Epilepsy & Seizures
Febrile seizures
Jun. 02, 2026
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Focal to bilateral tonic-clonic seizures …
- Updated 04.06.2026
- Released 12.16.2008
- Expires For CME 04.06.2029
Focal to bilateral tonic-clonic seizures
Introduction
Overview
Focal to bilateral tonic-clonic seizures begin as ictal discharges in a restricted focus of the brain and subsequently propagate to involve both hemispheres of the brain. In this article, clinical features suggesting lateralization and diagnostic techniques to localize the focus are discussed, and management options are briefly covered. Throughout this article, terminology based on the latest update of the ILAE seizure classification is used (12).
Key points
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• Seizures that clinically appear to be generalized may represent activation of specific pathways, dependent on the location of the focus, and may not be truly generalized. | |
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• Cardiac arrhythmias and sudden unexpected death in epilepsy can be associated with intractable focal to bilateral seizures. | |
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• Intracranial neurostimulation (responsive neurostimulation and deep brain stimulation) can be used as an adjunct therapy in patients with medically refractory epilepsy. | |
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• Stem cell and gene therapies are evolving new avenues for the treatment of epilepsy. |
Historical note and terminology
The earliest descriptions of tonic-clonic seizures appear in ancient Babylonian tablets around 600 to 700 BC. Focal onset seizures in which convulsions were restricted to one side of the body were systematically described by Louis François Bravais in his 1827 thesis and were referred to as hemiplegic epilepsy. In a paper published in 1870, John Hughlings Jackson, unlike Bravais, accepted that convulsions that are initially unilateral could spread to involve both sides of the body. He also believed that loss of consciousness could occur before the spread of convulsions to the contralateral side of the body.
The terminology and classification of seizures and epilepsy by ILAE have undergone several revisions since 1970. In 2017, the revised ILAE operational classification of seizure types suggested that the term “secondarily generalized” be replaced by “focal to bilateral tonic-clonic” seizures (20). The appropriateness of this change in terminology was emphasized again in the latest update of the ILAE seizure classification (12).
Clinical manifestations
Presentation and course
• The main phases of the clinical manifestation of focal to bilateral tonic-clonic seizures are aura, onset of generalization, tonic, clonic, and postictal. | |
• Seizures can start with auras that are focal preserved consciousness seizures characterized by perceived symptoms and absence of observable signs. | |
• Auras can proceed to impaired consciousness, eventually propagating bilaterally and leading to tonic and then clonic phases. | |
• Certain localizing and lateralizing signs can be seen during bilateral propagation (generalization). |
Focal to bilateral tonic-clonic seizures have been typically divided into specific stages. Marked heterogeneity exists in phase durations and clinical expression, suggesting multiple cortical and subcortical routes of spread. The most commonly described stages are as follows (41).
Aura. About 40% to 70% of patients may experience an antecedent focal preserved consciousness seizure characterized by localized or nonlocalized symptoms in the absence of observable manifestations. When an observable manifestation is present, the convention is to categorize that phenomenon as a focal seizure with an observable manifestation rather than aura. In the 2025 update to the ILAE seizure classification, auras are referred to as non-observable manifestations of seizures and considered as part of the “descriptor” of seizures. Common auras, such as auditory, olfactory, gustatory, and somatosensory auras, are classified under sensory phenomena, and anxiety, anger, and fear are classified under affective (emotional) phenomena. Auras may progress to focal seizures with impaired consciousness or directly to generalized tonic-clonic seizures.
Focal seizures with observable manifestations. Focal impaired consciousness seizures with observable manifestations are focal seizures with clinical signs, “alteration of consciousness,” and amnesia. Clinically, these are often associated with automatisms, such as orofacial grimacing, chewing, lip-smacking, fumbling, picking, or repetitive movements of the hands and arms. They may also include unresponsiveness and staring.
Onset of bilateral propagation (generalization). The transition between the aura or antecedent seizure and the remaining phases of generalized tonic-clonic seizures can sometimes be identified by the presence of localizing or lateralizing signs, such as head version. More information is provided in the Localization section. Clonic jerks that are usually irregular and asymmetric may precede the tonic phase.
Tonic phase. The tonic phase begins with a rigid muscular contraction that usually consists of a brief phase of flexion followed by a longer phase of extension. The flexion phase usually begins in the head and trunk and then extends to the extremities and is usually symmetric. The extension phase usually begins with axial muscle contractions, along with laryngeal spasm that may produce an ictal cry and apnea. Autonomic signs such as tachycardia, hypertension, and diaphoresis may begin during this phase. The tonic phase usually lasts for 10 to 30 seconds.
Clonic phase. The tonic phase gives way to clonic convulsive movements, in which rhythmic jerking lasts for a variable period. During the clonic phase, muscle relaxation interrupts tonic contraction and produces generalized rhythmic jerks, which slow down until the seizure ends. Deep, often stertorous respiration occurs at the end of the clonic phase, as other muscles relax. Urinary incontinence and tongue biting may occur in this phase. The clonic phase usually lasts for 30 to 50 seconds.
Postictal state. The postictal state includes a period during which the patient becomes quiet in deep sleep, begins breathing deeply, and then gradually wakes up, often confused, with some automatic behaviors; the patient may later complain of feeling stiffness, generalized soreness, and headache.
Localization. Generalized seizures have long been thought to involve the entire brain. Research has indicated that focal to bilateral generalized or even idiopathic seizures may not result in diffuse cortical activation and may activate only specific circuits. A complex model of epileptogenic circuitry involving cortical and subcortical “nodes” may be instrumental in propagating seizure activity (29).
Several clinical manifestations have been found to have localizing or lateralizing value for focal onset seizures, including forced versive head-turning, ictal aphasia, dystonic limb posturing, asymmetric tonic limb posturing, unilateral automatisms, ictal spitting, ictal vomiting, unilateral eyelid blinking, peri-ictal water drinking, and postictal nose wiping (30; 16; 11). In some cases, particularly in the frontal and parietal lobes, the spread of the ictal discharge is rapid, and localizing features may not be apparent.
In focal to bilateral tonic-clonic seizures, head (and eye) version has a reliable lateralizing value in frontal and temporal lobe epilepsies, with the seizure onset zone being contralateral to the direction of head turning when it is forced and immediately precedes bilateral generalization. This is most likely the result of activation of frontal eye and motor areas anterior to the precentral gyrus.
