Simple Partial Seizures 

Updated: Feb 22, 2016
Author: Jane G Boggs, MD, FACS, FAES; Chief Editor: Selim R Benbadis, MD 



All partial seizures are characterized by onset in a limited area, or focus, of one cerebral hemisphere. The 1989 International Classification of Epileptic Seizures (ICES) remains the most widely accepted classification system, although several recent modifications of terminology have been proposed.[1] In all these classifications systems, however, simple partial seizures (SPS) are defined as those that are not associated with any alteration of consciousness.[2] Although the ability to respond may be preserved, motor manifestations or anxiety relating to the seizure symptoms may prevent a patient from responding appropriately.

The level of consciousness may be difficult to determine during a partial seizure, especially in infants, cognitively impaired individuals, and aphasic patients. The lack of availability of trained persons to interact directly with the patient during and after the seizure can make distinctions between simple and complex partial seizures difficult, even with high-resolution video-EEG.

The ICES defines an aura as "that portion of the seizure which occurs before consciousness is lost, and for which memory is retained afterwards." Auras without subsequent seizures should be considered a type of SPS.

Simple partial status epilepticus (SPSE) includes epilepsia partialis continua (ie, Kojewnikoff syndrome). Some researchers also have included periodic lateralized epileptiform discharges (PLEDs) and the spectrum of Landau-Kleffner syndrome as types of SPSE.

The suspicion of SPS is based on a history consistent with the typical, reproducible patterns seen with the various SPS categories (see Clinical Presentation). An electroencephalogram (EEG) fortuitously obtained during the patient's symptoms can provide clear support for a diagnosis. EEGs obtained soon after a suspected seizure often record nonspecific patterns or may be normal (see Workup).

In most patients with SPS, antiepileptic drug therapy is appropriate. Selected patients with SPS refractory to AEDs may be candidates for surgical treatment (see Treatment and Management).

Go to Epilepsy and Seizures for an overview of this subject.


Any structural lesion of the brain that causes an electrical variation in the surrounding tissue can provide an adequate substrate for epileptogenesis. The epileptogenic zone is the area that generates seizures, but may itself be clinically silent; instead, the clinical and EEG manifestations may be due to secondary activation of another cortical area.[3]

The anatomical pathways involved in SPS determine the clinical symptoms. SPS may be characterized by motor, sensory, psychic, or autonomic symptoms. Motor or sensory SPS are caused by ictal discharges in the somatotopically representative gyri of the contralateral hemisphere,[4] or by ictal discharges that spread to the sensorimotor cortex from the parietal, occipital, or temporal lobes.

Interestingly, the areas of the cortex with the lowest threshold for electrical stimulation are those that correspond to the body segments most commonly observed to be the regions responsible for motor or sensory SPS. Penfield and Jasper identified the perioral area, thumb, index finger, and great toe as the areas that usually are affected first in partial seizures. These are all anatomical parts having a disproportionately large area of representation in the cortical homunculus.[5]

Psychic SPS are characterized by complex cognitive or affective symptoms, such as déjà vu. They more commonly arise in temporal rather than extratemporal regions. Electrical stimulation experiments have demonstrated that similar psychic manifestations can be elicited from noncontiguous locations.[6] This suggests that this type of SPS may have a more diffuse rather than a discrete localization.

The origin of autonomic SPS is hypothesized to be hypothalamus. The clinical manifestations are determined by the pattern of activation of the central autonomic network and the higher-order autonomic control areas of the insula and prefrontal cortices.[7]


Any localized structural lesion of the brain can result in SPS, including the following:

  • Developmental abnormalities

  • Vascular lesions

  • Meningitis/focal encephalitis

  • Trauma

  • Tumors

  • Hypoxic insults

  • Postsurgical changes

  • Metabolic and electrolyte shifts

  • Endocrine disorders

  • Medications and toxins


Among all seizures, partial seizures have the highest incidence after the first year of life. In the United States, the incidence of all partial seizures for subjects aged 1-65 years is approximately 20 cases per 100,000 population. Although observational classification studies are imprecise, an estimated 6-12% of patients with epilepsy have SPS exclusively.[8]

The proportions of sensory, motor, special sensory, psychic, and autonomic SPS differ among various population studies. Most authors agree, however, that SPS are found most frequently in association with other types of seizures.

Not enough studies are available to indicate the incidence of SPS worldwide as compared with that in the United States. In general, the incidence of epilepsy and the proportion of partial epilepsy are expected to be higher in developing countries because of the higher rates of infection and overall lower standard of health.

