Highlights
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Vagus nerve stimulation may contribute to seizure termination in super-refractory status epilepticus.
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Clinical response to VNS in SRSE can be delayed.
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Prolonged SRSE may lead to focal cortical atrophy beyond the mesial temporal lobe.
Keywords: Vagus nerve stimulation, Brain atrophy, Neuromodulation, Case report
Abstract
Super-refractory status epilepticus (SRSE), defined as seizure activity persisting > 24 h despite anesthetic treatment, remains a therapeutic challenge with high morbidity and mortality. We report a 42-year-old man with Crohn’s disease who developed SRSE following a right posterior cerebral artery infarction. Despite treatment with multiple antiseizure medications, immunotherapy, intravenous anesthetics, and barbiturate coma, seizures persisted for 80 days. A vagus nerve stimulator (VNS) was implanted on day 57 after status epilepticus onset. Clinical improvement began within days, and complete cessation of clonic seizures occurred 23 days after implantation, allowing withdrawal of anesthetic agents. The patient was discharged with mild residual deficits and achieved good long-term functional recovery. Follow-up MRI revealed progressive focal atrophy of the right postcentral gyrus, correlating with cortical sensory deficits.
This case highlights that VNS may contribute to seizure termination in SRSE even when implanted late, although clinical effects may be delayed. It also illustrates that prolonged SRSE can lead to focal cortical atrophy beyond the mesial temporal lobe.
1. Introduction
Status epilepticus (SE) is a neurological emergency and is currently defined by the International League Against Epilepsy (ILAE) as: “a condition resulting either from the failure of the mechanisms responsible for seizure termination or from the initiation of mechanisms, which lead to abnormally, prolonged seizures (after time point t1). It is a condition which can have long-term consequences (after time point t2), including neuronal death, neuronal injury, and alteration of neuronal networks, depending on the type and duration of seizures” [1]. Prompt therapeutic intervention is required to prevent irreversible neuronal injury [2]. The mainstay of treatment consists of antiseizure medications (ASM) combined with anesthetic agents when needed. Super-refractory status epilepticus (SRSE), defined as seizure activity persisting for more than 24 h despite anesthetic treatment, is a rare and highly challenging condition for which evidence-based therapeutic strategies remain limited [3].
In addition to escalating ASM and continued anesthesia, further treatments are often tried sequentially or in combination. These include barbiturate-induced coma, administration of ketamine, therapeutic hypothermia, or metabolic therapies such as a ketogenic diet [3], [4]. Another potential option is implantation of a vagus nerve stimulator (VNS), which provides retrograde stimulation of the left vagus nerve to help disrupt seizure activity. Proposed mechanisms of action include modulation of neurotransmitter release and desynchronization of epileptic networks [5], [6]. While there are some uncontrolled case series suggesting that VNS may be effective in SRSE [7], its success in this emergency situation is far from guaranteed.
2. Case presentation
We report on a 42-year-old patient with a 24-years history of Crohn’s disease. After unsuccessful treatment with upadacitinib, he received immunotherapy with the anti-interleukin 23 antibody risankizumab. The evening following the first dose, he suddenly appeared disoriented and presented to our department. On clinical examination, he was awake and fully oriented but could not recall the episode. During the examination, he suddenly became confused again.
Emergency brain MRI revealed a right hemispheric infarction in the territory of the posterior cerebral artery, already demarcated on FLAIR sequences, also seen on CT the following day (Fig. 1A). Full work-up for juvenile stroke, including sonography of cervical and intracranial arteries, transthoracic and transesophageal echocardiography, extensive vasculitis and thrombophilia screening, as well as lumbar puncture, did not reveal a cause of stroke. Clinically, left-sided hemianopia persisted.
Fig. 1.
(A): Axial head CT demonstrating right posterior cerebral artery infarction one day after admission. (B) and (C): Axial Diffusion-weighted imaging showing marked cortical diffusion restriction in the right centrotemporo-parietal region. (D): Axial FLAIR at admission showing preserved cortical volume in the right postcentral gyrus. (E): Axial FLAIR three months later demonstrating focal atrophy of the right postcentral gyrus, correlating with deficits of the contralateral upper limb. (F): Axial FLAIR seventeen months later demonstrating progressed and now severe focal atrophy of the right postcentral gyrus.
