A complex partial seizure, now known as a focal impaired awareness seizure according to the updated classification system from the International League Against Epilepsy (ILAE),[1] starts focally within the brain and causes impairment of consciousness. In most patients, focal impaired awareness seizures represent underlying temporal lobe epilepsy. See the image below.
View Image
Left temporal lobe seizure.
Signs and symptoms
Focal impaired awareness seizures typically last 30 seconds to 2 minutes. Longer seizures may occur when seizures become generalized with full-body convulsions or transform to a state of partial status epilepticus.
Aura
Typically of brief duration, rarely lasting longer than seconds
Eight different varieties are recognized: somatosensory, visual, auditory, gustatory, olfactory, autonomic, abdominal, and psychic
Auras precede temporal lobe seizures in approximately 80% of cases; the most common are abdominal (a rising epigastric sensation) and psychic (fear, déjà vu, jamais vu)
Parietal lobe seizures may begin with a contralateral sensation, usually of the positive type (electrical sensation, tingling)
Occipital lobe seizures may begin with contralateral visual changes, usually of the positive type (eg, colored lines, spots, or shapes) or a loss of vision
Temporal-parietal-occipital seizures may produce more formed auras
Impaired consciousness
Usually, during a focal impaired awareness seizure, the patient is unresponsive and does not remember events that occurred
Although patients typically do not respond to external stimuli, they may make simple verbal responses; follow simple commands; or continue to perform simple or, less commonly, complex motor behaviors (eg, operating a car)
Automatisms
Automatisms are nonpurposeful, stereotyped, and repetitive behaviors that commonly accompany complex partial seizures
The behavior is inappropriate for the situation
Patients are usually amnestic to their automatisms
Verbal automatisms range from simple vocalizations, such as moaning, to more complex, comprehensible, stereotyped speech
The most common automatisms, at least in temporal lobe epilepsy, are oral (eg, lip smacking, chewing, swallowing) and manual (eg, picking, fumbling, patting[2] )
Unilateral manual automatisms accompanied by contralateral arm dystonia usually indicates seizure onset from the cerebral hemisphere ipsilateral to the manual automatisms
Automatisms can also be more elaborate, coordinated movements involving bilateral extremities (eg, cycling movements of the legs, stereotyped swimming movements)
Bizarre automatisms (eg, alternating limb movements, right-to-left head rolling, sexual automatisms) may occur with frontal lobe seizures
Seizure features by site of origin
Temporal lobe seizures often begin with a motionless stare followed by oral or manual automatisms
Frontal lobe seizures often begin with vigorous motor automatisms or stereotyped clonic or tonic activity[3]
Extratemporal lobe seizures may spread quickly to the frontal lobe and produce motor behaviors similar to those associated with complex partial seizures of the frontal lobe
In temporal lobe seizures, lateralizing signs with corresponding sensitivities include the following[4, 5] :
Laboratory studies aim to rule out potential causes or, more often, triggers for seizures. Routine workup for all patients should include EEG and MRI of the brain; most of the time, the results will be normal. A patient with seizures that are difficult to control should be reassessed for a possible alternative diagnosis or temporal lobe epilepsy, using prolonged EEG-video monitoring to record patient events. Lumbar puncture may be indicated for a patient with new-onset seizure when an acute inflammatory or infectious process is being considered, but it is not indicated in patients with chronic epilepsy.
Laboratory studies
Electrolyte levels
Concentrations of antiepileptic drugs, if being used
Consider a urine drug screen
Brain MRI
Used to exclude an obvious structural lesion as the cause[6, 7]
Should include contrast with gadolinium to allow assessment of possible neoplastic and vascular etiologies
MRI with temporal cuts measures hippocampal volumes in assessment for temporal lobe epilepsy
Increased signal on fluid-attenuation inversion recovery (FLAIR) T2-weighted MRI can detect sclerosis of the mesial temporal lobe in 80-90% of cases
Electroencephalography
EEG within 24 hours is more sensitive for diagnosing epileptiform abnormalities than later EEG is (51% sensitivity vs 34%), but it is often impractical
Epileptiform discharges, when present, help localize the seizure focus
A negative interictal EEG does not exclude a diagnosis of epilepsy
If the waking EEG is negative, a sleep-deprived EEG may demonstrate epileptiform abnormalities
See Workup for more detail.
