- Email: [email protected]
18[F]-FDG PET study on the Idiopathic Parkinson's disease from several parkinsonian-plus syndromes
Parkinsonism and Related Disorders 18S1 (2012) S60–S62
Contents lists available at ScienceDirect
Parkinsonism and Related Disorders journal homepage: www.elsevier.com/locate/parkreldis
18 [F]-FDG
PET study on the Idiopathic Parkinson’s disease from several parkinsonian-plus syndromes Ping Zhaoa,b , Benshu Zhanga, *, Shuo Gaoc a Department
of Neurology, Second Hospital of Tianjin Medical University, Tianjin, China of Neurology, General Hospital of Tianjin Medical University, Tianjin, China c Department of Nuclear Medicine, General Hospital of Tianjin Medical University, Tianjin, China b Department
article info
summary
Keywords: Parkinson’s disease Parkinsonism-plus syndrome 18 F-FDG PET Differential diagnosis Neurodegenerative disease
Objective: To investigate the difference in glucose metabolism on 18 F-fluorodeoxyglucose positron emission tomography (18 F-FDG PET) imaging for differential diagnosis of idiopathic Parkinson’s disease (IPD) from several parkinsonian-plus syndromes using SPM2 approach. Methods: 18 F-FDG PET was performed for 18 IPD patients, 22 multiple system atrophy (MSA) patients, 13 progressive supranuclear palsy (PSP) patients, 5 corticobasal degeneration (CBD) patients, 7 dementia with Lewy bodies (DLB) patients and 1 normal pressure hydrocephalus (NPH) patient. Imaging-based diagnosis was obtained by statistical parametric mapping (SPM2) software to analyze the differences and overlaps among these groups. Result: The 18 F-FDG PET images analyzed with SPM2 demonstrated that a reduction in glucose metabolism occurred in bilateral parietal area for IPD, in bilateral putamen for MSA-P, in bilateral cerebellum for MSA-C, in midbrain and the middle frontal cortex for PSP, in asymmetrical metabolism of the cortex and the basal ganglia for CBD, in bilateral occipital and parieto-occipital areas for DLB. The metabolic reductions in a patient of NPH group were observed in the ventricular system. Conclusions: This study identifies different patterns of glucose metabolism in parkinsonism. 18 F-FDG PET imaging may contribute to early differential diagnosis in clinically ambiguous cases of parkinsonism. © 2011 Elsevier Ltd. All rights reserved.
1. Introduction The diagnosis of IPD can be straightforward in patients with typical clinical presentation of cardinal signs, but misdiagnosis of IPD is not uncommon. In a clinical pathological study, the accuracy of a clinical diagnosis of IPD is not high, with only 76% of post-mortem confirmed cases being diagnosed correctly [1]. The most common misdiagnoses are related with parkinsonism-plus syndromes (PPS) such as multiple system atrophy (MSA), progressive supranuclear palsy (PSP), corticobasal degeneration (CBD) and dementia with Lewy bodies (DLB) [2–4]. Since prognosis and treatment options of IPD and PPS are substantially different, differential diagnosis of IPD from PPS is critical for clinicians. Metabolic brain imaging by 18 F-FDG PET has showed characteristic reduction in glucose metabolism in the different areas in neurodegenerative diseases such as IPD and PPS [5,6]. 18 F-FDG PET can be used to differentiate various kinds of PPS patients from IPD patients, especially at the early disease stages when no
characteristic features occur on MRI. In this study, we aimed to characterize the differences in glucose metabolism on 18 F-FDG PET for differential diagnosis among IPD, MSA, PSP, CBD and DLB. In addition, one normal pressure hydrocephalus (NPH) patient was included in this study. 2. Subjects and Methods 2.1. Subjects This study included 18 IPD patients, 10 MSA-P patients and 12 MSAC patients, 13 PSP patients, 5 CBD patients, 7 DLB patients, 1 NPH patient and 40 age-matched healthy controls. The study was approved by the Medical Ethics Committee of the Tianjin Medical University, and all subjects gave their informed consent. Subjects were selected from patients with a clinical diagnosis of neurodegenerative disease. 2.2.
* Corresponding author. Benshu Zhang, Department of Neurology, General Hospital of Tianjin Medical University, No. 154, Anshan Road, Heping District, Tianjin, 300052, China. E-mail address: [email protected] (B. Zhang). 1353-8020/$ – see front matter © 2011 Elsevier Ltd. All rights reserved.
