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F‑18 fluoro‑d‑glucose positron emission tomography/computed tomography in a patient with corticobasal degeneration Alejandro Marti1,2 1
National Cancer Institute, 2IDIME, Medical Diagnosis Institute, Bogota, Colombia
ABSTRACT Corticobasal degeneration is a rare neurodegenerative disorder that often eludes clinical diagnosis.
The present case shows the F‑18 fluoro‑d‑glucose positron emission tomography/computed tomography (PET/CT) of a 62‑year‑old man with a progressive movement disorder with asymmetric features. PET/CT examination showed a markedly right‑brain hemispheric hypometabolism also involving basal ganglia.
Keywords: Corticobasal degeneration, fluoro‑d‑glucose, parkinsonian syndromes, positron emission tomography
A 62‑year‑old man complaining of dystonia, akinesia and rigidity, ideomotor apraxia, alien limb phenomena with left‑sided predominance, also impairments of speech, language and gait difficulty with little response to levodopa‑carbidopa. He was referred for F‑18 fluoro‑d‑glucose (FDG) positron emission tomography (PET) with a diagnosis of parkinsonian syndrome. The examination showed a markedly right‑brain hemispheric hypometabolism also involving basal ganglia [Figure 1]. These types of abnormalities have been described and tend to be dominant in the contra‑lateral hemisphere to the most affected body side in corticobasal degeneration.[1] The left‑brain metabolism is also abnormal although a little less dramatic than right. Right basal ganglia and thalamus showed hypometabolism [Figure 2]. This is also a known feature of advanced corticobasal degeneration.[1] This disorder is thought to be caused by the deposition of abnormally phosphorylated tau protein in cortex and basal ganglia.[2] The characteristic pattern of hypometabolism in corticobasal degeneration is contra‑lateral posterior frontal/anterior parietal hypometabolism, which involves the basal ganglia also. Depending on the extent of tau deposition this can be hemispheric as in this case. FDG
Figure 1: Severe asymmetrical right hemisphere hypometabolism
Access this article online Quick Response Code: Website: www.ijnm.in
DOI: 10.4103/0972-3919.152991 Figure 2: Right basal ganglia and thalamus showing severe hypoglycolisis
Address for correspondence: Dr. Alejandro Marti, Calle 106A# 13A-40 Bogota, Colombia. E‑mail: [email protected]
Indian Journal of Nuclear Medicine | Vol. 30: Issue 2 | April-June, 2015
185
Marti: FDG PET/CT in patient with corticobasal degeneration
REFERENCES 1. 2. 3. 4. 5. Figure 3: Transaxial and coronal images showing severe hypometabolism in the left cerebellar hemisphere compared to the right (crossed cerebellar diaschisis)
PET is a powerful imaging tool for differentiating idiopathic Parkinson’s disease from Parkinson plus syndromes.[2‑5] Severe hypometabolism in the left cerebellar hemisphere compared to the right (crossed cerebellar diaschisis) was also noticed [Figure 3]. This phenomenon is thought to be caused by interruption of cortico‑ponto‑cerebellar tract with secondary deafferentation and a transneural metabolic depression of the contra‑lateral cerebellar hemisphere.[6] Differential diagnosis includes other Parkinson plus syndromes namely: Multiple system atrophy, progressive supranuclear palsy [7,8] and Creutzfeldt–Jakob disease.[9]
186
6. 7. 8. 9.
Eckert T, Barnes A, Dhawan V, Frucht S, Gordon MF, Feigin AS, et al. FDG PET in the differential diagnosis of parkinsonian disorders. Neuroimage 2005;26:912‑21. Tolosa E, Calandrella D, Gallardo M. Caribbean parkinsonism and other atypical parkinsonian disorders. Parkinsonism Relat Disord 2004;10 Suppl 1:S19‑26. Akdemir ÜÖ, Tokçaer AB, Karakuş A, Kapucu LÖ. Brain 18F‑FDG PET imaging in the differential diagnosis of parkinsonism. Clin Nucl Med 2014;39:e220‑6. Hosaka K, Ishii K, Sakamoto S, Mori T, Sasaki M, Hirono N, et al. Voxelbased comparison of regional cerebral glucose metabolism between PSP and corticobasal degeneration. J Neurol Sci 2002;199:67-71. Juh R, Kim J, Moon D, Choe B, Suh T. Different metabolic patterns analysis of parkinsonism on the 18F‑FDG PET. Eur J Radiol 2004;51:223‑33. Agrawal KL, Mittal BR, Bhattacharya A, Khandelwal N, Prabhakar S. Crossed cerebellar diaschisis on F‑18 FDG PET/CT. Indian J Nucl Med 2011;26:102‑3. 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. Mahapatra RK, Edwards MJ, Schott JM, Bhatia KP. Corticobasal degeneration. Lancet Neurol 2004;3:736‑43. Zhang Y, Minoshima S, Vesselle H, Lewis DH. A case of Creutzfeldt‑Jakob disease mimicking corticobasal degeneration: FDG PET, SPECT, and MRI findings. Clin Nucl Med 2012;37:e173‑5.
How to cite this article: Marti A. F-18 fluoro-d-glucose positron emission tomography/computed tomography in a patient with corticobasal degeneration. Indian J Nucl Med 2015;30:185-6. Source of Support: Nil. Conflict of Interest: None declared.
Indian Journal of Nuclear Medicine | Vol. 30: Issue 2 | April-June, 2015
Copyright of Indian Journal of Nuclear Medicine is the property of Medknow Publications & Media Pvt. Ltd. and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use.