Management
Treatment of focal impaired awareness seizures may involve pharmacologic therapy and, in certain cases, epilepsy surgery.[8, 9, 10, 11, 12, 13, 14, 15, 16, 17] Special considerations apply to women with childbearing potential.
Anticonvulsant therapy
Treatment with antiepileptic medication should always be initiated once a diagnosis of epilepsy is made
All current antiepileptic drugs (AEDs), with the exception of ethosuximide, can be used in the treatment of complex partial seizures
The best-tolerated AED should be selected for the patient on the basis of side effects and drug interactions
Monotherapy is always initially preferred over polytherapy for treating seizures
High dosages of a single agent may be required to achieve seizure control before adding a second agent
Women of childbearing age should be educated regarding the drug interactions between AEDs and contraceptive therapy
Women who become pregnant and have a history of seizures should be continued on current AED therapy that controls seizures and should not be switched to a secondary agent simply because of pregnancy
Surgical treatment
Epilepsy surgery is indicated for patients who have frequent, disabling seizures despite adequate trials of 2 or more anticonvulsants
Video EEG should be used before surgical referral to qualify events, assess severity, and aid in localization
Surgical procedures include temporal lobectomy, extratemporal resections, corpus callosotomy, placement of a vagus nerve stimulator, hemispherectomy, and multiple subpial transection
Broadly, seizures may be classified as either generalized or focal. The term “complex partial seizure” was originally defined by the International League Against Epilepsy (ILAE) in 1981. In 2017, the ILAE updated its seizure classification system and complex partial seizures are now known as focal impaired awareness seizures.[1] A focal impaired awareness seizure starts focally within the brain and causes impairment of consciousness. This definition is based on both clinical and electroencephalographic (EEG) data.
On the other hand, seizures may also be described in accordance with a pure semiologic approach that uses patient symptoms alone. Thus, seizures are classified solely on the basis of their predominant symptom type (motor, sensory, etc). (See Clinical Presentation.) This approach relies on clinical data alone and underscores the importance of obtaining an accurate history.
A seizure, in and of itself, does not constitute a diagnosis of epilepsy. Recognizing a seizure is the first step in the workup for a diagnosis of possible epilepsy. A focal impaired awareness seizure is most commonly a manifestation of temporal lobe epilepsy, but the term is so broadly defined (ie, as any focal seizure with impairment of consciousness) that it is very nonspecific. For this reason, many clinicians make a point of distinguishing between temporal and extratemporal complex partial seizures.
For more information, see Epilepsy and Seizures and Simple Partial Seizures.
Single-photon emission computed tomography (SPECT) ictal studies show hypoperfusion of the bilateral frontal and parietal association cortex and hyperperfusion of the mediodorsal thalamus and rostral brainstem. Ictal effects on these structures resulting from the spread of epileptic discharges or a transsynaptic mechanism may mediate impaired consciousness during complex partial seizures.[18]
In most patients, focal impaired awareness seizures are representative of underlying temporal lobe epilepsy. Over time, patients with temporal lobe epilepsy have increased neuroexcitability within the mesial temporal lobes. Pathologic studies suggest focal changes that include neuronal loss,[19] reorganization, neurogenesis, and altered neurotransmitter receptors.
The prevalence of epilepsy is approximately 0.5–1 case per 100 persons.[21] Focal impaired awareness seizures occur in about 35% of persons with epilepsy. Partial seizures are more common in countries where cysticercosis is prevalent.
The incidence of partial seizures, now called focal aware seizures[1] , in people younger than 60 years is 20 cases per 100,000 person-years. This figure rises to 80 cases per 100,000 person-years in people aged 60–80 years.
The mortality rate in individuals with epilepsy is 2-3 times that in the general population.[22] Most deaths are due to the underlying cause (ie, epilepsy) with the remainder due to accidents, sudden unexpected death in epilepsy (SUDEP), and suicides. SUDEP has no apparent cause. It occurs in 1 in 2500 persons with mild epilepsy and 1 in 250 persons with severe epilepsy. SUDEP is most common among those with frequent or medically intractable seizures.[23]
Individuals with epilepsy are at increased risk for trauma, burns, and aspiration.
The predominant symptoms occurring during a seizure event determine the seizure type. These can be assessed from direct observation or from video recordings (see the video below), but this is relatively rare because most patients with epilepsy never have video recordings. Thus, in most situations, symptom assessment is based on history alone.
