Resolution of bilateral temporal lobe epilepsy via minimally invasive stereoelectroencephalogram-guided asymmetric radiofrequency thermocoagulation: a case report

Abstract

Bilateral temporal lobe epilepsy (TLE) is a complex form of epilepsy, characterized by seizures originating from both temporal lobes. Its intricate nature presents significant challenges for both medical and surgical treatment, often necessitating a multidisciplinary approach. While resective surgery is generally unsuitable for bilateral TLE, neuromodulation offers more of a remission-focused approach, which better preserves neuropsychological function. In this study, we presented the case of a 45-year-old female with a 16-years history of recurrent seizures, diagnosed as drug-resistant bilateral TLE. After a comprehensive multidisciplinary epilepsy evaluation—encompassing detailed patient history, neurological examination, scalp audiovisual electroencephalogram monitoring, high-resolution brain magnetic resonance imaging, neuropsychological testing, and cerebrospinal fluid analysis—stereoelectroencephalogram (SEEG) confirmed the diagnosis. The patient subsequently underwent asymmetric radiofrequency thermocoagulation guided by SEEG results, targeting bilateral temporal lobes. Despite experiencing transient psychiatric symptoms postprocedure, she achieved seizure freedom and showed improved neuropsychological function over a 3-year follow-up period. This case demonstrates that, with thorough evaluation, seizure freedom is attainable in bilateral TLE patients, even when bilateral injury is present, without significant impairment to neuropsychological function.

Plain language summary

Treatment of bilateral temporal lobe epilepsy using a less-invasive method: a case report on stereoelectroencephalography-guided radiofrequency ablation

Bilateral temporal lobe epilepsy (BTLE) is a complicated type of epilepsy that causes seizures to start in both temporal lobes of the brain. Treating this condition can be challenging, so a team of specialists is often needed. Standard surgery to remove parts of the brain is usually not an option for BTLE, but neuromodulation offers a way to focus on reducing seizures while protecting brain function. In this study, we discuss the case of a 45-year-old woman who had been experiencing repeated seizures for 16 years, which were resistant to treatment. After a thorough evaluation by a team of specialists, including a detailed medical history, neurological exams, scalp audiovisual EEG monitoring, high-resolution brain MRI, neuropsychological tests, and cerebrospinal fluid analysis, the diagnosis was confirmed through stereoelectroencephalogram (SEEG). The patient then had asymmetric radiofrequency thermocoagulation, guided by SEEG findings, to treat both temporal lobes. Although she had temporary psychiatric symptoms after the procedure, she became seizure-free and showed improvements in her brain function during a follow-up period of three years. This case shows that with a careful evaluation, it is possible for patients with BTLE, even with damage in both lobes, to achieve freedom from seizures without significantly harming their brain function.

Keywords

bilateral temporal lobe epilepsy neural compensation neuropsychological function radiofrequency thermocoagulation stereoelectroencephalogram

Introduction

Stereoelectroencephalogram (SEEG)-guided radiofrequency thermocoagulation (RFTC) is a minimally invasive technique used to treat drug-resistant epilepsy. By generating heat through an oscillating current between two leads in an implanted electrode, RFTC induces a small, controlled lesion, typically around 50 mm³ per target.¹ It is applied following SEEG recordings to identify epileptogenic zones. However, due to its limited lesion size, the average seizure-free rate after 2 years is approximately 10%, though it allows for better preservation of neurological function.^1,2

Bilateral temporal lobe epilepsy (TLE), characterized by bilateral (simultaneous or independent) seizure onset in both temporal lobes, represents a subset that is particularly refractory to treatment.³ While unilateral TLE is often managed effectively with surgery, bilateral involvement complicates resective procedures due to the need to preserve critical neurological functions. Neuromodulation therapies such as vagus nerve stimulation (VNS), deep brain stimulation (DBS), and responsive neurostimulation (RNS) have been developed as alternatives, but achieving both seizure freedom and full neurological function preservation remains challenging.^4–6 We now present our experience in using SEEG-guided asymmetric bilateral RFTC to treat drug-resistant bilateral TLE without neurological function deficits for a patient. The case might bring new direction for research of this complex epilepsy and neural compensation.

