eMedicine Specialties > Neurology > Seizures and Epilepsy

Partial Epilepsies

Author: Selim R Benbadis, MD, Professor, Director of Comprehensive Epilepsy Program, Departments of Neurology and Neurosurgery, University of South Florida School of Medicine, Tampa General Hospital
Coauthor(s): Vikas K Agrawal, MD, Staff Physician, Department of Neurology, University of South Florida
Contributor Information and Disclosures

Updated: Jan 2, 2009

Introduction

Background

Partial epilepsies are epileptic disorders in which seizure semiology or findings at investigation disclose localized origin of seizures.

For more information on epilepsy, see Medscape's Epilepsy Resource Center.

Pathophysiology

Most partial epilepsies are the result of a localized brain abnormality, even though in most patients it cannot be seen with imaging techniques.

Only a few partial epilepsies are genetic; most are lesional. Unfortunately, in the current classification, they are referred to as idiopathic. The term idiopathic is often misunderstood in this setting. While generally idiopathic means "of unknown cause," idiopathic epilepsies are not truly of unknown cause. This terminology most likely will be corrected in the upcoming classification system of the International League Against Epilepsy (ILAE). Idiopathic epilepsies are determined genetically and have no apparent structural cause, with seizures as the only manifestation of the condition.

Frequency

United States

The prevalence of epilepsy is approximately 1% of the population. Most adult-onset epilepsies are partial epilepsies.

International

The international prevalence of epilepsy is similar to that in the United States.

Mortality/Morbidity

In the United States, the mortality rate from epilepsy was 0.8 deaths per 100,000 persons in 1979. The rate in 1986 was 0.7 deaths per 100,000 persons overall; it was 0.6 deaths per 100,000 persons for white males and females but 1.7 deaths per 100,000 persons for black males and 1 death per 100,000 persons for black females. No specific data are available for partial epilepsy.

Sex

Males and females are equally affected.

Age

The age-related incidence follows a U-shaped curve, with a peak in the first year of life and an increase during the sixth and seventh decades (see Media file 1).

Clinical

History

Obtain a description of the seizures from the patient and witnesses, as it is critical.

• Partial seizures are divided into simple, complex, and those that evolve into secondary generalized seizures.
• Simple and complex seizures are distinguished solely on the basis of the state of consciousness. Consciousness usually is assessed by the ability of the patient to respond to external stimuli (ie, responsiveness). This is intact in simple partial seizures (SPS) and impaired in complex partial seizures (CPS).
• SPSs are subdivided further into 4 categories according to the symptoms present (motor, sensory, autonomic, psychic).
  • Motor symptoms can vary and include motor signs with or without march, versive movements, posturing, and phonatory symptoms.
  • Sensory symptoms include all 5 senses and a vertiginous sensation. With the exception of vertigo, these usually are characterized by elementary hallucinations.
  • Autonomic symptoms include the common rising epigastric sensation (typically observed in mesial temporal lobe epilepsy) and less frequent symptoms (eg, vasomotor phenomena, mydriasis).
  • Psychic symptoms are characterized by various experiences involving memory (déjà-vu, jamais-vu), affect (fear, pleasure), or other complex psychic phenomena such as illusions.
• CPS includes some complex symptomatology and, by definition, an impairment of consciousness. Automatism is a better term for complex symptomatology. These consist of involuntary but coordinated motor activity, which tends to be purposeless and repetitive.
  • Common automatisms include lip smacking, chewing, fidgeting, and walking.
  • CPS can begin as SPS and seizures with impaired consciousness at onset.
  • CPSs are not subdivided according to coexisting symptoms, no matter how prominent.
• The third kind of partial seizure evolves into a generalized seizure.
  • This is divided further according to what precedes generalization (SPS only, CPS only, SPS evolving into CPS).
  • For clinical purposes, however, the partial phase of the seizure often is missed and many patients simply present with a convulsion (secondarily generalized tonic-clonic seizure).

Physical

In most focal epilepsies, examination is unrevealing. Direct neurologic examination should be done to elicit any cortical abnormality or dysfunction, which would depend on etiology and lesion site.