Ictal aphasia. Ictal aphasia is related to the ictal activity in the language-dominant hemisphere.
Dystonic posturing. Dystonic posturing of the contralateral extremities is a reliable lateralizing sign to the contralateral hemisphere in temporal lobe seizures. The proposed mechanism includes propagation of ictal discharges to involve the sensory motor area, anterior cingulate gyrus, ventral striatum, and pallidum.
Asymmetric tonic limb posturing. Asymmetric tonic limb posturing, where one elbow is extended while the other is flexed (figure-of-4 sign), has been described as a lateralizing sign with a positive predictive value of about 90%. The extended elbow is contralateral to the side of ictal onset. Activation of the supplemental motor area (SMA) is believed to be the underlying mechanism.
Unilateral automatism. Unilateral automatism (usually in association with dystonic limb) posturing in the opposite limb is predominantly ipsilateral to the seizure onset zone in mesial temporal lobe epilepsy, and contralateral in neocortical temporal lobe epilepsy.
Ictal spitting. Ictal spitting is a rare semiological event in right temporal lobe epilepsy that probably involves the autonomic networks.
Ictal vomiting. Ictal vomiting initially was reported to be associated with a very small percentage of seizures from the right temporal lobe; however, studies have cast doubt on the reliability of lateralization of ictal nausea and vomiting.
Unilateral eye blinking. Unilateral eye blinking has been reported to be associated with ipsilateral ictal discharges and is thought to result from the involvement of the inferior postcentral cortex.
Peri-ictal water drinking. Peri-ictal water drinking might be considered a rare automatism during or within 2 minutes of an electrographical seizure that can be seen in temporal lobe epilepsy in the nondominant right hemisphere in the majority.
Postictal nose wiping. Postictal nose wiping can be associated with temporal lobe seizures more than frontal lobe seizures on the ipsilateral side of the hand that is used to wipe the nose.
Postictal paresis (Todd paralysis) is another lateralizing feature that is reported in around 3% to 16% of focal to bilateral tonic-clonic seizures, indicating onset in the contralateral hemisphere. Postictal features can be transient and must be assessed shortly after the seizure.
Table 1. Summarizing Clinical Features Suggesting Lateralization in Focal to Bilateral Tonic-Clonic Seizures
Clinical Feature | Localization or Lateralization |
Forced head version | Contralateral hemisphere |
Ictal aphasia | Language-dominant hemisphere |
Dystonic limb posturing | Contralateral hemisphere |
Figure-of-4 sign | Contralateral hemisphere to extended elbow |
Unilateral motor automatism | Ipsilateral hemisphere |
Ictal spitting | Right hemisphere |
Ictal vomiting | Possibly right hemisphere |
Unilateral eye blinking | Ipsilateral hemisphere |
Peri-ictal water drinking | Possibly nondominant right hemisphere |
Postictal nose wiping | Ipsilateral temporal lobe (less frequent extratemporal) |
Postictal paresis | Contralateral hemisphere |
Prognosis and complications
The available prognostic data are conflicting because of differing design, classification, duration of follow-up in different studies, and etiology of the seizures. The prognosis for individuals with focal to bilateral tonic-clonic seizures is less favorable than that of patients with most types of idiopathic generalized tonic-clonic seizures.
Many studies have found that two of the strongest predictors of seizure recurrence in focal to bilateral tonic-clonic seizures are focal changes in brain imaging and abnormal interictal discharges in EEG (08; 26). In its evidence-based guideline of management of an unprovoked first seizure in adults, the American Academy of Neurology (AAN) lists the following four factors as having the strongest evidence for increased risk of recurrence of seizures: a prior brain insult, epileptiform abnormalities in EEG, abnormal brain imaging, and a nocturnal seizure (27).
In a large cohort for prognostic patterns and predictors in epilepsy, 1006 children and adults were followed for a median of 16 years (09). During follow-up, the 1-year remission was 91.7%, and the 5-year remission was 77.1%. Factors confirmed to be associated with 5-year remission were fewer seizures (one or two seizures) before diagnosis, generalized epilepsy, absence of psychiatric comorbidity, and treatment with one to two antiseizure medications.
Complications that may occur in the ictal or immediate postictal period following a tonic-clonic seizure include:
• Oral trauma |
The most important risk factors for sudden unexpected death in epilepsy include a high frequency of generalized tonic-clonic seizures and living alone, especially not sharing a bedroom with anyone (23). It seems the SUDEP risk is highest in the first 5 years after diagnosis and decreases thereafter (40).
As the relationship between SUDEP, cardiac arrhythmias, and ictal asystole is further clarified, close attention to cardiac arrhythmias on video-EEG monitoring becomes of prime importance (39). A pacemaker may be indicated in some patients with ictal asystole or bradycardia.
There is growing information about the complex genetic interactions predisposing individuals to SUDEP, both in genetic and acquired epilepsies (33). In addition, the role of hypothalamic–pituitary–adrenal (HPA) axis dysfunction and its role in SUDEP have been receiving increasing attention (44).
Biological basis
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• Etiology of focal epilepsies is categorized as “known,” broken down to structural, genetic, infectious, metabolic, and immune etiologies, and “unknown.” | |
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• Excitatory positive feedback is characteristic of epileptic networks. Neuronal loss or damage and sprouting new connections can lead to excitatory positive feedback. | |
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• Inflammatory and immunological mechanisms are thought to be involved in the pathogenesis of not only autoimmune epilepsies but also epilepsies with other etiologies. | |
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• Synchronization of inhibitory interneurons by synchronized ictal excitation eventually can lead to inhibitory termination of seizures. |
Etiology and pathogenesis
In their 2017 epilepsy classification, the ILAE included the etiological classification of epilepsy, and some changes in terminology were proposed (37). In previous ILAE classifications, the term “cryptogenic” referred to unknown or suspected etiology other than possible hereditary predisposition, and idiopathic generalized epilepsies (IGE) encompassed four epilepsy syndromes: childhood absence epilepsy syndromes, juvenile absence epilepsy, juvenile myoclonic epilepsy, and generalized tonic-clonic seizures alone. The newer classification proposes that using genetic generalized epilepsies (GGE), where the clinician is comfortable with invoking a genetic etiology, is more meaningful. In addition, instead of using the terms symptomatic (known structural lesions) and cryptogenic (unknown causes), the etiology is referred to either as “known,” which is broken down into five subgroups, and “unknown.” The five subgroups of known etiologies include structural, genetic, infectious, metabolic, and immune.
