|Year : 2011 | Volume
| Issue : 2 | Page : 67-77
Spectrum of neurocognitive dysfunction in Indian population on FDG PET/CT imaging
Rajnish Sharma1, Madhavi Tripathi1, Maria M D'Souza1, Abhinav Jaimini1, Raunak Varshney2, Puja Panwar2, Aruna Kaushik2, Sanjeev Saw1, Romana Seher1, Santosh Pandey1, Dinesh Singh1, Yachna Solanki1, Anil K Mishra2, Anupam Mondal1, RP Tripathi1
1 Division of Pet Imaging, Molecular Imaging Research Center, INMAS, Delhi, India
2 Division of Cyclotron and Radiopharmaceutical Sciences, Molecular Imaging Research Center, INMAS, Delhi, India
|Date of Web Publication||25-Nov-2011|
Division of PET Imaging, Molecular Imaging Research Center, INMAS, Lucknow Road, Timarpur, Delhi-110 054
Source of Support: DRDO Project No. (ST-P1-2008/INM-311), Conflict of Interest: None
| Abstract|| |
Background : A variety of neurodegenerative disorders produce significant abnormal brain function which can be detected using fluorodeoxyglucose positron emission tomography (FDG PET) scan even when structural changes are not detected on CT or MRI Scan. A study was undertaken at our institute to evaluate the FDG PET/CT findings in Indian population suffering from mild cognitive impairment (MCI), Alzheimer's disease (AD), fronto-temporal dementia (FTD), dementia with lewy body disease (DLBD) and other miscellaneous causes of dementia. Materials and Methods : 117 0 subjects having neurocognitive deficits and 36 normals were included in our study. All patients underwent a detailed history and clinical examination. This was followed by a mini mental state examination. Subsequently an FDG brain PET scan and an MRI were done. Results :In the patient population included in our study group 36 were normal, 39 had MCI, 40 had AD, 14 had FTD, and 13 had DLBD and 11 dementia due to other miscellaneous causes. MCI patients showed primarily reduced tracer uptake in the mesio-temporal cortex. AD patients showed reduced tracer concentration in temporo-parietal lobes, while patients with advanced diseases showed frontal lobe disease additionally. In subjects of FTD, reduced radiotracer uptake in the fronto-temporal lobes was noted. In addition, FTD patients also showed basal ganglia defects. In contrast the DLBD patients showed globally reduced FDG uptake including severely affecting the occipital cortices. Conclusion :In the current study the F18-FDG PET scans have been shown to be highly useful in the diagnosis of various neurocognitive disorders of the brain. AD was found to be the most common dementia in the Indian population followed by MCI. Diffuse Lewy body disease, FTD and other miscellaneous categories of dementia had a near similar incidence.
Keywords: Dementia, F18-FDG scan, Indian population
|How to cite this article:|
Sharma R, Tripathi M, D'Souza MM, Jaimini A, Varshney R, Panwar P, Kaushik A, Saw S, Seher R, Pandey S, Singh D, Solanki Y, Mishra AK, Mondal A, Tripathi R P. Spectrum of neurocognitive dysfunction in Indian population on FDG PET/CT imaging. Indian J Nucl Med 2011;26:67-77
|How to cite this URL:|
Sharma R, Tripathi M, D'Souza MM, Jaimini A, Varshney R, Panwar P, Kaushik A, Saw S, Seher R, Pandey S, Singh D, Solanki Y, Mishra AK, Mondal A, Tripathi R P. Spectrum of neurocognitive dysfunction in Indian population on FDG PET/CT imaging. Indian J Nucl Med [serial online] 2011 [cited 2022 Jan 20];26:67-77. Available from: https://www.ijnm.in/text.asp?2011/26/2/67/90255
| Introduction|| |
One of the most important uses of PET in neurosciences has been in the work up of the patients of various dementing disorders. Criteria for diagnosis of AD were defined by the National institute of neurological and communicative disorders and the Alzheimer's disease and related disorders.  These require evidence of progressive, chronic cognitive deficits in middle aged and elderly patients with no identifiable cause. It is very difficult to differentiate between AD and various other causes of dementia. , It has been reported that there is 20-30% decrease in the brain FDG uptake values in patients with various dementias when compared with the normal healthy population. 
