eMedicine Specialties > Neurology > Seizures and Epilepsy

Simple Partial Seizures

Author: Jane G Boggs, MD, Associate Professor of Neurology, Wake Forest University; Clinical Associate Professor, Virginia Commonwealth University School of Medicine (Medical College of Virginia)
Contributor Information and Disclosures

Updated: Sep 3, 2009

Introduction

Background

All partial seizures are characterized by onset in a limited area, or focus, of one cerebral hemisphere. The International Classification of Epileptic Seizures (ICES) classifies simple partial seizures (SPS) as those that are not associated with any impairment of consciousness.¹ 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.

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 syndromes as types of SPSE.

Pathophysiology

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 it may in fact be clinically silent. The clinical and EEG manifestations may be due to secondary activation of another cortical area.²

• 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.³
• Sensory or motor symptoms also can be caused 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.⁴

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.⁵ 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, and its 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.⁶

Frequency

United States

Among all seizures, partial seizures have the highest incidence after the first year of life. 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.⁷ The proportions of sensory, motor, special sensory, psychic, and autonomic SPS differ among various population studies, but most agree that SPS are found most frequently in association with other types of seizures.

International

Not enough studies are available to indicate the incidence of SPS 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.

Mortality/Morbidity

• 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 accidents and aspiration leading to pneumonia are less common with SPS, morbidity and mortality rates are expected to be lower than in seizures that affect consciousness.
• SPS are frequently the result of symptomatic lesions; 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.

Race

SPS have no reported predilection for any race or ethnic group.

Sex

Males and females are affected equally.

Age

• 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.

Clinical

History

The ICES lists 18 categories of SPS. All types of SPS can be seen with subsequent complex partial secondarily generalized seizures. The suspicion of SPS is based on the history of typical, reproducible patterns as outlined here.

• Motor simple partial seizures⁸
  • Clonic discharges in the sensorimotor cortex cause jerky, rhythmic movements that may remain restricted to one body segment or spread by "jacksonian march."
  • 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.
  • Another subtype, epilepsia partialis continua (ie, Kojewnikoff syndrome), includes stereotypical periodic to semiperiodic clonic activity that may persist for years and is often refractory to treatment.⁹
    • Clonic jerking usually involves the thumb or great toe, and may or may not spread to other body parts.
    • This activity 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-supplementary motor area (SMA) and premotor region discharges produce sustained contractions and unusual postures of a limb.¹⁰
    • 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 seizures³
  • Somatosensory-primary sensory cortex seizures usually elicit positive or negative sensations contralateral to the discharge.
  • Symptoms associated with seizures from the postcentral gyrus include tingling, numbness, pain, heat, cold, agnosia, phantom sensations, or 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.
    • Includes the déjà vu and jamais vu phenomena
    • Emotional: Fear is usual, but SPS can elicit happiness, sexual arousal, anger, and similar responses.
    • Cognitive: These responses include feelings of depersonalization, unreality, forced thinking, or feelings that may defy description.
• Autonomic simple partial seizures¹¹
  • Abdominal sensation phenomena
    • These 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).
  • Cardiovascular sensations¹²
    • The most common cardiac manifestation of any seizure is sinus tachycardia with arrhythmias, with bradycardia occurring infrequently.
    • 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.¹³
  • Pupillary symptoms - Miosis, mydriasis, hippus, and unilateral pupillary dilatation
  • Urogenital symptoms
    • 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.¹⁴
  • Other autonomic symptoms - Rarely 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

The physical examination may show subtle or obvious neurological focality.

• Immediately following a SPS, the focality may become more pronounced owing to postictal inhibition (eg, Todd paralysis).
• If an examination is performed during a 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.
  • Responsiveness may appear to be impaired because of interference by the motor manifestations of the SPS.
  • This is best established by asking the patient to perform simple, unilateral and bilateral neurological functions during the SPS.
  • If the patient is unable to perform a task because of the manifestations of the SPS, recollection of the instructions implies 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.

Causes

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

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