View Video
Note oral and hand automatisms at initiation of event. Patient is not following commands or answering questions during the event.
For this reason, a purely semiologic classification has been proposed and is in use at some centers.[24, 25, 26] In this system, seizure types include autonomic, dialeptic, simple motor (clonic, tonic, tonic-clonic, epileptic spasm, myoclonic, versive), complex motor (automotor, hypermotor, gelastic), and negative (aphasic, astatic, atonic, akinetic, hypomotor, negative myoclonic). Focal impaired awareness seizures, as defined by the International League Against Epilepsy (ILAE) classification can be equivalent to various categories of the semiologic classification.[1]
A thorough history should be obtained from the patient, the family members, and any relevant witnesses. It is the most important part of investigating a seizure event.
Question the patient regarding any family history of seizures, febrile seizures as an infant, or previous history of traumatic or other brain insults, which may place the patient at a higher risk for seizures. If the patient has a history of seizures, include his or her responses to previous anticonvulsants or surgery and the results of previous cranial magnetic resonance imaging (MRI), electroencephalography (EEG), and video-EEG recordings.
Focal impaired awareness seizures typically last 30 seconds to 2 minutes. Longer seizures may occur when seizures become generalized with full body convulsions or transform to a state of partial status epilepticus.
In particular, ask detailed questions designed to elicit and assess seizure-type behaviors, such as aura, impairment of consciousness, automatisms, focal symptoms (eg, weakness, sensory changes), and postictal behaviors.
Aura
An aura is a subjective sensation and is a simple partial seizure (ie, the initial part during which the patient is aware). Typically, it is of brief duration, rarely lasting longer than seconds. Determining the type of aura present is critical for identifying the site of cortical onset. Eight different varieties are recognized: somatosensory, visual, auditory, gustatory, olfactory, autonomic, abdominal, and psychic.
Auras precede temporal lobe seizures in approximately 80% of cases. The most common auras in temporal lobe seizures are abdominal (a rising epigastric sensation) and psychic aura (fear, déjà vu, jamais vu).
Parietal lobe seizures may begin with a contralateral sensation, usually of the positive type (electrical sensation, tingling). Occipital lobe seizures may begin with contralateral visual changes, usually of the positive type, such as colored lines, spots, or shapes, or even a loss of vision. Temporal-parietal-occipital seizures may produce more formed auras.
Impaired consciousness
Focal impaired awareness seizures, in the ILAE classification, are defined by impairment of consciousness.[1] This implies decreased responsiveness and awareness of one’s self and surroundings. Usually, during a focal impaired awareness seizure, a patient is unresponsive and does not remember events that occurred.
Consciousness may not be impaired completely, however. Although patients typically do not respond to external stimuli, they may make simple verbal responses, follow simple commands, or continue to perform simple or, less commonly, complex motor behaviors (eg, operating a car). Impairments in consciousness should be contrasted with psychic automatisms, in which the patient experiences intense feelings of strangeness.
Focal impaired awareness seizures are roughly equivalent to what used to be known as psychomotor seizures. In the semiologic classification, they are equivalent to automotor seizures (automatisms), whereas seizures with alteration of consciousness without motor phenomena are known as dialeptic seizures.
Automatisms
Automatisms are nonpurposeful, stereotyped, and repetitive behaviors that commonly accompany focal impaired awareness seizures (in the semiologic classification, they define automotor seizures). The behavior is inappropriate for the situation. Patients are usually amnestic to their automatisms. Verbal automatisms range from simple vocalizations, such as moaning, to more complex, comprehensible, stereotyped speech.
The most common automatisms, at least in temporal lobe epilepsy, are oral (eg, lip smacking, chewing, swallowing) and manual (eg, picking, fumbling, patting[2] ). Unilateral manual automatisms accompanied by contralateral arm dystonia usually indicates seizure onset from the cerebral hemisphere ipsilateral to the manual automatisms.
Automatisms can also be more elaborate, coordinated movements involving bilateral extremities. Examples of complex motor automatisms are cycling movements of the legs and stereotyped swimming movements. Bizarre automatisms, such as alternating limb movements, right-to-left head rolling, or sexual automatisms, may occur with frontal lobe seizures.