Pathophysiology
Pathophysiology can be divided broadly into three main processes: epileptogenesis, mechanisms of spread, and termination of seizures.
Epileptogenesis. Epileptogenesis refers to processes that alter the function of a normal brain network in a way that enhances the probability of the brain to generate spontaneous recurrent seizures (SRSs). Several molecular and cellular plasticity mechanisms that are involved in generating the first unprovoked seizure continue beyond the initial seizure and contribute to the progression of the epileptic condition. Several broad mechanisms may be involved in the epileptogenesis of focal onset seizures, including excitatory positive feedback, which is a characteristic of epileptic networks, enabling them to switch back and forth between normal and epileptic modes of activity. One of the mechanisms that leads to this phenomenon is possibly uncovering preexisting positive feedback because of the loss of inhibitory circuits due to neuronal cell loss or damage, for example, in the hippocampus. Another mechanism is the development of positive feedback in sprouting new synaptic connections, for example, after brain injury (15).
Various mechanisms have been proposed for tumor-associated epilepsy, including altered intrinsic properties of the tumor cell membranes and gap junctions, high concentration of glutamate in extracellular space, GABA receptor downregulation, changes in potassium and chloride receptors and transporters, and inflammation (03).
Inflammatory and immunological mechanisms are thought to be involved in the pathogenesis of autoimmune epilepsies and epilepsies with other etiologies (21). In a large cohort study, the plasma levels of various cytokines (interleukins and interferons), inflammatory markers, and neurotrophic factors were found to be abnormal in 446 patients with epilepsy of various etiologies compared to 166 healthy controls. Among these, soluble tumor necrosis factor receptor 1 (sTNFr1) was found to have a relation with seizure frequency and was proposed as a potential biomarker for epilepsy (02).
Mechanisms of spread. Epileptic discharges may remain localized to a small area due in part to “surround inhibition” and other less clear mechanisms. In cases of focal to bilateral seizures, the epileptic focus propagates through fibers of cortico-cortical networks and multiple brain circuits to reach larger cortex areas and subcortical structures. Spread occurs when the focal seizure is adequately intense and when the surrounding activity is less inhibitory. White matter network abnormalities have a significant role in the spread of seizures. In a study of 83 patients with refractory temporal lobe epilepsy, patients with and without focal to bilateral tonic-clonic seizures had altered subnetworks, and the alteration was more widespread in the former group (38). Some studies suggest that mesial temporal lobe epilepsy consists of distinct electroclinical phenotypes due to divergent seizure propagation dynamics. Understanding this heterogeneity may have implications in the presurgical evaluation of the mesial temporal lobe epilepsy (05).
Termination of seizures. Potential mechanisms involved in seizure termination are complex (17). It is generally presumed that when the synchronous post-burst depression outweighs the possibility of burst re-excitation, the seizures stop. This process is facilitated by thalamic-limbic interactions, changes in metabolic environment such as pH shifts, exhaustion of presynaptic glutamate release, increased GABAergic drive, ATP depletion, and release of neuromodulators (eg, adenosine) that act as endogenous anticonvulsants (07).
Epidemiology
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• A meta-analysis reports the point prevalence of active epilepsy to be 6.38 per 1000 persons and the incidence rate of epilepsy to be 61.44 per 100,000 persons. | |
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• There was no clear difference between the point prevalence or cumulative incidence of epilepsy in low-middle income countries (LMIC) vs. high-income countries (HIC); however, the incidence rate was higher in LMIC compared to HIC. |
A meta-analysis of the incidence and prevalence of epilepsy from reported worldwide data was published in 2017 (19). The pooled point prevalence of active epilepsy was 6.38 per 1000 persons (95% CI, 5.57-7.30), and the pooled lifetime prevalence was 7.60 per 1000 persons (95% CI, 6.17-9.38). The annual cumulative incidence of epilepsy was 67.77 per 100,000 persons (95% CI, 56.69-81.03). The incidence rate was 61.44 per 100,000 persons (95% CI, 50.75-74.38). There was no clear difference between the point prevalence or cumulative incidence of epilepsy in low-middle-income countries versus high-income countries. However, the incidence rate was higher in low-middle-income countries compared to high-income countries, possibly explained by higher rates of CNS infections, greater exposure to perinatal risks, and higher rates of traumatic brain injuries.
The incidence of epilepsy tends to be higher in males than females and is thought to be at least partially due to a higher rate of concealment of epilepsy in females in certain sociocultural environments. The incidence of epilepsy is generally higher in the youngest and oldest age groups.
The distribution of epilepsy syndromes in newly diagnosed patients has been reported in several studies. One of the largest cohort studies in France reported 47.4% of newly diagnosed epilepsy cases with a history of more than one seizure are focal, including focal to bilateral tonic-clonic seizures, comprising 13.5% with known structural etiology (symptomatic), 29.2% with unknown etiology (cryptogenic), and 4.7% idiopathic with genetic etiology, whereas 33.8% were genetic (primary) generalized (24).
Differential diagnosis
Confusing conditions
The diagnosis of seizures relies critically on history. Usually, it is not difficult to distinguish generalized tonic-clonic seizures from other epileptic disorders. However, it is often difficult to distinguish focal to bilateral tonic-clonic from generalized tonic-clonic seizures. The focal seizure is usually recognized when a slow onset with a well-defined characteristic evolves into a generalized tonic-clonic seizure. However, the spread of the seizure can be extremely rapid, making it difficult to appreciate clinical or even electroencephalographical propagation. A focal seizure can sometimes arise from a focus deeper in the cortex or with a dipole orientation not detectable by recording scalp electrodes. Differentiation is then helped by indirect evidence, such as semiology of seizures, focal brain lesions on imaging, or focal interictal epileptiform activity. If needed, other tests such as long-term video EEG monitoring, intracranial monitoring, ictal SPECT, PET, or MEG can be used for further evaluation and localization.
