• Intractable epilepsy;
  • Epilepsy surgery;
  • Reoperation;
  • Surgical outcome;
  • Positron emission tomography;
  • α−[11C]Methyl-l-tryptophan


  1. Top of page
  2. Abstract
  6. Acknowledgments

Summary: Purpose: Reoperation after failed cortical resection can alleviate seizures in patients with intractable neocortical epilepsy, provided that previously nonresected epileptic regions are accurately defined and removed. Most imaging modalities have limited value in identifying such regions after a previous surgery. Positron emission tomography (PET) using α−[11C]methyl-l-tryptophan (AMT) can detect epileptogenic cortical areas as regions with increased tracer uptake. This study analyzed whether increased cortical AMT uptake can detect nonresected epileptic foci in patients with previously failed neocortical resection.

Methods: Thirty-three young patients (age 3–26 years; mean age, 10.8 years) with intractable epilepsy of neocortical origin, and a previously failed cortical resection performed at various epilepsy centers, underwent further presurgical evaluation for reoperation. AMT-PET scans were performed 6 days to 7 years after the first surgery. Focal cortical areas with increased AMT uptake were objectively identified and correlated to ictal EEG data as well as clinical variables (age, postsurgical time, etiology).

Results: Cortical increases of AMT uptake were detected on the side of the previous resections in 12 cases. In two patients scanned shortly (within a week) after surgery, diffuse hemispheric increases were observed, without any further localization value. In contrast, in 10 (43%) of 23 patients scanned >2 months but within 2.3 years after surgery, focal cortical increases occurred, concordant with seizure onset on ictal EEG. Age, etiology (lesional vs. cryptogenic), epileptiform EEG activity during PET, or time of the last seizure were not significantly related to the presence of increased AMT uptake. All patients with localizing AMT-PET, who underwent reoperation, became seizure free (n = 5) or showed considerable improvement of seizure frequency (n = 2).

Conclusions: AMT-PET can identify nonresected epileptic cortex in patients with a previously failed neocortical epilepsy surgery and, with proper timing for the scan, can assist in planning reoperation.

Partial epilepsy is refractory to medical treatment in ≤20% of cases, and resective epilepsy surgery can effectively alleviate seizures in these patients. The outcome of epilepsy surgery varies widely depending on the type of epilepsy and operation performed, and the ultimate results with respect to seizures remain far from optimal. In particular, the success rate of cortical resections in epilepsies of neocortical origin (which are especially common among children), continues to be disappointingly low at 50 to 60% (1–6).

Further resection (reoperation) of epileptogenic brain regions after an initial failed epilepsy surgery can result in seizure freedom. Several studies have shown good results after reoperation (7–12), especially when additional resections included incompletely removed lesions or previous resections were extended based on ictal EEG recordings. However, Schwartz and Spencer (13) recently reported disappointingly low surgical success when the second surgery was performed in patients in whom seizures recurred after comprehensive preoperative evaluation and resection; only 19% of such patients remained seizure free after a 1-year follow-up. In that series, successful outcomes resulted from removal of recurrent tumors, completion of a functional hemispherectomy, or repeated invasive monitoring to correct a previous sampling error. Magnetic resonance imaging (MRI) can reveal missed or incompletely resected lesions, but it is not helpful in cryptogenic cases. Scalp ictal EEG can be difficult to interpret in patients with previous resection because of alterations of the original brain anatomy, shifting, intracranial cavities, as well as effects of skull and dural scarring.

A real need exists for innovative neuroimaging approaches to localize nonresected epileptic cortex after failed resective epilepsy surgery. Functional neuroimaging, including positron emission tomography (PET) and ictal single-photon emission computed tomography (SPECT) may be beneficial in this regard. However, functional imaging studies after epilepsy surgery are scarce, perhaps also reflecting some limitations of these imaging modalities after cortical resection. For example, interictal 2-deoxy-2-[18F]fluoro-d-glucose (FDG) PET can detect hypometabolism in nonresected cortex, but it is difficult to determine whether the observed hypometabolism indicates epileptogenic tissue rather than postsurgical tissue damage or deafferentation. The value of ictal SPECT also remains to be documented in such cases. One case report describes a recurrent epileptogenic oligodendroglioma detected by [11C]l-methionine PET, when it was not visible on MRI (14). Recently the PET tracer α−[11C]methyl-l-tryptophan (AMT) has been reported to be selectively accumulated in and around epileptogenic cortical regions (15–17). AMT was originally developed for the measurement of serotonin synthesis in vivo (18). Subsequent studies indicated that increased cortical AMT uptake can occur either because of increased rate of serotonin synthesis or of induction of the kynurenine pathway (19,20). Increased cortical AMT uptake appears to be highly specific for epileptogenic regions, although its sensitivity depends on the underlying pathology: it was found to be most sensitive (≤70%) in children with tuberous sclerosis or other developmental cortical malformations, and less sensitive (<40%) in cryptogenic epilepsy (15–17,21). A recent study (22) also showed that increased AMT uptake can lateralize the seizure focus in patients with temporal lobe epilepsy without hippocampal atrophy, thus further extending the clinical potential of this imaging method.