F‑18 fluoro‑d‑glucose positron emission tomography/computed tomography in a patient with corticobasal degeneration Alejandro Marti1,2 1
National Cancer Institute, 2IDIME, Medical Diagnosis Institute, Bogota, Colombia
ABSTRACT Corticobasal degeneration is a rare neurodegenerative disorder that often eludes clinical diagnosis.
The present case shows the F‑18 fluoro‑d‑glucose positron emission tomography/computed tomography (PET/CT) of a 62‑year‑old man with a progressive movement disorder with asymmetric features. PET/CT examination showed a markedly right‑brain hemispheric hypometabolism also involving basal ganglia.
Keywords: Corticobasal degeneration, fluoro‑d‑glucose, parkinsonian syndromes, positron emission tomography
A 62‑year‑old man complaining of dystonia, akinesia and rigidity, ideomotor apraxia, alien limb phenomena with left‑sided predominance, also impairments of speech, language and gait difficulty with little response to levodopa‑carbidopa. He was referred for F‑18 fluoro‑d‑glucose (FDG) positron emission tomography (PET) with a diagnosis of parkinsonian syndrome. The examination showed a markedly right‑brain hemispheric hypometabolism also involving basal ganglia [Figure 1]. These types of abnormalities have been described and tend to be dominant in the contra‑lateral hemisphere to the most affected body side in corticobasal degeneration.[1] The left‑brain metabolism is also abnormal although a little less dramatic than right. Right basal ganglia and thalamus showed hypometabolism [Figure 2]. This is also a known feature of advanced corticobasal degeneration.[1] This disorder is thought to be caused by the deposition of abnormally phosphorylated tau protein in cortex and basal ganglia.[2] The characteristic pattern of hypometabolism in corticobasal degeneration is contra‑lateral posterior frontal/anterior parietal hypometabolism, which involves the basal ganglia also. Depending on the extent of tau deposition this can be hemispheric as in this case. FDG
Figure 1: Severe asymmetrical right hemisphere hypometabolism
Access this article online Quick Response Code: Website: www.ijnm.in
DOI: 10.4103/0972-3919.152991 Figure 2: Right basal ganglia and thalamus showing severe hypoglycolisis
Address for correspondence: Dr. Alejandro Marti, Calle 106A# 13A-40 Bogota, Colombia. E‑mail: [email protected]
Indian Journal of Nuclear Medicine | Vol. 30: Issue 2 | April-June, 2015
185
Marti: FDG PET/CT in patient with corticobasal degeneration
REFERENCES 1. 2. 3. 4. 5. Figure 3: Transaxial and coronal images showing severe hypometabolism in the left cerebellar hemisphere compared to the right (crossed cerebellar diaschisis)
PET is a powerful imaging tool for differentiating idiopathic Parkinson’s disease from Parkinson plus syndromes.[2‑5] Severe hypometabolism in the left cerebellar hemisphere compared to the right (crossed cerebellar diaschisis) was also noticed [Figure 3]. This phenomenon is thought to be caused by interruption of cortico‑ponto‑cerebellar tract with secondary deafferentation and a transneural metabolic depression of the contra‑lateral cerebellar hemisphere.[6] Differential diagnosis includes other Parkinson plus syndromes namely: Multiple system atrophy, progressive supranuclear palsy [7,8] and Creutzfeldt–Jakob disease.[9]
186
6. 7. 8. 9.
Eckert T, Barnes A, Dhawan V, Frucht S, Gordon MF, Feigin AS, et al. FDG PET in the differential diagnosis of parkinsonian disorders. Neuroimage 2005;26:912‑21. Tolosa E, Calandrella D, Gallardo M. Caribbean parkinsonism and other atypical parkinsonian disorders. Parkinsonism Relat Disord 2004;10 Suppl 1:S19‑26. Akdemir ÜÖ, Tokçaer AB, Karakuş A, Kapucu LÖ. Brain 18F‑FDG PET imaging in the differential diagnosis of parkinsonism. Clin Nucl Med 2014;39:e220‑6. Hosaka K, Ishii K, Sakamoto S, Mori T, Sasaki M, Hirono N, et al. Voxelbased comparison of regional cerebral glucose metabolism between PSP and corticobasal degeneration. J Neurol Sci 2002;199:67-71. Juh R, Kim J, Moon D, Choe B, Suh T. Different metabolic patterns analysis of parkinsonism on the 18F‑FDG PET. Eur J Radiol 2004;51:223‑33. Agrawal KL, Mittal BR, Bhattacharya A, Khandelwal N, Prabhakar S. Crossed cerebellar diaschisis on F‑18 FDG PET/CT. Indian J Nucl Med 2011;26:102‑3. 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. Mahapatra RK, Edwards MJ, Schott JM, Bhatia KP. Corticobasal degeneration. Lancet Neurol 2004;3:736‑43. Zhang Y, Minoshima S, Vesselle H, Lewis DH. A case of Creutzfeldt‑Jakob disease mimicking corticobasal degeneration: FDG PET, SPECT, and MRI findings. Clin Nucl Med 2012;37:e173‑5.
How to cite this article: Marti A. F-18 fluoro-d-glucose positron emission tomography/computed tomography in a patient with corticobasal degeneration. Indian J Nucl Med 2015;30:185-6. Source of Support: Nil. Conflict of Interest: None declared.
Indian Journal of Nuclear Medicine | Vol. 30: Issue 2 | April-June, 2015
Copyright of Indian Journal of Nuclear Medicine is the property of Medknow Publications & Media Pvt. Ltd. and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use.