Functional (psychogenic nonepileptic) seizures are the most common differential diagnosis. Some of the features suggestive of functional seizures include:
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• Triggers that are unusual for epileptic seizures (conditions promoting feelings of anxiety or guilt) |
Phenomena strongly associated with functional seizures include gradual onset or termination, pseudo sleep, irregular or asynchronous activity, including side-to-side head movements, pelvic thrusting, opisthotonic posturing, stuttering, weeping, preserved consciousness with bilateral motor activity, and persistent eye closure.
In contrast, symptoms in favor of epileptic seizures include occurrence out of sleep, incontinence, significant injuries, tongue bites of the lateral part of the tongue, and postictal confusion. The definite diagnosis requires video-EEG monitoring, which is the “gold standard” for diagnosis. Provocative techniques, activation procedures, or induction can be useful for the differential diagnosis of functional seizures, particularly when no spontaneous episodes occur during monitoring, although some controversies in the utilization of these techniques exist (14).
Associated and underlying disorders
Focal to bilateral tonic-clonic seizures can occur in focal epilepsies with known structural, genetic, or unknown etiologies. Common pathological conditions that can cause focal epilepsies in adults include:
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• Malformations of cortical development |
Benign focal epilepsies causing focal to bilateral tonic-clonic seizures, mainly in children, include:
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• Benign childhood epilepsy with centrotemporal spikes (also known as Self-limited epilepsy with centrotemporal spikes or SeLECTS) |
Diagnostic workup
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• A complete history and physical examination are essential in the diagnostic workup of epilepsy. | |
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• The yield of EEG in finding interictal abnormalities increases with repeated studies. | |
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• Various imaging modalities, such as MRI, fMRI, PET, DTI, and MEG, are utilized in the workup of focal epilepsies. |
Diagnosis of epilepsy starts with a complete history and physical examination of the patient. A detailed history of the semiology of the seizure can help identify signs or symptoms before bilateral propagation. Focal neurologic abnormalities are useful, especially if they correlate with the localization of the initial ictal manifestations (see localization under the clinical manifestations section). Various diagnostic tools can then be used to confirm the location of the epileptic focus or functional deficit, including EEG and imaging studies such as PET, SPECT, MEG, fMRI, and DTI.
Electroencephalogram (EEG). EEG is an important diagnostic tool for the diagnosis, localization, and determination of an epilepsy syndrome. The EEG abnormalities that can be observed in focal to bilateral tonic-clonic seizures include interictal, ictal, and postictal patterns.
Interictal pattern. The interictal pattern includes spikes, sharp waves, and, less often, polyspike and spike-and-wave complexes. Up to 40% of patients with epilepsy do not demonstrate any interictal epileptiform EEG findings on initial EEGs; however, with repeated studies, including sleep-deprived EEG and EEG with additional leads (eg, subtemporal), the yield approaches 90%.
Ictal pattern. During the tonic phase of convulsion, a progressively higher amplitude and lower frequency discharge pattern is seen simultaneously in cortical hemispheres. This pattern then becomes slower and intermixed with bilateral high-amplitude spikes and a progressively greater amount of rhythmic delta activity. During the clonic phase, progressive repetitive complexes of high-amplitude spike-and-slow waves are observed.
Postictal pattern. EEG generally shows a period of diffusely slow and low-amplitude activities; focal or lateralized slowing indicates focal onset.
Imaging studies. MRI and CT have been used routinely in the diagnosis and management of epilepsy. MRI is recommended for patients in whom focal epilepsy is suspected. Coronal FLAIR and T1 and T2 sequences with 1 to 3 mm cuts should be used to detect hippocampal sclerosis, and 3D volumetric studies, including SPGR sequences with multiple planes of reconstruction, are best for detecting cortical dysplasias.
Positron emission tomography (PET). PET scans produce metabolic maps of the brain. The most commonly used tracer is 18F-flourodeoxyglucose (FDG), although flumazenil is also useful. Epileptic foci and surrounding areas may have decreased metabolism during the interictal period, with sensitivities ranging from 30% to 90%, depending on location.
Single-photon emission computed tomography (SPECT). Stabilized technetium 99m is most commonly used in focal onset seizures. Ictal SPECT requires injection during or shortly after the seizure onset, usually during video-EEG monitoring. The isotope distribution is proportional to blood flow, and regions of maximal seizure activity show hyperperfusion.
Magnetoencephalography (MEG). This technique detects the magnetic fields associated with electrical discharges in the cortex. It is complementary in detecting some dipoles not seen on scalp EEG.
Functional magnetic resonance imaging (fMRI). Rarely, seizures have been captured during scanning and showed clear areas of seizure involvement. The fMRI is usually used in conjunction with neuropsychological testing and invasive cortical stimulation to identify eloquent language areas as well as the sensory and motor cortex to guide electrode placement and to delimit surgical resection.
Diffusion tensor imaging (DTI). DTI is an MRI imaging that allows visualization of the white matter anatomy of the brain. This modality has been used in guiding the plan for epilepsy surgery, especially in temporal lobe epilepsies (10).
Management
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• Medications, neurostimulation, and surgery are the main therapeutic options. | |
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• Monotherapy with a single antiseizure medication is preferred, although rational polytherapy, combining antiseizure medications with different mechanisms of action for better efficacy, is a common practice in refractory epilepsy. | |
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• Vagus nerve stimulation, brain-responsive neurostimulation, and deep brain stimulation are FDA-approved neurostimulations for adjunct therapy in medically refractory focal epilepsy. Vagus nerve stimulation is the only neurostimulator that is approved for children (and only those older than the age of 4). | |
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• Epilepsy surgery should always be considered in patients with medically refractory focal epilepsy. | |
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• Common disorders that can be successfully addressed with surgery include low-grade tumors, vascular lesions, cortical dysplasia, and mesial temporal or hippocampal sclerosis. |
Therapeutic options for focal to bilateral tonic-clonic seizures include medical therapy, surgery, and neurostimulation. Furthermore, management should include counseling the patient about their condition and educating them on standard seizure precautions.