The goal of the present study was to determine the usefulness of AMT-PET in patients with recurrent seizures after resective epilepsy surgery. We hypothesized that increased AMT uptake will identify epileptogenic cortex in at least some patients with previously failed cortical resection. We also evaluated which factors (such as age, etiology, or timing of the PET scan) may help predict which patients will most likely benefit from AMT-PET, when reoperation is being contemplated after failed neocortical resective epilepsy surgery.


  1. Top of page
  2. Abstract
  6. Acknowledgments


Thirty-three young patients (21 male patients; age range, 3–26 years; mean age, 10.8 years) with intractable epilepsy of neocortical origin who had undergone previous cortical resections because of intractable epilepsy in our institution (n = 27) or other epilepsy centers (n = 6), but continued to have seizures, were included in the study. These patients were selected from 75 subjects who had undergone previous epilepsy surgery and were evaluated for further surgery with PET scanning (using various tracers) in our center during a 7-year period (1996–2002). Patients with tuberous sclerosis as well as those with a previous hemispherectomy were not included in the study. Previous surgical resections of the selected 33 patients included portions of one lobe (n = 10), two lobes (n = 10), or three lobes (n = 13). All patients underwent postsurgical AMT-PET scan 6 days to 7.0 years after surgery (mean, 2.1 years; median, 1.3 years) and additional presurgical evaluation including prolonged interictal and ictal scalp EEG monitoring. One patient had two operations and underwent two consecutive AMT-PET scans 8 months after the first resection, and 6 days after the reoperation (which was an extension of the first resection). Thirteen patients had a lesion on presurgical MRI (six cortical developmental malformations (including three cortical dysplasia, one heterotopia, one pachygyria, one hemimegalencephaly, mostly affecting the posterior half of the hemisphere), two had encephalomalacias, and one each had dysembryoplastic neuroepithelial tumor (DNET), glioma, cyst, Rasmussen encephalitis, and temporal lesion for which histology was not available). All patients were taking antiepileptic medication (AED) including carbamazepine (CBZ; n = 17), valproate (VPA; n = 11), lamotrigine (LTG; n = 9), topiramate (TPM; n = 8), levetiracetam (LEV; n = 8), phenytoin (PHT; n = 7), vigabatrin (VGB; n = 7), oxcarbazepine (OXC; n = 4), phenobarbital (PB; n = 3), zonisamide (ZNS; n = 3), diazepam (DZP; n = 2), clonazepam (CZP; n = 2), or clorazepate (CLP; n = 1) used as mono- or polytherapy at the time of PET scanning.


PET scanning procedure

PET studies were performed by using the CTI/Siemens EXACT/HR whole-body positron tomograph (Knoxville, TN, U.S.A.) located in the Children's Hospital of Detroit, Michigan. This scanner has a 15-cm field of view and generates 47 image planes with a slice thickness of 3.125 mm. The reconstructed image in-plane resolution obtained is 7.5 ± 0.38 mm at full width, half maximum (FWHM) and 7.0 ± 0.49 mm in the axial direction (reconstruction parameters: Hanning filter with 1.26 cycles/cm cutoff frequency). The procedure for AMT-PET scanning has been described previously (23). In brief, patients were fasted for 6 h before the AMT-PET studies. This ensured stable plasma tryptophan and large neutral amino acid levels during the study. A venous line was established for injection of AMT (0.1 mCi/kg) as a slow bolus over a 2-min period. Scalp-recorded EEG was monitored and recorded during the AMT-PET scanning during the uptake period with surface EEG electrodes placed according to the International 10–20 system, by using the Nicolet Voyageur Digital EEG equipment (Nicolet Biomedical, Madison, WI, U.S.A.). EEG recording during AMT-PET was available in 24 patients, whereas the others were closely observed during the AMT uptake to ensure that no clinical seizures occurred. Children were sedated intravenously with either pentobarbital (PTB; Nembutal; 5 mg/kg) or midazolam (0.2–0.4 mg/kg), if necessary. Prior studies performed in our laboratory on five adults, each scanned twice (once without and once with sedation with midazolam), found that global differences of AMT uptake were <10% between the two testing conditions (24).Twenty-five minutes after tracer injection, a dynamic emission scan of the brain (7 × 5 min) was acquired in three-dimensional mode. Measured attenuation and decay correction were applied to the PET images. Summed images representing five frames of the dynamic scan (30–55 min after injection) were used for this study. All AMT-PET studies were performed in compliance with the regulations of Wayne State University Human Investigation Committee, and written informed consent of the patient, parent, or legal guardian was obtained.