18
F-FDG PET imaging
The PET scans were performed in a 3 dimensional mode using GE Discovery LS PET/CT system. Subjects were administered with an intravenous bolus injection of 1.85–3.7 MBq (5–10 mCi/)
P. Zhao et al. / Parkinsonism and Related Disorders 18S1 (2012) S60–S62
S61
Fig. 1. 18 F-FDG PET images from SPM analysis in these groups. (A) In the IPD group, the hallmark of glucose metabolism is a decreased metabolism in bilateral parietal lobe.(B) In the MSA-P group, the distinguishing feature is the decreased metabolism in bilateral basal ganglia. (C) In the MSA-C group, the distinguishing feature is the presence of a glucose hypometabolism in bilateral cerebellum. (D) In the PSP group, the distinguishing feature is a decreased metabolism in midbrain and the middle frontal cortex. (E) In the CBD group, the distinguishing feature is the presence of a glucose hypometabolism in asymmetrical metabolism of the cortex and the basal ganglia. (F) In the DLB group, the distinguishing feature is the presence of a glucose hypometabolism in bilateral occipital and parieto-occipital areas. 18 F-FDG and 18 F-FDG scan were obtained. Three-dimensional data acquisition mode was performed, and images were collected with slice thickness of 2 mm collected in 128 × 128 matrix. Changes of 18 F-FDG metabolism in regions of interest were analyzed using visual inspection and SPM2 methods.
2.3. Statistical analysis Analyses were performed using SPSS 11.5. All values were presented as mean and standard deviation. Student t test was used to compare the difference among IPD patients and PPS patients. Categorical data were compared with chi square. Probability values less than 0.05 were considered statistically significant. 3. Results 3.1. Clinical characteristics 18 IPD patients (13 males, age 61.33±10.70 years), 10 MSAP patients (4 males, age 66.20±7.36 years), 12 MSA-C patients (5 males, age 58.83±8.98 years), 13 PSP patients (9 males, age 66.15±11.77 years), 5 CBD patients (3 males, age 58.40±11.59 years), 7 DLB patients (5 males, age 74.86±7.01 years), 1 NPH patient (male, age 48 years) and 40 normal controls (22 males, age 60.94±11.09 years) underwent 18 F-FDG PET studies. Patient age, gender and disease duration did not differ significantly among these groups. 3.2.
18
F-FDG PET imaging
For visual inspection of 18 F-FDG PET images, we did not identify a significant characteristic pattern of glucose metabolism between IPD group and other groups. We performed SPM2 analysis of the differences in 18 F-FDG PET images among these groups. In the IPD group, the hallmark of glucose metabolism was a decreased metabolism in parietal areas (Fig. 1A). 11 (61.11%) of 18 IPD patients showed a bilateral reduction in glucose metabolism. Hypometabolic areas in these patients were also observed in parieto-occipital, frontal, occipital, and temporal cortical areas in 3, 3, 2 and 2 IPD patients, respectively. The glucose metabolism was not significantly different in 3 IPD patients compared with controls. Hypometabolic areas in MSA-P patients were observed in bilateral putamen and caudate (Fig. 1B). This finding was found in 7 of 10 patients, and 2 of them also had a mild and
local reduction in glucose metabolism in bilateral cerebellum. In addition, hypometabolic areas were also observed in bilateral frontal, parietal, occipital, and insular cortical areas. Hypometabolic areas in MSA-C patients were observed in bilateral cerebellum (Fig. 1C). All 12 patients had this distinct characteristics, and 8 (66.67%) of them also showed a hypometabolism in the middle cerebellar peduncle. In addition, hypometabolic areas were also observed in pons and oblongata, frontal area, parietal and occipital area in 1, 4 and 2 of MSA-C patients, respectively. Hypometabolic areas in PSP patients were observed in midbrain. 12 (92.31%) of 13 PSP patients showed a hypometabolism in the midbrain, and also 5 (38.46%) patients showed a reduction in glucose metabolism in bilateral frontal areas, specially in the middle frontal cortex and cingulate gyrus (Fig. 1D). In addition, 1 patient also showed a reduction in glucose metabolism in superior cerebellar peduncle. Hypometabolic areas in CBD patients were observed in asymmetrical frontal, parietal, temporal and insular lobe, as well as in putamen contralateral to the clinically most affected side (Fig. 1E). 1 patient exhibited a decreased metabolism in thalamus contralateral to the affected side. Hypometabolic areas were observed in bilateral occipital and parieto-occipital areas in all DLB patients (Fig. 1F). Hypometabolic areas were also observed in bilateral frontal and temporal areas in 2 DLB patients. The comparison of the NPH patient with the normal controls showed a statistically significant decrease in glucose metabolism in the periventricular areas such as bilateral parietal, temporal, occipital and insular lobe, as well as the cingulate gyrus and basal ganglia. 4. Discussion In this study, we seek to study the images of IPD and other parkinsonian disorders to find possible discriminating patterns of 18 F-FDG PET imaging. The glucose hypometabolism was found mainly in the parietal areas in our IPD patients with no sign of dementia. This finding agrees with a previous report that the glucose metabolism was decreased in the parietal and parietooccipital regions in non-demented Parkinson’s patients [7]. In addition, very few patients in MSA-P and MSA-C patients exhibits a hypometabolism in parietal area, suggesting that it is a good parameter for differentiation of IPD form MSA.