Medical therapy. Medical therapy with a single antiseizure medication is the initial primary approach to the management of focal to bilateral tonic-clonic seizures. The use of a single antiseizure medication reduces the risks of idiosyncratic and dose-related toxic reactions, the cost of medications, and the chances of drug-drug interactions, and it increases therapy compliance. The initial drug selection is based on consideration of syndrome and seizure type, potential side effects, cost, comorbidities, and drug interactions. According to the 2004 American Academy of Neurology guidelines of efficacy and tolerability of antiepileptic drugs, use of lamotrigine, gabapentin, topiramate, and oxcarbazepine, in addition to the well-established carbamazepine and phenytoin, are effective in new-onset focal epilepsy (22). Additional recommendations in the 2018 update to the 2004 AAN guidelines include that lamotrigine, levetiracetam, and zonisamide may be considered in decreasing seizure frequency in adults with new-onset focal epilepsy (25). The recommended medication for patients 60 years of age or above is lamotrigine, and gabapentin can also be considered. A few newer-generation medications have been approved for monotherapy in focal epilepsies, such as lacosamide, eslicarbazepine, perampanel, and cenobamate. Table 2 lists the medications available for monotherapy or adjunct therapy in focal epilepsies, along with recommended adult doses and common or important side effects (01).
Rational polytherapy, combining antiseizure medications with different mechanisms of action for better efficacy, is a common practice in refractory epilepsy, although there are no robust guidelines and little evidence-based data for clinicians to follow (43).
Achieving seizure control is inversely correlated with the number of failed drug regimens. ILAE proposed a definition for drug-resistant epilepsy as failure of adequate trials of two tolerated, appropriately chosen, and used antiseizure medications (whether as monotherapies or in combination) to achieve sustained seizure freedom. Wrong diagnosis, non-compliance, and inadequate or inappropriate treatment are common reasons for pseudo-resistance that need to be identified in cases of drug-resistant epilepsy (28). Early identification of patients with drug-resistant epilepsy is important to consider other modalities to achieve seizure control, including vagal nerve stimulation, surgical intervention, and responsive intracranial stimulation.
Table 2. Medications for Focal Epilepsy
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Medication |
Monotherapy (M) vs. adjunct (A) |
Adult Initial dose |
Adult Maintenance dose |
Common or serious side effects |
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Brivaracetam |
M |
50 mg bid |
100 mg bid |
Sedation, dizziness, fatigue, mood change |
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Carbamazepine |
M |
200 mg bid |
400 to 800 mg bid |
Sedation, ataxia, dizziness, fatigue, hyponatremia, bone marrow suppression |
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Cenobamate |
M |
12.5 mg/day |
200 to 400 mg/day |
Sedation, dizziness, fatigue, diplopia, shortening of QT interval |
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Eslicarbazepine |
M |
400 mg/day |
800 to 1200 mg/day |
Sedation, ataxia, fatigue |
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Felbamate |
M |
600 mg bid |
600 to 1200 mg tid |
GI irritation, aplastic anemia, fulminant hepatitis |
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Gabapentin |
A |
300 to 400 mg/day |
600 to 1200 mg tid |
Sedation, dizziness, ataxia, fatigue |
|
Lacosamide |
M |
50 mg bid |
100 to 300 mg bid |
Sedation, dizziness, headache, ataxia, prolonging PR interval |
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Lamotrigine |
M |
25 mg/day |
100 to 600 mg/day |
Sedation, dizziness, diplopia, tremor, Stevens-Johnson syndrome |
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Levetiracetam |
M |
500 mg/day |
3000 to 4000 mg/day divided bid |
Sedation, dizziness, fatigue, mood change, irritability |
|
Oxcarbazepine |
M |
150 to 300 mg bid |
800 to 1200 mg bid |
Sedation, ataxia, fatigue, hyponatremia |
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Perampanel |
M |
2 mg/day |
8 to 12 mg/day |
Sedation, dizziness, ataxia, headache, mood changes |
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Phenobarbital |
M |
30 to 60 mg/day |
1 to 2.5 mg/kg/day |
Sedation, osteoporosis |
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Phenytoin |
M |
200 to 400 mg/day |
Keep the serum level at 10 to 20 mg/L |
Ataxia, nystagmus, osteoporosis |
|
Pregabalin |
A |
75 mg/day |
75 to 300 mg bid |
Sedation, dizziness, weight gain, peripheral edema |
|
Rufinamide |
A |
400 mg/day |
800 to 1600 mg bid |
Sedation, dizziness, fatigue, shortening of QT interval |
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Tiagabine |
A |
4 mg/night |
8 to 16 mg tid |
Dizziness, mood changes, nonconvulsive status epilepticus, encephalopathy |
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Topiramate |
M |
25 mg/day |
50 to 200 mg bid |
Sedation, dizziness, cognitive slowing, renal stone, weight loss |
|
Valproate |
M |
500 mg/day |
1000 to 2000 mg/day |
Sedation, tremor, weight gain, hair loss, pancreatitis |
|
Vigabatrin |
A |
500 mg bid |
1500 mg bid |
Sedation, dizziness, ataxia, mood changes, concentric visual field constriction |
|
Zonisamide |
M |
100 mg/night |
300 to 600 mg/night |
Sedation, dizziness, ataxia, irritability, weight loss, Stevens-Johnson syndrome |
Neurostimulation. Vagus nerve stimulation, brain-responsive neurostimulation, and deep brain stimulation are the main Food and Drug Administration-approved adjunctive therapies available for patients with medically refractory focal epilepsies.
Vagus nerve stimulation. Vagus nerve stimulation was the first neurostimulation device approved for treating epilepsy. It consists of a pulse generator usually implanted below the left clavicle and a lead that is wrapped around the left vagus nerve. In a meta-analysis, the pooled odds ratio from three randomized controlled trials and three comparative observational studies for experiencing a 50% or more reduction in seizure frequency with implantation of vagus nerve stimulation was 2.27 (06). In addition, the pooled odds ratio from two randomized controlled trials and three comparative observation studies for experiencing a 75% or more reduction in seizure frequency was 3.56. There was no difference in odds of seizure freedom. Despite studies in animals and humans, which show changes in brain electrophysiology, metabolism, and neurochemistry, the mode of action remains uncertain. The programmable generator allows adjustments in current, pulse, frequency, and duty cycle. Adverse surgical outcomes are acceptably low in experienced hands. Stimulation-induced effects, such as hoarseness, cough, and dysphagia, are intensity-dependent, diminish over time, and are usually not treatment-limiting. The current generation of vagus nerve stimulation devices includes the ability to detect ictal tachycardia and deliver enhanced stimuli to try to interrupt the seizures. Although the rate of rise in heart rate is rapid in seizures, adequate reliability of ictal detection and response must be balanced with tolerability of intermittent stimuli from other instances of rapid tachycardia.
