is a Clinical Fellow and
is a Professor, Division of Nuclear Medicine, Department of
Radiology and Biomedical Imaging, University of California, San
The combination of positron emission tomography (PET) and
computed tomography (CT) provides an extremely valuable tool for
interpreting molecular and physiologic information in the context
of its corresponding anatomy. While the majority of PET-CT scanners
are geared toward oncologic applications, the utilization of
combined PET-CT scanners for neurological and cardiovascular
imaging is still evolving. Given that the majority of PET imaging
units now sold are incorporated into combined PET-CT scanners,1
the question arises as to when CT information could add useful
additional clinical information, particularly considering the risks
of additional CT radiation. Herein, we will review the current
state of common PET applications in neurological and cardiovascular
imaging with discussion of potential benefits of incorporating
diagnostic CT in the imaging evaluation.
Several PET radiopharmaceuticals are available for nuclear
cardiac imaging (Table 1) in the evaluation of coronary artery
disease and myocardial viability. Some of these agents are still
under investigation, while others require an onsite or nearby
cyclotron for production- limiting their availability to most PET
facilities. Our discussion will focus on rubidium-82 (Rb-82) and
18F fluorodeoxyglucose (FDG) as they are the most commonly used
agents for cardiac PET imaging and they have widespread commercial
Myocardial perfusion imaging
Myocardial perfusion imaging (MPI) is primarily performed on
widely available single photon emission computed tomography (SPECT)
systems. The increasing prevalence of PET scanners will soon
challenge this bias based on increasing access to PET imaging.
Moreover, PET addresses potential pitfalls in image interpretation
from attenuation artifacts inherent in SPECT myocardial perfusion
imaging such as from breast attenuation in women as well as in
large patients, given the increasing trend of obesity in the United
PET-CT offers the ability to use CT for attenuation correction
of PET images. This method requires less time than performing
attenuation correction using a transmission source used in stand
alone PET scanners. However, the appropriate implementation of CT
for attenuation correction of PET images requires close attention
to the fusion and raw images to ensure appropriate registration and
to avoid potential artifacts leading to false diagnoses.2
Furthermore, the ability to perform CT in conjunction with PET
allows one to acquire CT images for coronary calcium scoring (risk
stratification) and CT angiography (anatomic evaluation). The
combined acquisition of both PET MPI and coronary CT angiography
provides a complete view of both physiology (PET) and anatomy (CT),
and may be appropriate for select individuals. However, this
population has yet to be defined and the risks of additional
radiation exposure from coronary CT angiography should be
considered before performing a concurrent cardiac PET and CT
Rb-82 is produced from a U.S. Food and Drug Administration
approved strontium-82 generator, making PET MPI available to
facilities without access to an onsite or nearby cyclotron. Like
thallium, Rb-82 is a potassium analogue that is extracted
proportional to myocardial blood flow in living cells, and thus has
a better extraction fraction at higher coronary flow rates when
compared with traditional technetium (99mTc) labeled SPECT agents (e.g. sestamibi, CardioLite, Lantheus
Medical Imaging, North Billerica, MA; and, tetrofosmin, Myoview, GE
Healthcare, Chalfont St. Giles, UK). Given these favorable
extraction characteristics, Rb-82 is theoretically less likely to
result in false-negative studies for ischemia at high relative
coronary flow rates.
Additional advantages of using PET vs. SPECT include better
attenuation correction, counting efficiency and higher spatial
resolution, thus resulting in overall improved perfusion imaging
quality and less equivocal exam interpretations. This is
particularly pertinent for patients who are more likely to have
false-positive exams with SPECT from breast attenuation or
attenuation from an overall large body habitus, as well as with
improved accuracy for the identification of patients with
Given the short half-life of 75 seconds for Rb-82, MPI is performed
under pharmacologic stress such as with dipyridamole or adenosine.
Furthermore, technical orchestration and acquisition times need to
accommodate this rapid decay rate, as most counts will be acquired
in the first 4 to 5 minutes following injection. A sample PET-CT
protocol and Rb-82 MPI exam are shown in Figures 1 and 2.