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P. Zhao et al. / Parkinsonism and Related Disorders 18S1 (2012) S60–S62
Our study also showed that glucose hypometabolism mainly occurs in bilateral putamen for MSA-P patients and in cerebellum for MSA-C patients, suggesting that it has a good parameter for differential diagnosis of MSA and IPD. This character of PET image is consistent with neuropathologic feature of MSA-P (predominated in basal ganglia) and MSA-C (predominated in cerebellum) [8]. Furthermore, the hypometabolism in cerebellum show the highest specificity in diagnosis of MSA-C, since this feature is present in all MSA-C patients, but not in IPD patients. The neurological features of PSP include an impaired ocular motility, pseudobulbar palsy and dystonia [3,9]. A diminished blood flow in the midbrain and the middle frontal cortex is consistently observed in patients with PSP. In addition, a reduction in glucose metabolism in superior cerebellar peduncle suggests that cerebellum may be involved. CBD can present clinically as unilateral parkinsonism but also with any of a variety of asymmetrical cortical degeneration syndromes such as asymmetrical ideomotor apraxia, alien-limb phenomenon and non-fluent aphasia [10]. Our finding that asymmetrical reduction in glucose metabolism is observed in frontal, parietal, temporal, insular lobe and putamen is consistent with the clinical signs of CBD patients. This finding agrees with previous PET studies that the patients with CBD showed an asymmetrical decrease in the brain metabolism in the cortical and subcortical regions [11]. Visual hallucinations are the most characteristic neuropsychiatric features of DLB [12], and our finding that greater metabolic reduction occurs in bilateral occipital cortex is compatible with neurodegenerative changes in visual occipital cortex in DLB. Our study suggests that abnormality of visual cortex and visual association cortex function exist at an early stage of dementia. In addition, hypometabolism of periventricular areas in 18 F-FDG PET may be the character pattern of NPH patient. In our study, the overall correct diagnosis rate 18 F-FDG PETbase diagnosis with clinical diagnosis was 86.36%. This may be result from 3 IPD patients who did not exhibit any difference in glucose metabolism from controls. These 3 IPD patients with normal glucose metabolism are needed to be confirmed with the progression of the disease to exclude the possibility of other parkinsonism-plus syndromes. In summary, 18 F-FDG PET imaging is helpful for differentiating IPD from PPS, especially at the early disease stages when the symptom and signs are not typical for differential diagnosis.
Acknowledgements We thank Department of Neurology and Department of Nuclear Medicine at General Hospital of Tianjin Medical University for collaboration.
Conflict of interests The authors have not received any kind of financial assistance and fellowships, and have no relevant conflicts of interest to disclose.