SPS have no reported predilection for any race or ethnic group. Males and females are affected equally.

The incidence of SPS is lowest in children younger than 1 year and increases gradually up to approximately age 65 years, after which it rises exponentially. The increase in SPS corresponds to the increase in all partial seizures with age, particularly those due to cerebrovascular disease.


The risk for seizure recurrence after a single seizure has been reported to be higher in patients with partial seizures than in those with generalized seizures. However, the recurrence rates of simple and complex partial seizures appear to differ little, if at all.

As consciousness is preserved throughout the ictal event in SPS, these patients are less likely to suffer from seizure-related accidents and aspiration leading to pneumonia than are patients with seizures that affect consciousness. Consequently, morbidity and mortality rates are expected to be lower in SPS than in those other syndromes. However, focal motor SPS can result in falls and risk of trauma. In addition, SPS are frequently the result of symptomatic lesions, and the underlying etiology may impart additional risk for morbidity or mortality.

Individuals with idiopathic, complex partial epilepsy may have a higher survival rate than those with symptomatic epilepsy and SPS.

The prognosis of patients with SPS is similar to that of patients with complex partial seizures.

Poorly controlled seizures can result in chronic neurological and cognitive complications, the severity of which is largely dependent on the underlying etiology of the seizures.

Patient Education

Patients with SPS have the same requirement for education concerning epilepsy as those individuals with other seizure types. SPS can resemble many other disorders, and reassurance about the diagnosis may be necessary. Education should not be limited only to the patients, but should include family members, caretakers, and employers to limit unnecessary stigmatization and discrimination.

For patient education information, see the Brain and Nervous System Center, as well as Epilepsy.




The International Classification of Epileptic Seizures (ICES) lists 18 categories of simple partial seizures (SPS).[9] All types of SPS can be seen with subsequent complex partial, secondarily generalized seizures. The suspicion of SPS is based on a history consistent with the typical, reproducible patterns seen with the various SPS categories.

Motor simple partial seizures

In motor SPS, clonic discharges in the sensorimotor cortex cause jerky, rhythmic movements that may remain restricted to one body segment or spread by "jacksonian march."[10] Subtypes of motor SPS are as follows:

  • Benign focal epilepsy of childhood

  • Epilepsia partialis continua

  • Tonic supplementary motor area (SMA) and premotor region discharges

Benign focal epilepsy of childhood accounts for 15-25% of childhood epilepsy and eventually remits by age 16 years. Typical seizures are simple and motor, affect the face or arm, and occur soon after falling asleep or awakening. As it usually remits by age 16 years, this syndrome does not always require treatment.

Epilepsia partialis continua (ie, Kojewnikoff syndrome) includes stereotypical periodic to semiperiodic clonic activity that may persist for years and is often refractory to treatment.[11] Clonic jerking usually involves the thumb or great toe, and may or may not spread to other body parts.

Epilepsia partialis continua has been associated with stroke, tumor, trauma, hypoxia, Rasmussen encephalitis, syndrome of mitochondrial encephalomyopathy, lactic acidosis, and stroke (MELAS), subacute sclerosing panencephalitis (SSPE), and adult nonketotic hyperglycinemia.

Tonic SMA and premotor region discharges produce sustained contractions and unusual postures of a limb[11] . In 72% of cases, SMA seizures are not associated with impaired consciousness. Versive-smooth or jerky, tonic contractions of head and eye muscles, usually on the side contralateral to the discharge, often are followed by a secondarily generalized tonic-clonic seizure. Phonatory activation of the primary or supplementary motor cortex produces vocalizations, speech arrest, or aphasia.

Sensory simple partial seizures

Somatosensory-primary sensory cortex seizures usually elicit positive or negative sensations contralateral to the discharge.[4] Symptoms associated with seizures from the postcentral gyrus include the following:

  • Tingling

  • Numbness

  • Pain

  • Heat

  • Cold

  • Agnosia

  • Phantom sensations

  • Sensations of movement

Abdominal pain usually originates from the temporal lobe, and genital pain from the mesial parietal sensory cortex. The posterior parietal cortex is the likely origin of limb agnosia.

Supplemental sensory-secondary sensory cortex seizures may have ipsilateral or bilateral positive or negative sensations or vague axial or diffuse sensations.

Visual-calcarine cortex discharges produce elemental hallucinations including scintillations, scotomata, colored lights, visual field deficits, or field inversion. The visual association cortex is the probable location of origin of complex visual hallucinations and photopsias.

