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Simple Partial Seizures

  • Author: Jane G Boggs, MD; Chief Editor: Selim R Benbadis, MD  more...
Updated: Feb 22, 2016


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.

Contributor Information and Disclosures

Jane G Boggs, MD Associate Professor of Neurology, Wake Forest University School of Medicine; Clinical Associate Professor, Virginia Commonwealth University School of Medicine, Medical College of Virginia

Jane G Boggs, MD is a member of the following medical societies: American Academy of Neurology, American Clinical Neurophysiology Society, American Epilepsy Society

Disclosure: Nothing to disclose.

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 Morsani 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, American Medical Association

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 (Livanova); Eisai; Lundbeck; Sunovion; UCB<br/>Received research grant from: Cyberonics (Livanova); GW, Lundbeck; Sunovion; UCB; Upsher-Smith.

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