Automatisms may also occur during nonepileptic states of confusion (eg, metabolic encephalopathy), after ictus, and during absence seizures, especially when prolonged.
Temporal versus extratemporal seizures
Focal impaired awareness seizures can arise from any location but most commonly arise from the temporal lobe (60%). Temporal lobe seizures have highly specific behaviors as compared with extratemporal seizures.
Focal impaired awareness seizures of temporal lobe origin often begin with a motionless stare followed by oral or manual automatisms. Frontal lobe seizures often begin with vigorous motor automatisms or stereotyped clonic or tonic activity.[3] Extratemporal lobe seizures may spread quickly to the frontal lobe and produce motor behaviors similar to those associated with focal impaired awareness seizures of the frontal lobe.
Temporal lobe type seizures (temporal lobe epilepsy) require a treatment approach emphasizing early surgical referral. Careful notation of seizure aura, seizure semiology, and postictal phenomena can give highly sensitive localizable signs and further provide high preoperative value in these cases.
Lateralizing signs with corresponding sensitivities include the following[4, 5] :
The physical examination is directed so as to elucidate focal cortical neurologic findings, such as aphasia, unilateral neglect, apraxia, or unilateral signs. In the vast majority of patients with focal epilepsies and focal impaired awareness seizures, the neurologic examination yields normal results.
Laboratory studies aim to rule out potential causes or triggers for seizures. These causes generally do not cause chronic epilepsy but may be triggers in patients with epilepsy. Routine workup for all patients should include electroencephalography (EEG) and magnetic resonance imaging (MRI) of the brain; most of the time, the results will be normal.
Workup after drug failure
A patient with seizures that are difficult to control should be reassessed for a possible alternative diagnoses or temporal lobe epilepsy. This is done with prolonged EEG-video monitoring to record patient events.
About 30% of patients thought to have focal impaired awareness seizures actually have psychogenic nonepileptic seizures. These events can be recorded and reviewed during monitoring. Recorded and confirmed cases of temporal lobe epilepsy via monitoring should be considered for possible surgery and undergo the remainder of the evaluation for surgery (eg, single-photon emission computed tomography [SPECT], positron emission tomography [PET]).
Electrolyte levels, including sodium, potassium, magnesium, and calcium concentrations, should be assessed. If antiepileptic drugs are being used, drug concentrations should be obtained. Consider a urine drug screen.
The purpose of the initial brain MRI is to exclude an obvious structural lesion as the cause.[6, 7] The procedure should include contrast with gadolinium to allow assessment of possible neoplastic and vascular etiologies. More subtle etiologies, such as mesial temporal sclerosis (MTS) and cortical dysplasia, only become important if the seizures prove intractable and surgery is considered.
MRI with temporal cuts gives attention to hippocampal volumes in assessment for temporal lobe epilepsy. Hippocampal atrophy predominates as seizures are maintained throughout the life of a patient with temporal lobe epilepsy. Increased signal on fluid-attenuation inversion recovery (FLAIR) T2-weighted MRI can detect sclerosis of the mesial temporal lobe in 80-90% of cases. Subtle cortical changes due to cortical dysplasia are often overlooked.
EEG within 24 hours is more sensitive for diagnosing epileptiform abnormalities than later EEG is (51% sensitivity vs 34%), but it is often impractical. When epileptiform discharges are present, they help localize the seizure focus (see the images below).
View Image
Left temporal sharp wave.
View Image
Left temporal lobe seizure.
A negative interictal EEG does not exclude a diagnosis of epilepsy. If the waking EEG is negative, a sleep-deprived EEG may demonstrate epileptiform abnormalities.
For more information, see EEG in Common Epilepsy Syndromes, EEG in Status Epilepticus, Epileptiform Normal Variants on EEG, Generalized Epilepsies on EEG, and Localization-Related Epilepsies on EEG.
Lumbar puncture may be indicated for a patient with new-onset seizure when an acute inflammatory or infectious process is being considered. However, it is not indicated in patients with chronic epilepsy.
Treatment of focal impaired awareness seizures may involve pharmacologic therapy and, in certain cases, epilepsy surgery.[8, 9, 10, 11, 12, 13, 14, 15, 16, 17] Special considerations apply to women with childbearing potential.
