The use of positron emission tomography in the clinical assessment of dementia*

https://doi.org/10.1016/S0001-2998(05)80118-7Get rights and content

A number of reasons can be cited for performing a test that identifies patients early in their course who have fatal and currently untreatable neurological disorders. At this stage of illness there is clinical ambiguity. The patient, family, and physician are typically faced with a battery of negative test results and an ambiguous clinical impression that can lead to periodic repetition of tests that involve cost, inconvenience, potential morbidity to the patient, and lack of definitive diagnosis. An accurate test would lead to the avoidance of these low-yield, repetitive, and costly evaluations. In addition, such studies can identify homogeneous groups of individuals with degenerative disorders leading to dementia who could be enrolled in experimental therapeutic programs. In these programs therapies could be monitored in an objective and noninvasive fashion using positron emission tomography (PET). The magnitude of the health problems resulting from the dementing illnesses is great in terms of medical practive, economics, and family hardship. The number of individuals with these disorders is predicted to increase dramatically in the future. The ability to provide an accurate diagnosis and more clear prognosis early in the disease course should diminish ambiguity for patients, families, and physicians. Ample evidence is cited in this article to show that PET hasthe ability to provide such information objectively and noninvasively.

References (164)

  • MazziottaJC

    Movement disorders

  • KetySS et al.

    The determination of cerebral blood flow in man by the use of nitrous oxide in low concentrations

    Am J Physiol

    (1945)
  • KetySS et al.

    The nitrous oxide method for the quantitative determination of cerebral blood flow in man: Theory, procedure and normal values

    J Clin Invest

    (1948)
  • FreyhanFA et al.

    Cerebral blood and metabolism in psychoses of senility

    J Nerv Ment Dis

    (1951)
  • LassenNA et al.

    Bilateral studies of cerebral oxygen uptake in young and aged normal subjects and in patients with organic dementia

    J Clin Invest

    (1960)
  • LassenNA et al.

    Mental function and cerebral oxygen consumption in organic dementia

    Arch Neuropsychiatr

    (1957)
  • ObristWD et al.

    Regional cerebral blood flow in senile and presenile dementia

    Neurology

    (1970)
  • IngvarDH et al.

    Regional cerebral blood flow in organic dementia with early onset

    Acta Neurol Scand

    (1970)
  • LenziGL et al.

    The relationship between regional oxygen utilisation and cerebral blood flow in multi-infarct dementia

    Acta Neurol Scand

    (1977)
  • PerryRH

    Recent advances in neuropathology

    Br Med Bull

    (1986)
  • McKhannG et al.

    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)
  • EslingerPJ et al.

    Examining the relationship between computed tomography and neuropsychological measures in normal and demented elderly

    J Neurol Neurosurg Psychiatr

    (1984)
  • WuS et al.

    Cognitive correlates of diffuse cerebral atrophy determined by computed tomography

    Neurology

    (1981)
  • FrackowiakR et al.

    Regional cerebral oxygen supply and utilization in dementia: A clinical and physiological study with oxygen-15 and positron tomography

    Brain

    (1981)
  • McGeerPL et al.

    Comparison of PET, MRI and CT with pathology in a proven case of Alzheimer's disease

    Neurology

    (1986)
  • CutlerNR et al.

    Clinical hisory, brain metabolism, and neurophysiological function in Alzheimer's disease

    Ann Neurol

    (1985)
  • KuhlDE et al.

    Local cerebral glucose utilization in elderly patients with depression, multiple infarct dementia and Alzheimer's disease

    J Cereb Blood Flow Metab

    (1983)
  • KuhlDE et al.

    Similarities of cerebral glucose metabolism in Alzheimer's and Parkinsonian dementia

    J Cereb Blood Flow Metab

    (1985)
  • de LeonMJ et al.

    Computed tomography and positron emission transaxial tomography evaluations of normal aging and Alzheimer's disease

    J Cereb Blood Flow Metab

    (1983)
  • FriedlandRP et al.

    Regional cerebral metabolic alterations in dementia of the Alzheimertype: Positron emission tomography with [18F]Fluorodeoxyglucose

    J Comp Assist Tomography

    (1983)
  • FosterNL et al.

    Alzheimer's disease: Focal cortical changes shown by positron emission tomography

    Neurology

    (1983)
  • BensonDF et al.

    The fluorodeoxyglucose 18F scan in Alzheimer's disease and multi-infarct dementia

    Arch Neurol

    (1983)
  • FosterNL et al.

    Cortical abnormalities in Alzheimer's disease

    Ann Neurol

    (1984)
  • ChaseTN et al.

    Weshsler adult intelligence scale performance

    Arch Neurol

    (1984)
  • FriedlandRP et al.

    The diagnosis of Alzheimer-type dementia: A preliminary comparison of positron emission tomography and proton magnetic resonance

    JAMA

    (1984)
  • CutlerNR et al.

    Brain metabolism as measured with positron emission tomography: Serial assessment in a patient with familial Alzheimer's disease

    Neurology

    (1985)
  • HaxbyJV et al.

    Relationship between neuropsychological and cerebral metabolic asymmetries in early Alzheimer's disease

    J Cereb Blood Flow Metab

    (1985)
  • HatazawaJ et al.

    Disturbance of cerebral oxidative metabolism in patients with Alzheimer's disease: A positron emission tomography study

    J Cereb Blood Flow Metab

    (1985)
  • DuaraR et al.

    Positron emission tomography in Alzheimer's disease

    Neurology

    (1986)
  • HaxbyJV et al.