We present a case of drug-resistant bilateral TLE successfully treated with SEEG-guided asymmetric bilateral RFTC, without any significant neurological deficits. This case provides a promising new avenue for research into the management of complex bilateral epilepsy and neural compensation mechanisms.

Case report

Ethical approval to report this case was obtained from by the Sanbo Brain Hospital Etiology Board, Beijing, China (SBNK-YJYS-2024-017-01). The patient provided written informed consent prior to participating. We used the CARE checklist when writing our report (Supplemental Material).⁷

Patient information

A 45-year-old woman was admitted to our epilepsy center with a 16-year history of progressively worsening seizures. Her symptoms first appeared when she was 29 years old, starting with ocular deviation, followed by tonic–clonic movements of the limbs and loss of consciousness. Initially, she was treated with phenytoin at a dose exceeding 300 mg daily, reducing her seizure frequency to once every 6 months. However, after 5 years of partial seizure control, the patient discontinued the medication on her own. By the eighth year of her condition, seizure frequency had worsened to nearly once a month, prompting her to undergo her first electroencephalogram (EEG) and magnetic resonance imaging (MRI) tests. Both investigations yielded negative results, based on the reports provided by the patient. She was then prescribed levetiracetam 500 mg twice daily (1000 mg daily), but after 6 years with no significant improvement, the patient stopped the medication again.

When she was 45 years old, the patient was admitted to our center for the first time. A 48-h EEG monitoring revealed interictal discharges in the bilateral temporal regions, while MRI results remained negative. At the time, she was not on any medication, so we initiated treatment with oxcarbazepine (OXC) 450 mg twice daily (900 mg daily). However, after 6 months, a new type of seizure emerged, characterized by sudden motion cessation and left-hand dystonia. Occasionally, these episodes were preceded by a sense of fear and agitation. Five months later, this second type of seizure had increased in frequency to one or two episodes per day, while the original seizures had remained stable. At this point, we decided to proceed with further evaluation of the patient.

Clinical findings

Initial long-term video EEG monitoring was conducted to capture the patient’s seizures, during which antiseizure medication was gradually tapered off. Over 72 h, seven seizures were recorded, classified into two distinct types (Figure 1). The patient reported no auras. She exhibited no responsiveness during seizures and had no recollection of events afterward.

Figure 1.

Presurgical long-term scalp EEG. (a) Seizure Type 1. After 22 s of the clinical symptoms appeared, rhythmic spikes were shown in the left temporal region, predominant in the anterior area (Sp1, F7). Annotations at the top indicate the time of clinical symptom onset (Clinical Seizure), the appearance of rhythmic spikes in the left temporal lobe (L Temporal Rhythmic Spikes), and the 22-s interval. (b) Seizure Type 2. After 16 s of the clinical symptoms appeared, rhythmic spikes were shown in right temporal region, predominant in the mid- and posterior area (T10, TP10, P8, in red dotted frame). Annotations at the top indicate the time of clinical symptom onset (Clinical Seizure), the appearance of rhythmic spikes in the right temporal lobe (R Temporal Rhythmic Spikes), and the 16-s interval. (c) Intermittent epileptiform discharges were shown in bilateral temporal region (red arrows).

Type 1 (five times): Characterized by autonomic symptoms, such as tachycardia, followed by involuntary movements and a subsequent reduction in movement. EEG recordings indicated seizure onset in the left temporal region, predominantly in the anterior area.

Type 2 (two times): Featured by involuntary movements followed by myoclonus of the left hand. EEG suggested seizure onset in the right temporal region, predominantly in the mid- and posterior areas.