Rb-82 PET MPI has demonstrated excellent results in prognosis
and risk stratification as well as diagnosing severe coronary
artery stenosis. Yoshinaga et al. showed increased cumulative rates
of death and myocardial infarction in pro-portion to summed stress
score (SSS) severity in 367 patients undergoing dipyridamole Rb-82
Lertsburapa et al. showed that summed stress score severity and
degree of left ventricular dysfunction with Rb-82 PET MPI were
significantly additive in predicting annual mortality rates.5
In diagnosing severe coronary artery stenosis (≥70% stenosis),
PET-CT with Rb-82 was shown to have a sensitivity and specificity
of 93% and 83%, respectively, with a normalcy rate of 100%,6
with diagnostic characteristics similar to traditional PET.7,8
Furthermore, comparison databases for PET-CT are being developed
and validated to assist in interpretation.9
Thus, Rb-82 PET-CT MPI has excellent diagnostic characteristics to
exclude patients with severe coronary artery stenosis.
Coronary blood flow, myocardial oxygen consumption and
contractile function are tightly coupled. Acute coronary occlusion
results in contractile dysfunction as a cardioprotective response.
In the setting of chronic coronary artery disease, there is an
adaptive downregulation of contractile function with reduced
resting perfusion, as a significant proportion of oxygen
utilization by myocytes is related to contractile performance. This
state of poor contractile function and poor perfusion in the
setting of living myocytes has been termed hibernating myocardium,
and is difficult to distinguish from myocardial infarct on MPI as
they have the same appearance of poor perfusion at both rest and
stress imaging. Assessment of myocardial viability with FDG
exploits the utilization of glucose by myocardium in a chronic
hypoxic state. Under normal well-perfused conditions, the
myocardium preferentially uses fatty acids as an energy substrate.
In the setting of hibernating myocardium, FDG is taken up by viable
myocardium helping distinguish it from myocardial infarction, hence
possibly being amenable to revascularization.
Performing PET viability imaging with FDG requires inducing a
relative hyperinsulinemic state within the patient to promote
maximal glucose utilization and thus FDG uptake within the
myocardium. Multiple methods have been advocated to achieve this
physiologic state and are detailed in the American Society of
Nuclear Cardiology and the Society of Nuclear Medicine guidelines
for PET imaging.10
In our experience, a protocol utilizing oral glucose loading with
adjustment of plasma glucose to less than 140 mg/dL with
intravenous regular insulin has proven to be logistically more
feasible than more technically challenging protocols such as the
hyperinsulinemic-euglycemic clamp method. Resting Rb-82 images are
acquired prior to FDG adminstration as a comparison map of
perfusion abnormalities. FDG imaging can also be combined with an
Rb-82 rest and stress imaging protocol as clinically appropriate. A
sample PET-CT protocol and Rb-82/FDG viability exam are shown in
Figures 1 and 2.
PET viability assessment with FDG has shown benefit in patient
management for predicting an increase in left ventricular function,
improving symptoms of angina and heart failure, and risk
stratification including survival following revascularization.11-17
The additive value of concurrent coronary CTA in conjunction with
FDG PET viability imaging needs further investigation. Additional
information gained from coronary CTA includes identifying patients
with extensive disease who are less amenable to percutaneous
interventions as well as assisting in preoperative coronary artery
bypass graft planning by defining anatomy and extent of coronary
PET has been used for neurological imaging for many decades. It
has grown in clinical importance, beyond its use in research,
particularly due to Centers for Medicare & Medicaid Services
(CMS) decision memorandum for reimbursement of select patients with
suspected dementia in 2004.18
While many promising radiopharmaceuticals are being developed for
application to neurological imaging, FDG constitutes the primary
agent currently used in clinical neurological imaging. Unlike the
myocardium, the grey matter of the brain preferentially uses
glucose as a metabolic substrate resulting in high levels of
baseline brain activity when using FDG. Thus, both increased and
decreased metabolism is used to evaluate intracranial
abnormalities. Our discussion will focus on the use of FDG in
evaluating suspected dementia, brain tumors and epilepsy. However,
many novel agents are under investigation and are likely to enter
clinical practice. Also, with the future realization of clinical
PET and magnetic resonance imaging (MRI) in a hybrid scanner,
concurrent PET and MRI acquisition will likely become the imaging
combination of choice for the evaluation of central nervous system
pathology with PET.