References 1. Rajput AH, Rozdilsky B, Rajput A. Accuracy of clinical diagnosis in parkinsonism – a prospective study. Can J Neurol Sci 1991;18:275–8. 2. Hughes AJ, Daniel SE, Ben-Shlomo Y, Lees AJ. The accuracy of diagnosis of parkinsonian syndromes in a specialist movement disorder service. Brain 2002;125:861–70. 3. Poewe W, Wenning G. The differential diagnosis of Parkinson’s disease. Eur J Neurol 2002;9(Suppl 3):23–30. 4. Savoiardo M. Differential diagnosis of Parkinson’s disease and atypical parkinsonian disorders by magnetic resonance imaging. Neurol Sci 2003; 24(Suppl 1):S35–7. 5. Kwon KY, Choi CG, Kim JS, Lee MC, Chung SJ. Comparison of brain MRI and 18F-FDG PET in the differential diagnosis of multiple system atrophy from Parkinson’s disease. Mov Disord 2007;22:2352–8. 6. Teune LK, Bartels AL, de Jong BM, Willemsen AT, Eshuis SA, de Vries JJ, et al. Typical cerebral metabolic patterns in neurodegenerative brain diseases. Mov Disord 2010;25:2395–404. 7. Hu MT, Taylor-Robinson SD, Chaudhuri KR, Bell JD, Labbe C, Cunningham VJ, et al. Cortical dysfunction in non-demented Parkinson’s disease patients: a combined (31)P-MRS and (18)FDG-PET study. Brain 2000;123(Pt 2):340–52. 8. Ozawa T, Paviour D, Quinn NP, Josephs KA, Sangha H, Kilford L, et al. The spectrum of pathological involvement of the striatonigral and olivopontocerebellar systems in multiple system atrophy: clinicopathological correlations. Brain 2004;127:2657–71. 9. Kato N, Arai K, Hattori T. Study of the rostral midbrain atrophy in progressive supranuclear palsy. J Neurol Sci 2003;210:57–60. 10. Kumar R, Bergeron C, Lang A. Cortical basal degeneration. In: Jankovic J, Tolosa E, editors. Parkinson’s disease and movement disorders. Baltimore, MD: Lippincott Williams and Wilkins; 2002, pp. 185–98. 11. Juh R, Pae CU, Kim TS, Lee CU, Choe B, Suh T. Cerebral glucose metabolism in corticobasal degeneration comparison with progressive supranuclear palsy using statistical mapping analysis. Neurosci Lett 2005;383:22–7. 12. McKeith IG, Dickson DW, Lowe J, Emre M, O’Brien JT, Feldman H, et al. Diagnosis and management of dementia with Lewy bodies: third report of the DLB Consortium. Neurology 2005;65:1863–72.
Contents lists available at ScienceDirect
Parkinsonism and Related Disorders journal homepage: www.elsevier.com/locate/parkreldis
18 [F]-FDG
PET study on the Idiopathic Parkinson’s disease from several parkinsonian-plus syndromes Ping Zhaoa,b , Benshu Zhanga, *, Shuo Gaoc a Department
of Neurology, Second Hospital of Tianjin Medical University, Tianjin, China of Neurology, General Hospital of Tianjin Medical University, Tianjin, China c Department of Nuclear Medicine, General Hospital of Tianjin Medical University, Tianjin, China b Department
article info
summary
Keywords: Parkinson’s disease Parkinsonism-plus syndrome 18 F-FDG PET Differential diagnosis Neurodegenerative disease
Objective: To investigate the difference in glucose metabolism on 18 F-fluorodeoxyglucose positron emission tomography (18 F-FDG PET) imaging for differential diagnosis of idiopathic Parkinson’s disease (IPD) from several parkinsonian-plus syndromes using SPM2 approach. Methods: 18 F-FDG PET was performed for 18 IPD patients, 22 multiple system atrophy (MSA) patients, 13 progressive supranuclear palsy (PSP) patients, 5 corticobasal degeneration (CBD) patients, 7 dementia with Lewy bodies (DLB) patients and 1 normal pressure hydrocephalus (NPH) patient. Imaging-based diagnosis was obtained by statistical parametric mapping (SPM2) software to analyze the differences and overlaps among these groups. Result: The 18 F-FDG PET images analyzed with SPM2 demonstrated that a reduction in glucose metabolism occurred in bilateral parietal area for IPD, in bilateral putamen for MSA-P, in bilateral cerebellum for MSA-C, in midbrain and the middle frontal cortex for PSP, in asymmetrical metabolism of the cortex and the basal ganglia for CBD, in bilateral occipital and parieto-occipital areas for DLB. The metabolic reductions in a patient of NPH group were observed in the ventricular system. Conclusions: This study identifies different patterns of glucose metabolism in parkinsonism. 18 F-FDG PET imaging may contribute to early differential diagnosis in clinically ambiguous cases of parkinsonism. © 2011 Elsevier Ltd. All rights reserved.
