for PSP. Typical for MSA-P were a hyperintense putaminal

rim, putaminal atrophy and hyperintensity, atrophy and signal decrease of

the globus pallidus (mainly on 1.5-T scans), thinning or smudging of the

substantia nigra, and infratentorial signal increase and atrophy. However,

midbrain atrophy and signal increase and dilatation of the third ventricle

was also seen. On the other hand, no patient had temporal or frontal lobe

atrophy, a midbrain diameter less than 17 mm, or signal increase of the

globus pallidus. Scans of patients with MSA-C all showed infratentorial

atrophy and signal change. The majority also had some atrophy of the

midbrain, but the midbrain diameter was smaller than 17 mm in only two of

them. Putaminal atrophy was found in 50%, and a hyperintense putaminal rim

in a third, and substantia nigra thinning or smudging in more than half of

all MSA patients. All CBD patients had global atrophy, but there was no

marked asymmetry. Most patients in this group had thinning or smudging of

the substantia nigra, signal change in the globus pallidus, and dilatation

of the third ventricle, and some had midbrain atrophy (marked only in one

patient) or signal increase, and infratentorial atrophy. However, no scan

showed infratentorial signal increase, temporal or frontal lobe atrophy

exceeding the global atrophy, a putaminal hyperintense rim or

hyperintensity, or globus pallidus atrophy.

Table 2. Abnormalities differentiating progressive supranuclear palsy from

multiple system atrophy Region Abnormality Sensitivity PPV Specificity p

Value

Midbrain Dilatation of third ventricle 77§ 71 80 <0.001

Signal increase 60§ 56 70 <0.01

Diameter < 17 mm 23§ 80 96 <0.05

Atrophy 77§ 44 37 NS

Supratentorial Frontal lobe atrophy 17 75 96 <0.05

Temporal lobe atrophy 20 78 96 <0.05

Globus pallidus Signal increase on 0.5-T scans * 35 82 94 <0.05

Red nucleus Atrophy 26§ 82 96 <0.005

Signal increase on 0.5 T scans * 13 100 100 NS

PPV = positive predictive value; NS = not significant.

* Results of 0.5- and 1.5-T (MRI scans combined apart from * = on 0.5-T

scans only.

p < 0.05, and §p < 0.001 compared with control subjects.

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Table 3. Abnormalities differentiating multiple system atrophy from

progressive supranuclear palsy Variable Abnormality Sensitivity PPV

Specificity p Value

Infratentorial signal increase Signal increase in cerebellum 30§ 100 100

<0.001

Signal increase in m.c. peduncles 50§ 93 94 <0.001

" Hot-cross bun " sign 50§ 97 97 <0.001

Signal increase in inferior olives 13 100 100 <0.05

Infratentorial atrophy Dilatation of fourth ventricle 56§ 94 94 <0.001

Dentate atrophy 48§ 97 97 <0.001

Atrophy of m.c. peduncles 56§ 84 83 <0.001

Medullary atrophy 44§ 88 91 <0.001

Atrophy of inferior olives 37§ 86 91 <0.001

Pontine atrophy 57§ 69 60 NS

Putamen Hyperintensity * 26 100 100 <0.01

Hyperintense rim 30§ 84 91 <0.05

PPV = positive predictive value; m.c. = middle cerebellar; NS = not

significant.

* Results of 0.5- and 1.5-T MRI scans combined apart from * = on 0.5-T scans

only, p < 0.05, p < 0.005, §p < 0.001 compared with control subjects.

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Abnormalities discriminating between PSP, MSA, and CBD.

Factors that differentiated PSP from MSA significantly were a midbrain

diameter of less than 17 mm, dilatation of the third ventricle and signal

increase of the midbrain (figure), frontal and temporal lobe atrophy, signal

increase in the globus pallidus (on 0.5-T scans), and atrophy of the red

nucleus. Signal increase of the red nucleus was seen exclusively in PSP and

only on 0.5-T scans, but this was not significant, probably due to small

numbers (see table 2). Abnormalities of the STN, which is pathologically

involved in PSP, were not seen, but we only evaluated axial scans, on which

this nucleus is not well visualized. The features that were seen

significantly more frequently in MSA-P than in PSP patients were the

presence of signal increase in cerebellum, middle cerebellar peduncles and

pons (hot-cross bun sign), dilatation of the fourth ventricle, atrophy of

the dentate nucleus, signal decrease in the globus pallidus (mainly on 1.5-T

scans), and a hyperintense rim or hyperintensity of the whole putamen (the

latter only on 0.5-T scans). MSA-C differed significantly from PSP in all

infratentorial abnormalities (signal increase and atrophy). Moderate

midbrain atrophy (with a midbrain diameter of more than 17 mm), atrophy of

globus pallidus or putamen, putaminal hypointensity, and smudging of the

substantia nigra did not help to differentiate between these conditions. The

only finding seen more frequently in CBD than in MSA-P patients was global

atrophy (100% versus 36%, p < 0.05) and hyperintensity of the globus

pallidus on 0.5-T scans (p < 0.05). Hyperintensity of the globus pallidus

was also more frequent than in PSP patients (p < 0.05). No other finding was

significantly different between CBD and PSP or MSA patients. This was most

likely due to the small number of patients with this rare disorder.