The prevalence of mild cognitive impairment (MCI) has been shown
to range between 3% and 19% in adults older than 65 years of age.19
Clinically classifying a patient with MCI and suspected dementia
can sometimes be difficult given the clinical overlap of many
dementias. In this subset of patients, correctly identifying the
underlying cause of dementia has therapeutic implications. FDG PET
has demonstrated the ability to detect and differentiate between
different types of dementias prior to significant cognitive
decline, particularly in distinguishing Alzheimer's disease (AD)
and frontotemporal dementia (FTD).20
Recently, a multicenter study demonstrated 92% to 95% accuracy in
classifying AD, FTD, and dementia with Lewy bodies (DLB) from
normal patients using a standardized automated analysis of FDG PET,21
and many commercial packages are now available comparing a
patient’s FDG PET with a reference population database allowing
additional quantitative assessments of regional changes of
In 2004, CMS approved the use of FDG PET for the evaluation of
select patients with suspected dementia given the proven efficacy
of cholinesterase inhibitors (tacrine, donepezil, rivastigmine,
galantamine) to delay progression of AD.22,23
However, specific patient criteria are required for payment, and
are outlined in the CMS memorandum.18
Briefly, patients must have:
- Documented cognitive decline for at least 6 months,
- Recently established diagnosis of dementia,
- Meet criteria for both AD and FTD,
- Have been evaluated for alternate causes of dementia,
- Have an unclear diagnosis.
Thus, FDG PET is used following an extensive inconclusive
clinical evaluation. Additionally, given the increasing utilization
of PET-CT for oncologic applications, incidental identification of
patterns of dementia may help referring clinicians in the
appropriate clinical context, particularly if the patient already
Patients with AD demonstrate a pattern of hypometabolism most
prominent in the parietotemporal cortex and posterior cingulate
cortex, and the pattern is more often symmetric though it can be
asymmetric. As AD becomes more clinically severe, regional
hypo-metabolism can extend anteriorly to involve the frontal lobes
and occasionally into the occipital lobes. In contrast, FTD
patients demonstrate a pattern of hypometabolism most prominent in
the frontotemporal cortex, although it can less often involve the
parietotemporal cortex and posterior cingulate cortex.
Occasionally, a patient presenting for FDG PET will not fit into
the AD or FTD pattern, thus awareness of other common dementia
patterns may help identify alternate etiologies of MCI. Dementia
with Lewy bodies often presents with regional areas of
hypometabolism most prominent in the parieto-occipital cortex,
however these patients are often clinically distinguishable by
clinical presentation, including visual hallucinations and
Parkinsonian motor features. Multi-infarct dementia classically
demonstrates peripheral wedge-shaped hypo-metabolic regions as
would be expected in the setting of chronic embolic disease. Given
the potential overlap of hypometabolic regions in different
dementias, quantitative analysis using a population database may
help in discriminating qualitatively equivocal metabolic patterns.