Causes

• Three genetic partial epilepsies are recognized.
  • Childhood epilepsy of occipital paroxysms
    • Age of onset is 15 months to 17 years.
    • One third of patients have a family history of epilepsy, especially rolandic epilepsy.
    • Symptoms include visual hallucination, blindness, hemianopia, visual illusions (eg, micropsia, macropsia, metamorphopsia), loss of consciousness, and unilateral clonic seizure, followed by migrainelike headache.
    • These attacks can occur while awake or while sleeping, more commonly during the transition period between wakefulness and sleep.
    • Sharp waves have a maximum occipital negativity, often occur in long bursts of spike-wave complexes, and are markedly activated by eye closure.
  • Benign childhood epilepsy with centrotemporal spikes
    • Age of onset is 2-12 years, with a strong peak at 8-9 years.
    • Characteristic ictal symptoms include guttural vocalizations, hypersalivation, drooling, sensations or movements of the mouth, dysphasia, and speech arrest.
    • Though these focal seizures are the most characteristic seizure types, they can be quite subtle and are missed easily; the most common mode of presentation is a nocturnal (secondary) generalized tonic-clonic seizure during sleep.
    • Neurologic examination is normal.
    • EEG findings are centrotemporal sharp waves with a characteristic morphology. They occur in repetitive bursts and are often bilateral. These sharp waves are activated markedly by nonrapid eye movement (non-REM) sleep. (For comparison, see the article Normal Sleep EEG.)
    • The natural history is benign. This syndrome has an excellent prognosis regardless of treatment, with spontaneous remission by 14-16 years. If treatment is required, options may include carbamazepine, gabapentin, or valproate. Antiepileptic drugs (AEDs) should always be weaned by 14-16 years.
  • Autosomal dominant nocturnal frontal lobe epilepsy (ADNFLE)
    • This is a recently described syndrome that appears to be a genetic localization-related epilepsy.
    • It is caused by an identified single gene mutation. Several mutations of the neuronal nicotinic acetylcholine receptor alpha4 subunit (CHRNA4) gene have been identified as the cause.
    • Onset is early in life.
    • Seizures are nocturnal and occur in clusters, mimicking parasomnias. They mostly are brief tonic seizures and rare tonic-clonic convulsions, often preceded by a nonspecific aura.
    • Interictal EEG may show epileptiform discharges with a frontal predominance, often observed only in sleep.
    • Despite its established genetic basis, the genetic findings are variable (locus heterogeneity); thus, definite diagnosis is difficult and largely one of exclusion.
    • Seizures often subside with age and may even disappear at adulthood. They usually are controlled with carbamazepine.
• Most partial epilepsies are caused by a localized brain abnormality, regardless of whether it is visible on imaging. This is the most common type of adult-onset epilepsy. These cases are characterized by seizures arising from a localized region of the brain. If the cause is found, they are said to be symptomatic. If imaging studies are normal, the cause remains elusive and they are said to be cryptogenic. The boundary between the two largely depends on diagnostic and imaging techniques, and etiologies such as low-grade tumors, hippocampal sclerosis, and subtle cortical dysplasias are identified more often because of advances in neuroimaging. Clinically, seizures may be simple partial or complex partial, with or without secondary generalization. Interictal EEG shows focal spikes or sharp waves, and ictal EEG shows a focal or regional discharge at onset. Because of dramatic differences in electroclinical semiology and management, localization-related epilepsies usually are divided into mesiotemporal and neocortical. The most common localization-related epilepsy in adults is mesiotemporal lobe epilepsy, but, in neonates and young children, this is less common than neocortical epilepsy.
  • Mesial temporal lobe epilepsy
    • The most common cause of temporal lobe epilepsy in candidates for epilepsy surgery in adults is hippocampal sclerosis, while in children, etiologies are dominated by cortical dysplasias and low-grade neoplasms.
    • Seizures typically are complex partial with automatisms, often preceded by a simple partial phase with sensory symptoms (ie, aura).
    • Auras commonly observed in temporal lobe epilepsy are epigastric (abdominal) and psychic auras, including déjà-vu or jamais-vu and fear.
    • CPSs of temporal lobe origin are semiologically automator with fine distal automatisms involving hands and/or fingers and orobuccal movements.
    • Interictal EEG typically shows temporal sharp waves maximal at anterior temporal or sphenoidal electrodes. Ictal EEG often shows well-defined rhythmic theta seizure patterns.
    • Diagnosis of mesial temporal lobe epilepsy often is confirmed by high-resolution MRI using dedicated epilepsy protocols. MRI is a strong predictor of a favorable surgical outcome, especially when concordant with ictal EEG, so much so that performing successful temporal lobectomies without ictal recordings may be possible. The availability and great sensitivity of MRI in this setting has greatly reduced the need for invasive EEG.
  • Neocortical seizures
    • Neocortical seizures may be simple partial or complex partial, with symptoms depending on the area of cortex affected.
    • Interictal EEG typically shows sharp waves or spikes outside of the anterior temporal region. Ictal EEG often shows regional or widespread discharges.
    • In general, localization of the epileptogenic zone by surface EEG (interictal and ictal) is less reliable for neocortical than for mesiotemporal epilepsy.
    • Epileptiform discharges can be absent on surface EEG when the focus is deep, as in supplementary sensorimotor area epilepsy.
    • Frontal discharges can spread rapidly and mimic primary generalized spike-wave complexes. This is referred to as secondary bilateral synchrony (with interictal epileptiform discharges that appear to be generalized but are in reality secondarily generalized focal discharges).
    • Strict criteria are required to attribute generalized discharges to secondary bilateral synchrony, focal or lateralized epileptiform discharges, or a structural lesion.
    • Neocortical extratemporal epilepsies may be difficult to localize precisely. Precise localization is important only when considering surgical treatment.
    • Certain syndromes are well characterized, including frontal, supplementary sensorimotor, parietal, and occipital lobe epilepsies.
    • Most adult-onset localization-related epilepsies do not have an identifiable etiology (ie, MRI is most often normal); this is well known. When a cause is found, it can include various structural lesions (eg, traumatic scars, neoplasms, vascular malformations, strokes, neuronal heterotopias).

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