There is no clear answer to the question of whether or not to treat after a single seizure. The risk of recurrent seizures is unchanged whether antiepileptic drugs are initiated after the first seizure or after the second. Attention to electroencephalographic (EEG) abnormalities, in addition to discussion with the patient and family, should be part of the decision-making process. In contrast, treatment with antiepileptic medication should always be initiated once a diagnosis of epilepsy is made.
All current antiepileptic drugs (AEDs), with the exception of ethosuximide, can be used in the treatment of complex partial seizures. The choice of an AED should be guided by certain general principles. The best-tolerated AED should be selected for the patient on the basis of side effects and drug interactions. Monotherapy is always initially preferred over polytherapy for treating seizures. High dosages of a single agent may be required to achieve seizure control before adding a second agent.
Treatment side effects
Side effects are common with all antiepileptic drugs.[27] All AEDs are central nervous system (CNS) depressants and therefore may cause sedation, dizziness, and changes in cognition. This side effect is more common in older AEDs. Certain medications may offer favorable side effects (eg, topiramate and weight loss), whereas other medications may be chosen solely on the basis of their route of excretion (eg, levetiracetam and renal excretion). Some side effects may treat comorbidities (eg, gabapentin and certain pain syndromes).
Certain AEDs have specific toxicities (eg, hepatic failure or bone marrow suppression) that necessitate periodic blood monitoring. Patients should also be educated about how to recognize the signs of a severe adverse drug reaction.
AED therapy can be continued in the face of mild elevations of transaminase levels and mild depressions of blood cell counts because these findings do not indicate pending hepatic failure or aplastic anemia.
Considerations in women
Women of childbearing age should be educated regarding the drug interactions between AEDs and contraceptive therapy. Women who become pregnant and have a history of seizures should be continued on current antiepileptic drug therapy that controls seizures and not switched to a secondary agent simply because of pregnancy.
Teratogenicity is possible with all AEDs. Most have the potential to cause minor anomalies (eg, fetal anticonvulsant syndrome). Major anomalies (eg, cardiac defects, cleft lip and palate, microcephaly, developmental delay, and neural tube defects) are more common with valproate therapy, especially at high dosages. AEDs impair folic acid metabolism, increasing the risk of NTDs, requiring initiation of folic acid supplementation for all women of childbearing age at a minimum dose of 0.4 mg/day; however, higher doses between 2-5 mg/day are encouraged.
Clinicians should document in writing that they have advised every woman of childbearing potential of the risks and benefits of anticonvulsant therapy, including the increased risk of congenital malformations.[28, 29, 30, 31] Patients should be initiated on folic acid supplementation. Clinicians should also document they have advised women of childbearing age on the risk of oral contraceptive failure that may occur with hepatic enzyme–inducing anticonvulsants.
For more information, see Women's Health and Epilepsy.
Bone health
Long-term anticonvulsant therapy with hepatic enzyme-inducing anticonvulsants also increases the risk for osteoporosis. Patients should undergo bone-density measurements every 2 years.
Monitoring
Anticonvulsant drug-level monitoring may be needed.[32] Consider drug-level monitoring when noncompliance is suspected, in patients at high risk for life-threatening adverse drug reactions, or in patients with mental impairments that limit their ability to communicate.
Anticonvulsant withdrawal
No strict criteria exist as to when anticonvulsant withdrawal is appropriate.[33] Patients who have been seizure free for at least 6 months may undergo consideration in discussion with their physician.
Epilepsy surgery is indicated for patients who have frequent, disabling seizures despite adequate trials of 2 or more anticonvulsants. Video EEG should be used before surgical referral to qualify events, assess severity, and aid in localization. Surgical procedures include temporal lobectomy, extratemporal resections, corpus callosotomy, placement of a vagus nerve stimulator, hemispherectomy, and multiple subpial transection.
All persons with uncontrolled seizures must be advised to refrain from high-risk activities that put themselves or others in danger in the event of a seizure. These activities include, but are not limited to, the following:
Operating a motor vehicle
Operating a stove or other dangerous machinery
Working at heights
Swimming in open/large bodies of water alone
Clinicians should document in writing that they have advised the patient not to operate a motor vehicle or dangerous machinery or to perform activities that would put the patient or others at risk of injury from a seizure. Persons with uncontrolled epilepsy should be advised to contact the appropriate state agency regarding driving regulations. Some states require physician reporting of drivers who experience seizures.