Brain-responsive neurostimulation. The brain-responsive neurostimulation system consists of a programmable neurostimulator that is implanted in the skull and is connected to depth or subdural cortical strip leads. The leads are placed in or close to the identified seizure focus or foci. Brain-responsive neurostimulation system provides responsive, closed-loop focal cortical stimulation when abnormal electrocorticographic (ECoG) activity is detected: the neurostimulator continually senses the ECoG activity and can detect specific patterns that have been previously programmed by the physician as ictal patterns. In response to detecting ictal patterns, the brain-responsive neurostimulation system delivers stimulus pulses. The initial 2-year randomized, blinded controlled trial showed a median 44% reduction in seizures at 1 year and 53% at 2 years (13). Out of the 256 patients treated in the initial trial, 230 participated in the long-term prospective open-label trial, and the data on safety, efficacy, and quality of life (QOL) over the additional 7 years were published in 2020 (32). The results showed 73% of patients responded to the device with a median 75% reduction in seizure frequency. In addition, there was a significant improvement in the quality of life and some aspects of cognitive function. Suggested mechanisms involved in the effectiveness of direct stimulation include changes in cellular inhibition or excitation, changes in synaptic plasticity, neurogenesis, or cortical reorganization. The main adverse events include infection (4.1% risk per procedure), intracranial hemorrhage (2.7%), and status epilepticus (8.2%; more than half were nonconvulsive). The percentage of patients who reported adverse effects related to depression was 1.6%, but the majority of them were not considered to be device-related.
Deep brain stimulation. Bilateral stimulation of the anterior nucleus of thalamus, delivered from a pulse generator via implanted electrodes, has been approved as an adjunctive therapy for refractory focal epilepsy in adults. In the initial clinical trial study (SANTE) of 110 patients who underwent bilateral anterior thalamic stimulation, 41% experienced a median reduction in seizure frequency at 1 year and 69% at 5 years (36). Patients with temporal lobe epilepsy experienced the most benefit from deep brain stimulation. Most complications included hemorrhage (4.9%), infection (1.7%), worsening or new seizures, neurologic symptoms such as paresthesia (22.7%), and memory and cognitive changes (4%).
Surgical therapy. Surgery should be considered as a treatment option in patients with medically refractory epilepsy. Common disorders that can be successfully addressed with surgery include low-grade tumors, vascular lesions, cortical dysplasia, and mesial temporal or hippocampal sclerosis. The key to successful epilepsy surgery is multimodal localization of the seizure focus. Video-EEG recording with scalp, and if needed, intracranial recording plays a vital role in localization. Several imaging modalities, including PET scans, ictal SPECT, magnetic resonance spectroscopy, fMRI, and DTI, are being used to help localize and place intracranial electrodes. Seizures related to benign tumors and mesial temporal sclerosis respond best to surgery. Surgery is less effective if there is no lesion in the MRI or if the lesion is in an extratemporal location. A randomized trial of early surgical therapy for drug-resistant mesial temporal lobe epilepsy showed 2-year seizure freedom in 11 of 15 surgically treated patients when compared to 0 of 23 in the medical arm (18).
Less invasive surgical techniques, such as stereotactic radiosurgery, radiofrequency ablation or laser ablation, have been used to target specific epileptogenic foci (31). Laser ablation is undergoing an increasing role in treatment.
Treatments on the horizon. Stem cell and gene therapies are progressing and may play a role in treating intractable epilepsy in the future. Several neuronal and glial precursor lines can now be synthesized in vitro, and research is ongoing in molding differentiation, survival, and integration of these precursors (35). Grafting primary GABAergic cells in the epileptogenic areas of the brain has shown promising results in animal models and in a clinical trial in humans (04).
Outcomes
Complete control with antiseizure medications can be achieved in approximately 45% to 55% of patients with focal to bilateral tonic-clonic seizures. The remaining cases have varying responses to treatment based on the etiology, location, and treatment modality.
Special considerations
Pregnancy
There are various challenges in the medical care of women of childbearing age with epilepsy. There are over one million patients with epilepsy in the United States who are of childbearing age. Seizures during pregnancy can have potentially harmful effects on a fetus. On the other hand, the teratogenic effects of antiseizure medications are always of great concern to the patient and healthcare providers.
About 84% to 92% of patients who had no seizures at least 9 to 12 months before the pregnancy remain seizure-free during pregnancy. Pregnancy registries have provided key information that usually guides the counseling and treatment of women with epilepsy in their reproductive years (34).
The major congenital malformation rate in the general population is estimated to be around 1.6% to 3.2%. With exposure to antiseizure medications during pregnancy, this rate can increase 2- to 3-fold higher, depending on the specific medication exposure. The available data confirm that the risk of major congenital malformation in antiseizure medication polytherapy is higher compared to monotherapy.
Valproate is well recognized to be associated with a higher risk of major congenital malformations and adverse effects on cognitive function in the offspring of women with epilepsy. This medication has a higher risk of causing spina bifida and hypospadias than other antiseizure medications. The absolute risk of major congenital malformation is about 6% to 9% of exposed pregnancies during the first trimester, which appears to be dose-related. Therefore, this medication should be avoided in this population of patients as much as possible.
An association of exposure to topiramate in the first trimester and risk of facial cleft has been reported from several pregnancy registries and studies. In utero exposure to carbamazepine has been confirmed to be associated with spina bifida with an odds ratio of 2.6% (CI 1.2 to 53). Levetiracetam seems to be associated a low risk of major congenital malformations, with a rate of about 2.4%.
Data from the European and International Registry of Antiepileptic Drug and Pregnancy (EURAP) revealed a close relationship between the dose of most antiseizure medications and risk of associated major congenital malformations. These data also showed the lowest risk was with lamotrigine at doses less than 325 mg/day. The associated risks with levetiracetam and oxcarbazepine were not dose-dependent and were approximately the same as the risk of a lower dose of lamotrigine and lower than a high dose (greater than 700 mg/day) of carbamazepine (42).
An adverse effect of fetal exposure to some antiseizure medications on the IQ, namely valproate and phenobarbital, has been demonstrated in retrospective and prospective studies. Data about other antiseizure medications are emerging.