Determination of cortical PET abnormalities

First, all PET images were inspected by two of the authors to ensure that no focal cortical increases were present contralateral to the previous resections. Subsequently, regional cortical increases of AMT uptake were identified and marked by using an objective method based on a semiautomated software package applied to all supratentorial planes of the PET image volumes (25). The method has been applied in several recent PET studies on patients with epilepsy, and the method of identifying increased AMT uptake has been described in a recent AMT-PET study (17). In brief, cortical regions with abnormal asymmetry of AMT uptake were objectively marked on the side of the resection, if they exceeded an 8% cutoff threshold (established based on magnitude of asymmetry in normative data) (17), and were higher than the uptake in contralateral homologous brain regions. As a result of this marking procedure, a new “marked” image PET file was created that included all 47 planes of the original frame. Subsequently we verified that the marked AMT-PET abnormalities indeed represented true increases of AMT uptake (rather than decreases in contralateral cortex) by using a region-of-interest (ROI) analysis. For this procedure, activity in the marked regions, as well as in nonresected cortex outside the marked area in the same hemisphere, were measured by drawing ROIs in each plane where marked regions were seen. Percentage increase of AMT uptake was calculated in marked cortex as compared with average uptake in the nonmarked cortex. Increases of >8% were considered to be abnormal.

Concordance between AMT-PET and ictal EEG findings

The localization of the marked and ROI-verified cortical regions with increased AMT uptake was considered to be concordant with the ictal EEG localization (seizure-onset zone) if both indicated the same lobe, or when ictal EEG abnormalities involved more than one lobe and AMT increase was detected objectively in at least one of these involved lobes.

Measurement of quinolinic acid concentration in resected epileptogenic brain tissue

To explore whether increased AMT uptake on PET can be attributed to increased quinolinic acid concentration, quinolinic acid concentrations were measured from resected tissue obtained during reoperation in one patient with increased AMT uptake on PET. The tissue samples were obtained from cortical areas showing epileptiform activity (seizure onset or frequent interictal spiking) on intracranial EEG monitoring, and quinolinic acid measurements were performed as described previously (26).

Statistical analysis

Age and time between surgery and PET scanning were compared in patients with increased AMT uptake and those with no increase on AMT-PET by using the Mann–Whitney U test. Further, patients were grouped according to the time of PET scanning after surgery, according to time between last seizure and AMT-PET scanning, as well as according to etiology (lesional vs. nonlesional, based on their preoperative MRI findings), and frequency of increased AMT uptake was compared between these groups by using the χ2 test. A value of p < 0.05 was considered to be significant.


  1. Top of page
  2. Abstract
  6. Acknowledgments

Localizing value of AMT-PET

On visual assessment, none of the patients had focally increased AMT uptake contralateral to the resection(s). In the objective analysis, 12 PET scans showed increased AMT uptake in the hemisphere that had undergone previous resection. In two patients in whom postoperative PET scans were performed shortly (6 days in both cases) after the resection, cortical increases of AMT uptake involved the operated-on hemisphere diffusely, giving no localization information (Fig. 1). These diffuse hemispheric increases were considered to be due to acute postsurgical (possibly inflammatory) changes; therefore these two scans were excluded from further comparisons. The remaining 10 AMT-PET scans with increased uptake were all performed >2 months after the resection and showed well-localized cortical increases (range, 8–46%; mean, 19%) affecting only a portion of nonresected hemisphere (Table 1). These focal increases occurred in the nonresected part of a previously partially resected lobe or lobes in all cases: nine of them were located close to the original resection margin (see examples in Fig. 2), whereas in patient 10 (Table 1), increased AMT uptake was present in a distant (inferior) part of the frontal lobe that had previously undergone resection in its superior portion (Fig. 3). Postsurgical ictal EEG data (including intracranial EEG monitoring data in six cases) were concordant with the location of increased AMT uptake on PET (Table 1).


