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. 2008 Nov 11;71(20):1594-601.
doi: 10.1212/01.wnl.0000334752.41807.2f.

FDG-PET/MRI coregistration improves detection of cortical dysplasia in patients with epilepsy

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FDG-PET/MRI coregistration improves detection of cortical dysplasia in patients with epilepsy

N Salamon et al. Neurology. .

Abstract

Objective: Patients with cortical dysplasia (CD) are difficult to treat because the MRI abnormality may be undetectable. This study determined whether fluorodeoxyglucose (FDG)-PET/MRI coregistration enhanced the recognition of CD in epilepsy surgery patients.

Methods: Patients from 2004-2007 in whom FDG-PET/MRI coregistration was a component of the presurgical evaluation were compared with patients from 2000-2003 without this technique. For the 2004-2007 cohort, neuroimaging and clinical variables were compared between patients with mild Palmini type I and severe Palmini type II CD.

Results: Compared with the 2000-2003 cohort, from 2004-2007 more CD patients were detected, most had type I CD, and fewer cases required intracranial electrodes. From 2004-2007, 85% of type I CD cases had normal non-University of California, Los Angeles (UCLA) MRI scans. UCLA MRI identified CD in 78% of patients, and 37% of type I CD cases had normal UCLA scans. EEG and neuroimaging findings were concordant in 52% of type I CD patients, compared with 89% of type II CD patients. FDG-PET scans were positive in 71% of CD cases, and type I CD patients had less hypometabolism compared with type II CD patients. Postoperative seizure freedom occurred in 82% of patients, without differences between type I and type II CD cases.

Conclusions: Incorporating fluorodeoxyglucose-PET/MRI coregistration into the multimodality presurgical evaluation enhanced the noninvasive identification and successful surgical treatment of patients with cortical dysplasia (CD), especially for the 33% of patients with nonconcordant findings and those with normal MRI scans from mild type I CD.

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Figures

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Figure 1 Examples of difficult-to-identify type I cortical dysplasia from two patients with epilepsy (A and B) This 15-year-old patient began with seizures at age 4 years. Interictal scalp EEG disclosed synchronous spikes from F4, C4, and T4 and rarer independent spikes from F3 and C3. Ictal events were associated with broad EEG changes over the right frontal–temporal electrodes. Two previous outside MRI scans had been read as normal, as had his initial fluorodeoxyglucose (FDG)-PET scan (grayscale). FDG-PET/MRI coregistration indicated a well-defined area of focal hypometabolism in the right superior temporal gyrus (B, arrow). Closer inspection of the structural MRI indicated less white matter signal on T2 imaging in the same area (A, arrow). (C and D) This 8-year-old patient presented with seizure onset at age 3 years. The seizures were characterized by right leg and arm tonic events with eye fluttering lasting from 15 to 45 seconds. Scalp EEG showed fairly regular synchronous interictal discharges coming from the Cz, C3, and Pz electrodes, with rarer spikes from C4. Scalp EEG ictal onsets were difficult to localize secondary to movement artifacts. A previous outside MRI scan had been read as normal. University of California, Los Angeles MRI was read as showing a subtle lesion consistent with CD (C, arrow). FDG-PET/MRI coregistration indicated a focal area of hypometabolism in the left superior parietal region just behind the sensory cortex (D, arrow).
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Figure 2 Example of mesial temporal lobe epilepsy without hippocampal sclerosis from type I cortical dysplasia This 17-year-old patient presented with a history of seizure onset at age 7 years. Scalp EEG found rare interictal T1 spikes, and ictal events were associated with 4- to 5-Hz high amplitude slowing over the T1 and T3 electrodes. Two previous MRI scans performed at outside hospitals had been read as normal. Fluorodeoxyglucose-PET/MRI coregistration indicated an area of well-defined hypometabolism involving the left anterior mesial temporal region (B and D, arrows). Structural MRI indicated slightly increased fluid-attenuated inversion recovery changes in the same region without increased T2 signal in the hippocampus (A and C, arrows).
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Figure 3 Example of multilobar type I cortical dysplasia with normal structural MRI This 11-year-old patient began with seizures at age 5 years. Scalp EEG disclosed intermittent background slowing over the temporal–parietal–central region, with interictal spikes localized to C4, T4, T6, and O2 electrodes. Initial ictal onsets were difficult to localize, but after a few seconds, there were phase reversals at T6 through O2. MRI was read as normal within the University of California, Los Angeles (B and C). However, fluorodeoxyglucose-PET/MRI coregistration demonstrated multiple areas of hypometabolism involving the right temporal and parietal regions (B and D).

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References

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