The magnitude and extent of hypometabolism correlates with the severity of dementia symptoms. ,, MCI is used as a diagnostic classification concept for patients with decline in cognitive performance, which is in excess of the expected age related changes but does not completely fit into the diagnosis of dementia.  It has been reported that a substantial proportion of MCI patients subsequently may develop dementing disorder of the Alzheimer type (DAT).  Hence, it is important to detect patients of MCI as it includes a sizeable number of subjects with pre-dementia of AD. , If patients of MCI are diagnosed on the basis of clinical diagnosis only, then there is a very high possibility of including the population suffering from cerebro vascular disease or depression. 
FDG PET assessment of cerebral glucose metabolism is a measure of synaptic activity and can identify the presence and localization of a neurodegenerative process in the brain. Different criteria have been laid down for differential diagnosis of dementia. ,,,,,,
AD patients typically show hypometabolism in parieto - temporal cortices and in frontal lobe in the advanced stage of the disease.  While the FTD patients show hypometabolism in the frontal and temporal cortices, ,, the DLBD patients show primary hypometabolism in the parieto-occipital cortex. , The present study was undertaken to evaluate the spectrum of various neurocognitive dysfunction in the Indian population.
| Materials and Methods|| |
The study comprised of 117 subjects including 39 MCI, 40 AD, 14 FTD, 13 DLBD patients and 11 belonging to miscellaneous group.
The subjects were referred from a tertiary neurological centre after detailed history (corroborated by a close informant), clinical examination and mini mental state examination (MMSE). All patients were subjected to FDG PET scan and MRI of brain. All participants provided written informed consent. Approval of the local ethics committee was taken. None of the patients had any evidence of organic brain pathology or organic illness affecting the brain, significant head injury, systemic illness, psychosis or history of drug or alcohol intake.
The control normal population included in our study had no functional impairment based on detailed neurological examination. These subjects had a clinical dementia rating (CDR) = 0 or global deterioration scale (GDS) ≤ 2. They all had a MMSE score of more than 28. The subjects were matched to the cases on the basis of age, sex and educational status.
The criteria for MCI were based on clinical examination showing impaired cognitive function, ability to perform normal daily activities, no evidence of dementing disease. They had a CDR = 0.5 or GDS = 3 and they all had normal activity of daily living (ADL). The MMSE score of these patients was equal to or more than 24.
All subjects fulfilled the diagnostic and statistical manual of mental disorders (DSM -IV),  criteria for dementia. They all had significant ADL defects, and had a CDR ≥ 1 or GDS ≥ 4. Standard clinical criteria were used to characterize the type of dementia. Consensus criteria were used for the diagnosis of DLB  and FTD. 
All patients were fasting for at least 4 hours before the study and advised adequate hydration for rapid tracer excretion. The studies were done in a resting state with eyes closed. Ear plugs were used to prevent any auditory stimulus. The PET/CT study was performed on a Discovery STE 16 (GE) camera. F18-FDG was injected intravenously in a dose of 370 M Bq and a brain scan was obtained after an interval of 60 minutes with patient in supine position and head immobilized in a head rest. An initial scout of the head with localizer positioning was followed by a low dose CT acquisition at 110mA and 120 KV for attenuation correction. This was followed by a static 20 minute single bed position 3 dimensional emission scan. Data was reconstructed using 3-dimensional VUE algorithm (GE) and images were viewed for interpretation on a Xeleris workstation using volumetrix protocol (GE). Visual image interpretation was independently performed by 3 PET physicians (Dr. MT, Dr. RS and Dr. AJ) for FDG PET brain scans using fused PET/CT images. Any tracer activity which was noted as abnormal by all the 3 physicians was reported as abnormal.