Figure 1. Diffuse hemispheric increase of α−[11C]methyl-l-tryptophan (AMT) uptake ipsilateral to the resection 6 days postoperatively in a 3-year-old girl. Arrows, multiple areas of nonresected cortex with AMT increase.

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Table 1. Clinical, imaging, and ictal EEG data of the 10 patients with localizing increase of AMT uptake
Patient sex/Age (yr)Preoperative MRI/Postop. histologyPrevious resectionAMT increaseIctal EEG focus(reoperation)Outcome class (reoperation)
  1. AMT, α−[11C]methyl-l-tryptophan; M, male; F, female; L, left; R, right; post. HME, hemimegalencephaly (mostly affecting the posterior half of the hemisphere); DNET, dysembryoplastic neuroepithelial tumor; F, frontal; T, temporal; O, occipital; P, parietal; C, central; HME, hemimegalencephaly.

  2. aConfirmed by intracranial EEG monitoring.

  3. bHistology was not available. Outcome class (>1 year after reoperation): I, seizure free; III, >75% improvement in seizure frequency.

1. M/6R F/dysplasiaR T, FR F12R FaI
2 M/11R F/dysplasiaR FR F13R F-P
3. M/7L TO post. HME/dysplasiaL TPOL TO24L TOIII
4. M/17R F/focal encephalitisR CR F30R F
5. M/12L TP lesionbL TP, FL T46L hemisph.
6. F/20L T DNETL TL T25L TaI
7. M/16Normal/gliosisR F, T, PR FP 8R FPaI
8. F/18Normal/gliosisL TL T10L F-TaI
9. F/5Normal/dysplasiaR F, PR F 8R FaI
10. M/10Normal/gliosisL F,T,PL F15L FaIII

Figure 2. Focal increases of α−[11C]methyl-l-tryptophan (AMT) uptake (arrows) at the resection margin. A: Right frontoparietal (but not temporal) cortical increase in a patient (no. 7) 2 months after a failed right-sided resection including multiple areas. After intracranial EEG monitoring, the patient underwent further frontoparietal resection and became seizure free. B: Focal increase of AMT uptake (arrow) confined to the left temporal lobe adjacent to the previous resection margin in a patient (no. 5) who had undergone a left temporoparietal lesionectomy and frontal resection (based on intracranial EEG data) 1 year before the positron emission tomography scan. Postsurgical magnetic resonance imaging did not show any residual lesion. Ictal EEG suggested left hemispheric onset without clear localization. No further resection has been performed thus far.

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Figure 3. Focal increase of α−[11C]methyl-l-tryptophan (AMT) uptake (arrow) remote from the resection margin. This patient (no. 10) underwent a previous left frontal (see first image), parietal (second image), and anterior temporal resection. Preoperative magnetic resonance imaging was normal. The AMT–positron emission tomography (PET) scan was performed 8 months after surgery and showed increase in the inferior part of the previously resected frontal lobe (arrow). Note that the original resection margins did not show abnormal increases. Intracranial ictal EEG showed right inferior frontal seizure onset consistent with the AMT-PET abnormality.

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So far, 17 of 33 patients, including seven patients with localizing AMT-PET, have undergone reoperation (further focal cortical resection) in our institution. In the seven reoperated-on patients with localizing increase of AMT uptake, subdural electrodes were applied in six cases and covered the area with increased AMT uptake. Resections included the ictal EEG focus in all seven cases, including the area with increased AMT uptake. Five (71%) of the reoperated-on patients with increased AMT uptake (including three with normal preoperative MRI) became and remained seizure free >1 year after reoperation, whereas the two others showed considerable (>75%) improvement of seizure frequency. Histologic examination confirmed the MRI diagnosis in those with cortical developmental malformations and showed gliosis (n = 3) or microscopic cortical dysplasia (n = 1) in those with normal preoperative MRI.

