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Functional neuroimaging using F-18 FDG PET/CT in amnestic mild cognitive impairment: A preliminary study.

Tripathi M, Tripathi M, Sharma R, Jaimini A, Md'souza M, Saw S, Mondal A, Kushwaha S - Indian J Nucl Med (2013)

Bottom Line: Seven patients had hypometabolism in at least one AD related territory and were classified as intermediate likelihood for PTAD.SPM analysis of these cases confirmed the areas hypometabolism in all 13 patients compared to a normal subgroup (P < 0.05).A longer follow-up of patients with hypometabolism in single AD territories is needed to predict their clinical behavior.

View Article: PubMed Central - PubMed

Affiliation: Department of Nuclear Medicine and Positron emission Tomography, All India Institute of Medical Sciences, New Delhi, India.

ABSTRACT

Background and objective: People with amnestic mild cognitive impairment (aMCI) are at a higher risk of developing Alzheimers Dementia (AD) than their cognitively normal peers. Decreased glucose metabolism with F-18 fluorodeoxyglucose (FDG) positron emission tomography (PET) is a downstream marker of neuronal injury and neurodegeneration. The risk of developing AD is higher in patients with aMCI who have a pattern of AD related glucose metabolic changes on FDG-PET than those who do not have these changes. We evaluated the utility of visual and 'statistical parametric mapping (SPM)-supported reading' of the FDG-PET scans of patients clinically classified as aMCI for identification of predementia patterns and for prediction of their progression to AD (PTAD).

Patients and methods: A total of 35 patients diagnosed as aMCI (mini mental state examination (MMSE) score ≥ 25) at the cognitive disorders and memory (CDM) clinic of speciality neurology centers were referred for a resting FDG-PET study. All patients had a detailed neurological, neuropsychological, and magnetic resonance imaging (MRI) evaluation prior to referral. Mean age of patients was 67.9 ± 8.7 (standard deviation (SD)) years, male: female (M: F) =26:9. Twenty healthy age-matched controls were included in the study for SPM (http://www.fil.ion.ucl.ac.uk/spm/). Scans were interpreted visually and using SPM. Each scan was classified as high, intermediate, or low likelihood for PTAD.

Results: On visual analysis, four scans were classified as high likelihood of PTAD and reveled hypometabolism in AD related territories. Seven patients had hypometabolism in at least one AD related territory and were classified as intermediate likelihood for PTAD. Two patients had hypometabolism in other than AD territories, while 22 patients did not show any significant hypometabolism on their FDG-PET scans and were classified as low likelihood for PTAD. SPM analysis of these cases confirmed the areas hypometabolism in all 13 patients compared to a normal subgroup (P < 0.05). On follow-up of 24 months, all four cases with high likelihood scans had progression of cognitive deficits and were confirmed as AD in the CDM clinic while none of the others showed cognitive decline.

Interpretation and conclusion: A pattern of AD hypometabolism on the FDG-PET study is useful for predicting PTAD. A longer follow-up of patients with hypometabolism in single AD territories is needed to predict their clinical behavior.

No MeSH data available.


Related in: MedlinePlus

(a) Statistical parametric mapping t map of this case superimposed on a transaxial T1 MRI template image showing hypometabolism (blue colour) in left parietal and posterior cingulate cortices (arrow). (b) SPM t maps superimposed on coronal magnetic resonance imaging T1 template showing hypometabolism in left parietal cortex and precuneus (arrow). (c) SPM t maps superimposed on saggital MRI T1 template showing hypometabolism in left temporal (arrow) and parietal cortices
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Figure 2: (a) Statistical parametric mapping t map of this case superimposed on a transaxial T1 MRI template image showing hypometabolism (blue colour) in left parietal and posterior cingulate cortices (arrow). (b) SPM t maps superimposed on coronal magnetic resonance imaging T1 template showing hypometabolism in left parietal cortex and precuneus (arrow). (c) SPM t maps superimposed on saggital MRI T1 template showing hypometabolism in left temporal (arrow) and parietal cortices

Mentions: Four scans were classified as high likelihood for PTAD. They had hypometabolism in unilateral parietal, mesial temporal, precuneus, and posterior cingulate cortices [Figures 1a–c]. Further SPM analysis confirmed significant hypometabolism (P ≤ 0.05) in these cortical regions [Figures 2a–c]. All four showed further cognitive deterioration and were diagnosed as AD by the specialist neurologist at the end of 24 months follow-up at the CDM clinic. Three of these cases underwent a repeat study at the end of 24 months. All three had metabolic evidence of disease progression [Figure 3a–c] which was well-visualized on the SPM analysis also [Figure 4a–c].


