Clinical Nuclear Medicine:
Nawas, Mohammed T. MD; Kubal, Wayne S. MD; Kuo, Phillip H. MD, PhD
From the Department of Medical Imaging, University of Arizona School of Medicine, Tucson, AZ.
Received for publication November 14, 2011; revision accepted May 23, 2012.
Conflicts of interest and sources of funding: none declared.
Reprints: Mohammed T. Nawas, MD, Department of Medical Imaging, University of Arizona School of Medicine, 1501 N Campbell Ave, Tucson, AZ 85724. E-mail: email@example.com.
Abstract: Cerebellar hypometabolism on FDG PET has been described in several conditions, for example, chronic alcohol abuse, antiepileptic medication use, multiple system atrophy, and cerebellar infarction. Corresponding cross-sectional examination is paramount in distinguishing possible etiologies because each condition has a relatively characteristic appearance. We present a case of an asymptomatic patient with diffuse cerebellar hypometabolism found incidentally on FDG PET/CT performed for suspected recurrence of gastric carcinoma. Accompanying CT images demonstrated calcification of the cerebellum and therefore confirmed the etiology of diffuse idiopathic cerebellar calcification. Identifying this diagnosis is critical for using the cerebellum as a standard to evaluate other brain structures.
1. Silverman DH, Mosconi L, Ercoli L. Positron emission tomography scans obtained for the evaluation of cognitive dysfunction. Semin Nucl Med. 2008; 38: 251–261.
2. Theodore WH, Fishbein D, Dietz M, et al.. Complex partial seizures: cerebellar metabolism. Epilepsia. 1987; 28: 319–323.
3. Gilman S, Adams K, Koeppe RA. Cerebellar and frontal hypometabolism in alcoholic cerebellar degeneration studied with positron emission tomography. Ann Neurol. 1990; 28: 775–785.
4. Lee PH, An YS, Yong SW, et al.. Cortical metabolic changes in the cerebellar variant of multiple system atrophy: a voxel-based FDG-PET study in 41 patients. Neuroimage. 2008; 40: 796–801.
5. Claassen DO, Lowe VJ, Peller PJ, et al.. Amyloid and glucose imaging in dementia with Lewy bodies and multiple systems atrophy. Parkinsonism Relat Disord. 2011; 17: 160–165.
6. Zhao P, Zhang B, Gao S. 18F-FDG PET study on the idiopathic Parkinson’s disease from several parkinsonian-plus syndromes. Parkinsonism Relat Disord. 2012; 18: S60–S62.
7. Savoiardo M, Strada L, Girotti F. Olivopontocerebellar atrophy: MR diagnosis and relationship to multisystem atrophy. Radiology. 1990; 174: 693–696.
8. Wang PS, Liu RS, Yang BH, et al.. Topographic brain mapping of the international cooperative ataxia rating scale. A positron emission tomography study. J Neurol. 2007; 254: 722–728.
9. Inagaki A, Iida A, Matsubara M, et al.. Positron emission tomography and magnetic resonance imaging in spinocerebellar ataxia type 2: a study of symptomatic and asymptomatic individuals. Eur J Neurol. 2005; 12: 725–728.
10. Soong BW, Liu RS. Positron emission tomography in asymptomatic gene carriers of Machado-Joseph disease. J Neurol Neurosurg Psychiatry. 1998; 64: 499–504.
11. Mittal A, Agrawal BK, Mittal A, et al.. Fahr’s syndrome: a rare case of idiopathic basal ganglia calcification. JIACM. 2010; 11: 239–241.
12. Koller WC, Klawans HL. Cerebellar calcification on computerized tomography. Ann Neurol. 1980; 7: 193–194.
13. Gomez CR, Luque A, Horenstein S. Microvasculopathy may precede idiopathic cerebral calcifications—case report. Angiology. 1989; 40: 67–72.
14. Burke JW, Williamson BR, Hurst RW. “Idiopathic” cerebellar calcifications: association with hypothyroidism? Radiology. 1988; 167: 533–536.
© 2012 Lippincott Williams & Wilkins, Inc.