F-18 fluoro-d-glucose positron emission tomography/computed tomography in a patient with corticobasal degeneration.

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.

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 PET is a powerful imaging tool for differentiating idiopathic Parkinson's disease from Parkinson plus syndromes.[2345] 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[78] and Creutzfeldt–Jakob disease.[9]

Figure 1

Severe asymmetrical right hemisphere hypometabolism

Figure 2

Right basal ganglia and thalamus showing severe hypoglycolisis

Figure 3

Transaxial and coronal images showing severe hypometabolism in the left cerebellar hemisphere compared to the right (crossed cerebellar diaschisis)