Subsequent magnetoencephalography (MEG) demonstrated epileptiform discharges localized to the left anterior temporal lobe (Figure 2). A re-examined MRI showed a suspicious enlargement of the left amygdala (Figure 3). Positron emission tomography (PET) scans demonstrated mild hypometabolism in the bilateral temporal lobes, with more pronounced abnormalities on the left side (Figure 4). Given the patient’s clinical aggravation in a short period of 1 year, a cerebrospinal fluid (CSF) analysis was performed to rule out encephalitis, including tests for infectious (antibodies including EB-VCA-IgA, EB-VCA-IgG, EB-VCA-IgM, EB-VEA-IgA, EB-VEA-IgG, EB-VEA-IgM, HSV-I-IgG, HSV-I-IgM, HSV-II-IgG, HSV-II-IgM, RV-IgG, RV-IgM, TOX-IgG, TOX-IgM, CMV-IgG, CMV-IgM), autoimmune (antibodies including anti-NMDAR, anti-AMPAR1, anti-AMPAR2, anti-CASPR2, anti-GABABR1/2, anti-LGI1, anti-IgLON5, anti-D2R, anti-DPPX, anti-GlyR, anti-GABAARα1, anti-GABAARα3, anti-mGluR5, anti-Neurexin3, anti-GAD65, anti-GABAARβ3, anti-GABAARγ2, anti-α3AchR), and paraneoplastic etiologies (antibodies including anti-HuD (ANNA1), anti-Yo (PCA-1), anti-Ri (ANNA2), anti-CV2, anti-Amphiphysin, anti-Ma1, anti-Ma2, anti-SOX1, anti-Tr (DNER), anti-Zic4, anti-GAD65, anti-PKCγ, anti-Recoverin, anti-Titin), all of which returned negative results.

Figure 2.

MEG demonstrated intermittent epileptiform discharges in the left anterior temporal lobe.

Figure 3.

Presurgical MRI, axial view, Flair. Suspicious enlargement of the left amygdaloid was demonstrated in the red rings.

Figure 4.

PET demonstrated mild low signal in bilateral temporal lobe and the abnormal in left temporal lobe was more severe. The max SUV was 12, and the minim was 0. (a) The SUV in the left temporal pole was 6.0, comparing to 6.4 in the right side. (b) Slices including bilateral amygdala. (c) Results of the whole brain.

A multidisciplinary case discussion concluded that the patient had drug-resistant epilepsy with focal seizures and impaired awareness. This diagnosis was based on her failure to achieve seizure control despite treatment with phenytoin at a dose exceeding 300 mg daily for approximately 5 years, levetiracetam at 1000 mg daily for over 6 years, and OXC at 900 mg daily for more than 11 months. The hypothesized seizure onset zone was likely the left temporal lobe, given the MEG and PET findings, although bilateral involvement could not be ruled out. Therefore, the team recommended and proceeded with the implantation of intracranial electrodes for SEEG monitoring in bilateral temporal lobes.

Intracranial electrodes implantation

Based on the hypothesis that seizure onset was predominantly left-sided, a total of nine electrodes were implanted on the left side and five on the right (Figure 5(a)). The target regions included the amygdala, hippocampus, parahippocampal gyrus, temporal pole, and superior, middle, and inferior temporal gyri bilaterally.

Figure 5.

(a) The SEEG electrodes. Nine electrodes were implanted in the left side, which were P (Temporal pole), A (Amygdala), B (Head of Hippocampus), C (Tail of Hippocampus), D (Isthmus of the cingulate), E (Para-hippocampus), G (Heschl’s gyrus), M (gyri breves insulae), N (gyri longus insulae). Five electrodes were implanted in the right side, which were A′ (Amygdala), B′ (Head of Hippocampus), C′ (Tail of Hippocampus), D′ (Isthmus of the cingulate), E′ (Para-hippocampus). (b) SEEG record of the Type 1 seizure. Seizure onset within electrodes B, C, P, and then spread to electrode A. (c) SEEG record of the Type 2 seizure. Seizure onset within electrodes A′, B′, C′, and then spread to electrode E′.

The left insular lobe was also covered due to the patient’s tachycardia during left-sided seizures. On the right, the primary target regions included the amygdala, hippocampus, parahippocampal gyrus, and the isthmus of the cingulate. The pars opercularis of the temporal lobe was initially considered as a target due to the patient’s left-hand myoclonus. However, high vascular density in the peri-Sylvian region led to the exclusion of electrodes in this area. Instead, the entry point for electrode D′, targeting the isthmus of the cingulate, was adjusted to be as close as possible to the Sylvian fissure.

Additionally, because ictal activity on both sides was delayed relative to the onset of clinical symptoms, suggesting possible extratemporal seizure origins, preparations were made for a secondary electrode implantation in case the initial implantation failed to detect seizure onset.