Four and seven days after admission, the patient experienced two focal to bilateral tonic-clonic seizures, which responded promptly to 4 mg of intravenous lorazepam. ASM with levetiracetam 2000 mg/d was initiated. EEG showed lateralized periodic discharges (LPDs) over the right hemisphere with maximum negativity over the right parieto-occipital region (Fig. 2).
Fig. 2.
EEG showing LPDs over the right hemisphere with maximum negativity over the right parieto-occipital region.
On day 17 after admission, the patient developed continuous clonic jerks of the left face and arm, consistent with focal motor status epilepticus with impaired consciousness. Despite sequential administration of lacosamide (400 mg/d), valproic acid (4000 mg/d), and perampanel (8 mg/d) in addition to levetiracetam over two days, seizure activity could not be adequately controlled.
MRI revealed marked laminar cortical diffusion restriction with sparing of the deep white matter, clearly extending beyond posterior cerebral artery vascular territory − involving the posterior temporal lobe, the lateral occipital lobe and the postcentral/parietal cortical regions of the right hemisphere. At this stage, pseudonormalization of the right hemispheric posterior cerebral artery infarction (occipitomesial and temporomesial regions) was noted, indicating the different timing of the described acute cortical changes (Fig. 1B and C). The patient was transferred to the intensive care unit (ICU) and intubated two days after the onset of status epilepticus. He received continuous midazolam sedation and a five-day course of high-dose prednisolone for possible autoimmune encephalitis. Corticosteroid treatment resolved the brain edema; however, the focal clonic jerks of the left face and arm and impaired consciousness persisted. A switch from valproic acid to phenytoin brought no improvement. Further diagnostic work-up, including a second lumbar puncture to exclude alternative etiologies, remained unremarkable. The patient was in a state of SRSE.
Repeated EEGs showed that boluses of midazolam led to a temporary cessation of epileptic activity. The continuous dose was therefore increased, but whenever the midazolam dose was tapered, clonic jerks of the left face and arm reemerged (Video segment 1). Subsequently, two cycles of barbiturate-induced coma with EEG burst suppression were administered in addition to midazolam, propofol, and corticosteroids, but this also failed to terminate the seizure activity. Other treatment attempts included administration of ketamine and intravenous immunoglobulins.
None of these measures succeeded in controlling the SE. At this point, the patient was receiving levetiracetam, lacosamide, perampanel, and phenytoin at high doses, adjusted according to regular plasma level monitoring. As a fifth antiseizure drug, cenobamate was initiated with an accelerated titration schedule (to 300 mg over a period of 51 days). For sedation, the patient received continuous midazolam, remifentanil, dexmedetomidine, and propofol.
Throughout the entire course, diagnostic steps and therapeutic strategies were regularly reviewed and discussed by a multidisciplinary expert panel (EpiCARE, https://epi-care.eu/). This ensured continuous external input and guidance for this highly challenging case. Among the various treatment options, emergency implantation of a vagus nerve stimulator (VNS), with an accelerated increase of stimulation parameters once implanted, was considered. The patient received a VNS (SenTivaTM Model 1000, LivaNova, Houston, TX, USA) on day 74 following hospital admission (57 days after SE onset). Two to four days after implantation, the patient showed improved consciousness and began to respond to visual and verbal stimuli at a basic level. Though vagus nerve stimulation appeared to help control epileptic activity, the patient also developed facial pain resulting in grimacing of the left side of the face during stimulation. Consequently, the stimulation voltage was reduced, stimulation intervals were shortened, and the settings adjusted to improve tolerability. Around the same time, phenytoin was replaced by high-dose oral topiramate, and pregabalin was added to support sleep.
Over the course of several days, the patient’s condition gradually improved, allowing for a slow tapering of anesthetic agents and subsequent weaning from mechanical ventilation and decannulation following tracheostomy. By day 89 following admission, the patient was awake, although some clonic jerks of the left face and arm persisted, predominantly during the day. On day 90, he was transferred to the neurological ward. At this point, the patient was awake and responsive, with slightly reduced vigilance and episodes of delusions and misidentifications. Mild left brachiofacial clonic jerking was still present.