Figure. Moderate midbrain atrophy and hyperintensity in a patient with

progressive supranuclear palsy on a 0.5-T scan.

The sensitivity (proportion of patients with a disease who have the abnormal

finding), specificity (proportion of patients who do not have the disease

who do not have the abnormality), and positive predictive value (likelihood

of a person with the abnormal finding to have the disease) for the

abnormalities are presented in table 2, table 3. Using the abnormalities

that differentiated MSA and PSP with a high positive predictive value and

good specificity as criteria for classification (table 4), a correct

classification could be made in the great majority of PSP and MSA-C patients

with either 1.5-T or 0.5-T scans (table 5). No patient in these groups was

misclassified. However, a substantial minority could not be classified

unequivocally (nine patients [26%] with PSP [two definite, four probable,

and three possible] and four patients [17%] with MSA-C), because either none

of the characteristic abnormalities was found or abnormalities

characteristic for both PSP and MSA were seen. Moreover, only half of the

patients classified clinically as having MSA-P could be classified correctly

by MRI findings, and 19% were classified incorrectly because of the presence

of at least one finding characteristic for PSP. We found no abnormalities

specific for CBD. Overall, 1.5-T scans were slightly more sensitive than

0.5-T scans because only one patient with possible PSP (8%) had no

abnormalities on 1.5-T scans, whereas one patient with possible PSP (4%) and

four patients with MSA (13%) had no abnormalities on 0.5-T scans.

Table 4. Criteria for the differentiation of progressive supranuclear palsy,

MSA-P, and MSA-C on routine MRI in a patient with atypical parkinsonism

Progressive supranuclear palsy MSA-P MSA-C

Midbrain diameter on axial scans < 17 mm Hyperintense putaminal rim

Dilatation of the fourth ventricle

Signal increase in the midbrain Putaminal hyperintensity * Atrophy of the

medulla, dentate nucleus, middle cerebellar peduncles, pons, inferior olives

Dilatation of the third ventricle Atrophy of the dentate nucleus Signal

increase in the cerebellum, middle cerebellar peduncles, pons (hot-cross bun

sign), inferior olives

Frontal or temporal lobe atrophy Dilatation of the fourth ventricle

Signal increase in the globus pallidus * Signal increase in the cerebellum,

middle cerebellar peduncles, pons (hot-cross bun sign)

Atrophy or signal increase of the red nucleus

MSA-P = multiple system atrophy with predominant parkinsonism; MSA-C = MSA

with predominant cerebellar features.

* On 0.5-T scan.

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Table 5. Correct classification using the proposed MRI criteria to

differentiate PSP and MSA patients Tesla PSP * MSA-P MSA-C

Percentage of patients who were classified correctly

0.5 78 44 80

1.5 67 57 89

Percentage of patients who were classified incorrectly

0.5 0 19 0

1.5 0 0 0

Percentage of patients who could not be classified unequivocally

0.5 22 38 20

1.5 33 43 11

PSP = progressive supranuclear palsy; MSA-P = multiple system atrophy with

parkinsonian features; MSA-C = MSA with cerebellar features.

* Presence of any of the following: midbrain diameter < 17 mm, signal

increase of midbrain, dilatation of the third ventricle, frontal or temporal

lobe atrophy, signal increase of globus pallidus on 0.5-T scan, or atrophy

of the red nucleus.

Presence of any of the following: hyperintense putaminal rim or putaminal

hyperintensity; signal increase in the cerebellum, middle cerebellar

peduncles, or pons (hot cross bun); atrophy of the dentate nucleus; or

dilatation of the fourth ventricle.

Presence of any of the following: signal increase or atrophy in the

cerebellum, middle cerebellar peduncles, pons (hot-cross bun), or inferior

olives; atrophy of the medulla or dentate nucleus; or dilatation of the

fourth ventricle.

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Clinical correlation.

Patients with parkinsonism in the MSA group had basal ganglia abnormalities

more frequently than those without parkinsonism (p < 0.01), and patients

with cerebellar dysfunction more often had infratentorial abnormalities (p <

0.05) than those without. In the PSP group, those who were later proved

pathologically to have PSP, or fulfilled criteria for probable PSP, [9] had

midbrain abnormalities more frequently than those who only fulfilled

possible criteria (p < 0.05). Disease duration was longer in PSP patients

with midbrain abnormalities (p < 0.01). However, disease duration, age, and

sex were not otherwise different between patients with the presence or

absence of basal ganglia, midbrain, or supra- or infratentorial findings in

the PSP or MSA groups. The numbers were too small to show any correlations

in the CBD group.

Patients with uncertain diagnosis.