Auditory SPS from the auditory cortex typically are perceived as simple sounds, rather than words or music. Olfactory-uncinate seizures originate from the orbitofrontal cortex and the mesial temporal area. Perceived odors are usually unpleasant, often with a burning quality.

Gustatory seizures usually are associated with temporal lobe origin, although the insula and parietal operculum also have been implicated. Perceived tastes are typically unpleasant, often with a metallic component.

Vestibular seizures originate from various areas, including frontal and temporal-parietal-occipital junction. Symptoms include vertigo, a tilting sensation, and vague dizziness.

Psychic SPS arise predominantly from the temporal and limbic region, including the amygdala, hippocampus, and parahippocampal gyrus. Perceptual hallucinations or illusions are usually complex, visual or auditory, and are rarely bimodal.

Déjà vu and jamais vu phenomena may occur. Fear is usual, but SPS can elicit happiness, sexual arousal, anger, and similar responses. Cognitive responses include feelings of depersonalization, unreality, forced thinking, or feelings that may defy description.

Autonomic simple partial seizures

Autonomic SPS can involve the following symptoms[12] :

  • Abdominal

  • Cardiovascular

  • Respiratory

  • Papillary

  • Urogenital

  • Other

Abdominal sensation phenomena are common in mesial temporal epilepsy but can arise from the operculum and occipital region. Symptoms include nausea, pain, hunger, warmth, and "epigastric rising" sensations, and may be associated with piloerection (ie, gooseflesh).

The most common cardiac manifestation of any seizure is sinus tachycardia with arrhythmias, with bradycardia occurring infrequently.[13] Some patients have chest pain or a sensation of palpitation that mimics cardiac disease.

Respiratory inhibition has been reported with electrical stimulation of the temporal regions.[14] Pupillary symptoms include miosis, mydriasis, hippus, and unilateral pupillary dilatation.

Seizures from the superior portion of the posterior central gyrus can result in genital sensations, while sexual auras arise more from the limbic or temporal regions. Ictal orgasms have been reported, although rarely, in association with seizures arising from various cerebral locations.[15]

Rare autonomic symptoms include perspiration, lacrimation, ictal enuresis, or flushing.

Postictal neurological deficits can occur after an SPS as a negative manifestation of the function affected by the seizure (eg, Todd paralysis).

Physical Examination

The physical examination may show subtle or obvious neurological focality. Immediately following SPS, the focality may become more pronounced owing to postictal inhibition (eg, Todd paralysis).

If an examination is performed during SPS, no impairment of awareness or responsiveness is observed. Preservation of awareness implies that a person is able to recount simple events that happen during the ictus. This is best established by giving a specific, uncommon 2-syllable word to the patient during the SPS and asking for its recall soon after the seizure has resolved.

Preservation of responsiveness implies that a person is able to carry out simple commands or directed volitional actions. This is best established by asking the patient to perform simple, unilateral and bilateral neurological functions during the SPS.

However, responsiveness may appear to be impaired because of interference by the motor manifestations of the SPS. If the patient is unable to perform a task because of the manifestations of the SPS but recollects the instructions afterwards, this recollection implies that responsiveness was preserved.

Motor, sensory, special sensory, psychic, and autonomic manifestations may begin in a small anatomical area and spread to a larger area of the body. This has been termed as "jacksonian march," and it typically progresses along contiguous parts of the body in a reproducible pattern.



Diagnostic Considerations

Other problems to be considered include the following:

  • Atypical facial pain

  • Benign epilepsy syndromes

  • Brainstem syndromes

  • Carcinoid syndrome

  • Cardiac disorders

  • Cervical disk syndromes

  • Gastrointestinal disorders

  • Hypoglycemic episodes

  • Transient ischemic attacks (TIAs)

  • Migraines

  • Myoclonus

  • Panic attacks

  • Psychosis

Differential Diagnoses



Approach Considerations

Lumbar puncture should be performed in all cases of suspected meningitis, unless neuroimaging or funduscopic examination suggests increased intracranial pressure.

Brain biopsy is strongly suggested to confirm the diagnosis in suspected cases of Rasmussen encephalitis, or in focal progressive lesions of unknown etiology.

Lab Studies

The following blood studies can be useful for excluding other disorders:

  • Electrolytes, including serum glucose

  • Thyroid-stimulating hormone and/or thyroid profile

  • Toxin and drug screen


An electroencephalogram (EEG) fortuitously obtained during the patient's symptoms can provide clear support for a diagnosis. EEGs obtained soon after a suspected seizure often record nonspecific patterns or may be normal.