One week later, 23 days after VNS implantation, the brachiofacial clonic jerks ceased completely. The antiseizure regimen at that time consisted of 3 g levetiracetam, 600 mg lacosamide, 800 mg topiramate, 300 mg cenobamate, and 150 mg pregabalin daily. VNS parameters were set to 1.5 mA with 21 s of stimulation alternating with 48 s of rest; all other settings followed the standard protocol. Tapering of levetiracetam resulted in reemergence of seizures, which responded promptly to lorazepam. Levetiracetam was therefore increased to its original dose. Since this episode, the patient remained seizure-free up to the time of writing (1.5 years after stroke and SE). Regular EEG examinations showed rare epileptic activity over the right hemisphere. Follow-up MRI, performed 3 months after onset of SRSE revealed distinct atrophy of the right postcentral gyrus (Fig. 1E). Seventeen months after initial presentation, MRI showed marked progression of atrophy, corresponding to a knife-blade atrophy of the post-central areas (Fig. 1F). In accordance with this MRI finding, the patient shows signs of a cortical sensory deficit with object agnosia and agraphesthesia as well as mild pseudoathetosis of the left upper limb (Video segment 2). A detailed overview of the clinical course and interventions is shown in Fig. 3.
Fig. 3.
Timeline summarizing the clinical course and therapeutic interventions in the presented case.
3. Discussion
This case highlights two clinically relevant aspects of SRSE. First, VNS may contribute to seizure termination even when initiated late in the disease course, although its clinical effects can be delayed. Second, prolonged SRSE may result in focal structural brain changes beyond the mesial temporal lobe, as illustrated by the selective cortical atrophy observed in our patient.
Management of SRSE typically involves escalation of anti-seizure medications, prolonged anesthetic therapy, and adjunctive measures such as immunotherapy or metabolic interventions [3], [8]. Neuromodulation techniques, including VNS, have emerged as potential rescue options when conventional treatments fail [7], [9].
VNS is an established therapy for drug-resistant epilepsy (DRE), while its use in SRSE remains off-label. Nevertheless, its potential to terminate SRSE is increasingly recognized. A recent systematic review [10] reported on 33 SRSE cases treated with VNS and found seizure cessation in 29 patients (88%). The median time from implantation to seizure cessation was 7 days. Implantation itself occurred between 5 and 420 days after seizure onset, suggesting that clinical benefit may be achievable even with delayed intervention. In our patient, VNS was implanted on day 57 after seizure onset, aligning with these reports.
While some reports describe seizure cessation within days of VNS implantation, others found a markedly delayed clinical response. Our patient showed no immediate resolution of epileptic activity after VNS implantation. Gradual improvement in consciousness and seizure control occurred over the following weeks, ultimately resulting in complete cessation of SE 23 days after implantation.
Another systematic review [9] reported on 20 case reports on patients with new-onset refractory status epilepticus (NORSE), including cases of febrile infection-related epilepsy syndrome (FIRES), who received neuromodulation therapies such as VNS, deep brain stimulation (DBS), or electroconvulsive therapy (ECT). In most cases, multiple other treatments, including immunosuppressive regimens, had been tried before. SRSE resolved in 17 of the 20 patients following initiation of neuromodulation. The time from SRSE onset to initiation of neuromodulation ranged from 5 to 435 days, with a tendency for a more rapid response following earlier intervention. The authors noted no clear superiority of one neuromodulation method over another. Our patient underwent VNS implantation relatively late in the disease course (day 74), yet still achieved seizure cessation, aligning with the reported range of initiation times and supporting the inclusion of neuromodulation in prolonged SRSE management strategies.