MRI studies were undertaken for all patients to rule out morphological abnormalities, vascular insults and intracranial space occupying lesions. This was undertaken on a 1.5 T- Magnetom Vision (Seimens) scanner with a standardized protocol consisting of axial T 1 weighted images (TR 665ms, TE 24 ms, NEX 2) axial and sagital, T 2 weighted images (TR - 3800 ms, TE 90 ms, NEX 2) and axial and coronal FLAIR images (TR - 9000 ms, TE 110ms, NEX 2).
| Results|| |
Details of the subjects included in the study have been depicted in [Table 1],[Table 2],[Table 3],[Table 4],[Table 5] for the MCI, AD, FTD, DLBD and Miscellaneous Dementia Category respectively. Among MCI patients 17 out of 39 (43.5%) showed cortical hypometabolism indicative of neurodegenerative disease. Mesio-temporal hypometabolism was the most common defect noted in patients of MCI [Figure 1]. The remaining 22 subjects did not show significant cortical hypometabolism. Out of 17 patients found to have abnormal FDG Brain scan 11 were labeled as MCI, 4 AD and 2 had FTD pattern. 2 (18.8%) MCI patients showed bilateral F18-FDG uptake reductions. 6 (54.5%) showed predominantly left and 3 (27.2%) showed a predominant right reductions. The AD group included 17 patients with mild and 23 patients with moderate to severe dementia. Among the AD patients 17/40 (42.5%) showed prominent parieto-temporal hypometabolism [Figure 2]. Symmetric F18-FDG uptake reductions were found in 26/40 (65%) AD, 8/40 (20%) showed severe hypometabolism in left hemisphere and 6/40 (15%) showed more severe hypometabolism in right hemisphere. 23/40 (57.5%) AD patients showed additional frontal cortex hypometabolism. No extension into occipital cortex was noted in AD patients in our series of patients.
|Table 5: Clinical and diagnostic characteristics of miscellaneous subjects |
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|Figure 1: 71-year-old male presented with the complaints of forgetfulness. His MMSE score was 24. Arrows in F18-FDG PET images show bilateral Mesio-temporal hypometabolism diagnostic of MCI, in this patient|
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|Figure 2: F18-FDG PET images in late AD. Brain images of a 50-year-old female demonstrate hypometabolism of the frontal, parietal and temporal lobes bilaterally with relative sparing of primary visual cortex, thalamus and basal ganglia|
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The DLBD group included 13 patients, out of which 4 were with mild dementia and 9 patients had moderate to severe dementia. Among the DLBD patients, all patients showed hypometabolism in the occipital cortex of the brain besides affecting temporal, parietal or frontal regions of the brain [Figure 3]. F18 FDG uptake reductions were bilateral in (9/13) 69.2% of the patients, more severe in left hemisphere in (1/13) 7.6 % and more severe in right hemisphere in 21% of the patients. (3/13) 23% patients had moderate to severe DLBD pattern.
|Figure 3: F18-FDG PET images of Creutzfeldt-Jakob disease More Details. This patient was 56-year-old female with a history of memory loss, personality changes and hallucinations. The MMSE Score was 24. The typical metabolic pattern of hypometabolism affecting the Fronto- parietal- temporal lobes, basal ganglia and thalamus bilaterally was noted|
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The FTD group included 14 subjects, out of which 9 had mild dementia and 5 patients had moderate to severe dementia. These patients showed a prominent frontal and temporal hypometabolism [Figure 4]. F18-FDG uptake reductions were bilateral in 1/14 (7.1%) of patients, more severe in left in 6/14 (42.8%) and more severe in right hemisphere in 7/14 (50%).
|Figure 4: F18-FDG PET images of FTD. This patient is a 55-year-old female with an MMSE score of 26. Arrows indicate bilateral hypometabolism of the frontal (a) & temporal (b) cortex|
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The miscellaneous group comprised of 7 patients of Parkinson's dementia (PD) [Figure 5], 2 of vascular dementia [Figure 6] and 2 of Creutzfeldt-Jakob disease [Figure 7].
