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Complex Partial Seizures

  • Author: Elizabeth Carroll, DO; Chief Editor: Selim R Benbadis, MD  more...
 
Updated: Feb 22, 2016
 

Practice Essentials

A complex partial seizure starts focally within the brain and causes impairment of consciousness. In most patients, complex partial seizures represent underlying temporal lobe epilepsy. See the image below.

Left temporal lobe seizure. Left temporal lobe seizure.

Essential update: FDA approves vigabatrin for adjunctive treatment of complex partial seizures in children

In October 2013, the FDA approved vigabatrin (Sabril) as add-on therapy for children aged 10 years and older with complex partial seizures that are refractory to several other treatments. Vigabatrin should be used in such cases only if the possible treatment benefit outweighs the risk for vision loss associated with the drug.

Vigabatrin is already approved as adjunctive therapy, but not first-line treatment, for adults with refractory complex partial seizures and for infants from 1 month to 2 years of age with infantile spasms for whom the possible benefit outweighs the potential risk for vision loss. Vigabatrin is available through a restricted program under a risk evaluation and mitigation strategy, the SHARE Program.[1]

Signs and symptoms

Complex partial 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 complex partial 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] :

  • Contralateral - Unilateral sensory aura (89%), hemifield visual/sensory aura (100%), motor version (100%), clonic activity (83%), tonic activity (100%); figure 4 sign (89%); unilateral dystonic posturing (100%); postictal palsy (93%)
  • Ipsilateral - Postictal nose wiping (92%)
  • Nondominant lobe - Ictal spitting (75%), ictal vomiting (81%), ictal speech (83%)
  • Dominant lobe - Ictal aphasia/dysphasia (100%)

See Clinical Presentation for more detail.

Diagnosis

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 complex partial 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

See Treatment and Medication for more detail.

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Background

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. A complex partial 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 complex partial 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.

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Pathophysiology

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, complex partial 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.

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Etiology

In the majority of cases, complex partial seizures are of unknown etiology (ie, cryptogenic). Potential causes include the following:

  • Hippocampal sclerosis (mesial temporal lobe)
  • Neoplasms
  • Cortical malformations
  • Vascular malformations
  • Central nervous system (CNS) infections
  • Immune-mediated CNS inflammation
  • Hypoxic-ischemic brain injury
  • Head trauma
  • Inheritable conditions

Febrile seizures, especially complex, are associated with an increased risk of later development of complex partial seizures and epilepsy.[20]

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Epidemiology

The prevalence of epilepsy is approximately 0.5-1 case per 100 persons.[21] Complex partial 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 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.

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Prognosis

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.

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Contributor Information and Disclosures
Author

Elizabeth Carroll, DO Resident Physician, Department of Neurology, University of South Florida College of Medicine

Elizabeth Carroll, DO is a member of the following medical societies: American Academy of Neurology, American Osteopathic Association, Florida Osteopathic Medical Association

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 College of Medicine

Selim R Benbadis, MD is a member of the following medical societies: American Academy of Neurology, American Medical Association, American Academy of Sleep Medicine, American Clinical Neurophysiology Society, American Epilepsy Society

Disclosure: Serve(d) as a director, officer, partner, employee, advisor, consultant or trustee for: Cyberonics; Eisai; Lundbeck; Sunovion; UCB; Upsher-Smith<br/>Serve(d) as a speaker or a member of a speakers bureau for: Cyberonics; Eisai; Glaxo Smith Kline; Lundbeck; Sunovion; UCB<br/>Received research grant from: Cyberonics; Lundbeck; Sepracor; Sunovion; UCB; Upsher-Smith.

Specialty Editor Board

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 College of Medicine

Selim R Benbadis, MD is a member of the following medical societies: American Academy of Neurology, American Medical Association, American Academy of Sleep Medicine, American Clinical Neurophysiology Society, American Epilepsy Society

Disclosure: Serve(d) as a director, officer, partner, employee, advisor, consultant or trustee for: Cyberonics; Eisai; Lundbeck; Sunovion; UCB; Upsher-Smith<br/>Serve(d) as a speaker or a member of a speakers bureau for: Cyberonics; Eisai; Glaxo Smith Kline; Lundbeck; Sunovion; UCB<br/>Received research grant from: Cyberonics; Lundbeck; Sepracor; Sunovion; UCB; Upsher-Smith.

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Note oral and hand automatisms at initiation of event. Patient is not following commands or answering questions during the event.
Left temporal sharp wave.
Left temporal lobe seizure.
 
 
 
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