Electrodes were implanted using a robot-assisted stereotactic system (Sino-precision). The SEEG depth electrodes, each with 8–16 contacts (2 mm in length, 0.8 mm in diameter, spaced 3.5 mm apart), were manufactured by ALCIS Co. Ltd. (Besançon, France).

Diagnostic assessment-results of SEEG

During the interictal period, epileptiform discharges were primarily recorded in temporal lobes bilaterally. A total of five seizures were monitored: four Type 1 seizures and one Type 2. In Type 1 seizures, the onset was recorded in the left temporal pole and hippocampus, with propagation to the left amygdala (Figure 5(b)). In Type 2 seizures, the onset was recorded in the right hippocampus and amygdala, with propagation to the right para-hippocampal gyrus (Figure 5(c)).

Cortical electrical stimulation was performed to further evaluate seizure onset regions. Both high-frequency stimulation (50 Hz, pulse width 0.3 ms, duration 5 s, current 1 mA) and low-frequency stimulation (1 Hz, pulse width 0.3 ms, duration 1 s, current 1 mA) were applied to all the electrode contacts overlying the cortices. High-frequency stimulation of the right amygdala induced Type 2 seizures, while low-frequency stimulation of the left hippocampus elicited symptoms of dizziness and abdominal discomfort. The patient reported that these symptoms were occasionally experienced preceding her habitual seizures, although they had not been reported prior to electrodes implantation. Consequently, these symptoms were considered possible habitual seizure manifestations of Type 1 seizures. Stimulation of other cortical regions yielded no significant responses even in the left temporal pole.

Based on SEEG findings, the diagnosis of bilateral TLE was confirmed, with distinct, independent seizure onsets in both hemispheres, though asymmetric in nature. The cortical stimulation results indicated that the right amygdala and left hippocampus might be more prone to seizure initiation.

Therapeutic interventions – radio frequency thermal coagulation

Following confirmation of bilateral TLE via SEEG, a plan for bilateral hippocampal DBS was proposed. However, before proceeding with DBS, a two-stage approach using RFTC was recommended. This not only aimed to further validate the diagnosis but also offered the potential for seizure-free, particularly given the absence of secondary generalized tonic–clonic seizures. The patient agreed to this strategy.

In the first stage, RFTC was performed on the leads within the left temporal pole and hippocampus using the following parameters: power 3.0 W, duration 60 s, interval 30 s, repeated three times. Afterward, 16-h SEEG monitoring captured a Type 2 seizure originating from the right hippocampus and amygdala, while no epileptiform discharges were shown in the left side. In the second stage, RFTC was selectively applied to the right amygdala, using the same parameters, to minimize the risk of symmetrical brain damage (Figure 6).

Figure 6.

The 4 months postsurgical MRI. Coronal view, Flair. (a) Arrow pointed the RFTC lesion in the left mesial temporal pole; (b) Arrow pointed the RFTC lesion in the right amygdala, which was close to the head of hippocampus; (c) Arrow pointed the RFTC lesion in the left head of hippocampus; (d) Arrow pointed the RFTC lesion in in the left tail of hippocampus.

Follow-up and outcomes

In the first few weeks following surgery, the patient experienced transient psychiatric symptoms, including agitation, and had no memory of the first postsurgical month. After the RFTC, the patient maintained OXC 450 mg twice daily, which is the same as presurgical. Over the course of 3 years of follow-up, the patient experienced only one seizure, which occurred during a COVID-19 infection in the 12th postsurgical month. Cognitive assessments using the Wechsler Adult Intelligence Scale and Wechsler Memory Scale were performed in the 4th and 24th postsurgical months, both showing improvement compared to presurgical scores (Table 1). Additionally, 16-h EEG monitoring was conducted at the 4th, 12th, and 24th months postsurgery, with all results remaining within the normal range.

Table 1.

Presurgical and postsurgical neurological test, WAIS-IV and WMS-IV.

