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Advanced Neuroimaging for Modern Epilepsy Surgery


Figure 3: Magnetic Resonance Imaging Demonstrates Subtle Signs of Cortical Dysplasia


AB


Figure 4: Positron Emission Tomography and Single Photon Emission Computed Tomography


AB


Axial fluid-attenuated inversion recovery sequence (A) and fast spin echo (B) showing focal cortical thickening and increased subcortical signal intensity (arrows) in the left frontal lobe of a 33-year-old male with medically refractory epilepsy. Pathology revealed type IIB focal cortical dysplasia.


Malformation of Cortical Development


Besides having an important role in identifying MTS, conventional MRI is crucial in identifying neocortical lesions in malformation of cortical development (MCD). MCD encompasses a spectrum of developmental disorders that are thought to result from abnormal neuronal proliferation and/or migration during cortical development. These disorders include mild MCD, focal cortical dysplasia, polymicrogyria, hemimegencephalay, schizencephaly, and lissencephaly. MCD is one of the most common causes of medically refractory epilepsy in children and young adults. Some of the characteristic findings on imaging include abnormal gyration, thickened cortex, loss of gray–white junction, heterotopia, and signal changes on T2 (see Figure 3).25–27


In a recent retrospective study of 143 patients with MCD, complete resection of structural lesions on MRI and/or electrocortigraphic abnormality was strongly associated with freedom from seizures (72 % at two years).28


In addition, gray–white blurring


on MRI and smaller lesions are favorable prognostic factors for post-operative outcome.


In another study, the authors found that patients with focal cortical dysplasia have a strong tendency to have identifiable MRI abnormalities and better surgical outcome compared with those with MCD.29 Because detection of epileptogenic focal cortical malformation is the most reliable predictor of freedom from seizures, sensitive and specific pre-surgical detection of these abnormalities is critical for improving surgical outcome.


Automated MRI imaging analysis such as VBM or surface-based morphometry (SBM) can be employed to identify subtle anatomic anomalies. One study showed that SBM was able to identify 92 % of cortical lesions with 96 % specificity, successfully discriminating patients from controls 94 % of the time.30


However, this method failed


to adequately describe the extent of the lesion in most of the cases. Future efforts can aim at improving these imaging analysis methods for detection of MCD lesions.


US NEUROLOGY


A: 18-fluorodeoxyglucose-positron emission tomography (18FDG-PET). This axial slice through the temporal lobes demonstrates moderate hypometabolism involving the right medial, anterior, and lateral temporal cortex in a 32-year-old woman with temporal lobe epilepsy without magnetic resonance imaging (MRI) evidence of mesial temporal sclerosis. Pathologic evaluation was consistent with mesial temporal sclerosis, with neuron loss especially prominent in the dentate gyrus; B: Ictal ethyl cysteinate diethylester single photon emission tomography overlying axial MRI. This axial slice shows focal hyperperfusion of the right insular cortex in a 43-year-old man with frequent nocturnal focal seizures.


Functional Imaging


While MRI is an essential work-up for epilepsy, it does not capture the dynamic physiologic processes that occur in the brain during ictal and interictal periods. Furthermore, what can be done when the MRI is normal? In this next section, we discuss the utility of functional imaging in detecting epileptogenic foci.


Positron Emission Tomography


PET detects pairs of photons emitted indirectly by a positron that collides with an electron in the surrounding environment. The majority of PET uses 18-fluorodeoxyglucose (18FDG), which is taken up by the neurons and reflects the local cerebral metabolic rate of glucose. 18FDG-PET is used primarily to reflect dynamic seizure-related changes in cerebral cellular functions during interictal states.31


Numerous studies have reported


the utility of PET in patients with TLE, with a sensitivity of 70–85 %.32,33 Interestingly, PET studies in patients with TLE demonstrated hypometabolic regions ipsilateral to seizure onset beyond the region of MRI abnormalities, which included lateral temporal (78 %), mesial temporal (70 %), thalamic (63 %), basal ganglia (41 %), frontal (30 %), parietal (26 %), and occipital (4 %) regions.34


This widespread hypometabolism may reflect subtle network dysfunctions that are not seen by static structural imaging.


In the same study cohort, the adjusted odds ratio for concordant, localized PET as a predictor of seizure-free outcome was 7.1, although the negative predictive value was low.35,36


This is consistent


with the results of a meta-analysis showing that in TLE, ipsilateral focal hypometabolism was a predictor of good surgical outcome.37


One 171


In patients with good MRI and electroencephalography (EEG) concordance, PET may be largely redundant. However, in the 20–25 % of patients with refractory focal epilepsy who have normal MRI scans, focal PET hypometabolism can provide useful data towards the decision to carry out invasive intracranial EEG recording (see Figure 4A). In a prospective study of patients with non-localizing EEG and MRI findings, sensitivity for PET imaging to detect lesions as revealed by the gold standard of intracranial EEG was reported to be 58–64 % with a specificity of 53–63 %.35,36


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