1. Introduction The diagnosis of IPD can be straightforward in patients with typical clinical presentation of cardinal signs, but misdiagnosis of IPD is not uncommon. In a clinical pathological study, the accuracy of a clinical diagnosis of IPD is not high, with only 76% of post-mortem confirmed cases being diagnosed correctly [1]. The most common misdiagnoses are related with parkinsonism-plus syndromes (PPS) such as multiple system atrophy (MSA), progressive supranuclear palsy (PSP), corticobasal degeneration (CBD) and dementia with Lewy bodies (DLB) [2–4]. Since prognosis and treatment options of IPD and PPS are substantially different, differential diagnosis of IPD from PPS is critical for clinicians. Metabolic brain imaging by 18 F-FDG PET has showed characteristic reduction in glucose metabolism in the different areas in neurodegenerative diseases such as IPD and PPS [5,6]. 18 F-FDG PET can be used to differentiate various kinds of PPS patients from IPD patients, especially at the early disease stages when no
characteristic features occur on MRI. In this study, we aimed to characterize the differences in glucose metabolism on 18 F-FDG PET for differential diagnosis among IPD, MSA, PSP, CBD and DLB. In addition, one normal pressure hydrocephalus (NPH) patient was included in this study. 2. Subjects and Methods 2.1. Subjects This study included 18 IPD patients, 10 MSA-P patients and 12 MSAC patients, 13 PSP patients, 5 CBD patients, 7 DLB patients, 1 NPH patient and 40 age-matched healthy controls. The study was approved by the Medical Ethics Committee of the Tianjin Medical University, and all subjects gave their informed consent. Subjects were selected from patients with a clinical diagnosis of neurodegenerative disease. 2.2.
* Corresponding author. Benshu Zhang, Department of Neurology, General Hospital of Tianjin Medical University, No. 154, Anshan Road, Heping District, Tianjin, 300052, China. E-mail address: [email protected] (B. Zhang). 1353-8020/$ – see front matter © 2011 Elsevier Ltd. All rights reserved.
18
F-FDG PET imaging
The PET scans were performed in a 3 dimensional mode using GE Discovery LS PET/CT system. Subjects were administered with an intravenous bolus injection of 1.85–3.7 MBq (5–10 mCi/)
P. Zhao et al. / Parkinsonism and Related Disorders 18S1 (2012) S60–S62
S61
Fig. 1. 18 F-FDG PET images from SPM analysis in these groups. (A) In the IPD group, the hallmark of glucose metabolism is a decreased metabolism in bilateral parietal lobe.(B) In the MSA-P group, the distinguishing feature is the decreased metabolism in bilateral basal ganglia. (C) In the MSA-C group, the distinguishing feature is the presence of a glucose hypometabolism in bilateral cerebellum. (D) In the PSP group, the distinguishing feature is a decreased metabolism in midbrain and the middle frontal cortex. (E) In the CBD group, the distinguishing feature is the presence of a glucose hypometabolism in asymmetrical metabolism of the cortex and the basal ganglia. (F) In the DLB group, the distinguishing feature is the presence of a glucose hypometabolism in bilateral occipital and parieto-occipital areas. 18 F-FDG and 18 F-FDG scan were obtained. Three-dimensional data acquisition mode was performed, and images were collected with slice thickness of 2 mm collected in 128 × 128 matrix. Changes of 18 F-FDG metabolism in regions of interest were analyzed using visual inspection and SPM2 methods.
2.3. Statistical analysis Analyses were performed using SPSS 11.5. All values were presented as mean and standard deviation. Student t test was used to compare the difference among IPD patients and PPS patients. Categorical data were compared with chi square. Probability values less than 0.05 were considered statistically significant. 3. Results 3.1. Clinical characteristics 18 IPD patients (13 males, age 61.33±10.70 years), 10 MSAP patients (4 males, age 66.20±7.36 years), 12 MSA-C patients (5 males, age 58.83±8.98 years), 13 PSP patients (9 males, age 66.15±11.77 years), 5 CBD patients (3 males, age 58.40±11.59 years), 7 DLB patients (5 males, age 74.86±7.01 years), 1 NPH patient (male, age 48 years) and 40 normal controls (22 males, age 60.94±11.09 years) underwent 18 F-FDG PET studies. Patient age, gender and disease duration did not differ significantly among these groups. 3.2.