These activity restrictions should be reviewed in detail (and documented in the medical record) with the patient, family, and/or caregivers.
Refer the patient to an epilepsy specialist if the patient has seizures despite previous trials with 2 or 3 anticonvulsants. Consultation with such a specialist is indicated if the patient is a possible candidate for epilepsy surgery.
Numerous different anticonvulsants may be used in the treatment of focal impaired awareness seizures. These agents tend to share certain properties but may have differing (or, in some cases, unknown) mechanisms of action.
Clinical Context:
Carbamazepine is effective for treatment of complex partial seizures. It appears to act by reducing polysynaptic responses and blocking posttetanic potentiation. Its major mechanism of action is reducing sustained, high-frequency, repetitive neural firing.
Clinical Context:
The primary site of action of hydantoins appears to be the motor cortex, where they may inhibit spread of seizure activity. Phenytoin may reduce maximal activity of the brainstem centers responsible for the tonic phase of grand mal seizures. Individualize the dose. If the daily dose cannot be divided equally, a large dose should be taken at bedtime. A phosphorylated formulation (fosphenytoin) is available for parenteral use and may be given intramuscularly (IM) or intravenously (IV).
Clinical Context:
Valproic acid is chemically unrelated to other drugs used to treat seizure disorders. Its mechanism of action is not established, but its activity may be related to increased brain levels of gamma-aminobutyric acid (GABA) or enhanced GABA action. It may also potentiate postsynaptic GABA responses, affect potassium channels, or have a direct membrane-stabilizing effect.
For conversion to monotherapy, concomitant AED dosage is ordinarily reduced by approximately 25% every 2 weeks. Reduction may be started at the beginning of therapy or may be delayed 1-2 weeks if seizures are likely to occur with reduction. Monitor patients closely during this period for increased seizure frequency.
As adjunctive therapy, divalproex sodium 10-15 mg/kg/d may be added to the regimen; the dosage may be increased 5-10 mg/kg/d every week to the optimal clinical response (usually with < 60 mg/kg/d).
Clinical Context:
Gabapentin has properties in common with other anticonvulsants, but its exact mechanism of action is unknown. It is structurally related to GABA but does not interact with GABA receptors.
Clinical Context:
Lamotrigine is a triazine derivative that is useful in treatment of seizures and neuralgic pain. It inhibits release of glutamate and inhibits voltage-sensitive sodium channels, which stabilizes the neuronal membrane. Follow the manufacturer's recommendations for dose adjustments.
Clinical Context:
Topiramate is a sulfamate-substituted monosaccharide with a broad spectrum of antiepileptic activity; it may have state-dependent sodium channel blocking action; it potentiates the inhibitory activity of GABA. It may block glutamate activity. Monitoring of plasma concentrations is not necessary to optimize therapy. If topiramate is added to phenytoin, the phenytoin dose may have to be adjusted to achieve optimal clinical outcome.
Clinical Context:
Tiagabine's mechanism of action in the antiseizure effect is unknown but is thought to be related to its ability to enhance activity of GABA, the major inhibitory neurotransmitter in the central nervous system (CNS). It may block GABA uptake into presynaptic neurons, increasing GABA for receptor binding on surfaces of postsynaptic cells and possibly preventing propagation of neural impulses that contribute to seizures by GABAergic action. Modification of concomitant AED doses is not necessary unless clinically indicated.
Clinical Context:
Felbamate is an oral AED that has weak inhibitory effects on GABA receptor binding and benzodiazepine receptor binding but interacts as antagonist at strychnine-insensitive glycine recognition site of N-methyl-D-aspartate (NMDA) receptor-ionophore complex. It is not indicated as first-line antiepileptic treatment. It is recommended only in those patients whose epilepsy is so severe that the benefits outweigh the risks of aplastic anemia or liver failure.
Clinical Context:
Phenobarbital has anticonvulsant activity at anesthetic doses and can be administered orally. If the IM route is chosen, the drug should be injected into a large muscle (eg, gluteus maximus or vastus lateralis) or other areas with little risk of encountering a nerve trunk or major artery. Injection into or near peripheral nerves may result in permanent neurologic deficit.
Restrict IV use to conditions in which other routes are not feasible because the patient is unconscious (eg, cerebral hemorrhage, eclampsia, status epilepticus) or in which prompt action is imperative.