|Figure 5: F18-FDG PET Images of Dementia with Lewy body disease. A 75-year-male had a MMSE score of 19 and symptoms of cognitive dysfunction and hallucinations. PET scan shows bilaterally reduced tracer uptake in frontal, parietal and occipital cortices|
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|Figure 6: 18F-FDOPA images of PD dementia. FDOPA scans shows reduced tracer uptake bilaterally in the basal ganglia (L > R). While the FDG scan shows hypometabolism in the right frontal cortex|
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|Figure 7: F18-FDG PET images of vascular dementia in 60-year-old female. Patient presented with irritability, violent behavior and visual hallucinations. Hypometabolism is noted in right frontal cortex, right temporal cortex and right thalamus|
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| Discussion|| |
The importance of PET imaging in the management of the dementia patient is to help in the early diagnosis of the dementia disease process. Early detection of patients of MCI is essential as one third of MCI patients proceed to manifest DAT while more than half do not show progression to dementia. These results confirm that MCI patients even when selected carefully after clear cut inclusion criteria, represent a very heterogeneous patient population with regard to prognosis. Our study group comprised of 39 patients referred to our institute after being diagnosed to have MCI on clinical and MMSE test examination. Out of these MCI patients 13 were found to be normal. This itself highlights the importance of PET examination in patients having a neurocognitive disorder. Mosconi et al, reported that out of 37 patients screened for MCI, 12 were found to be normal on PET study.  Our study findings also show that F18- FDG PET can differentiate MCI from normal patients quite efficiently making it an effective tool to distinguish between these two groups which cause a lot of diagnostic issues as clinically it is quite difficult to distinguish age related cognitive deterioration from MCI which is a diagnostic dilemma for the clinician. Various F18-FDG PET profiles have been reported in the MCI group of patients which is due to the spectrum of cognitive deficits reported in this patient group.  In the present PET study AD PET pattern was found in 4 subjects and FTD pattern was noted in 2 patients. In previously reported PET studies 22-41% of the MCI patients with an AD PET pattern eventually converted to AD within a time period of 1-3 years. ,,,,,
F18-FDG PET scan has played an important role in the diagnosis of AD. Patients of AD present with parieto-temporal defects in the cortices when compared to their age equivalent healthy subjects.  It has already been highlighted that patients of MCI are at high risk of developing AD in future. 
Diagnosis can be made in patients of AD when clinical symptoms are not being fully expressed by the patient, in very early stage of AD. There is definitive evidence to show that generalized atrophy of brain is present in elderly patients, years before they actually developed AD. ,,,0,
In our study, 42.5% of the patients had a mild AD while the rest had a severe form of the disease. The patient with the milder form of the disease had temporo-parietal defects while those with severe form the disease also had defects in the frontal region. In contrast, the western literature has reported that 99% of the patients had mild form of disease while 1 had severe AD pattern.  Thus the Indian population in contrast appears to be affected from a more severe form of the disease. On further analysis it was found that 65% population had bilaterally symmetrical defects, while 15% had right dominant pattern and 20% had a left dominant hypometabolism. None of the AD patients were found to have occipital lesions on FDG PET scans.
FTD is one of the most common forms of cortical dementia, accounting for about 20% of presenile dementia. Diagnosis of FTD is difficult as these groups of patients have a variegated clinical and pathological picture. , Patients suffering from this form of dementia have been reported to suffer from forgetfulness and a variety of behavior disorders and hence are difficult to separate out from patients of AD, vascular dementia and psychiatric illnesses. It has been reported earlier that FTD results in finding of cerebral atrophy on CT and MR studies and hypo-perfusion in PET studies in frontal and temporal regions of the brain. , We found additional hypometabolism in the basal ganglia region which are known to be involved in a variety of brain activities.  It has been suggested that asymmetric hemispheric degeneration is common in patients with FTD. ,,, We found a hemispheric metabolic asymmetry in 92.8% of our FTD patients. Thus it can be inferred that FTD is a disorder that causes asymmetrical degeneration of cerebral hemispheres.
Lewy body dementia More Details has been described as the second most common senile dementia after AD. ,, Till the advent of PET, the post mortem examination was the only tool available to provide the definitive diagnosis in this disease. ,, The clinical diagnosis is based on certain diagnostic criteria.  However these clinical criteria have high specificity (90-97%) and a very low sensitivity of the order of (22-75%).  The main clinical complaints noted in DLBD patients include a progressive and a fluctuating cognitive decline with delusion, hallucinations and PD like symptoms. Other symptom includes repeated falls, loss of consciousness and neuroleptic symptoms. In comparison in AD loss of memory and neuropsychiatric features are more common in late stages.  Moderate Parkinsonian signs are observed both in AD and DLBD.  Thus in such cases where there is overlapping of symptoms such as cognitive decline, psychiatric signs and Parkinsonism More Details, it is difficult to differentiate AD from DLBD. , In our study 64% of the patients were found to have a moderate to severe form of the disease. All these patients had a bilateral form of the disease. Besides 2 patients of DLBD showed hypometabolism in basal gangalia and thalamus region also.
