Clinical Neurophysiology xxx (2015) xxx–xxx
Contents lists available at ScienceDirect
Clinical Neurophysiology journal homepage: www.elsevier.com/locate/clinph
Letter to the Editor Nonconvulsive status epilepticus following implantation of subdural grid electrodes in a brain tumor patient
Implantation of subdural electrodes is considered to be safe and conventionally performed during epilepsy surgery. The application has been recently expanded into brain tumor surgery for the presurgical evaluation of the cerebral function, wherein no major complications have been reported (Kral et al., 2007; Little et al., 2008; Wellmer et al., 2012). We herein present a precautionary case in a patient with a high-grade glioma who showed transient neurological deficits after the implantation of subdural grid electrodes. A 69-year-old woman was admitted to our hospital with a complaint of mild speech and gait disturbance. Baseline laboratory investigations were normal. Contrast-enhanced magnetic resonance imaging (MRI) revealed a ring-enhanced tumor mass in the white matter under the speech and primary motor areas, which was associated with extensive vasogenic edema (Fig. 1A and B). Since malignancy was suspected, we elected to resect not only the tumor mass but the peripheral tissue. Due to the location of the tumor, functional cortical mapping was planned. Scalp electroencephalography showed infrequent spikes over the left parietal area, and Fostoin (750 mg/day for the first day followed by 375 mg/day) was preoperatively administered for seizure prevention. Craniotomy was performed with the aid of an intraoperative navigation system. Following the incision of the dura, mild brain swelling was observed. The primary motor area was identified using somatosensory and motor evoked potentials. A sheet of 5 6 channel subdural grid electrodes (measuring 39 47 mm in size) with a thickness of 0.8 mm (Unique Medical Co., Japan) was slipped into the subdural space to cover the cortical region of interest (Fig. 1C). No particular intraoperative complications were recognized. The follow-up head CT scan on the next morning was unremarkable. Spinal fluid leakage was not evident and the baseline laboratory investigations were normal. On that evening, however, the patient became slightly lethargic with worsened motor aphasia and right hemiparesis. An emergent head CT scan did not show any additional intracranial lesions (Fig. 1D). While no convulsive seizures were apparent, electrocorticography (ECoG) recorded from the subdural electrodes on the same day showed continuous slow waves, which were composed of triphasic and spike and slow waves across all regions covered by the electrodes (sampling rate of 4 kHz per channel, Fig. 1E and F), indicating nonconvulsive status epilepticus. Neurological deficits on the following day progressed to a stage where she was hardly able to
vocalize or move her right limbs, although the head CT scan was also unremarkable. Fostoin was administered daily throughout this period, and the neurological deficits were slightly improved by the administration of glycerol. Without performing functional mapping, tumor resection was performed on the following day with the aim of a prompt histological diagnosis. There were no particular intraoperative findings except moderate brain swelling to an extent comparable with that of the first surgery and a thin layer of subdural hematoma under the electrode. Avoiding Broca’s area with the conventional anatomical landmark, a small corticotomy was made on the frontal cortex and the ring-enhanced mass was selectively resected. The neurological deficits gradually ameliorated thereafter, which recovered almost to a preoperative level within 3 weeks. Fostoin was administered 2 days after the operation, which was subsequently replaced by oral administration of valproate acid (1200 mg/day). The histological diagnosis of the resected tumor was anaplastic astrocytoma (WHO grade 3), and chemoradiation was subsequently performed. To the best of our knowledge, this is the first case of a subdural electrode-associated major complication in a brain tumor patient, which may serve as a precaution. Despite the increasing popularity, less attention seems to have been placed on potential subdural electrode-associated complications. However, it is important to recognize that subdural electrode implantation in epileptic patients can cause various complications such as infection, edema, increased intracranial pressure, cerebrospinal fluid leak, epidural and subdural hematoma, intracranial hemorrhage, and transient neurological deficits (Hamer et al., 2002; Fountas, 2011). Furthermore, the use of subdural grid electrodes in epileptic patients is reported to have a significantly higher risk of complications than that of strip electrodes (Hamer et al., 2002). While there were no major subdural-electrode associated complications in brain tumor patients both in low- and high-grade glioma patients (Kral et al., 2007; Little et al., 2008; Wellmer et al., 2012), which were also observed with subdural grid electrodes (Kral et al., 2007; Little et al., 2008), these previous results require careful consideration given the substantial heterogeneity of brain tumors and limited number of samples. The neurological deficits in the present case appear to be associated with nonconvulsive status epilepticus, which could be induced by cerebral ischemic changes due to compressive factors such as grid electrodes, hematoma, and brain edema, in addition to an intrinsically increased metabolic demand through neuronal hyperexcitability. Currently, it is unknown whether the neurological deficits in the present case are caused by the same mechanisms as those observed during epilepsy surgery. Further investigation is required to clarify the mechanisms and conditions for the safe and reliable application of subdural grid electrodes.
http://dx.doi.org/10.1016/j.clinph.2015.05.010 1388-2457/Ó 2015 International Federation of Clinical Neurophysiology. Published by Elsevier Ireland Ltd. All rights reserved.
