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Decreased Cerebellar Activity on FDG PET/CT Secondary to Diffuse Idiopathic Cerebellar Calcification

Nawas, Mohammed T., MD; Kubal, Wayne S., MD; Kuo, Phillip H., MD, PhD

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doi: 10.1097/RLU.0b013e318262adb2
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Abstract

FIGURE 1
FIGURE 1:
A 50-year-old asymptomatic woman presented for an FDG PET/CT examination for suspected recurrence of gastric carcinoma. The patient reported no history of brain infarct, radiation therapy, head trauma, or family history of neurodegenerative disorder. Axial (A) and sagittal (C) PET images demonstrate diffusely decreased FDG uptake throughout the bilateral cerebellar hemispheres (arrows). Note the normal FDG uptake in the supratentorial compartment. Axial (B) and sagittal (D) images from the corresponding CT examination demonstrate diffuse coarse calcification throughout the cerebellar hemispheres (arrows). Parenchymal calcification was not present in the supratentorial brain. Normally, the cerebellum consistently demonstrates high activity and is often used as an internal reference for brain activity.1 The finding of cerebellar hypometabolism on FDG PET is nonspecific and may result from a number of varying entities including prior infarct, hemorrhage, and trauma. Although associated calcification may be present, these common conditions result in localized encephalomalacia and typically demonstrate a characteristic appearance. Chronic alcohol abuse and long-term usage of antiepileptic medications, most commonly phenytoin, also result in decreased FDG uptake throughout the cerebellum.2,3 The typical correlating finding on cross-sectional imaging is diffuse atrophy with prominence of the cerebellar sulci and ex vacuo expansion of the fourth ventricle. The differential diagnostic considerations for cerebellar hypometabolism also include neurodegenerative disorders such as multiple-system atrophy with predominate cerebellar symptoms (MSA-C) and multiple subtypes of spinocerebellar ataxia (SCA). PET examinations in MSA-C typically demonstrate hypometabolism in the cerebellar hemispheres, cerebellar vermis, and the brainstem.4–6 On corresponding cross-sectional imaging, the finding of cerebellar, pontine, and middle cerebellar peduncle atrophy is common.7 MRI may also demonstrate abnormal signal intensity in these regions. Cerebellar hypometabolism was also noted in multiple subtypes of SCA, particularly subtypes 2 and 3.8–10 In addition to hypometabolism, specific neurodegenerative disorders may also result in abnormal brain calcification.11 Although cerebellar calcification may be seen with idiopathic basal ganglia calcification (Fahr disease), this condition is characterized primarily by extensive bilateral and symmetric basal ganglia calcification, which was absent in this case. Cerebellar parenchymal calcifications may occur physiologically, typically in the dentate nucleus.12 Cerebellar calcification has also been hypothesized to occur as a result of microvasculopathy.13 In a case series of 6 patients, a potential association of hypothyroidism has been described with idiopathic cerebellar calcification.14 Thyroid function tests obtained 2 weeks after our patient’s FDG PET/CT revealed a thyroid-stimulating hormone level of 0.8 μIU/mL (reference range, 0.35–4 μIU/mL) and a thyroxine level of 6.8 μg/dL (reference range, 4.8–11.7 μg/dL). Although normal in our case, given the reported association with hypothyroidism as well as the inexpensive nature and wide availability of thyroid function tests, thyroid function testing is likely worth obtaining. Recognizing this entity avoids a potential misdiagnosis of one of the other causes of cerebellar hypometabolism and is also critical in the case of using the cerebellum as a standard to evaluate other brain structures.

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                              Keywords:

                              diffuse idiopathic cerebellar calcification; cerebellar hypometabolism; FDG PET/CT; cerebellum; multiple system atrophy

                              © 2012 Lippincott Williams & Wilkins, Inc.