Effect of timing of AMT-PET, age, and etiology

Patients with localizing AMT-PET had shorter time (1.0 ± 0.8 years) elapsed since surgery than did those with nonlocalizing AMT-PET (2.7 ± 2.2 years; p = 0.02), although overlaps were found between the two groups. None of the patients with localizing AMT-PET had >2.3 years between the resection and postoperative PET, and patients with early postoperative PET scanning (i.e., within 2.3 years after surgery) had significantly higher chances for a localizing AMT-PET (10 of 23; 43.5%) than did those scanned >2.3 years after surgery (none of nine; χ2= 5.69; p = 0.017).

The age of patients with localizing AMT-PET (12.2 ± 5.3 years) did not differ from that of the others (10.6 ± 4.7 years; p = 0.43). Six of the 10 patients with localizing AMT-PET had a structural lesion detected by MRI before surgery, including a patient with a DNET that had not been completely resected. Increased AMT uptake occurred more commonly in patients with structural lesions (six of 13; 46.1%), as compared with those with no lesion on MRI (four of 19; 21.1%), but the difference was not significant (χ2= 2.26; p = 0.13).

Effect of epileptiform activity during AMT uptake and time of last seizures

Among the 24 EEGs recorded during the AMT uptake period, three showed evidence of electrographic seizures, 16 showed interictal epileptiform activity, whereas no epileptiform activity was recorded in five cases. Increased AMT uptake occurred in each of these three groups of patients (in one of three patients with electrographic seizures during PET, in four of 16 patients with interictal epileptiform activity, and in two of five cases with no epileptiform activity), without any obvious group differences. The time of the last seizure before AMT-PET scanning could be reliably determined in 27 cases. In most of these patients (19 of 27, 70.3%), seizures were noted within 24 h before the PET scanning, whereas only five patients were seizure free within 1 week before the PET scan. Occurrence of increased AMT uptake in patients with recent (≤24 h) seizures versus in those with no recent seizure(s) was not significantly different (eight of 19 vs. two of eight, respectively; p = 0.66).

Quinolinic acid concentration in resected epileptogenic tissue

Quinolinic acid concentrations measured in the resected tissues of patient 6 were increased (2,790, 3,700, and 163 pmol/g; normal value is <100 pmol/g) in all three samples obtained from cortex showing epileptiform activity on subdural EEG monitoring.


  1. Top of page
  2. Abstract
  6. Acknowledgments

This study demonstrates that AMT-PET can identify additional epileptogenic cortical areas and assist successful reoperation in patients with a previously failed cortical resection. When performed after the acute postsurgical period, but within 2 to 3 years after surgery, AMT-PET was able to identify well-localized cortical increases in ∼40% of the cases. These increases were concordant with ictal EEG localizations, and removal of the affected areas resulted in sustained seizure freedom or considerable improvement in all cases. The results are consistent with two recent studies documenting that increased cortical AMT uptake can detect epileptic regions in patients with neocortical epilepsy (16,17). Similar to these previous studies, the present findings indicate that abnormal increases of cortical AMT uptake are highly specific for epileptogenic brain regions and can occur in patients with and without structural lesions. Consistent with findings on patients with no previous resection (17), focal increase of AMT uptake did not appear to be related to epileptiform activity (including electrographic seizures) recorded during the tracer-uptake period, or to the time elapsed since the last clinical seizure before PET scanning. Thus it is unlikely that in these patients, increased AMT uptake in the epileptic focus was due to ictal or postictal activity, or even to active interictal spiking.

In addition to demonstrating the clinical utility of AMT-PET after failed cortical resections, our results provide clues regarding the optimal timing of postsurgical PET scanning. As demonstrated in two of our patients, early (within a week, or possibly even beyond) postoperative PET scanning with AMT may show widespread nonlocalized hemispheric increases, presumably due to transient postoperative inflammatory reactions. The reason for very high AMT uptake in such cases most likely stems from activation of the kynurenine pathway of tryptophan metabolism (27). This can lead to overproduction of toxic and convulsant tryptophan metabolites, particularly quinolinic acid (19,27). Previous studies showed increased levels of quinolinic acid in brain tissues resected from cortical regions showing increased AMT uptake in patients with epilepsy associated with tuberous sclerosis or brain tumors (19,20,28). Tissue quinolinic acid levels can increase under certain pathologic conditions, via induction of the key enzyme indoleamine 2,3-dioxygenase (by infections, viruses, or interferons), leading to significant metabolism of tryptophan along the kynurenine pathway (27,29,30). If the cortical increases on AMT-PET scans taken shortly after cortical resection reflect this pathway, it raises the possibility that increased quinolinic acid (or other convulsant tryptophan metabolites) levels may contribute to early postoperative seizures in such cases. Early postoperative seizures can occur in as many as 25% of patients after pediatric epilepsy surgery and, although these early seizures predict worse long-term outcome, approximately half of these patients become and remain seizure free in the prolonged postoperative period (31). It remains unclear, but would be useful to explore, whether similar widespread increases of AMT uptake occur shortly after resection in patients with no postoperative seizures.