Examples of suspected (non-pathologically proven) cases of AD and
FTD are shown in Figure 3. These examples were found incidentally
on PET-CT for oncology indications. The development of PET amyloid
specific imaging agents are currently under development for the
evaluation of dementia, though their clinical use and application
need further investigation.24,25
While MRI is the current gold standard for evaluating CNS
neoplasms, FDG PET has been shown to be useful in evaluating the
posttreatment brain for recurrence in the setting of an equivocal
contrast-enhanced MRI. As previously discussed, given the normal
physiologic uptake of FDG in the brain, lesions which are
isometabolic to adjacent brain parenchyma may confound image
interpretation. However, the demonstration of decreased or
increased metabolism relative to adjacent brain parenchyma can
yield clinically relevant information. FDG is actively transported
across the blood-brain barrier into the brain, with uptake usually
higher in higher grade tumors. Furthermore, increased FDG uptake
correlates with transformation of a low-grade tumor into a
While this information can be clinically useful, the use of FDG PET
has not supplanted the use of contrast-enhanced MRI and biopsy for
FDG PET can be used to troubleshoot equivocal MRI findings,
particularly in the setting of nonspecific enhancement after
stereotactic radiosurgery. Both radiation necrosis and recurrent
tumor can have a similar appearance on contrast-enhanced MRI. FDG
PET has been shown to have good sensitivity, from 81% to 86%, for
the detection of recurrent tumor in this setting. However,
specificity has been shown to vary from 40% to 94%, likely due to
the baseline high physiologic uptake of FDG in brain parenchyma
combined with differences in technique.27,28
In equivocal cases, the additional information provided by FDG PET
may guide follow-up or identify regions to target for biopsy in the
setting of high suspicion for tumor recurrence.29,30
The use of PET-CT for anatomic correlation of regions of
hypermetabolism has not been evaluated, and areas of contrast
enhancement on CT correlated with PET may improve specificity.
However, fusion of PET images with MRI may achieve the same goals
without acquiring additional imaging and thus could alleviate the
risks associated with intravenous contrast for contrast-enhanced
CT. Multiple investigational PET agents show promise for imaging
brain tumors, including F-18 fluorothymidine as well as various
amino acid PET tracers. These agents are likely to enter clinical
practice, particularly in the instance of evaluating early response
to treatment prior to changes seen with conventional anatomic
Patients refractory to medical treatment for seizures are often
considered for surgical resection of the epileptogenic focus.
Surgical candidates undergo a multitude of tests including
electroencephalography (EEG), MRI, and sometimes SPECT or PET.
SPECT or PET imaging can add value in settings such as,
- Discordant MRI and EEG,
- Normal MRI where precise anatomic localization of an
epileptogenic focus is difficult, and
- When multiple anatomic lesions are seen on MRI and the
identification of an offending epileptogenic focus could help
limit the extent of surgery.
During a seizure, there is a coupled increase in regional
cerebral blood flow (CBF) and glucose metabolism.35-38
Thus, in the ictal state both SPECT imaging measuring CBF and FDG
PET imaging measuring glucose metabolism are similarly useful,
demonstrating increased activity relative to adjacent brain
parenchyma. However, due to the shorter half-life of FDG compared
99mTc-labeled SPECT agents, SPECT is considered logistically easier to
perform for ictal imaging. Also, with FDG, activation of secondary
and tertiary seizure foci may result in decreased FDG accumulation,
whereas SPECT regional CBF agents create a “snapshot” of blood flow
focused only on the primary epileptogenic focus.
In the interictal state, both regional CBF and glucose
metabolism are decreased through a mechanism that is not fully
understood, resulting in a relative decrease in activity relative
to adjacent brain parenchyma. Futhermore, regional CBF and glucose
metabolism are uncoupled with a greater reduction in glucose
metabolism compared with CBF during interictal imaging, making FDG
PET more favorable for interictal imaging.39-41
Furthermore, the intrinsic better spatial resolution of PET allows
improved anatomic localization and detail when compared with
In comparison with MRI, FDG PET has been shown to be more
sensitive in identifying seizures originating in the temporal
lobes, adding laterality and localization in approximately 60% to
90% of patients with temporal lobe epilepsy.42-44
However, in patients with mesial temporal sclerosis demonstrated on
MRI, FDG PET has reduced sensitivity with normal PET exams in 10%
of these patients.45,46
Patients with extratemporal lobe epilepsy more often have normal
brain MRI’s and thus often have SPECT or PET imaging to help
localize the inciting epileptogenic focus-up to 73% sensitivity has
However, FDG PET is also limited, with low sensitivities as low as
44% in one study in MRI negative patients.48
Despite potential low sensitivities, when an abnormality is present
on PET, this may add valuable additional information in patient
management. An example of reduced metabolism in the setting of
temporal lobe epilepsy is shown in Figure 4.
