**5.1 Corticobasal degeneration**

220 12 Chapters on Nuclear Medicine

lesser symptom. In contrast to other dementias however, there is no (or less prominent) memory impairment associated with FTLD. Therefore, clinical differentiation from other diseases such as AD is usually relatively straightforward. The main difficulty associated with managing FTLD is that it is not typically diagnosed in its early stages because mild symptoms often go unnoticed, or are difficult to verify. To address this issue, FDG PET has been investigated as a possibility for diagnosing and staging the FTLD-related conditions by identifying areas of reduced glucose metabolism that are characteristic of these conditions.

Reduced glucose metabolism in the frontal (mostly the frontal cortex) and anterior temporal regions is the characteristic hallmark observed in FDG PET scans of FTD patients. Such impairment is not always symmetric, and thought to be related to the aphasia and semantic memory deficits common in such patients. This (mostly) frontal impairment allows distinction of FTD from AD. For example, Foster and co-workers were recently able to distinguish FTD from AD with 86% specificity and 97.6% sensitivity, beyond clinical features alone (Foster, et al., 2007). Frontal metabolic decline, however, is not limited to FTD and can be apparent in certain cases of AD. In such cases where there is FTD / AD overlap in the FDG PET scans, it is recommended to conduct additional scans exploring microglial activation or amyloid deposits (see Section 2). For example, microglial activation characteristic of FTD has been investigated (A. Cagnin, et al., 2004). Alternatively, an amyloid positive scan would strongly suggest AD, whilst an amyloid negative scan would

Fig. 5. High PIB retention was observed in patient with AD (A) and patient with DLB (B). In contrast, low PIB retention was observed in patient with PD (not demented) (C) and in patient with FTD (D). *(Parts A and B reprinted with permission from Ahmadul K and Nordberg A, Targetspecific PET probes for neurodegenerative disorders related to dementia. J Nucl Med. 2010;51:1418- 1430; Part C reprinted with permission from A. Johansson, et al. [11C]-PIB imaging in patients with Parkinson's disease: preliminary results. Parkinsonism Relat. Disord. 2008;14:345-347; Part D courtesy* 

Other diseases (e.g. progressive supranuclear palsy, spino-cerebellar atrophy) or lifestyle choices (e.g. cocaine abuse) can also lead to frontal metabolic impairment. Consequently, other

*of Professor Henry Engler, Uppsala PET Center, Academical Hospital, Uppsala, Sweden).*

**4.2 FDG PET for imaging frontotemporal dementia** 

indicate FTD (Figure 5) (Kadir and Nordberg, 2010).

Corticobasal degeneration (CBD) is a progressive dementia in which patients have cognitive decline, significant dementia and unique motor symptoms such as akineto-rigid syndrome (Ishii, 2002). In FDG PET of CBD patients, there is a decrease in absolute glucose metabolism in several regions of the brain, and distinct asymmetry in glucose metabolism patterns that is characteristic of the condition. For example, Hirono and colleagues showed that CBD patients had greater glucose metabolic asymmetries in the lateral frontal, lateral temporal, central and lateral parietooccipital regions than did the corresponding healthy controls (Hirono, et al., 2001). In the same study it was reported that the most significant pathologic changes in CBD appear in the pre- and post-central gyri, and parietal association cortices. Moreover, the associated metabolic asymmetries in the pre- and post-central gyri, as well as the thalamus, were larger in CBD than AD allowing differentiation of these conditions using FDG PET.