18
F-FDG PET imaging
For visual inspection of 18 F-FDG PET images, we did not identify a significant characteristic pattern of glucose metabolism between IPD group and other groups. We performed SPM2 analysis of the differences in 18 F-FDG PET images among these groups. In the IPD group, the hallmark of glucose metabolism was a decreased metabolism in parietal areas (Fig. 1A). 11 (61.11%) of 18 IPD patients showed a bilateral reduction in glucose metabolism. Hypometabolic areas in these patients were also observed in parieto-occipital, frontal, occipital, and temporal cortical areas in 3, 3, 2 and 2 IPD patients, respectively. The glucose metabolism was not significantly different in 3 IPD patients compared with controls. Hypometabolic areas in MSA-P patients were observed in bilateral putamen and caudate (Fig. 1B). This finding was found in 7 of 10 patients, and 2 of them also had a mild and
local reduction in glucose metabolism in bilateral cerebellum. In addition, hypometabolic areas were also observed in bilateral frontal, parietal, occipital, and insular cortical areas. Hypometabolic areas in MSA-C patients were observed in bilateral cerebellum (Fig. 1C). All 12 patients had this distinct characteristics, and 8 (66.67%) of them also showed a hypometabolism in the middle cerebellar peduncle. In addition, hypometabolic areas were also observed in pons and oblongata, frontal area, parietal and occipital area in 1, 4 and 2 of MSA-C patients, respectively. Hypometabolic areas in PSP patients were observed in midbrain. 12 (92.31%) of 13 PSP patients showed a hypometabolism in the midbrain, and also 5 (38.46%) patients showed a reduction in glucose metabolism in bilateral frontal areas, specially in the middle frontal cortex and cingulate gyrus (Fig. 1D). In addition, 1 patient also showed a reduction in glucose metabolism in superior cerebellar peduncle. Hypometabolic areas in CBD patients were observed in asymmetrical frontal, parietal, temporal and insular lobe, as well as in putamen contralateral to the clinically most affected side (Fig. 1E). 1 patient exhibited a decreased metabolism in thalamus contralateral to the affected side. Hypometabolic areas were observed in bilateral occipital and parieto-occipital areas in all DLB patients (Fig. 1F). Hypometabolic areas were also observed in bilateral frontal and temporal areas in 2 DLB patients. The comparison of the NPH patient with the normal controls showed a statistically significant decrease in glucose metabolism in the periventricular areas such as bilateral parietal, temporal, occipital and insular lobe, as well as the cingulate gyrus and basal ganglia. 4. Discussion In this study, we seek to study the images of IPD and other parkinsonian disorders to find possible discriminating patterns of 18 F-FDG PET imaging. The glucose hypometabolism was found mainly in the parietal areas in our IPD patients with no sign of dementia. This finding agrees with a previous report that the glucose metabolism was decreased in the parietal and parietooccipital regions in non-demented Parkinson’s patients [7]. In addition, very few patients in MSA-P and MSA-C patients exhibits a hypometabolism in parietal area, suggesting that it is a good parameter for differentiation of IPD form MSA.