Clinical Context:
Oxcarbazepine exerts its pharmacologic activity primarily via 10-monohydroxy derivative (MHD). It may block voltage-sensitive sodium channels, inhibit repetitive neuronal firing, and impair synaptic impulse propagation. The anticonvulsant effect may occur by affecting potassium conductance and high-voltage activated calcium channels. Pharmacokinetics are similar in children older than 8 years and in adults. Children younger than 8 years have 30-40% increased clearance. Use in children younger than 2 years has not been studied in controlled clinical trials.
Clinical Context:
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 action may inhibit repetitive firing and may decrease the propagation of synaptic impulses. It may also increase potassium conductance and modulate the activity of high-voltage activated calcium channels. It is indicated as adjunctive treatment or monotherapy for partial-onset seizures in adults.
Clinical Context:
Levetiracetam is used for adjunctive treatment of partial seizures. It binds to presynaptic vesicle protein (SV2A). It blocks high-voltage calcium currents and suppresses several negative modulators of GABA and glycine-gated currents.
Clinical Context:
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).
Clinical Context:
Pregabalin binds to the alpha2-delta subunit site of voltage-gated calcium channels in CNS tissues. It modulates calcium channel function and reduces release of multiple neurotransmitters.
Clinical Context:
Zonisamide may block sodium channels and reduce voltage-dependent, T-type Ca2+ currents and transient inward currents. It binds to the allosteric GABA/benzodiazepine receptor ionophore. It has weak carbonic anhydrase inhibiting activity.
Clinical Context:
Vigabatrin's precise mechanism is unknown. It is an irreversible inhibitor of GABA transaminase (GABA-T). GABA-T metabolizes GABA, an inhibitory neurotransmitter, thereby increasing CNS GABA levels. Use of vigabatrin must be weighed against the risk of permanent vision loss. Vigabatrin is available only from a restricted access program. It is indicated for adjunctive treatment of complex partial seizures in adults and children aged 10 y or older who have had inadequate response to first-line therapy.
Clinical Context:
Ethotoin shares the actions of the hydantoin-derivative anticonvulsants; however, the drug apparently does not have the antiarrhythmic properties demonstrated by phenytoin.
Clinical Context:
Lacosamide selectively enhances slow inactivation of voltage-gated sodium channels, resulting in stabilization of the hyperexcitable neuronal membranes and inhibition of repetitive neuronal firing. It is indicated for adjunctive therapy for partial-onset seizures.
Clinical Context:
Methsuximide shares the actions of the succinimide-derivative anticonvulsants. It is indicated for the control of absence (petit mal) seizures refractory to other medications.
Clinical Context:
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.
Clinical Context:
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.
All current antiepileptic drugs (AEDs), with the exception of ethosuximide, can be used in the treatment of complex partial seizures. The choice of an AED should be guided by certain general principles. The best-tolerated AED should be selected for the patient on the basis of side effects and drug interactions. Certain medications may offer favorable side effects (eg, topiramate and weight loss), whereas others may be chosen solely on the basis of route of excretion (eg, levetiracetam and renal excretion).
Monotherapy is always initially preferred over polytherapy for treating seizures. High dosages of a single agent may be required to achieve seizure control before adding a second agent.