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Letter to the Editor / Clinical Neurophysiology xxx (2015) xxx–xxx
Fig. 1. Contrast-enhanced MRI showing a ring enhancement of the tumor (A). Flair MRI showed tumor-associated extensive edema (B). An X-ray image of the implanted grid electrodes (C). Post-operative CT image showing no particular intracranial lesion other than the tumor (D). Postoperatively recorded ECoG (bipolar montage) over Broca’s area, showing continuous slow waves (
Contents lists available at ScienceDirect
Clinical Neurophysiology journal homepage: www.elsevier.com/locate/clinph
Letter to the Editor Nonconvulsive status epilepticus following implantation of subdural grid electrodes in a brain tumor patient
Implantation of subdural electrodes is considered to be safe and conventionally performed during epilepsy surgery. The application has been recently expanded into brain tumor surgery for the presurgical evaluation of the cerebral function, wherein no major complications have been reported (Kral et al., 2007; Little et al., 2008; Wellmer et al., 2012). We herein present a precautionary case in a patient with a high-grade glioma who showed transient neurological deficits after the implantation of subdural grid electrodes. A 69-year-old woman was admitted to our hospital with a complaint of mild speech and gait disturbance. Baseline laboratory investigations were normal. Contrast-enhanced magnetic resonance imaging (MRI) revealed a ring-enhanced tumor mass in the white matter under the speech and primary motor areas, which was associated with extensive vasogenic edema (Fig. 1A and B). Since malignancy was suspected, we elected to resect not only the tumor mass but the peripheral tissue. Due to the location of the tumor, functional cortical mapping was planned. Scalp electroencephalography showed infrequent spikes over the left parietal area, and Fostoin (750 mg/day for the first day followed by 375 mg/day) was preoperatively administered for seizure prevention. Craniotomy was performed with the aid of an intraoperative navigation system. Following the incision of the dura, mild brain swelling was observed. The primary motor area was identified using somatosensory and motor evoked potentials. A sheet of 5 6 channel subdural grid electrodes (measuring 39 47 mm in size) with a thickness of 0.8 mm (Unique Medical Co., Japan) was slipped into the subdural space to cover the cortical region of interest (Fig. 1C). No particular intraoperative complications were recognized. The follow-up head CT scan on the next morning was unremarkable. Spinal fluid leakage was not evident and the baseline laboratory investigations were normal. On that evening, however, the patient became slightly lethargic with worsened motor aphasia and right hemiparesis. An emergent head CT scan did not show any additional intracranial lesions (Fig. 1D). While no convulsive seizures were apparent, electrocorticography (ECoG) recorded from the subdural electrodes on the same day showed continuous slow waves, which were composed of triphasic and spike and slow waves across all regions covered by the electrodes (sampling rate of 4 kHz per channel, Fig. 1E and F), indicating nonconvulsive status epilepticus. Neurological deficits on the following day progressed to a stage where she was hardly able to
vocalize or move her right limbs, although the head CT scan was also unremarkable. Fostoin was administered daily throughout this period, and the neurological deficits were slightly improved by the administration of glycerol. Without performing functional mapping, tumor resection was performed on the following day with the aim of a prompt histological diagnosis. There were no particular intraoperative findings except moderate brain swelling to an extent comparable with that of the first surgery and a thin layer of subdural hematoma under the electrode. Avoiding Broca’s area with the conventional anatomical landmark, a small corticotomy was made on the frontal cortex and the ring-enhanced mass was selectively resected. The neurological deficits gradually ameliorated thereafter, which recovered almost to a preoperative level within 3 weeks. Fostoin was administered 2 days after the operation, which was subsequently replaced by oral administration of valproate acid (1200 mg/day). The histological diagnosis of the resected tumor was anaplastic astrocytoma (WHO grade 3), and chemoradiation was subsequently performed. To the best of our knowledge, this is the first case of a subdural electrode-associated major complication in a brain tumor patient, which may serve as a precaution. Despite the increasing popularity, less attention seems to have been placed on potential subdural electrode-associated complications. However, it is important to recognize that subdural electrode implantation in epileptic patients can cause various complications such as infection, edema, increased intracranial pressure, cerebrospinal fluid leak, epidural and subdural hematoma, intracranial hemorrhage, and transient neurological deficits (Hamer et al., 2002; Fountas, 2011). Furthermore, the use of subdural grid electrodes in epileptic patients is reported to have a significantly higher risk of complications than that of strip electrodes (Hamer et al., 2002). While there were no major subdural-electrode associated complications in brain tumor patients both in low- and high-grade glioma patients (Kral et al., 2007; Little et al., 2008; Wellmer et al., 2012), which were also observed with subdural grid electrodes (Kral et al., 2007; Little et al., 2008), these previous results require careful consideration given the substantial heterogeneity of brain tumors and limited number of samples. The neurological deficits in the present case appear to be associated with nonconvulsive status epilepticus, which could be induced by cerebral ischemic changes due to compressive factors such as grid electrodes, hematoma, and brain edema, in addition to an intrinsically increased metabolic demand through neuronal hyperexcitability. Currently, it is unknown whether the neurological deficits in the present case are caused by the same mechanisms as those observed during epilepsy surgery. Further investigation is required to clarify the mechanisms and conditions for the safe and reliable application of subdural grid electrodes.
http://dx.doi.org/10.1016/j.clinph.2015.05.010 1388-2457/Ó 2015 International Federation of Clinical Neurophysiology. Published by Elsevier Ireland Ltd. All rights reserved.
2
Letter to the Editor / Clinical Neurophysiology xxx (2015) xxx–xxx
Fig. 1. Contrast-enhanced MRI showing a ring enhancement of the tumor (A). Flair MRI showed tumor-associated extensive edema (B). An X-ray image of the implanted grid electrodes (C). Post-operative CT image showing no particular intracranial lesion other than the tumor (D). Postoperatively recorded ECoG (bipolar montage) over Broca’s area, showing continuous slow waves (