There is some evidence that taking folic acid supplementation during pregnancy reduces the risk of major congenital malformations, especially neural tube defects and cognitive disabilities in offspring of women with epilepsy who are taking antiseizure medications. The recommended dose is 4 mg/day. However, the data from EURAP did not provide confirmatory data about the protective effect of folic acid.
The blood level of antiseizure medications may decrease during pregnancy due to multiple factors, including induced metabolism of some medications secondary to hormonal changes. Therefore, frequent monitoring and dose adjustment are of importance in these cases.
Anesthesia
Anesthesia-induced seizures are rare. Enflurane, sevoflurane, and etomidate are among the anesthetic agents that can induce epileptiform discharges and seizures; therefore, it is recommended that these agents be avoided in patients with epilepsy, if possible.
References
- 01
- Abou-Khalil BW. Update on antiseizure medications 2022. Continuum (Minneap Minn) 2022;28(2):500-35.** PMID 35393968
- 02
- Alvim MKM, Morita-Sherman ME, Yasuda CL, et al. Inflammatory and neurotrophic factor plasma levels are related to epilepsy independently of etiology. Epilepsia 2021;62(10):2385-94. PMID 34331458
- 03
- Aronica E, Ciusani E, Coppola A, et al. Epilepsy and brain tumors: two sides of the same coin. J Neurol Sci 2023;446:120584. PMID 36842341
- 04
- Babu H, Beach R, Ben-Haim S, et al. First-in-Human Trial of NRTX-1001 GABAergic Interneuron Cell Therapy for Treatment of Focal Epilepsy - Emerging Clinical Trial Results (S19.002). Available online at : https://doi.org/10.1212/WNL.0000000000206002. Neurology 2024.
- 05
- Bae H, Seo DW, Hong SB, Park HR, Shon YM. Divergent propagation networks define two pathophysiologically distinct electroclinical phenotypes in mesial temporal lobe epilepsy. J Clin Neurol 2026;22(2):203-11. PMID 41775375
- 06
- Batson S, Shankar R, Conry J, et al. Efficacy and safety of VNS therapy or continued medication management for treatment of adults with drug-resistant epilepsy: systematic review and meta-analysis. J Neurol 2022;269(6):2874-91. PMID 35034187
- 07
- Beamer E, Kuchukulla M, Boison D, Engel T. ATP and adenosine-Two players in the control of seizures and epilepsy development. Prog Neurobiol 2021;204:102105. PMID 34144123
- 08
- Beghi E, Giussani G, Sander JW. The natural history and prognosis of epilepsy. Epileptic Disord 2015;17(3):243-53. PMID 26234761
- 09
- Beghi E, Beretta S, Carone D, et al. Prognostic patterns and predictors in epilepsy: a multicentre study (PRO-LONG). J Neurol Neurosurg Psychiatry 2019;90(11):1276-85. PMID 31248935
- 10
- Ben Dor N, Sighinolfi G, Rosetti V, et al. Diffusion tensor imaging biomarkers to predict neurological outcomes in brain surgery: a systematic review. Life (Basel) 2026;16(1):115. PMID 41598270
- 11
- Beniczky S, Tatum WO, Blumenfeld H, et al. Seizure semiology: ILAE glossary of terms and their significance. Epileptic Disord 2022;24(3):447-95.** PMID 35770761
- 12
- Beniczky S, Trinka E, Wirrell E, et al. Updated classification of epileptic seizures: position paper of the International League Against Epilepsy. Epilepsia 2025;66(6):1804-23. PMID 40264351
- 13
- Bergey GK, Morrell MJ, Mizrahi EM, et al. Long-term treatment with responsive brain stimulation in adults with refractory partial seizures. Neurology 2015;84(8):810-7. PMID 25616485
- 14
- Chen DK, Izadyar S, Collins RL, Benge JF, Lemaire AW, Hrachovy RA. Induction of psychogenic nonepileptic events: success rate influenced by prior induction exposure, ictal semiology, and psychological profiles. Epilepsia 2011;52(6):1063-70. PMID 21371022
- 15
- Chen L, Wang Y, Chen Z. Adult neurogenesis in epileptogenesis: an update for preclinical finding and potential clinical translation. Curr Neuropharmacol 2020;18(6):464-84. PMID 31744451
- 16
- Chowdhury FA, Silva R, Whatley B, Walker MC. Localisation in focal epilepsy: a practical guide. Pract Neurol 2021;21(6):481-91. PMID 34404748
- 17
- de Curtis M, Suffczynski P, Lévesque M, et al. Mechanisms leading to initiation, development, and termination of focal seizures. In: Noebels JL, Avoli M, Rogawski MA, Vezzani A, Delgado-Escueta AV, editors. Jasper's Basic Mechanisms of the Epilepsies. Chapter 8. 5th ed. New York: Oxford University Press, 2024. PMID 39637112
- 18
- Engel J Jr, McDermott MP, Wiebe S, et al. Early surgical therapy for drug-resistant temporal lobe epilepsy: a randomized trial. JAMA 2012;307(9):922-30. PMID 22396514
- 19
- Fiest KM, Sauro KM, Wiebe S, et al. Prevalence and incidence of epilepsy: A systematic review and meta-analysis of international studies. Neurology 2017;88(3):296-303.** PMID 27986877
- 20
- Fisher RS, Cross JH, French JA, et al. Operational classification of seizure types by the International League Against Epilepsy: Position Paper of the ILAE Commission for Classification and Terminology. Epilepsia 2017;58(4):522-30.** PMID 28276060
- 21
- Flammer J, Neziraj T, Rüegg S, Pröbstel AK. Immune mechanisms in epileptogenesis: update on diagnosis and treatment of autoimmune epilepsy syndromes. Drugs 2023;83(2):135-58. PMID 36696027
- 22
- French JA, Kanner AM, Bautista J, et al. Efficacy and tolerability of the new antiepileptic drugs I: treatment of new onset epilepsy: report of the Therapeutics and Technology Assessment Subcommittee and Quality Standards Subcommittee of the American Academy of Neurology and the AES. Neurology 2004;62(8):1252-60. PMID 15111659
- 23
- Harden C, Tomson T, Gloss D, et al. Practice guideline summary: sudden unexpected death in epilepsy incidence rates and risk factors: report of the Guideline Development, Dissemination, and Implementation Subcommittee of the American Academy of Neurology and the American Epilepsy Society. Neurology 2017;88(17):1674-80. PMID 28438841
