Alzheimer disease is the most common cause of dementia (23%) and usually shows a classical pattern of metabolic abnormality.PET has also been found to help predict conversion from MCI(4%) to early Alzheimer disease .It is followed by movement disorder and vascular dementia in about (16%) of patients.Four cases were of Paraneoplastic limbic encephalitis and six were of immune mediated encephalitis.Nine cases were of Prion disease.In our series 11% cases were unidentifiable and could represent mixed pattern of dementia.

In healthy subjects, the most intense FDG uptake occurs in the  putamen, caudate nucleus and thalamus followed by high uptake in the cortical gray matter. The globus pallidus typically demonstrates mild uptake and the white matter is relatively photopenic. Two key structures to recognize are the cingulate gyrus and the overlying precuneus cortex . The cingulate gyrus, located adjacent to the corpus callosum,is affected early in many neurodegenerative disorders. The precuneus lies cephalad to the posterior cingulate gyrus and is bounded anteriorly by the cingulate marginal sulcus and posteriorly by the parieto-occipital sulcus (Fig 3). Both structures should be actively sought and evaluated when analyzing images obtained for the workup of patients with dementia.

Alzheimer disease is characterized by early neuronal loss and gliosis in the mesiotemporal cortex. Pathologic hallmarks include b-amyloid plaques and neurofibrillary tangles . The earliest changes of hypometabolism are often seen in the posterior cingulate gyrus (2). The classic pattern of impaired metabolism consists of involvement of the posterior cingulate gyri, precuneus and posterior temporal and parietal association cortices (fig 4, 5).

In more advanced Alzheimer disease, hypometabolism extends to involve the prefrontal association cortices. Metabolism is typically relatively preserved in the visual and anterior cingulate cortices, basal ganglia, thalamus and posterior fossa in Alzheimer disease.

Dementia with Lewy body (DLB )  is the second most common neurodegenerative disorder in patients over 65 years of age. DLB manifests with a pattern of hypometabolism similar to that seen in Alzheimer disease . However, there is associated involvement of the occipital lobes, which are spared in Alzheimer disease(3). This involvement of the occipital lobes is compatible with the clinical diagnosis of DLB (fig 6).Imaging with dopamine transporter(4) agents can also help distinguish DLB from Alzheimer disease when clinical and FDG findings are inconclusive. An Alzheimer disease pattern of hypometabolism and a positive dopamine transporter scan indicate that DLB is the most likely diagnosis.

The 'cingulate island ' sign is a highly specific radiological sign described in DLB. On FDG-PET, there is occipital hypometabolism with relative sparing of the posterior cingulate cortex thus creating the appearance of an 'island' of normal metabolism in the posterior cingulate region which can help differentiate DLB from Alzheimer.

In Fronto-temporal dementia (FTD)patients often present with social impairment and disinhibitive and impulsive behavior(5).Classic FTD is characterized by hypometabolism in the frontal and anterior temporal lobes with involvement of the anterior cingulate gyrus.

The frontal-predominant form of FTD (fig7) shows sparing of the temporal lobes, with patients typically demonstrating behavioral changes, including disinhibition. Patients with temporal variant FTD (semantic dementia) have problems with language and often cannot find the words to describe an object. These patients tend to have primarily temporal lobe hypometabolism(6)(fig8).

FDG allows for a highly accurate distinction between Parkinson disease (PD) and atypical parkinsonian syndromes(APS) including multiple-system atrophy, progressive supranuclear palsy and corticobasal degeneration.

The APSs are a heterogeneous group of neurodegenerative disorders characterized by levodopa-refractory parkinsonism and distinctive atypical clinical features(7) . Patients of MSA, may have various combinations of progressive autonomic failure, parkinsonian, cerebellar features, and pyramidal features. MSA is classified as of the parkinsonian subtype (MSA-P) if parkinsonism is the most prominent feature and as of the cerebellar subtype (MSA-C) if cerebellar ataxia predominates(8).(fig 9,10)

Recent Movement Disorder Society proposed 4 core clinical diagnostic criteria in functional domains to diagnose progressive supranuclear palsy(PSP)—ocular motor dysfunction (Richardson syndrome), postural instability, akinesia, and cognitive dysfunction.In cases of PSP, regional hypometabolism (9)is consistently noted in the medial, dorsal, and ventrolateral frontal areas ,thalamus and upper brain stem( fig.11)

Corticobasal degeration (CBD) is characterized by a usually highly asymmetric hypometabolism of the fronto-parietal areas, striatum and thalamus contralateral to the most affected body side(10). Cortical hypometabolism may be pronounced in the parietal cortex and usually extends across the sensorimotor cortex into the cingulate gyrus and premotor–to posterior prefrontal areas.(fig12)

Creutzfeldt-Jakob disease (sCJD) is an infrequent cause of rapidly progressive dementia. Its major symptoms are cognitive dysfunction, myoclonus and pyramidal syndrome. Most of the abnormalities on 18F-FDG PET scan are consistent with those found on DWI and FLAIR images and are believed to correspond with areas of neuronal loss(11). Other foci of low uptake on PET/CT images that do not match MRI might be indicative of early cortical involvement.(fig 13)

Autoimmune encephalitis (AE)  is an antibody-mediated brain inflammatory process. Autoimmune encephalitis can be divided broadly into two groups

• Paraneoplastic encephalitis: antibodies are against intracellular antigens and they show poor response to immunotherapy.

• Non-neoplastic autoimmune encephalitis: antibodies are against extracellular antigens, usually with a reversible neuronal dysfunction and show better response to immunotherapy.

Specific patterns of metabolism have been observed on FDG-PET in certain AE syndromes(13,14) these patterns of metabolism are dependent on the differential distribution of the antigenic receptors in the brain and the degree of receptor dysfunction caused by the specific autoantibody.Temporal hypermetabolism with increased basal ganglia uptake is a common finding seen in AE (fig 14,15,16,17). 

FDG PET is also specific to identify lymphoproliferative disease or to exclude atypical presentation of primary CNS lymphoma as even the small focus of disaese involvement will show significant FDG avidity( fig 18).