Functional neuroimaging using F-18 FDG PET/CT in amnestic mild cognitive impairment: A preliminary study.

Tripathi M, Tripathi M, Sharma R, Jaimini A, Md'souza M, Saw S, Mondal A, Kushwaha S - Indian J Nucl Med (2013)

(a) Statistical parametric mapping t map of this case superimposed on a transaxial T1 MRI template image showing hypometabolism (blue colour) in left parietal and posterior cingulate cortices (arrow). (b) SPM t maps superimposed on coronal magnetic resonance imaging T1 template showing hypometabolism in left parietal cortex and precuneus (arrow). (c) SPM t maps superimposed on saggital MRI T1 template showing hypometabolism in left temporal (arrow) and parietal cortices
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC3822410&req=5

Figure 2: (a) Statistical parametric mapping t map of this case superimposed on a transaxial T1 MRI template image showing hypometabolism (blue colour) in left parietal and posterior cingulate cortices (arrow). (b) SPM t maps superimposed on coronal magnetic resonance imaging T1 template showing hypometabolism in left parietal cortex and precuneus (arrow). (c) SPM t maps superimposed on saggital MRI T1 template showing hypometabolism in left temporal (arrow) and parietal cortices
Mentions: Four scans were classified as high likelihood for PTAD. They had hypometabolism in unilateral parietal, mesial temporal, precuneus, and posterior cingulate cortices [Figures 1a–c]. Further SPM analysis confirmed significant hypometabolism (P ≤ 0.05) in these cortical regions [Figures 2a–c]. All four showed further cognitive deterioration and were diagnosed as AD by the specialist neurologist at the end of 24 months follow-up at the CDM clinic. Three of these cases underwent a repeat study at the end of 24 months. All three had metabolic evidence of disease progression [Figure 3a–c] which was well-visualized on the SPM analysis also [Figure 4a–c].

Bottom Line: Seven patients had hypometabolism in at least one AD related territory and were classified as intermediate likelihood for PTAD.SPM analysis of these cases confirmed the areas hypometabolism in all 13 patients compared to a normal subgroup (P < 0.05).A longer follow-up of patients with hypometabolism in single AD territories is needed to predict their clinical behavior.

View Article: PubMed Central - PubMed

Affiliation: Department of Nuclear Medicine and Positron emission Tomography, All India Institute of Medical Sciences, New Delhi, India.

ABSTRACT

Background and objective: People with amnestic mild cognitive impairment (aMCI) are at a higher risk of developing Alzheimers Dementia (AD) than their cognitively normal peers. Decreased glucose metabolism with F-18 fluorodeoxyglucose (FDG) positron emission tomography (PET) is a downstream marker of neuronal injury and neurodegeneration. The risk of developing AD is higher in patients with aMCI who have a pattern of AD related glucose metabolic changes on FDG-PET than those who do not have these changes. We evaluated the utility of visual and 'statistical parametric mapping (SPM)-supported reading' of the FDG-PET scans of patients clinically classified as aMCI for identification of predementia patterns and for prediction of their progression to AD (PTAD).

Patients and methods: A total of 35 patients diagnosed as aMCI (mini mental state examination (MMSE) score ≥ 25) at the cognitive disorders and memory (CDM) clinic of speciality neurology centers were referred for a resting FDG-PET study. All patients had a detailed neurological, neuropsychological, and magnetic resonance imaging (MRI) evaluation prior to referral. Mean age of patients was 67.9 ± 8.7 (standard deviation (SD)) years, male: female (M: F) =26:9. Twenty healthy age-matched controls were included in the study for SPM (http://www.fil.ion.ucl.ac.uk/spm/). Scans were interpreted visually and using SPM. Each scan was classified as high, intermediate, or low likelihood for PTAD.

Results: On visual analysis, four scans were classified as high likelihood of PTAD and reveled hypometabolism in AD related territories. Seven patients had hypometabolism in at least one AD related territory and were classified as intermediate likelihood for PTAD. Two patients had hypometabolism in other than AD territories, while 22 patients did not show any significant hypometabolism on their FDG-PET scans and were classified as low likelihood for PTAD. SPM analysis of these cases confirmed the areas hypometabolism in all 13 patients compared to a normal subgroup (P < 0.05). On follow-up of 24 months, all four cases with high likelihood scans had progression of cognitive deficits and were confirmed as AD in the CDM clinic while none of the others showed cognitive decline.

Interpretation and conclusion: A pattern of AD hypometabolism on the FDG-PET study is useful for predicting PTAD. A longer follow-up of patients with hypometabolism in single AD territories is needed to predict their clinical behavior.

No MeSH data available.


Related in: MedlinePlus