What are complex partial seizures (focal impaired awareness seizures)?What are the signs and symptoms of complex partial seizures (focal impaired awareness seizures)?How are complex partial seizures (focal impaired awareness seizures) diagnosed?How are complex partial seizures (focal impaired awareness seizures) treated?What is included in anticonvulsant therapy for complex partial seizures (focal impaired awareness seizures) treated?Which surgical interventions are used in the treatment of complex partial seizures (focal impaired awareness seizures) treated?How are complex partial seizures (focal impaired awareness seizures) classified?What is the pathophysiology of complex partial seizures (focal impaired awareness seizures)?What causes complex partial seizures (focal impaired awareness seizures)?What is the prevalence of complex partial seizures (focal impaired awareness seizures)?Which age groups have the highest prevalence of complex partial seizures (focal impaired awareness seizures)?What is the prognosis of complex partial seizures (focal impaired awareness seizures)?Which clinical history findings are characteristic of complex partial seizures (focal impaired awareness seizures)?How is aura characterized in complex partial seizures (focal impaired awareness seizures)?How is impaired consciousness characterized in complex partial seizures (focal impaired awareness seizures)?How are automatisms characterized in complex partial seizures (focal impaired awareness seizures)?Which findings indicate complex partial seizures (focal impaired awareness seizures) arise from the temporal lobe?Which physical findings are characteristic of complex partial seizures (focal impaired awareness seizures)?Which psychiatric disorders are included in the differential diagnoses of complex partial seizures (focal impaired awareness seizures)?What are the differential diagnoses for Complex Partial Seizures?What is the role of lab testing in the workup of complex partial seizures (focal impaired awareness seizures)?What is the role of EEG-video monitoring in the workup of complex partial seizures (focal impaired awareness seizures)?Which lab tests are included in the workup of complex partial seizures (focal impaired awareness seizures)?What is the role of MRI in the workup of complex partial seizures (focal impaired awareness seizures)?What is the role of EEG in the workup of complex partial seizures (focal impaired awareness seizures)?What is the role of lumbar puncture in the workup of complex partial seizures (focal impaired awareness seizures)?What is the role of antiepileptic drugs (AEDs) in the treatment of complex partial seizures (focal impaired awareness seizures)?What are the possible adverse effects of antiepileptic drugs (AEDs) for the treatment of complex partial seizures (focal impaired awareness seizures)?How should women with complex partial seizures (focal impaired awareness seizures) be treated during pregnancy?How do antiepileptic drugs (AEDs) for the treatment of complex partial seizures (focal impaired awareness seizures) affect bone health?What is included in the monitoring of patients taking antiepileptic drugs (AEDs) for the treatment of complex partial seizures (focal impaired awareness seizures)?When should antiepileptic drug (AED) treatment of complex partial seizures (focal impaired awareness seizures) cease?When is surgery indicated in the treatment of complex partial seizures (focal impaired awareness seizures)?Which activity modifications are used in the treatment of complex partial seizures (focal impaired awareness seizures)?Which specialist consultations are beneficial to patients with complex partial seizures (focal impaired awareness seizures)?What is the role of medications in the treatment of complex partial seizures (focal impaired awareness seizures)?Which medications in the drug class Anticonvulsants are used in the treatment of Complex Partial Seizures?
Elizabeth Carroll, DO, Resident Physician, Department of Neurology, University of South Florida College of Medicine
Disclosure: Nothing to disclose.
Coauthor(s)
Selim R Benbadis, MD, Professor, Director of Comprehensive Epilepsy Program, Departments of Neurology and Neurosurgery, Tampa General Hospital, University of South Florida Morsani College of Medicine
Disclosure: Serve(d) as a director, officer, partner, employee, advisor, consultant or trustee for: Ceribell, Eisai, Greenwich, Growhealthy, LivaNova, Neuropace, SK biopharmaceuticals, Sunovion<br/>Serve(d) as a speaker or a member of a speakers bureau for: Eisai, Greenwich, LivaNova, Sunovion<br/>Received research grant from: Cavion, LivaNova, Greenwich, Sunovion, SK biopharmaceuticals, Takeda, UCB.
Specialty Editors
Francisco Talavera, PharmD, PhD, Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference
Disclosure: Received salary from Medscape for employment. for: Medscape.
Chief Editor
Selim R Benbadis, MD, Professor, Director of Comprehensive Epilepsy Program, Departments of Neurology and Neurosurgery, Tampa General Hospital, University of South Florida Morsani College of Medicine
Disclosure: Serve(d) as a director, officer, partner, employee, advisor, consultant or trustee for: Ceribell, Eisai, Greenwich, Growhealthy, LivaNova, Neuropace, SK biopharmaceuticals, Sunovion<br/>Serve(d) as a speaker or a member of a speakers bureau for: Eisai, Greenwich, LivaNova, Sunovion<br/>Received research grant from: Cavion, LivaNova, Greenwich, Sunovion, SK biopharmaceuticals, Takeda, UCB.
Annegers JF. The epidemiology of epilepsy. Wyllie E, ed. The Treatment of Epilepsy: Principles and Practice. Baltimore, Md: Williams & Wilkins; 1997. 165-2.
Jeffrey S. FDA Okays Vigabatrin as Add-on for Seizures in Children. Available at http://www.medscape.com/viewarticle/813666. Accessed: November 2, 2013.
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