Thus in the majority of AD patients temporo-parietal defects were noted, in FTD patients more prominent hypometabolism in frontal and temporal cortex was noted and in DLBD patients though a global hypo-perfusion in the cortex was noted, the hypometabolism was most profound in the occipital cortex, which corresponds to the results of earlier workers. , This characteristic pattern of cortical hypometabolism including the occipital areas could be a result of diaschisis due to disruption of intracortial connections. Diaschisis is defined as depression of regional neuronal metabolism and cerebral blood flow caused by dysfunction in anatomically separate but functionally related neuronal regions.  Typically, sparing of primary sensori-motor cortex was noted. All the patients from this group showed prominent hypometabolism in the occipital region as reported in previous reports. ,,,, Thus, it is concluded that the most common cause of dementia in Indian population is AD followed by MCI. FTD and DLBD had almost same incidence patterns.
| Conclusion|| |
The present study illustrates the utility of F18-FDG PET in the diagnosis and characterization of neurocognitive dysfunction. AD has been found to be the most prevalent form of dementia in the Indian subcontinent, which is in conformity with the global trend. A significantly higher proportion of frontal lobe involvement was noted in the Indian population, as compared to that documented in the world-wide literature. These new findings, and epidemio-pathological reasons thereof, would merit further investigation. F18 FDG PET scans provide an objective and sensitive support to the diagnosis of early dementia.
| References|| |
|1.||McKhann G, Drachman D, Folstein M, Katzman R, Price D, Stadlan EM. Clinical diagnosis of Alzheimer's disease: Report of the NINCDS- ADRDA work group under the auspices of department of health and human services task force on Alzheimer's disease. Neurology 1984;34:939-44. |
|2.||Tierney MC, Fisher RH, Lewis AJ, Zorzitto ML, Snow WG, Reid DW, et al. The NINCDS-ADRDA Workgroup Criteria for the clinical diagnosis of probable Alzheimer's disease: A clinical pathological study of 57 cases. Neurology 1988;38:359-64. |
|3.||Joachim CL, Morris JH, Selkow DJ. Clinical diagnosed Alzheimer's disease: Autopsy results in 150 cases. Ann Neurol 1988;24:50-6. |
|4.||Alavi A, Reivich M, Ferris S, Christman D, Fowler J, MacGregor R, et al. Regional cerebral glucose metabolism in aging and senile dementia as determined by F18-deoxyglucose and positron emission tomography. In: h0 oyer S, editor. The aging brain: Physiological and pathophysiological aspects. Berlin Springer-Verlag; 1982. p. 87-195. |
|5.||Newberg A, Cotter A, Udeshi M, Alavi A, Clark C. Metabolic imaging severity rating scale (MISRS) for the assessment of patients with cognitive impairment. Clin Nucl Med 2003;28:565-70. |
|6.||Culter NR, Haxby J, Duara R, Grady CL, Kay AD, Kessler RM, et al. Clinical history, brain metabolism, and neurophysiological function in Alzheimer's disease. Ann Neurol 1985;18:298-309. |
|7.||Friedland RP, Jagust WJ, Huesman RH, Koss E, Knittel B, Mathis CA, et al. Regional cerebral glucose transport and utilization in Alzheimer's disease. Neurology 1989;39:1427-34. |
|8.||Peter RC. Mild cognitive impairment, and early Alzheimer's disease. Neurologist 1995;1:326-44. |