It is important to note that in many reported cases of SRSE, the final therapeutic intervention is often attributed a decisive role in seizure termination, despite the presence of multiple simultaneously evolving treatments. In our case, VNS was introduced after prolonged multimodal therapy, including several antiseizure medications, anesthetics, and immunomodulatory treatments. Therefore, a causal relationship between VNS implantation and seizure cessation cannot be definitively established. However, the temporal association with subsequent clinical improvement suggests that VNS may have contributed to seizure control in this setting. Current evidence for VNS in SRSE is limited, with inherent risk of publication bias, limited validity of outcomes in individual cases due to multiple concurrent treatment interventions in an emergency situation and lack of randomized controlled trials. Optimal timing, stimulation parameters, and patient selection remain to be established. In addition, patient groups are extremely heterogeneous. A better understanding of the underlying mechanisms of VNS in SRSE may allow for more targeted application and optimized patient selection.
Interestingly, 2 follow-up MRIs revealed progressive focal cortical atrophy ipsilateral to the seizure generating hemisphere with corresponding clinical findings. A retrospective study investigated 19 patients with SRSE who developed diffuse brain atrophy due to prolonged SRSE [11]. The degree of atrophy corresponded with SRSE duration. In a retrospective observational study of 39 patients with NORSE, 82% had structural abnormalities on follow-up imaging. The most common finding was hippocampal atrophy (58%), which was significantly associated with unfavorable outcomes [12]. These data underline the relevance of structural sequelae for long-term prognosis, although most reports emphasize mesial temporal lobe involvement rather than focal structural changes in cortical regions such as in our patient. These structural changes may persist but also be reversible in individual cases [13], [14], [15]. To our knowledge, no previous case has described a selective atrophy of the postcentral gyrus following SRSE of this degree, highlighting the unusual topography of structural damage in our patient. The mechanisms underlying structural changes following SE remain to be fully clarified. Animal models of epilepsy suggest excitotoxicity due to excessive glutamate release during SE as potential trigger. However, inflammatory and immunological mechanisms have to be considered as well [16].
4. Conclusion
This case underscores that VNS may represent a valuable adjunctive treatment option in super-refractory status epilepticus, even when applied late, although delayed clinical responses should be anticipated. Furthermore, it highlights that prolonged SRSE can lead to focal cortical atrophy beyond the mesial temporal lobe. Further studies are needed to better define patient selection, optimal timing, and stimulation parameters, as well as the mechanisms underlying both treatment response and structural brain changes.
Data availability statement.
No datasets were generated or analyzed for this study.
Ethics statement.
The patient provided written informed consent for the publication of this case report, including any potentially identifiable clinical data or images.
Author contributions.
W.P. and A.P. conceptualized and planned the manuscript. A.P., A.H., and S.P. assisted in the acquisition, analysis, and interpretation of data for the work. A.P. screened the literature and prepared the first draft of the manuscript, with important contributions from S.P., G.K., E.T., and W.P. All authors critically reviewed and commented on the manuscript and approved the final version. All authors agree to be accountable for all aspects of the work, ensuring that questions related to the accuracy or integrity of any part of the work are appropriately investigated and resolved.
Ethical statement.
This case report was conducted in accordance with ethical guidelines. Written informed consent was obtained from the patient directly for the publication of this report and associated images. No identifying details have been disclosed to maintain the patient’s confidentiality.
Funding statement
The authors did not receive any specific funding for this work.
CRediT authorship contribution statement
Ario Parak: Writing – original draft, Investigation, Data curation, Conceptualization. Alexander Holzhausen: Writing – review & editing, Investigation. Susanne Pirker: Writing – review & editing, Supervision, Investigation, Formal analysis. Gregor Kasprian: Writing – review & editing, Supervision, Methodology, Data curation. Eugen Trinka: Writing – review & editing, Validation, Supervision, Formal analysis. Walter Pirker: Writing – review & editing, Supervision, Project administration, Methodology, Investigation.
