eMedicine Specialties > Neurology > Seizures and Epilepsy

Complex Partial Seizures

Author: Anthony M Murro, MD, Laboratory Director, Professor, Department of Neurology, Medical College of Georgia
Contributor Information and Disclosures

Updated: Oct 11, 2006

Introduction

Background

Complex partial seizures cause impaired consciousness and arise from a single brain region. Impaired consciousness implies decreased responsiveness and awareness of self and surroundings. During a complex partial seizure, the patient may not communicate, respond to commands, or remember events that occurred. Consciousness might not be impaired completely. During a complex partial seizure, some patients may make simple verbal responses, follow simple commands, or continue to perform simple or, less commonly, complex motor behaviors such as operating a car. Complex partial seizures typically arise from the temporal lobe but may arise from any cortical region.

Automatisms are quasi-purposeful motor or verbal behaviors that commonly accompany complex partial seizures. The behavior is called quasi-purposeful because it is repeated inappropriately or is inappropriate for the situation. Verbal automatisms range from simple vocalizations, such as moaning, to more complex, comprehensible, stereotyped speech.

Automatisms also may occur during nonepileptic states of confusion (eg, metabolic encephalopathy), after ictus, and during absence seizures. Motor automatisms are classified as simple or complex. Simple motor automatisms include oral automatisms (eg, lip smacking, chewing, swallowing) and manual automatisms (eg, picking, fumbling, patting). Unilateral manual automatisms accompanied by contralateral arm dystonia usually indicates seizure onset from the cerebral hemisphere ipsilateral to the manual automatisms.

Complex motor automatisms are more elaborate, coordinated movements involving bilateral extremities. Examples of complex motor automatisms are cycling movements of the legs and stereotyped swimming movements. De novo automatisms often begin after seizure onset. In other cases, perseverative automatisms occur as repetitions of motor activity that began before the seizure. Bizarre automatisms such as alternating limb movements, right-to-left head rolling, or sexual automatisms may occur with frontal-lobe seizures.

Seizures often begin with a brief aura (simple partial seizure) lasting seconds and then becomes a complex partial seizure. The type of aura is related to the site of cortical onset. Temporal-lobe seizures often begin with a rising abdominal sensation, fear, unreality, or déjà vu. Parietal-lobe seizures may begin with an electrical sensation, tingling, or numbness. Occipital-lobe seizures may begin with visual changes, such as the perception of colored lines, spots, or shapes or even a loss of vision.

Complex partial seizures of the temporal lobe often begin with a motionless stare followed by simple oral or motor automatisms. In contrast, frontal-lobe seizures often begin with vigorous motor automatisms or stereotyped clonic or tonic activity. 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. Tonic and dystonic arm posturing may occur in the arm contralateral to the seizure focus. Sustained head or eye turning contralateral to the seizure focus may occur immediately before or simultaneously with clonic or tonic activity elsewhere.

Complex partial seizures often last 30 seconds to 2 minutes. Longer seizures may occur, particularly when the seizures become generalized convulsions. Complex partial status epilepticus may also occur with prolonged episodes of waxing and waning of consciousness.

Pathophysiology

Single photon emission CT (SPECT) ictal studies show hypoperfusion of bilateral frontal and parietal association cortex, and hyperfusion of the mediodorsal thalamus and rostral brainstem. Ictal effects on these structures by means of the spread of epileptic discharges or a transsynaptic mechanism may mediate impaired consciousness during complex partial seizures.

Frequency

United States

For people younger than 60 years, the incidence of partial seizures is 20 cases per 100,000 person-years. For people aged 60-80 years, incidence increases to 80 cases per 100,000 person-years. The prevalence of epilepsy is 0.5-1 case per 100 persons. Complex partial seizures occur in about 35% of persons with epilepsy.

International

Partial seizures are more common in countries where cysticercosis is prevalent.

Mortality/Morbidity

  • The mortality rate among individuals with epilepsy is 2-3 times that of the general population.
  • Most deaths are due to the underlying cause of epilepsy. Sudden unexpected death in epilepsy (SUDEP) occurs with no apparent cause. The incidence of SUDEP is 1 case per 370-1110 patient-years among people with epilepsy. SUDEP is most common among those with frequent, medically intractable seizures.
  • Individuals with epilepsy are at increased risk for trauma, burns, and aspiration.