|9.||Bruscoli M, Lovestone S. Is MCI really just early dementia? A systematic review of conversion studies. Int Psychogeriatr 2004;16:129-40. |
|10.||Small GW, Rabins PV, Barry PP, Buckholtz NS, DeKosky ST, Ferris SH, et al. Diagnosis and treatment of Alsheimer disease and related disorders: Consensus statement of the American Association for Geriatric Psychiatry, The Alzheimer's Association, and the American Geriatrics Society. JAMA 1997;278:1363-71. |
|11.||Small GW. Differential diagnosis ad early detection of dementia. Am J Geriatr Psychiatry 1998;6:S26-33. |
|12.||Friedrich MJ. Mild cognitive impairment raises Alzheimer disease risk. JAMA 1999;282:621-2. |
|13.||Salmon E, Sadzot B, Maquet P, Degueldre C, Lemaire C, Rigo P, et al. Differential diagnosis of Alzheimer disease with PET. J Nucl Med 1994;35:391-8. |
|14.||Mazziotta JC, Frackowiak RS, Phelps ME. The use of positron emission tomography in the clinical assessment of dementia. Semin Nucl Med 1992;22:233-46. |
|15.||Herholz K. FDG PET and differential diagnosis of dementia. Alzheimer Dis Assoc Discord 1995;9:9-16. |
|16.||Minoshima S, Giordani B, Berent S, Frey KA, Foster NL, Kuhl DE. Metabolic reduction in the posterior cingulated cortex in very early Alzheimer's disease. Ann Neurol 1997;42:85-94. |
|17.||Nordberg A. Application of PET in dementia disorders. Acta Neurol Scand Suppl 1996;168:71-6. |
|18.||Small GW, Leiter F. Neuroimaging for diagnosis of dementia. J Clin Psychiatr 1998;59(suppl 11):4-7. |
|19.||Mosconi L, Brain glucose metabolism in the early and specific diagnosis of Alzheimer's disease: FDG-PET studies in MCI and AD. Eur J Nucl Med Imaging 2005;32:486-510. |
|20.||Ishii K, Sakamoto S, Sasaki M, Kitagaki H, Yamaji S, Hashimoto M, et al. Cerebral glucose metabolism in patients with frontotemporal dementia. J Nucl Med 1998;39:1875-8. |
|21.||Jeong Y, Cho SS, Park JM, Kang SJ, Lee JS, Kang E, et al. F18-FDG PET finding in frontotemporal dementia: An SPM analysis of 29 patients. J Nucl Med 2005;46:233-9. |
|22.||Diehl-Schmid J, Grimmer T, Drzezga A, Bornschein S, Riemenschneider M, Förstl H, et al. Decline of cerebral glucose metabolism in frontotemporal dementia: A longitudinal F18-FDG-PET-study. Neurobiol Aging 2007;28:42-50. |
|23.||Albin RL, Minoshima S, D'Amato CJ, Frey KA, Kuhl DE, Sima AA. Fluorodeoxyglucose positron emission tomography in diffuse Lewy body disease. Neurology 1996;47:462-6. |
|24.||Minoshima S, Foster NL, Sima AA, Frey KA, Albin RL, Kuch DE, Alzheimer's disease versus dementia with Lewy bodies: Cerebral metabolic distinction with autopsy confirmation. Ann Neurol 2001;50:358-65. |
|25.||American Psychiatric Association. Diagnostic and Statistical Manual of Mentall Disorders (DSM- IV), 4 th ed. Washington, D.C.: American Psychiatric Assocaition; 1994. |
|26.||McKeith IG, Galasko D, Kosaka K, Perry EK, Dickson DW, Hansen LA, et al. Consensus guidelines for the clinical and pathologic diagnosis of dementia with Lewy bodies (DLB): Report of the Consortium on DLB International Workshop. Neurology 1996;47:1113-24. |
|27.||McKhann G, Albert MS, Grossman M, Miller B, Dickson D, Trojanowski JQ. Clinical. Clinical and pathological diagnosis of frontotemporal dementia. Ann Neurol 2001;58:1803-9. |
|28.||Mosconi L, Tsui WH, Pupi A, De Santi S, Drzezga A, Minoshima S, et al. F18 -FDG PET database of longitudinally confirmed healthy elderly individuals improves detection of mild cognitive impairment and Alzheimer's Disease. J Nucl Med 2007;48:1129-34. |