Declaration of competing interest
The authors declare the following financial interests/personal relationships which may be considered as potential competing interests: Walter Pirker reports a relationship with Stada that includes: consulting or advisory, speaking and lecture fees, and travel reimbursement. Walter Pirker reports a relationship with AbbVie Pharma that includes: consulting or advisory, speaking and lecture fees, and travel reimbursement. Walter Pirker reports a relationship with Merz Pharma that includes: consulting or advisory and speaking and lecture fees. Walter Pirker reports a relationship with Bial that includes: consulting or advisory, speaking and lecture fees, and travel reimbursement. Walter Pirker reports a relationship with AOP Health that includes: travel reimbursement. Eugen Trinka reports a relationship with EVER Pharma Holding that includes: speaking and lecture fees. Eugen Trinka reports a relationship with Marinus Pharmaceuticals Inc that includes: speaking and lecture fees. Eugen Trinka reports a relationship with Arvelle Therapeutics GmbH that includes: speaking and lecture fees. Eugen Trinka reports a relationship with Angelini Pharma SpA that includes: speaking and lecture fees. Eugen Trinka reports a relationship with Alexion that includes: speaking and lecture fees. Eugen Trinka reports a relationship with Argenx Us, Inc. that includes: speaking and lecture fees. Eugen Trinka reports a relationship with Medtronic that includes: speaking and lecture fees. Eugen Trinka reports a relationship with Biocodex SAS that includes: speaking and lecture fees. Eugen Trinka reports a relationship with BIAL Portela & CA SA that includes: speaking and lecture fees. Eugen Trinka reports a relationship with NewBridge Pharmaceuticals FZ LLC that includes: speaking and lecture fees. Eugen Trinka reports a relationship with GL Pharma that includes: speaking and lecture fees. Eugen Trinka reports a relationship with GlaxoSmithKline that includes: speaking and lecture fees. Eugen Trinka reports a relationship with Boehringer Ingelheim Pharma GmbH & Co KG that includes: speaking and lecture fees. Eugen Trinka reports a relationship with LivaNova USA, Inc. that includes: speaking and lecture fees. Eugen Trinka reports a relationship with Eisai Inc that includes: funding grants and speaking and lecture fees. Eugen Trinka reports a relationship with Epilog that includes: speaking and lecture fees. Eugen Trinka reports a relationship with UCB Pharma GmbH that includes: funding grants and speaking and lecture fees. Eugen Trinka reports a relationship with Biogen that includes: funding grants and speaking and lecture fees. Eugen Trinka reports a relationship with Sanofi that includes: speaking and lecture fees. Eugen Trinka reports a relationship with Jazz Pharmaceuticals Inc that includes: speaking and lecture fees. Eugen Trinka reports a relationship with Actavis Inc that includes: speaking and lecture fees. Eugen Trinka reports a relationship with Jubiläumsfond der Österreichischen Nationalbank that includes: funding grants. Eugen Trinka reports a relationship with Red Bull GmbH that includes: funding grants. Eugen Trinka reports a relationship with Merck Pharma and Chemicals that includes: funding grants. Eugen Trinka reports a relationship with Bayer AG that includes: funding grants. Eugen Trinka reports a relationship with European Union that includes: funding grants. Eugen Trinka reports a relationship with Oesterreichischer Fond zur Wissenschaftsforderung Bundesministerium für Wissenschaft und Forschung that includes: funding grants. If there are other authors, they declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.
Acknowledgements
The authors used OpenAI’s ChatGPT (GPT-5.1, accessed via chat.openai.com) to assist with language refinement and stylistic editing. All factual content, interpretations, references, and figures were generated by the authors, who assume full responsibility for the accuracy and integrity of the final manuscript.
E.T. has received personal honoraria for lectures and educational activities from EVER Pharma, Marinus, Arvelle, Angelini, Alexion, Argenx, Medtronic, Biocodex, Bial‐Portela & Ca, NewBridge, GL Pharma, GlaxoSmithKline, Boehringer Ingelheim, LivaNova, Eisai, Epilog, UCB, Biogen, Sanofi, Jazz Pharmaceuticals, and Actavis; his institution has received research grants from Biogen, UCB Pharma, Eisai, Red Bull, Merck, Bayer, the European Union, FWF Osterreichischer Fond zur Wissenschaftsforderung Bundesministerium für Wissenschaft und Forschung, and Jubiläumsfond der Österreichischen Nationalbank.
The remaining authors declare that the case report was prepared in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
Footnotes
Supplementary data to this article can be found online at https://doi.org/10.1016/j.ebr.2026.100871.
Contributor Information
Eugen Trinka, Email: eugen@trinka.at.
Walter Pirker, Email: walter.pirker@gesundheitsverbund.at.
Appendix A. Supplementary data
The following are the Supplementary data to this article:
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