Test time	IQ	GAI	CPI	VCI	PRI	WMI	PSI	WCST	RPM	MQ	AMI	VMI	IMI	DMI
Pre-surgical	75	77	78	65	80	64	91	65	66	72	71	70	65	75
4 Months post-surgical	84	84	86	76	85	74	96	76	65	77	79	74	70	77
24 Months post-surgical	86	84	86	77	85	75	97	75	64	81	84	80	77	78

AMI, auditory memory; CPI, Cognitive Proficiency Index; DMI, delayed memory; GAI, General Ability Index; IMI, immediate memory; IQ, intelligence quotient; MQ, memory quotient, PRI, perceptual reasoning; PSI, processing speed; RPM, Raven’s Progressive Matric; VCI, verbal comprehension; VMI, visual memory; WAIS-IV, Wechsler Adult Intelligence Scale fourth edition; WCST, Wisconsin Card Sorting Test; WMS-IV, Wechsler Memory Scale fourth edition.

Discussion

We presented a two-stage SEEG-guided RFTC therapy for a patient with bilateral TLE. This approach utilized the focused lesioning effect created by the current oscillation between two electrode leads.

Compared to unilateral TLE, which boasts a high seizure-free rate following resective surgery,⁸ bilateral TLE remains more difficult to treat.³ Due to the potential for significant neurological deficits, resective surgery is not a viable option. Neuromodulation therapies, while preserving neurological function, generally result in seizure reduction rather than seizure-free. For bilateral TLE, seizure-free rates are low with VNS,⁹ at 14.3% for DBS,¹⁰ and between 15% and 20% for RNS.^4,11 This underscores the importance of exploring targeted lesioning approaches, such as RFTC.

Although the seizure-free rate of RFTC is lower compared to resective surgery due to its limited lesioning area,^1,2 it can still be effective when the epileptic focus is well-defined. In studies of RFTC for periventricular nodular heterotopia epilepsies, seizure-free rates reached 76%.¹² In our case, SEEG revealed focal seizure onsets in the left temporal pole and hippocampus, as well as the right amygdala and hippocampus, creating the potential for seizure-free.

However, the primary goal remained to avoid neurological deficits. Under SEEG guidance, we were able to prevent symmetrical brain injuries. Although the patient experienced temporary psychiatric symptoms and memory loss of the first postsurgical month, these were likely caused by postsurgical edema and were expected to resolve. Follow-up evaluations confirmed the resolution of these symptoms.

In the development of bilateral TLE treatment, there are few studies exploring bilateral amygdala RFTC,¹³ and although no permanent neurological deficits have been reported, avoiding symmetric injuries remains a general principle. Some physicians have recently attempted ablating the dominant mesial temporal structures of bilateral TLE following a period of responsive neuromodulation and signal recording,^14,15 with encouraging results, though long-term studies are still needed.

A limitation of our case is the small sample size and the unexplained outcome: why did RFTC of the right amygdala alone lead to the cessation of right-sided seizures, given that SEEG recorded seizure onsets from both the amygdala and the hippocampus? This unexpected seizure-free warrants further clinical and mechanistic investigation.

Conclusion

SEEG-guided RFTC led to seizure freedom in this bilateral TLE case without causing neurological deficits. Further research is required to understand and refine this therapeutic approach. In this case, our patient is satisfied with the result.

Supplemental Material

sj-docx-1-tan-10.1177_17562864251321255 – Supplemental material for Resolution of bilateral temporal lobe epilepsy via minimally invasive stereoelectroencephalogram-guided asymmetric radiofrequency thermocoagulation: a case report

Supplemental material, sj-docx-1-tan-10.1177_17562864251321255 for Resolution of bilateral temporal lobe epilepsy via minimally invasive stereoelectroencephalogram-guided asymmetric radiofrequency thermocoagulation: a case report by Zhao Liu, Guoming Luan, Mengyang Wang, Jing Wang, Pengfei Teng, Yuguang Guan, Xiongfei Wang, Tianfu Li, Tianyi Cui and Jian Zhou in Therapeutic Advances in Neurological Disorders

Footnotes

Acknowledgements

This work was supported by Laboratory for Clinical Medicine, Capital Medical University.

Declarations

ORCID iDs

Zhao Liu

Tianfu Li

Supplemental material

Supplemental material for this article is available online.

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