In these nine patients with atypical parkinsonism in whom a differentiation

between MSA and PSP could not be made according to published criteria, the

MR image revealed findings typical for PSP in three patients (33%) and

typical for MSA in two patients (22%). In the four remaining patients (44%),

no specific abnormality was found.

Discussion.

In this study routine MRI revealed characteristic findings that can be used

in clinical practice to help differentiate between PSP and MSA. Using the

proposed criteria (see table 4) most patients in the PSP and MSA-C groups

could be classified unequivocally with either 1.5-T or 0.5-T scans (74% and

83%). However, in the MSA-P group only slightly more than half of the

patients could be classified using 1.5-T scans, and less than 50% could be

classified using 0.5-T scans. Moreover, 0.5-T scans misclassified 19% of MSA

patients as having PSP. Although in all patients this was due to one or two

abnormalities seen mostly by one rater, 0.5-T scans seem unsuitable for

differentiating between MSA-P and PSP. On the 1.5-T scans, 47% of patients

still could not be classified unequivocally, even though a clinical

diagnosis was already possible. The only clinical factors that discriminated

patients who had characteristic findings on MRI from those who did not were

disease duration and diagnostic certainty in the PSP group, which correlated

with the presence of midbrain atrophy. This comparatively low sensitivity of

MRI abnormalities in MSA-P is in accordance with our previous finding [3] of

a high specificity, but lower sensitivity, of these MRI findings in

comparison with IPD and control subjects. In the current study, specific

changes were seen on all MR images of patients with MSA who had a 1.5-T

scan, and in 87% of those who had 0.5-T scans, which is more than in the

previous study. [3] This improved sensitivity may be due to the learning

curve, a change of investigators, and a slightly different patient group.

Our findings of high specificity, but limited sensitivity, of the described

MRI abnormalities in patients with MSA are in accordance with those of

Savoiardo et al. [4] On the other hand, unlike some other authors, [4] we

have also found MRI useful in supporting a diagnosis of PSP in the great

majority of patients. PSP could be differentiated from MSA by the presence

of hyperintensity and marked atrophy of the midbrain (<17 mm diameter) as

well as atrophy of the frontal or temporal lobes, signal increase in the

globus pallidus (on 0.5-T scans only), and atrophy of the red nucleus.

The only abnormality seen significantly more frequently in CBD patients than

in MSA patients in this study was global atrophy. However, the presence of

infratentorial signal change, a hyperintense putaminal rim, or putaminal

hyperintensity, which were characteristic for MSA, and atrophy of the globus

pallidus as well as frontal or temporal lobe atrophy exceeding the global

atrophy, which were characteristic for PSP and were not seen in any patient

with CBD, appear to make a diagnosis of CBD unlikely. There was no obvious

asymmetry in any of the paired abnormalities, but subtle changes may have

been missed because they were not sought specifically, and coronal scans,

which demonstrate asymmetric atrophy best, [8] were not performed.

Like others, we found considerable overlap in some findings between the

disease groups. This included thinning of the substantia nigra pars compacta

(which has been found in MSA and other types of parkinsonism including PD,

but not in control subjects [15] ), atrophy of the globus pallidus or

putamen, and midbrain atrophy (apart from marked midbrain atrophy with a

diameter of less than 17 mm on axial scans, which was characteristic for

PSP). Similar to our results in patients with MSA, others also found not

only atrophy of the cerebellum and pons, but also of the midbrain. [16]

These abnormalities, although differentiating atypical parkinsonism from

control subjects, are therefore not helpful in differentiating between

atypical parkinsonian syndromes with routine MRI. In addition, a higher

putaminal iron content than in IPD, as reflected in (mainly posterior)

putaminal hypointensity, has been shown in quantitative MRI studies in MSA,

[17] [18] but on visual evaluation of routine scans in this and other

studies [3] [15] [19] this was not a discriminating factor between MSA and

IPD or control subjects, or between different atypical parkinsonian

syndromes.

There are some limitations to this study. Most importantly, the same group

of patients was used to determine the abnormalities characteristic for the

diseases and to test the value of these findings in differentiating them.

Thus, the criteria may be less effective in a different group of patients

than shown in this sample in table 5. Therefore, the proposed criteria

should be used to support diagnostic classification but should be

interpreted with caution. Because none of the findings had optimal

sensitivity, specificity, positive and negative predictive values, and may

not be equally effective in differentiating other diseases (e.g., Pick's

disease), they should always be interpreted in a clinical context. Second,

the size of the disease groups probably does not reflect the proportions of

patient groups in a typical movement disorder clinic, where PSP is as

frequent as MSA. CBD is rare, and the small size of this group precluded

valid statistical comparisons. Furthermore, cortical asymmetry in CBD could

have been missed as a discriminating factor for this condition because it

was not sought specifically, and coronal scans were not performed. Lastly,

the sensitivity of MRI findings in MSA and PSP might have been slightly

higher if only 1.5-T scans had been used, particularly in patients with

MSA-P. However, sensitivity and specificity differed only slightly between

0.5- and 1.5-T scans.

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