    Neocortical metabolic abnormalities precede nonmemory cognitive defects in early Alzheimer's-type dementia

    Arch Neurol

    (1986)
  • FosterNL et al.

    Cerebral mapping of apraxia in Alzheimer's disease by positron emission tomography

    Ann Neurol

    (1986)
  • LoewensteinDA et al.

    Predominant left hemisphere metabolic dysfunction in dementia

    Arch Neurol

    (1989)
  • JagustWJ et al.

    Longitudinal studies of regional cerebral metabolism in Alzheimer's disease

    Neurology

    (1988)
  • HaxbyJV et al.

    Heterogeneous anterior-posterior metabolic patterns in dementia of the Alzheimer type

    Neurology

    (1988)
  • SheridanPH et al.

    Relations of EEG alpha background to parietal lobe function in Alzheimer's disease as measured by positron emission tomography and psychometry

    Neurology

    (1988)
  • FriedlandRP et al.

    Regional cerebral glucose transport and utilization in Alzheimer's disease

    Neurology

    (1989)
  • FazekasF et al.

    Comparison of CT, MR, and PET in Alzheimer's dementia and normal aging

    J Nucl Med

    (1989)
  • FosterNL et al.

    The pattern of cerebral hypometabolism studied with positron emission tomography is similar in sporadic and familial Alzheimer's disease

    Ann Neurol

    (1989)
  • FriedlandRP et al.

    Family history of dementia and regional cerebral glucose utilization (rCMRglc) in dementia of the Alzheimer type (AD)

    Neurology

    (1989)
  • KuhlDE et al.

    Cerebral metabolic patterns before the diagnosis of probable Alzheimer's disease

    J Cereb Blood Flow Metab

    (1987)
  • Cited by (95)

    • Positron Emission Tomography-Based Assessment of Cognitive Impairment and Dementias, Critical Role of Fluorodeoxyglucose in such Settings

      2022, PET Clinics
      Citation Excerpt :

      A large number of foundational studies show that this pattern of temporo-parietal hypometabolism has a sensitivity of approximately 85% to 90%, a specificity of approximately 60% to 70%, and a negative predictive value ranging from 77% to 95% in screening for AD.16 However, because this pattern can be observed in patients with other conditions including Parkinson disease, DLB, bilateral parietal stroke, bilateral parietal subdural hematomas, and bilateral parietal radiation therapy ports, it is not considered to be pathognomonic for AD.17 Furthermore, recent findings suggest that other patterns of hypometabolism, such as that within the entorhinal cortex, may be more specific to AD and thus provide more accurate diagnostic biomarkers of AD.18

    • Cognitive Impairment and Dementias

      2018, Seminars in Nuclear Medicine
      Citation Excerpt :

      Based on a large number of studies, this temporo-parietal hypometabolism pattern has a sensitivity of approximately 85%-90% and specificity of approximately 60%-70%. However, the pattern is not pathognomonic for AD since it can be observed in patients with other conditions including Parkinson's disease, bilateral parietal stroke, bilateral parietal subdural hematomas, and bilateral parietal radiation therapy ports.17 In reviewing the extant data from resting FDG-PET studies, regional glucose hypometabolism is a prominent indicator of disease in AD patients.

    • Fluorodeoxyglucose positron emission tomography/magnetic resonance imaging: Current status, future aspects

      2014, PET Clinics
      Citation Excerpt :

      Although high physiologic uptake can limit FDG cerebral PET value, there is much ongoing research with newer PET tracers. Neurodegenerative disorders such as Alzheimer dementia (AD) affect a large percentage of the aging population.66 The dementia spectrum includes several different dementias with distinct clinical features and treatments.

    • Neuroimaging and Human Genetics

      2005, International Review of Neurobiology
      Citation Excerpt :

      Alzheimer's disease (AD) is a complex polygenic disorder in most cases (Emahazion et al., 2001; Farrer et al., 1991) and is the most common form of dementia in adults, affecting approximately 7% of people older than 65 and perhaps 40% of people older than 80 (Price, 2000). The disease is typically characterized by a severe decline in memory performance (American Psychiatric Association, 1995), and from an imaging perspective, slowing of resting EEG in the temporoparietal region (Dierks et al., 1991; Duffy et al., 1984), prolonged latency (and amplitude reduction) of the temporoparietal P300 event‐related potential component (Brown et al., 1983; Syndulko et al., 1982), volume reduction of the medial temporal lobe in MRI or CT scans (Jack et al., 1992; Jobst et al., 1992; Scheltens et al., 1992), a decline of white and gray matter tissue anisotropy that is most prominent in the temporal lobe (Bozalli et al., 2001), and decreased parietotemporal regional blood flow and glucose‐uptake in PET and SPECT scans (Benson et al., 1981; Herholz et al., 2002a,b; Mazziotta et al., 1992). To some extent, comparable, but more subtle, abnormalities are also observed in subjects at familial risk for the disease (Boutros et al., 1995; Burggren et al., 2002; Green and Levey, 1999; Ponomareva et al., 1998) or in early stages of the illness (De Santi et al., 2001; Fellgiebel et al., 2004; Grundmann et al., 2002; Huang et al., 2000; Killiany et al., 2002).

    View all citing articles on Scopus
    *

    Supported in part by grants from the National Institute of Neurological Disease and Stroke (NS-15654, NS-20867), Biomedical Research (447145-MP24188), UCLA School of Medicine (USHHS RR5354), and the National Institute of Mental Health (MH-37916), and a contract from the Department of Energy (#DE-AC03-SF-7600012)

    View full text