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Our study also showed that glucose hypometabolism mainly occurs in bilateral putamen for MSA-P patients and in cerebellum for MSA-C patients, suggesting that it has a good parameter for differential diagnosis of MSA and IPD. This character of PET image is consistent with neuropathologic feature of MSA-P (predominated in basal ganglia) and MSA-C (predominated in cerebellum) [8]. Furthermore, the hypometabolism in cerebellum show the highest specificity in diagnosis of MSA-C, since this feature is present in all MSA-C patients, but not in IPD patients. The neurological features of PSP include an impaired ocular motility, pseudobulbar palsy and dystonia [3,9]. A diminished blood flow in the midbrain and the middle frontal cortex is consistently observed in patients with PSP. In addition, a reduction in glucose metabolism in superior cerebellar peduncle suggests that cerebellum may be involved. CBD can present clinically as unilateral parkinsonism but also with any of a variety of asymmetrical cortical degeneration syndromes such as asymmetrical ideomotor apraxia, alien-limb phenomenon and non-fluent aphasia [10]. Our finding that asymmetrical reduction in glucose metabolism is observed in frontal, parietal, temporal, insular lobe and putamen is consistent with the clinical signs of CBD patients. This finding agrees with previous PET studies that the patients with CBD showed an asymmetrical decrease in the brain metabolism in the cortical and subcortical regions [11]. Visual hallucinations are the most characteristic neuropsychiatric features of DLB [12], and our finding that greater metabolic reduction occurs in bilateral occipital cortex is compatible with neurodegenerative changes in visual occipital cortex in DLB. Our study suggests that abnormality of visual cortex and visual association cortex function exist at an early stage of dementia. In addition, hypometabolism of periventricular areas in 18 F-FDG PET may be the character pattern of NPH patient. In our study, the overall correct diagnosis rate 18 F-FDG PETbase diagnosis with clinical diagnosis was 86.36%. This may be result from 3 IPD patients who did not exhibit any difference in glucose metabolism from controls. These 3 IPD patients with normal glucose metabolism are needed to be confirmed with the progression of the disease to exclude the possibility of other parkinsonism-plus syndromes. In summary, 18 F-FDG PET imaging is helpful for differentiating IPD from PPS, especially at the early disease stages when the symptom and signs are not typical for differential diagnosis.
Acknowledgements We thank Department of Neurology and Department of Nuclear Medicine at General Hospital of Tianjin Medical University for collaboration.
Conflict of interests The authors have not received any kind of financial assistance and fellowships, and have no relevant conflicts of interest to disclose.
References 1. Rajput AH, Rozdilsky B, Rajput A. Accuracy of clinical diagnosis in parkinsonism – a prospective study. Can J Neurol Sci 1991;18:275–8. 2. Hughes AJ, Daniel SE, Ben-Shlomo Y, Lees AJ. The accuracy of diagnosis of parkinsonian syndromes in a specialist movement disorder service. Brain 2002;125:861–70. 3. Poewe W, Wenning G. The differential diagnosis of Parkinson’s disease. Eur J Neurol 2002;9(Suppl 3):23–30. 4. Savoiardo M. Differential diagnosis of Parkinson’s disease and atypical parkinsonian disorders by magnetic resonance imaging. Neurol Sci 2003; 24(Suppl 1):S35–7. 5. Kwon KY, Choi CG, Kim JS, Lee MC, Chung SJ. Comparison of brain MRI and 18F-FDG PET in the differential diagnosis of multiple system atrophy from Parkinson’s disease. Mov Disord 2007;22:2352–8. 6. Teune LK, Bartels AL, de Jong BM, Willemsen AT, Eshuis SA, de Vries JJ, et al. Typical cerebral metabolic patterns in neurodegenerative brain diseases. Mov Disord 2010;25:2395–404. 7. Hu MT, Taylor-Robinson SD, Chaudhuri KR, Bell JD, Labbe C, Cunningham VJ, et al. Cortical dysfunction in non-demented Parkinson’s disease patients: a combined (31)P-MRS and (18)FDG-PET study. Brain 2000;123(Pt 2):340–52. 8. Ozawa T, Paviour D, Quinn NP, Josephs KA, Sangha H, Kilford L, et al. The spectrum of pathological involvement of the striatonigral and olivopontocerebellar systems in multiple system atrophy: clinicopathological correlations. Brain 2004;127:2657–71. 9. Kato N, Arai K, Hattori T. Study of the rostral midbrain atrophy in progressive supranuclear palsy. J Neurol Sci 2003;210:57–60. 10. Kumar R, Bergeron C, Lang A. Cortical basal degeneration. In: Jankovic J, Tolosa E, editors. Parkinson’s disease and movement disorders. Baltimore, MD: Lippincott Williams and Wilkins; 2002, pp. 185–98. 11. Juh R, Pae CU, Kim TS, Lee CU, Choe B, Suh T. Cerebral glucose metabolism in corticobasal degeneration comparison with progressive supranuclear palsy using statistical mapping analysis. Neurosci Lett 2005;383:22–7. 12. McKeith IG, Dickson DW, Lowe J, Emre M, O’Brien JT, Feldman H, et al. Diagnosis and management of dementia with Lewy bodies: third report of the DLB Consortium. Neurology 2005;65:1863–72.