Activation by sleep deprivation, photic stimulation, and/or hyperventilation increases the ability to detect abnormalities on a single recording. Repeat or prolonged recording may increase the chance of recording interictal or ictal patterns of diagnostic significance.

Although interictal spikes in an appropriate anatomical location for the symptoms of the suspected seizure are highly suggestive of epilepsy, EEG abnormalities may be distant in location from the actual area of seizure onset, giving poor localizing information for possible epilepsy surgery. EEG performed with extra scalp electrodes or intracranial electrodes is necessary if involvement of mesial structures is suspected.

Single or rare interictal sharp waves may be normal variants, and further diagnostic confirmation should be pursued. Normal EEG findings do not exclude the possibility of epilepsy.


EEG-video monitoring is often necessary to record typical clinical events and to correlate them with any electrographic changes. Many SPS are characterized by EEG patterns that are difficult to record, and the diagnosis may depend entirely on video analysis of reproducible ictal semiology of multiple events, or on observation by trained personnel.

Electrocardiographic Studies

Routine 12-lead ECG and a rhythm strip should be obtained in all subjects with cardiac, thoracic, gastrointestinal, or focal positive and negative sensations. Twenty-four–hour Holter monitoring and inpatient telemetry are appropriate if daily episodes are expected (based on history). A telephone transmittal cardiac recorder can be useful for episodes occurring infrequently.

Imaging Studies

CT scan of the brain, with and without contrast, is primarily useful and appropriate in an emergency setting or for patients unable to have MRI studies. Coronal T2-weighted MRI with fluid-attenuated inversion recovery (FLAIR) and careful attention to the mesial temporal structures is more likely to demonstrate abnormalities if a diagnosis of SPS already has been established.

Low-resolution MRI, under 1.5 T, should be discouraged in any evaluation of epilepsy. This typically makes the use of "open MRI" inadequate.

Histologic Findings

Various microscopic abnormalities, including the following, can be found in the epileptogenic zone:

  • Focal cortical dysplasia

  • Hippocampal sclerosis

  • Neoplasia

  • Cortical inflammation

  • Encephalomalacia

  • Vascular malformation



Approach Considerations

Benign focal epilepsy of childhood is usually a self-limited condition; if no seizures with secondarily generalization occur, patient care need not include antiepilepsy drugs (AEDs). In other patients, AED treatment is appropriate for simple partial seizures (SPS). Selected patients with SPS refractory to AEDs may be candidates for surgical treatment.

Go to Epilepsy and Seizures for an overview of this topic.

Antiepileptic Drug Therapy

Numerous AEDs currently are approved worldwide with indications for SPS, and others are in development. No one drug of choice is recommended for SPS, since in clinical trials all the drugs have demonstrated similar levels of efficacy. Selection of the most appropriate medication is based on potential side effects, dosing schedules, available formulations, and individual factors.[16, 17, 18, 19, 20]

Go to Antiepileptic Drugs for complete information on this topic.

Surgical Care

Patients with medically refractory seizures may be candidates for epilepsy surgery, especially if they have a well-localized seizure onset documented by video-EEG and a corresponding lesion on neuroimaging. Such cases should be carefully evaluated preoperatively with the resection properly planned by the epilepsy surgical team to minimize the risk of postoperative deficit.

Focal cortical resection, amygdalo-hippocampectomy, lesionectomy, thermal laser ablation, or gamma knife surgery may be the most appropriate procedure. The specific procedure should be tailored individually to the features of each case. Implantable responsive neurostimulation (RNS) can be an alternative to focal resection in some patients.

Rasmussen encephalitis responds poorly to medical treatment and usually is treated by hemispherectomy to prevent involvement of the contralateral hemisphere.

Patients whose seizures are medically refractory but are not good candidates for epilepsy surgery may be candidates for implantation of a device to provide vagus nerve stimulation.

Go to Epilepsy Surgery for complete information on this topic.

Treatment During Pregnancy

Although often perceived to be less severe than complex partial and generalized seizures, SPS in pregnancy can be associated with fetal distress. Every effort must be made to control seizures during pregnancy by using appropriate doses of the most successful agent for the individual. If possible, avoid AED drug changes.

Go to Women's Health and Epilepsy for complete information on this topic.


Cardiac, gastrointestinal, psychiatric, or endocrine consultation, depending on individual cases, may be necessary in diagnostically difficult cases.

Psychiatric consultation may be necessary for management of concurrent depression, anxiety, and/or non-epileptic events.


