 Hello everyone, I am Dr. Sikandar. Today I will be speaking on PET City Neurology applications. Now coming to the Neurology applications on the PET. The most common and important is Neuro oncology which shows the tumor recurrence versus radiation necrosis. This is one of the important thing which is very difficult to be identified even on contrast MR, MR spectroscopy and other MR applications. So here PET is very important in distribution between the tumor recurrence versus radiation necrosis. Second is for the diagnosis, then grading, then seizure focal identification is one of the important entity, dementia. So this is the important aspect which I will be covering today. A lot of dementia groups are there. How PET is useful in identifying and quantifying the different applications on the PET and their presentations in the dementia. Other applications like brain injury, vascular trauma, psychiatric applications like depression, schizophrenia, movement disorders with 18 fdopa and miscellaneous infections like substance abuse. So coming to the PET imaging studies of the central nervous system, they are global or regional changes in the brain function such as glucose utilization, cerebral blood flow and oxygen metabolism, then development of specific probes, neurotransmitter receptors, second messenger systems and neuronal networks in the brain pattern karma. As everybody knows the molecular changes precede the structural changes and thus we can do early diagnosis and there is a targeted treatment management which is based on functional rather than structural measures. PET tracers allow the study of numerous brain functions in the normal and pathological conditions, then measurement of regional blood flow, glucose metabolism, enzyme activity, protein accumulation and receptor density in the central nervous system. So coming to dementia, this is a wide variety of applications in this. So it is a wide entity. Lot of conditions are there. So it is for assessment of patient with symptoms of dementia, early diagnosis of dementia, then differential diagnosis between Alzheimer's disease, dementia with levy bodies, frontotemporal, low dementia and vascular dementia. And another important application which I will be showing today is epilepsy. For pre-surgical evaluation of refractory epilepsy, lateralize and localize the functional impaired region with normal MRI findings. So Parkinson's disorders. Differential diagnosis of Parkinsonism because Parkinsonism can be a typical and atypical and the diagnosis of atypical Parkinsonism such as corticobasal degeneration, multiple system atrophy and progressive supranuclear palsy. So coming to psychiatry, you have depression, bipolar disorders, schizophrenia, stroke and assessment of the neuronal plasticity. So coming to positioning, it is normal as that of a CT brain. And the important thing is to avoid or minimize head movements. Head fixation may be useful. Orbitumenital line in parallel to the detector range and standardization of the positioning will be done. So how you are going to quantify this? We have a standard as uptake values that is a CV value helping assessment of the uptake patterns and a CV ratios are created using an unaffected re-affirmed region. So quantification of CMR can be performed using arterial or arterialized blood input. And the regional analysis should use manual or atlas-based regions of interest or voxel-based analysis, ideally created or co-resisted with the MR images. So in the healthy brain, you have subcortical, cortical gray matter and subcortical level, caudate nucleus, vitamin and the thalamine which shows the highest uptake, FDG uptake. Then cerebellar cortex and brainstem, usually they are lower in uptake compared to the cerebellar parenchyma, basal ganglia and thalamine. And white matter generally shows low uptake and can hardly be visually distinguished from the adjacent ventricular system. So coming to the different conditions of dementia, you have Alzheimer's disease, you have frontotemporal dementia and the DLB which I will be showing in different cases. Then you have Christopher Jacob disease in Parkinson's dementia and atypical Parkinson's. So coming to the first case today, it is temporal lobe epilepsy. You have diffuse hypermetabolism which is seen in the pet and fused pet city images. CT is not that much useful, you see normal temporal lobe. But if you see the temporal uptake in both sides, there is reduced compared to the other parietal, posterior parietal and occipital lobes. So this is definitely a case of temporal lobe epilepsy. Coming to Parkinsonism, you see Parkinsonism, dementia, there is hypermetabolism in the parietal and temporal lateral cortices similar to the pattern in Alzheimer's disease. But only the thing is you have preserved glucose uptake in the basal ganglia. So that is the important differential between the Alzheimer's disease and the Parkinsonism. So this is another case which shows the diffuse evaluation of the functional evaluation of the brain parenchyma which shows multiple areas of orange and yellow and followed by the blue areas. So all blue areas which are seen in bilateral regions are the hypermetabolic regions while the orange and the yellow one is a normal cortex which shows normal metabolism. So that is how though you will be easily identifying the hypermetabolism which is seen in different lobes of the cerebral parenchyma. Coming to Alzheimer's disease, you have hypermetabolism in the parietal, medial and posterior lateral temporal cortex and posterior singulum. So frontal hypermetabolism may also be seen as a progression of the disease in bilateral but can be unilateral. So preserved metabolism in occipital and sensory motor cortex basal ganglia and cerebellum is one of the important hallmarks of the Alzheimer's disease which differentiates from the Parkinsonism. So frontal temporal dementia, you have hypermetabolism in the frontal cortex, anterior singulum and anterior lateral temporal cortex. And the hypermetabolism can affect the caudate nuclei. So the cortex hypermetabolism may vary in different forms of the frontal temporal dementia but most important frontal temporal name itself depicts so you have to be way easier for analyzing the frontal and temporal cortex. Coming to DLB, DLB there is parietal and temporal lateral hypermetabolism similar to the pattern in Alzheimer's disease and occipital and parietal visual cortex involvement is important in differential diagnosis. So hypermetabolism may also be present in the basal ganglia. Sometimes it is like variation of the DLB. Now coming to crucifold Jacob disease there is distinct hypermetabolism in the large areas of brain involving the right or the left hemisphere or bilateral in the most cases only the differentiation with other dementia groups is temporal lobes are usually less affected in CJD. Now coming to Parkinsonism hypermetabolism in the parietal and temporal lateral cortex is similar to the pattern in Alzheimer's disease but here the hallmark is preserved glucose uptake in the basal ganglia. So that is how you can differentiate with the Alzheimer's disease. So coming to temporal lobe epilepsy already I have shown this is another case of a typical Parkinsonism. A typical means there is disparity between the right and left and it is not classical of the Parkinsonism. So there is a lot of hypermetabolism seen in the cortices in the bilateral frontal and parietal which is more prominent on the right side as compared to the left side. So coming to the important aspect which I want to show how the quantification of the metabolic uptake is seen in the bilateral cerebral parankaima and based on the SCV values. If you see the left side there is a chart which shows frontal lobe, L frontal lobe, R and then you have mean SCV value on the adjacent to it. You have temporal lobes, you have parietal lobes, you have singulate areas, then you have central region, occipital lobe, calcarean, fissure, basal ganglia, measles temporal lobe and cerebellum. All are having left and right L is left, R is right and you have mean SCV values and the disparity of the difference between the right and left is the mean which is being shown in the chart here. So here important is the quantification L is left, R is right and SCV values. So with the SCV values we can see the disparity between the right and left and that is how you are able to identify easily the metabolic activity of the cerebral cortex. So this is automated structure by the software previously we used to quantify it but nowadays it is coming automated in the recent advanced machines. So with this I hope you have learned how to differentiate between the different dementia groups especially the role of it which is very viable and very important clinically. Sometimes there can be overlap on findings even in imaging also sometimes difficult but here PET can easily distinguish between the Parkinson's disease, Alzheimer's disease and other forms of the dementia group.