AMT-PET did not provide localization information in nine patients in whom the PET scans were performed beyond 2.3 years after resection, although all of these patients had intractable seizures. The reason for the low sensitivity of AMT-PET in these patients remains unclear, and the limited number of patients precludes general conclusions regarding the clinical usefulness of AMT-PET performed beyond 2-3 years after epilepsy surgery. Nevertheless, our findings suggest that AMT-PET can be very helpful to localize epileptic foci in almost half of the patients with previously failed neocortical resection, if the PET is performed beyond the acute postsurgical period but within 2–3 years after resection. This finding represents an advance in seizure-focus localization in patients who have had a previously failed cortical resection. Currently no reliable imaging methods can detect missed epileptogenic cortex in these patients, and one must rely heavily on scalp-EEG data to guide subdural electrode placements, an approach that is not optimal.

The biologic basis of increased AMT uptake localized to the epileptic focus remains unclear. In the present study, increased quinolinic acid concentrations were found in the resected epileptogenic brain tissue of one reoperated-on patient with localized increase of AMT uptake. This is consistent with similar findings in children with tuberous sclerosis and intractable epilepsy (18). However, increased AMT uptake can also result from increased serotonin synthesis in or around the epileptogenic tissue. In support of this possibility, human epileptic tissue studies showed serotonergic hyperinnervation in dysplastic tissue but not in cortex from patients with cryptogenic epilepsy (32). Our recent PET study also found a significant association between presence of increased AMT uptake and cortical developmental malformations (17). In the present study, the number of patients with developmental abnormalities was too low, and such an association could not be confirmed. To address the role of serotonergic mechanisms in epileptogenic brain regions further, PET studies using a tracer for 5-HT1A receptors have recently become available (33).

Another important issue for further study is whether resection of cortex with increased AMT uptake leads to seizure-free outcome or, conversely, nonresection of it predicts seizure recurrence after surgery. Our previous study with intracranial EEG correlations demonstrated that cortical areas immediately adjacent to increased AMT uptake are often epileptogenic and should be addressed by subdural EEG monitoring. Analysis of surgical outcomes suggested that the best surgical results occurred when the resection included both cortex with increased AMT uptake and the surrounding epileptogenic region (17). With this consideration, increased AMT uptake can be a powerful guide for grid placement. In the present study, all but one reoperation in patients with increased AMT uptake was guided by intracranial EEG monitoring, and regions including the AMT-PET abnormality as well as intracranial seizure onset were resected. This resulted in seizure freedom in five patients and has led to a considerable improvement in the remaining two. One of these three patients had a hemimegalencephaly with mostly posterior quadrant involvement, and focal resection rather than hemispherectomy was performed in an attempt to spare the functioning motor cortex. A recent study described a series of 11 patients with a similar malformation (called “hemi-hemimegalencephaly”), in whom temporoparietooccipital resections (but not occipital or parietal resection alone) decreased but did not always abolish seizures (34). It is likely that, in such cases, complete, sustained seizure freedom could be achieved only by hemispherectomy. Nevertheless, all patients in the present series benefited greatly from reoperation assisted by AMT-PET. Thus the clinical utility of AMT-PET can be extended to the most challenging patients with previously failed neocortical resection; with proper timing, accurate focus localization facilitating successful reoperation can be achieved by applying AMT-PET in almost half of such patients. Conversely, the fact that more than half of patients did not show increased AMT uptake indicates that much work remains to be done in developing other neuroimaging approaches to define their remaining epileptogenic cortex.


  1. Top of page
  2. Abstract
  6. Acknowledgments

Acknowledgment:  This work was supported by NIH grant NS34488 (to H.T.C.) and NS38324 (to D.C.C.). We thank Galina Rabkin, CNMT, Teresa Jones, CNMT, and Mei-li Lee, MS, Anna Deboard, RN, and Kris Baird, BS, for their expert technical assistance in performing the PET studies.


  1. Top of page
  2. Abstract
  6. Acknowledgments
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