Although a ketogenic diet has been used successfully in refractory seizures, it is not used commonly for patients exhibiting SPS exclusively (except children) who are not responding to medication.[21]

The medium-chain triglyceride diet is more convenient and palatable, and it does not result in hypercholesterolemia, although it appears to be less successful in the treatment of refractory seizures.[22] The Atkins diet has also been reported to have some adjunctive benefit to some patients with refractory seizures.[23]


As SPS do not impair consciousness, activity may not need to be restricted severely as with other types of seizures. Compliant patients with a consistent, exclusively SPS pattern that does not interfere with the ability to manipulate the controls of a motor vehicle are legally allowed to drive in states in which the motor vehicle authority approves exceptions to complete seizure control. Compliance with state guidelines may require self-reporting by patients or specific documentation of patient symptoms, compliance, and medications by the treating physician.

The safety of swimming and other potentially hazardous recreational or employment activities should be evaluated on an individual basis. The ability of an affected patient to care for infants in an unsupervised setting should be evaluated on an individual basis.

Long-Term Monitoring

At least monthly outpatient follow-up is recommended when seizures are not well controlled. As seizure control improves, the interval between evaluations can be increased.

Seizure-free patients may be monitored by a neurologist once or twice annually. Outpatient laboratory studies should be performed to monitor metabolic effects of the medications used to treat SPS, and to monitor underlying medical conditions.

AED levels should be performed when toxicity is suspected, or to confirm adequate compliance or absorption of medications. In the absence of side effects of medication, metabolic changes, or breakthrough seizures, routine monitoring of AED levels usually is not justified.

Patients diagnosed with SPS may require follow-up inpatient care if new patterns of seizures develop. EEG or video-EEG studies are often necessary to clarify the nature of the new seizure type. Neuroimaging and laboratory studies may help in identifying reasons for seizure exacerbations. In addition, medications usually can be adjusted more quickly in inpatients, and hospitalization in a video-EEG-monitoring unit optimizes the safety of rapid adjustment in the doses of medication.



Medication Summary

Many anticonvulsants currently are approved by the US Food and Drug Administration (FDA) for partial seizures with and without secondary generalization. These drugs have approval for treatment of single partial seizures (SPS) as well. No single agent is the drug of choice for SPS.

Also see Antiepileptic Drugs.


Class Summary

These agents prevent seizure recurrence and terminate clinical and electrical seizure activity.

Ezogabine (Potiga)

Neuronal potassium channel opener. Stabilizes neuronal KCNQ (Kv7) channels in the open position, increasing the stabilizing membrane current and preventing bursts of action potentials during the sustained depolarizations associated with seizures. Indicated as adjunctive therapy in partial-onset seizures uncontrolled by current medications.

Carbamazepine (Tegretol, Tegretol-XR, Carbatrol, Epitol)

Carbamazepine is a tricyclic compound extensively metabolized to its active metabolite, carbamazepine-epoxide. This agent markedly induces its own metabolism and is highly bound to plasma proteins. It is indicated in the treatment of partial seizures with complex symptomatology (psychomotor, temporal lobe), generalized tonic-clonic seizures (grand mal), or mixed seizure patterns.

Divalproex sodium (Depacon, Depakene, Depakote, Depakote-ER)

This is a branched-chain fatty acid that undergoes oxidative metabolism and is highly protein bound. The amount of protein binding increases with dose. This agent is available as 250-mg/5 mL syrup; 250-mg capsules; 125-mg sprinkle capsules; 125-, 250-, and 500-mg delayed-release tablets; 250- and 500-mg extended-release tablets; and 100-mg/mL injectable solution.

Gabapentin (Neurontin)

Gabapentin has saturable gastric absorption with virtually no protein binding and no metabolism; excretion is primarily renal. This agent is available as 100-, 300-, and 400-mg capsules; 600- and 800-mg tablets; and 50-mg/mL solution.

Lamotrigine (Lamictal)

Lamotrigine is hepatically metabolized and moderately protein bound. Its half-life is shorter -life in the presence of enzyme-inducing compounds. It is available as 2-, 5-, and 25-mg dispersible tablets and 25-, 100-, 150-, and 200-mg tablets.

Phenytoin (Dilantin, Phenytek)/ Fosphenytoin (Cerebyx)

Phenytoin is a poorly soluble compound that is highly protein bound, metabolized by cytochrome P-450 system, and has nonlinear pharmacokinetics. It is available as a 125-mg/5 mL suspension; 50-mg chewable tablet; 30-mg capsules; 100-mg capsules; and 50-mg/mL injectable phenytoin solution (contains propylene glycol). Fosphenytoin is phosphorylated phenytoin, a prodrug that is highly soluble and converted rapidly to phenytoin; it contains 50 mg phenytoin equivalent per mL solution.