|29.||Petersen RC, Doody R, Kurz A, Mohs RC, Morris JC, Rabins PV, et al. Current concepts in mild cognitive impairment. Arch Neurol 2001;58:1985-92. |
|30.||Minoshima S, Giordani B, Berent S, Frey KA, Foster NL, Kuhl DE. Metabolic reduction in the posterior cingulate cortex in very early Alzheimer's disease. Ann Neurol 1997;42:85-94. |
|31.||Drzezga A, Lautenschlager N, Siebner H, Riemenschneider M, Willoch F, Minoshima S, et al. Cerebral metabolic changes accompanying conversion of mild cognitive impairment into Alzeheimer's disease: A PET follow-up study. Eur J Nucl Med Imaging 2003;30:1104-13. |
|32.||Mosconi L, Perani D, Sorbi S, Herholz K, Nacmias B, Holthoff V, et al. MCI conversion to dementia and the APOE genotype: A prediction study with FDG-PET. Neurology 2004;63:2332-40. |
|33.||Drzezga A, Grimmer T, Riemenchneider M, Lautenschlager N, Siebner H, Alexopoulus P, et al. Prediction of individual outcome in MCI by means of genetic assessment and F18-FDG PET. J Nucl Med 2005;46:1625-32. |
|34.||Herholz K, Nordberg A, Salmon E, Perani D, Kessler J, Mielke R, et al. Impairment of neocortical metabolism predicts progression in Alzheimer's disease. Dement Geriatr Cogn Disord 1999;10:494-504. |
|35.||Silverman DH, Small G, Chang CY, Lu CS, Kung De Aburto MA, Chen W, et al. Positron emission tomography in evaluation of dementia: Regional brain metabolism and long-term outcome. JAMA 2001;286:2120-7. |
|36.||Petersen RC, Doody R, Kurz A, Mohs RC, Morris JC, Rabins PV, et al. Current concepts in mild cognitive impairment. Arch Neurol 2001;58:1985- 92. |
|37.||de Leon MJ, Convit A, Wolf OT, Tarshish CY, DeSanti S, Rusinek H, et al. Pediction of cognitive decline in normal elderly subjects with 2-[F18]fluoro-2-deoxy-D-glucose/positron-emission tomography (FDG/PET). Proc Natl Acad Sci USA 2001;98:10966-71. |
|38.||Jagust W, Gitcho A, Sun F, Kuczynski B, Mungas D, Haan M. Brain imaging evidence of preclinical Alzheimer's disease in normal aging. Ann Neurol 2006;59:673-81. |
|39.||Rusinek H, De Santi S, Frid D, Tsui WH, Tarshish CY, Convit A, et al. Regional brain atrophy rate predicts future cognitive decline: 6 -year longitudinal MR imaging study of normal aging. Radiology 2003;229:691-6. |
|40.||Jack CR, Shiung MM, Gunter JL, O'Brien PC, Weigand SD, Knopman DS, et al. Comparison of different MRI brain atrophy rate measures with clinical disease progression in AD. Neurology 2004;62:591-600. |
|41.||Masconi L, De Santi S, Li J, Tsui WH, Li Y, Boppana M, et al. Hippocampal hypometabolism predicts cognitve decline from normal aging. Neurobiol Aging 2008;29:676-92. |
|42.||Mosconi L, Tsui WH, Herholz K, Pupi A, Drzezga A, Lucignani G, et al. Multicenter standardized F18-FDG PET diagnosis of mild cognitive impairment, Alzheimer's disease, and other dementias. J Nucl Med 2008;49:390-8. |
|43.||Lund And Manchester Groups. Clinical and neuropathological crieteria for fronto-temporal dementia. J Neurol Neurosurg Pcychiatry 1994;57:416-8. |
|44.||Neary D, Snowden JS, Gustafson L, Passant U, Stuss D, Black S, et al. Frontotemporal lobar degeneration: A consensus on clinical diagnostic criteria. Neurology 1998;51:1546-54. |
|45.||Miller Bl, Cumming JL, Villanueva-Meyer J, Boone K, Mehringer CM, Lesser IM, et al. Frontal lobe degeneration: Clinical, neuropsychological, and SPECT characteristics, Neurology 1991;41:1374-82. |
