Complex Partial Seizures 

  • Author: Elizabeth Carroll, DO; Chief Editor: Selim R Benbadis, MD   more...
 
Updated: Jun 16, 2011
 

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.[1]

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,[2] 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
  • Stroke
  • 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.[3]

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Epidemiology

The prevalence of epilepsy is approximately 0.5-1 case per 100 persons.[4] 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.[5] 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.[6]

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, and 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 Academy of Sleep Medicine, American Clinical Neurophysiology Society, American Epilepsy Society, and American Medical Association

Disclosure: UCB Pharma Honoraria Speaking, consulting; Lundbeck Honoraria Speaking, consulting; Cyberonics Honoraria Speaking, consulting; Glaxo Smith Kline Honoraria Speaking, consulting; Pfizer Honoraria Speaking, consulting; Sleepmed/DigiTrace Honoraria Speaking, consulting

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: Medscape Salary Employment

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 Academy of Sleep Medicine, American Clinical Neurophysiology Society, American Epilepsy Society, and American Medical Association

Disclosure: UCB Pharma Honoraria Speaking, consulting; Lundbeck Honoraria Speaking, consulting; Cyberonics Honoraria Speaking, consulting; Glaxo Smith Kline Honoraria Speaking, consulting; Pfizer Honoraria Speaking, consulting; Sleepmed/DigiTrace Honoraria Speaking, consulting

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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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