The addition of CT to brain FDG PET for the evaluation of
epileptogenic foci is unlikely to provide additional information
anatomically, as most patients already have had a brain MRI. The
attenuation correction CT obtained during a brain PET-CT may
improve automated anatomic coregistration of the PET to MRI, using
the CT portion of the PET-CT exam as the reference series for image
fusion. However, as with brain tumor imaging, the implementation of
simultaneous PET-MR imaging will likely become the modality of
choice for fusion brain imaging of epilepsy.
PET-CT has many useful applications in cardiovascular and
neurological imaging. However, the benefit of concurrent diagnostic
CT imaging is unclear in most instances and needs further
investigation. CT for attenuation correction of PET images is still
an important part of PET imaging when performed utilizing a
dedicated PET-CT scanner. Attention should be paid to potential
artifacts introduced with CT attenuation correction. When
incorporating a diagnostic quality CT, the risks of additional
radiation exposure should be weighed with the benefits of this
additional anatomic information given the indication of the PET
- Townsend DW. Dual-Modality imaging: Combining anatomy and function. J Nucl Med. 2008;49(6):938-955.
Lautamäki R, Brown TL, Merrill J, Bengel FM. CT-based attenuation
correction in (82)Rb-myocardial perfusion PET-CT: Incidence of
misalignment and effect on regional tracer distribution. Eur J Nucl Med Mol Imaging. 2008;35(2):305-310.
Bateman TM, Heller GV, McGhie, et al. Diagnostic accuracy of
rest/stress ECG-gated Rb-82 myocardial perfusion PET: Comparison with
ECG-gated Tc-99m sestamibi SPECT.J Nucl Cardiol. 2006;13(1):24-33.
K, Chow BJ, Williams K, et al. What is the prognostic value of
myocardial perfusion imaging using rubidium-82 positron emission
tomography? J Am Coll Cardiol. 2006;48(5):1029-1039.
Lertsburapa K, Ahlberg AW, Bateman TM, et al. Independent and
incremental prognostic value of left ventricular ejection fraction
determined by stress gated rubidium 82 PET imaging in patients with
known or suspected coronary artery disease. J Nucl Cardiol. 2008;15(6):745-753.
Sampson UK, Dorbala S, Limaye A, et al. Diagnostic accuracy of
rubidium-82 myocardial perfusion imaging with hybrid positron emission
tomography/computed tomography in thedetection of coronary artery
disease. J Am Coll Cardiol. 2007;49(10): 1052-1058.
- Groves AM, Speechly-Dick ME, Dickson JC, et al. Cardiac 82Rubidium PET-CT: Initial European experience. Eur J Nucl Med Mol Imaging. 2007:34(12): 1965-1972.
Esteves FP, Sanyal R, Nye JA, et al. Adenosine stress rubidium-82
PET/computed tomography in patients with known and suspected coronary
artery disease. Nucl Med Commun. 2008;29(8):674-678.
Santana CA, Folks RD, Garcia EV, et al. Quantitative (82)Rb PET-CT:
Development and validation of myocardial perfusion database. J Nucl Med. 2007; 48(7):1122-1128.
Bacharach SL, Bax JJ, Case, J, et al. PET myocardial glucose metabolism
and perfusion imaging: Part 1-Guidelines for data acquisition and
patient preparation. J Nucl Cardiol. 2003;10(5):543-556.
vom Dahl J, Altehoefer C, Sheehaet FH, et al. Recovery of regional left
ventricular dysfunction after coronary revascularization. Impact of
myocardial viability assessed by nuclearimaging and vessel patency at
follow-up angiography. J Am Coll Cardiol. 1996;28(4):948-958.
Di Carli MF, Asgarzadie F, Schelbert HR, et al. Quantitative relation
between myocardial viability and improvement in heart failure symptoms
after revascularization in patients withischemic cardiomyopathy. Circulation. 1995;92(12):3436-3444.