Clinical

History

  • Confirm that the patient does not have a nonepileptic cause for episodes of loss of consciousness. Such causes may include psychogenic nonepileptic events, syncope, transient global amnesia, migraine, or certain parasomnias.
  • A history of typical seizure auras, blank staring with the eyes open, unresponsiveness, and automatisms suggest complex partial seizures.
  • Quantify the severity of epilepsy on the basis of previous complications and seizure frequency.
  • Include the patient's responses to previous anticonvulsants or surgery.
  • Include results of previous cranial MRIs, electroencephalograms (EEGs), and EEG-video recordings.
  • Screen the patient for possible etiologies, such as brain infection, trauma, hereditary epilepsy, stroke, perinatal brain injury, cerebral palsy, cortical dysplasia, neonatal convulsions, complex febrile seizure, or vascular malformation.
  • Obtain a history from patient and from witnesses of any lateralized seizure symptoms, such as versive head or eye turning, stereotyped posturing, or postictal focal symptoms.

Physical

Physical examination is directed to elucidate focal cortical neurologic findings, such as the following:

  • Aphasia
  • Unilateral neglect
  • Apraxia
  • Unilateral limb weakness
  • Unilateral facial weakness
  • Increased muscle tone
  • Increased deep tendon reflexes
  • Pronator drift
  • Extensor plantar reflex

Causes

  • Possible causes of complex partial seizures include the following:
    • Brain trauma
    • Encephalitis
    • Meningitis
    • Stroke
    • Perinatal brain injuries
    • Vascular malformations
    • Cortical dysplasia
    • Neoplasms
  • Febrile seizures that are unusually prolonged, frequent, or associated with focal neurologic features may increase risk for later development of complex partial seizures.
  • In most patients, complex partial seizures represent a symptom of underlying temporal-lobe epilepsy, the cause of which is unknown. Characteristic pathologic changes, called mesial temporal sclerosis, are most often visible on brain MRI.

More on Complex Partial Seizures

Overview: Complex Partial Seizures
Differential Diagnoses & Workup: Complex Partial Seizures
Treatment & Medication: Complex Partial Seizures
Follow-up: Complex Partial Seizures
Multimedia: Complex Partial Seizures
References

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Further Reading

Keywords

attacks, convulsions, fainting, spells, impaired consciousness, simple motor automatisms, manual automatisms, oral automatisms, perseverative automatisms, bizarre automatisms, temporal lobe complex partial seizures, parietal lobe seizures, frontal lobe seizures, extratemporal lobe seizures, occipital lobe seizures, complex partial status epilepticus, sudden unexpected death in epilepsy, SUDEP, brain trauma, encephalitis, meningitis, stroke, perinatal brain injuries, vascular malformations, cortical dysplasia, neoplasms, febrile seizures, temporal lobe epilepsy, mesial temporal sclerosis

Contributor Information and Disclosures

Author

Anthony M Murro, MD, Laboratory Director, Professor, Department of Neurology, Medical College of Georgia
Anthony M Murro, MD is a member of the following medical societies: American Academy of Neurology and American Epilepsy Society
Disclosure: Nothing to disclose.

Medical Editor

Joseph F Hulihan, MD, Vice President, Medical Affairs, Ortho-McNeil Janssen Scientific Affairs, LLC
Joseph F Hulihan, MD is a member of the following medical societies: American Academy of Neurology, American Clinical Neurophysiology Society, American Epilepsy Society, American Headache Society, and American Medical Association
Disclosure: Johnson & Johnson Salary Employment; Johnson & Johnson Stock Employment

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: Nothing to disclose.

Managing Editor

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
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: Nothing to disclose.

CME Editor

Matthew J Baker, MD, Consulting Staff, Collier Neurologic Specialists, Naples Community Hospital
Matthew J Baker, MD is a member of the following medical societies: American Academy of Neurology
Disclosure: Nothing to disclose.

Chief Editor

Nicholas Y Lorenzo, MD, Chief Editor, eMedicine Neurology; Consulting Staff, Neurology Specialists and Consultants
Nicholas Y Lorenzo, MD is a member of the following medical societies: Alpha Omega Alpha and American Academy of Neurology
Disclosure: Nothing to disclose.

 
 
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