Primidone (Mysoline)

Primidone is metabolized to phenobarbital and phenylethylmalonamide (PEMA), which also possesses some weak anticonvulsant activity. It is available as a 250-mg/5 mL suspension and 50- and 250-mg tablets.

Tiagabine (Gabitril)

Tiagabine is a gamma-aminobutyric acid (GABA) reuptake inhibitor, with its metabolism enhanced by cytochrome P-450 inducers. It is highly protein bound. It is available as a 2-, 4-, 12-, and 16-mg tablets.

Topiramate (Topamax)

Topiramate undergoes moderate hepatic metabolism and is excreted largely by the kidneys. It has low protein binding. Topiramate tablets and topiramate capsules are indicated as initial monotherapy or adjunctive therapy in patients 2 years of age and older with partial onset or primary generalized tonic-clonic seizures.

Oxcarbazepine (Trileptal)

The pharmacological activity of oxcarbazepine is primarily performed by the drug's 10-monohydroxy metabolite (MHD). Oxcarbazepine may block voltage-sensitive sodium channels, inhibit repetitive neuronal firing, and impair synaptic impulse propagation. An anticonvulsant effect may also occur by affecting potassium conductance and high-voltage activated calcium channels.

Drug pharmacokinetics are similar in older children (>8 y) and adults. Young children (< 8 y) have a 30-40% increased clearance compared with older children and adults. Oxcarbazepine is available as 150-, 300-, and 600-mg tablets and 300-mg/5 mL solution.

Eslicarbazepine acetate (Aptiom)

Eslicarbazepine acetate is a prodrug that is activated to eslicarbazepine (S-licarbazepine), the major active metabolite of oxcarbazepine. It stabilizes neuronal membranes by blocking sodium channels; this may inhibit repetitive firing and may decrease the propagation of synaptic impulses; may also increase potassium conductance and modulate the activity of high-voltage activated calcium channels. It is indicated as adjunctive therapy or monotherapy for partial-onset seizures in adults or children aged 4 years or older.

Levetiracetam (Keppra, Spritam)

The mechanism of action of levetiracetam is unknown. This agent is approved for treatment in partial epilepsy. It is available as 250-, 500-, 750-, and 1000-mg tablets and 100-mg/mL solution.

Brivaracetam (Briviact)

Precise mechanism of action is unknown. Brivaracetam displays a high and selective affinity for synaptic vesicle protein 2A (SV2A) in the brain, which may contribute to the anticonvulsant effect. It is indicated for the treatment of partial-onset seizures in children and adolescents (≤4 years).

Zonisamide (Zonegran)

Zonisamide is indicated for adjunctive treatment of partial seizures with or without secondary generalization. It is available as 25-, 50-, and 100-mg sprinkle capsules. Evidence suggests that it is also effective in myoclonic and other generalized seizure types.

Pregabalin (Lyrica)

A structural derivative of GABA, pregabalin has an unknown mechanism of action. It binds with high affinity to alpha2-delta site (a calcium channel subunit). In vitro, pregabalin reduces calcium-dependent release of several neurotransmitters, possibly by modulating calcium channel function. It is FDA approved for neuropathic pain associated with diabetic peripheral neuropathy or postherpetic neuralgia and as adjunctive therapy in partial-onset seizures. It is available as 25-, 50-, 75-, 100-, 150-, 200-, 225-, and 300-mg capsules.

Lacosamide (Vimpat)

Lacosamide selectively enhances slow inactivation of voltage-gated sodium channels, resulting in stabilization of hyperexcitable neuronal membranes and inhibition of repetitive neuronal firing. It is indicated for adjunctive therapy of partial-onset seizures in children and adults ≥4 years.

Ethotoin (Peganone)

Ethotoin may act in the motor cortex, where it may inhibit the spread of seizure activity. The activity of brain stem centers responsible for the tonic phase of grand mal seizures may also be inhibited. It is indicated for the control of tonic-clonic (grand mal) and complex partial (psychomotor) seizures.

Perampanel (Fycompa)

Perampanel is a noncompetitive antagonist of the alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) glutamate receptor. It is indicated as adjunct treatment for partial-onset seizures with or without secondary generalized seizures in adults and children aged 12 years or older.