Di Carli MF, Maddahi J, Rokhsar S, et al. Long-term survival of
patients with coronary artery disease and left ventricular dysfunction:
Implications for the role of myocardial viabilityassessment in
management decisions. J Thorac Cardiovasc Surg. 1998; 116(6):997-1004.
Rohatgi R, Epstein S, Henriquez J, et al. Utility of positron emission
tomography in predicting cardiac events and survival in patients with
coronary artery disease and severe left ventricular dysfunction. Am J Cardiol. 2001;87(9):1096-1099, A6.
Beanlands RS, Hendry PJ, Masters RG, et al. Delay in revascularization
is associated with increased mortality rate in patients with severe left
ventricular dysfunction and viable myocardium on fluorine
18-fluorodeoxyglucose positron emission tomography imaging. Circulation. 1998;98(19 Suppl): II51-II56.
- Di Carli MF. Predicting improved function after myocardial revascularization. Curr Opin Cardiol. 1998;13(6):415-424.
- Allman KC, Shaw LJ, Hachamovitch R, Udelson JE. Myocardial viability
testing and impact of revascularization on prognosis in patients with
coronary artery disease and left ventricular dysfunction: A
meta-analysis. J Am Coll Cardiol. 2002;39(7):1151-1158.
- CMS Manual System Department of Health & Human Services, Pub.
100-04 Medicare Claims Processing Centers for Medicare & Medicaid
Services. CMS Transmittal R310CP,Billing Requirements for Positron
Emission Tomography (PET) Scans for Dementia and Neurodegenerative
Diseases, October 2004. Available at
http://www.cms.hhs.gov/transmittals/2004trans. Accessed May 13, 2009.
- Gauthier S, Reisberg B, Zaudig M, et al. Mild cognitive impairment. Lancet. 2006;367(9518):1262-1270.
Foster NL, Heidebrink JL, Clark CM, et al. FDG-PET improves accuracy in
distinguishing frontotemporal dementia and Alzheimer’s disease. Brain. 2007;130(Pt 10):2616-2635.
Mosconi L, Tsui WH, Herholz K, et al. Multicenter standardized 18F-FDG
PET diagnosis of mild cognitive impairment, Alzheimer’s disease, and
other dementias. J Nucl Med. 2008;49(3):390-398.
- Trinh NH, Hoblyn J, Mohanty S, Yaffe K. Efficacy of cholinesterase
inhibitors in the treatment of neuropsychiatric symptoms and functional
impairment in Alzheimer disease: A meta-analysis. JAMA. 2003; 289(2):210-216.
- Raina P, Santaguida P, Ismaila A, et al. Effectiveness of
cholinesterase inhibitors and memantine for treating dementia: Evidence
review for a clinical practice guideline. Ann Intern Med. 2008;148(5):379-397.
Butters MA, Klunk WE, Mathis CA, et al. Imaging Alzheimer pathology in
late-life depression with PET and Pittsburgh Compound-B. Alzheimer Dis Assoc Disord. 2008;22(3):261-268.
- Herholz K, Carter SF, Jones M. Positron emission tomography imaging in dementia. Br J Radiol. 2007; 80(Spec No 2):S160-167.
De Witte O, Levivier M, Violon P, et al. Prognostic value of positron
emission tomography with [18F]fluoro-2-deoxy-D-glucose in the low-grade
glioma. Neurosurgery. 1996;39(3):470-476; discussion 476-477.
- Langleben DD, Segall GM. PET in differentiation of recurrent brain tumor from radiation injury. J Nucl Med. 2000;41(11):1861-1867.
Henze M, Mohammed A, Schlemmer HP, et al. PET and SPECT for detection
of tumor progression in irradiated low-grade astrocytoma: A
receiver-operating-characteristic analysis. J Nucl Med. 2004; 45(4):579-586.
Messing-Jünger AM, Floeth FW, Pauleit D, et al. Multimodal target point
assessment for stereotactic biopsy in children with diffuse bithalamic
astrocytomas. Childs Nerv Syst. 2002;18(8):445-449.