- 24
- Jallon P, Loiseau P, Loiseau J. Newly diagnosed unprovoked epileptic seizures : Presentation at diagnosis in CAROLE Study. Coordination Active du Réseau Observatoire Longitudinal de l' Epilepsie. Epilepsia 2001;42(4):464-75. PMID 11440341
- 25
- Kanner AM, Ashman E, Gloss D, et al. Practice guideline update summary: efficacy and tolerability of the new antiepileptic drugs I: treatment of new-onset epilepsy: Report of the Guideline Development, Dissemination, and Implementation Subcommittee of the American Academy of Neurology and the American Epilepsy Society. Neurology 2018;91(2):74-81.** PMID 29898971
- 26
- Koutroumanidis M, Bruno E. Epileptology of the first tonic-clonic seizure in adults and prediction of seizure recurrence. Epileptic Disord 2018;20(6):490-501. PMID 30530414
- 27
- Krumholz A, Wiebe S, Gronseth GS, et al. Evidence-based guideline: management of an unprovoked first seizure in adults: Report of the Guideline Development Subcommittee of the American Academy of Neurology and the American Epilepsy Society. Neurology 2015;84(16):1705-13.** PMID 25901057
- 28
- Kwan P, Schachter SC, Brodie MJ. Drug-resistant epilepsy. N Engl J Med 2011;365(10):919-26.** PMID 21899452
- 29
- Lopes MA, Junges L, Woldman W, Goodfellow M, Terry JR. The role of excitability and network structure in the emergence of focal and generalized seizures. Front Neurol 2020;11:74. PMID 32117033
- 30
- Marashly A, Ewida A, Agarwal R, Younes K, Lüders HO. Ictal motor sequences: lateralization and localization values. Epilepsia 2016;57(3):369-75. PMID 26864781
- 31
- Mohsen Y, Sarhan K, Alawadi IS, et al. Efficacy and safety of laser interstitial thermal therapy versus radiofrequency ablation and stereotactic radiosurgery in the treatment of intractable mesial temporal lobe epilepsy: a systematic review and meta-analysis. Neurosurg Rev 2025;48(1):71. PMID 39836334
- 32
- Nair DR, Laxer KD, Weber PB, et al. Nine-year prospective efficacy and safety of brain-responsive neurostimulation for focal epilepsy. Neurology 2020;95(9):e1244-56.** PMID 32690786
- 33
- Noebels JL. Genetic and cellular mechanisms underlying SUDEP risk. In: Noebels JL, Avoli M, Rogawski MA, Vezzani A, Delgado-Escueta AV, editors. Jasper's Basic Mechanisms of the Epilepsies. Chapter 63. 5th ed. New York: Oxford University Press; 2024. PMID 39637214
- 34
- Perucca P, Battino D, Bromley R, et al. Epilepsy-pregnancy registries: an update. Epilepsia 2025;66(1):47-59. PMID 39540312
- 35
- Ramos-Fresnedo A, Perez-Vega C, Domingo RA, et al. Mesenchymal stem cell therapy for focal epilepsy: a systematic review of preclinical models and clinical studies. Epilepsia 2022;63(7):1607-18. PMID 35451066
- 36
- Salanova V. Deep brain stimulation for epilepsy. Epilepsy Behav 2018;88S:21-24.** PMID 30030085
- 37
- Scheffer IE, Berkovic S, Capovilla G, et al. ILAE classification of the epilepsies: Position paper of the ILAE Commission for Classification and Terminology. Epilepsia 2017;58(4):512-21.** PMID 28276062
- 38
- Sinha N, Peternell N, Schroeder GM, et al. Focal to bilateral tonic-clonic seizures are associated with widespread network abnormality in temporal lobe epilepsy. Epilepsia 2021;62(3):729-41. PMID 33476430
- 39
- Surges R, Shmuely S, Dietze C, Ryvlin P, Thijs RD. Identifying patients with epilepsy at high risk of cardiac death: signs, risk factors and initial management of high risk of cardiac death. Epileptic Disord 2021;23(1):17-39. PMID 33650492
- 40
- Sveinsson O, Andersson T, Carlsson S, Tomson T. Type, etiology, and duration of epilepsy as risk factors for SUDEP: further analyses of a population-based case-control study. Neurology 2023;101(22):e2257-65. PMID 37813583
- 41
- Theodore WH, Porter RJ, Albert P, et al. The secondarily generalized tonic-clonic seizure: a videotape analysis. Neurology 1994;44:1403-7. PMID 8058138
- 42
- Tomson T, Battino D, Bonizzoni E, et al. Comparative risk of major congenital malformations in children of women with eight different antiepileptic drugs: a prospective cohort study of the EURAP registry. Lancet Neurol 2018;17(6):530-8. PMID 29680205
- 43
- Verrotti A, Tambucci R, Di Francesco L, et al. The role of polytherapy in the management of epilepsy: suggestions for rational antiepileptic drug selection. Expert Rev Neurother 2020;20(2):167-73. PMID 31855066
- 44
- Wenker IC, Gehlbach BK, Isom LL, et al. Unraveling SUDEP: mechanisms of seizure-induced cardiac and respiratory impairment. Epilepsy Curr 2026;21:15357597261416723. PMID 41584903
Contributors
All contributors' financial relationships have been reviewed and mitigated to ensure that this and every other article is free from commercial bias.
Authors
-
Shahram Izadyar MD
Dr. Izadyar of Upstate Medical University in Syracuse received research grants from Otsuka Pharmaceuticals, Neurona Therapeutics, and Xenon Pharmaceuticals.
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Robert L Beach MD PhD
Dr. Beach of Upstate Medical University, has no relevant financial relationships to disclose.
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Editor
-
Jerome Engel Jr MD PhD
Dr. Engel of the David Geffen School of Medicine at the University of California, Los Angeles, has no relevant financial relationships to disclose.
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Former Authors
- Rajdeep Singh MD
- Peter J Struck MD
Patient Profile
- Age range of presentation
-
- 0 month to 65+ years
ICD & OMIM codes
- ICD-10
-
- Localization-related (focal) (partial) symptomatic epilepsy and epileptic syndromes with complex partial seizures, not intractable, without status epilepticus: G40.209
- ICD-11
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- Generalised tonic-clonic seizure: 8A68.4
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