|46.||Ishii K, Sakamoto S, Sakaki M, Kitagaki H, Yamaji S, Hashimoto M, et al. Cerebral glucose metabolism in patients with frontotemporal dementia. J Nucl Med 1998;39:1875-8. |
|47.||Cereda C, Ghika J, Maeder P, Bogousslavsky J. Strokes restricted to the insular cortex. Neurology 2002;59:1950-5. |
|48.||Santens P, De Bleecker J, Goethals P, Strijckmans K, Lemahieu I, Slegers G, et al. Differential regional cerebral uptake of F18-fluoro-2-deoxy-D-glucose in Alzheimer's disease and frontotemporal dementia at initial diagnosis. Eur Neurol 2001;45:19-27. |
|49.||Boone KB, Miller Bl, Lee A, Berman N, Sherman D, Stuss DT. Neuropsychological patterns in right versus left frontotemporal dementia. J Int Neuropsychol Soc 1999;5:616-22. |
|50.||Rosen HJ, Lengenfelder J, Miller Bl. Frontotemporal dementia. Neurol Clin 2000;18:979-92. |
|51.||Miller BL, Chang L, Mena I, Noone JK, Lesser IM, Progressive right frontotemporal denegration: Clinical, neuropsychological and SPECT characteristics. Dementia 1993;4:204-13. |
|52.||Byne EJ, Lennox G, Godwin-Anusten R. Diffuse Lewy body disease: Clinical features in 15 cases. J Neurol Neurosurg Psychiatry 1989;52:709-17. |
|53.||Hansen L, Salmon D, Galasko D, Masliah E, Katzman R, De Teresa R, et al. The Lewy body variant of Alzheimer's disease: A pathological and clinical entity. Neurology 1990;40:1-8. |
|54.||McKeith IG, Galasko D, Kosaka K, Perry EK, Dickson DW, Hansen LA, et al. Consensus guidelines for the clinical and pathologic diagnosis of dementia with Lewy bodies (DLB): Report of the consortium on DLB international workshop. Neurology 1996;47:1113-24. |
|55.||Hansen LA, Noville RL. Lewy body disease. Curr Opin Neurol Neurosurg 1992;5:889-94. |
|56.||Gibb WR, Luthert PJ, Janota I, Lantos PL. Cortical Lewy body dementia: Clinical features and classficiation. J Neurol Neurosurg Psychiatry 1989;52:85-192. |
|57.||Kosaka K, Yoshimura M, Ikeda K, Budka H. Diccuse type of Lewy disease: Progressive dementia with abundant cortial Lewy bodies and senile changes of varying degree - a new disease? Clin Neuropthol 1984;3:185-92. |
|58.||Ransmayr G, Wenning GK, Seppi K, Jellinger K, Poewe W. Dementia with Lewy bodies. Nevenarzt 2000;71:929-35. |
|59.||Mckhann G, Drachaman D, Folstein M, Katzman R, Price D, Stadlan EM. Clinical diagnosis of Alzhemier's disease: Report of the NINCDS- ADRDA Work Group under the auspices of Department of Health and Human Services Task Force on Alzheimer's disease. Neurology 1984;34:939-44. |
|60.||Soininen H, Laulumaa V, Helkala EL, Hartikainen P, Riekkinen PJ. Extrapyramidal signs in Alzheimer's disease: A 3-year follow-up study. J Neural Transm Park Dis Dement Sect 1992;4:107-19. |
|61.||Forerstl H, Burns A, Luther P, Cairns N, Levy R. The Lewy body variant of Alzheimer's disease: Clinical and pathological findings. Br J Psychiatry 1993;162:385-92. |
|62.||Minoshima S, Foster NL, Sima AA, Frey KA, Albin RL, Kuhl DE. Alzheimer's disease versus dementia with Lewy bodies: Cerebral metabolic distinction with autopsy confirmation. Ann Neurol 2001;50:358-65. |
|63.||Brunberg JA, Frey KA, Horton JA, Kuhl DE. Crossed cerebellar diaschisis: Occurrence and resolution demonstrated with PET during carotid temporary ballon occlusion. AJNR Am J Neuroradiol 1992;13:58-61. |
[Figure 1], [Figure 2], [Figure 3], [Figure 4], [Figure 5], [Figure 6], [Figure 7]
[Table 1], [Table 2], [Table 3], [Table 4], [Table 5]
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