- Wong TZ, van der Westhuizen GJ, Coleman RE. Positron emission tomography imaging of brain tumors. Neuroimaging Clin N Am. 2002;12(4):615-626.
Hatakeyama T, Kawai N, Nishiyama Y, et al. (11)C-methionine (MET) and
(18)F-fluorothymidine (FLT) PET in patients with newly diagnosed glioma.
Eur J Nucl Med Mol Imaging. 2008;35(11):2009-2017.
Ullrich R, Backes H, Li H, et al. Glioma proliferation as assessed by
3’-fluoro-3’-deoxy-L-thymidine positron emission tomography in patients
with newly diagnosed high-grade glioma.Clin Cancer Res. 2008;14(7):2049-2055.
- Schiepers C, Chen W, Dahlbom M, et al. 18F-fluorothymidine kinetics of malignant brain tumors. Eur J Nucl Med Mol Imaging. 2007;34(7):1003-1011.
- Saga T, Kawashima H, Araki N, et al. Evaluation of primary brain tumors with FLT-PET: Usefulness and limitations. Clin Nucl Med. 2006;31(12):774-780.
- Hougaard K, Oikawa T, Sveinsdottir E, et al. Regional cerebral blood flow in focal cortical epilepsy.Arch Neurol. 1976;33(8)527-535.
- Engel J, Kuhl DE, Phelps ME, et al. Local cerebral metabolism during partial seizures. Neurology. 1983; 33(4):400-413.
Kuhl DE, Engel J, Phelps ME, Selin C. Epileptic patterns of local
cerebral metabolism and perfusion in humans determined by emission
computed tomography of 18FDG and 13NH3.Ann Neurol. 1980;8(4): 348-360.
- Ingvar M. Cerebral blood flow and metabolic rate during seizures. Relationship to epileptic brain damage. Ann N Y Acad Sci. 1986;462:194-206.
- Bruehl C, Hagemann G, Witte OW. Uncoupling of blood flow and metabolism in focal epilepsy. Epilepsia. 1998;39(12):1235-1242.
Gaillard WD, Fazilat S, White S, et al. Interictal metabolism and blood
flow are uncoupled in temporal lobe cortex of patients with complex
partial epilepsy.Neurology. 1995;45(10):1841-1847.
- Lee SK, Lee SY, Kim KK, et al. Surgical outcome and prognostic factors of cryptogenic neocortical epilepsy.Ann Neurol. 2005;58(4):525-532.
Drzezga A, Arnold S, Minoshima S, et al. 18F-FDG PET studies in
patients with extratemporal and temporal epilepsy: Evaluation of an
observer-independent analysis. J Nucl Med. 1999;40(5):737-746.
Breier JI, Mullani NA, Thomas AB, et al. Effects of duration of
epilepsy on the uncoupling of metabolism and blood flow in complex
partial seizures. Neurology. 1997;48(4):1047-1053.
- Casse R, Rowe CC, Newton M, et al. Positron emission tomography and epilepsy.Mol Imaging Biol. 2002;4(5):338-351.
O’Brien TJ, Newton MR, Cook MJ, et al. Hippocampal atrophy is not a
major determinant of regional hypometabolism in temporal lobe epilepsy.Epilepsia. 1997;38(1):74-80.
- Foldvary N, Lee N, Hanson MW, et al. Correlation of hippocampal neuronal density and FDG-PET in mesial temporal lobe epilepsy. Epilepsia. 1999;40(1): 26-29.
- Kim YK, Lee DS, Lee SK, et al. (18)F-FDG PET in localization of frontal lobe epilepsy: Comparison of visual and SPM analysis. J Nucl Med. 2002;43(9): 1167-1174.
Lee DS, Lee JS, Kang KW, et al. Disparity of perfusion and glucose
metabolism of epileptogenic zones in temporal lobe epilepsy demonstrated
by SPM/SPAM analysis on 15O water PET, [18F]FDG-PET, and [99mTc]-HMPAO
SPECT. Epilepsia. 2001;42(12):1515-1522.