eMedicine Specialties > Neurology > Seizures and Epilepsy

Complex Partial Seizures

Author: Elizabeth Carroll, DO, Resident Physician, Department of Neurology, University of South Florida College of Medicine
Coauthor(s): 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
Contributor Information and Disclosures

Updated: Dec 11, 2009

Introduction

Background

Broadly, seizures can be classified into generalized or focal. The term complex partial seizure was originally defined by the International League Alliance on 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 EEG data.

In contrast, seizures may be described by patient symptoms alone, using a pure semiological approach. In this scheme, seizures are classified solely into their predominant symptom type (motor, sensory, etc) (see Clinical section on seizure semiology below). This relies on clinical data alone and underscores the importance of obtaining an accurate history.

Seizures do not constitute a diagnosis of epilepsy. Recognizing a seizure is the first step in the workup for a diagnosis of possible epilepsy. Complex partial seizures most commonly are a manifestation of temporal lobe epilepsy, but the term is so broad (any focal seizure with impairment of consciousness) that it is very nonspecific. For this reason, many distinguish between temporal and extratemporal complex partial seizures.

Pathophysiology

Single photon emission CT (SPECT) ictal studies show hypoperfusion of bilateral frontal and parietal association cortex, and hyperperfusion 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.

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 inclusive of neuronal loss, reorganization, neurogenesis, and altered neurotransmitter receptors.

Frequency

United States

  • Incidence of partial seizures for people younger than 60 years is 20 cases per 100,000 person-years.
  • Incidence of partial seizures for people aged 60-80 years increases to 80 cases per 100,000 person-years.
  • 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 with the remainder due to accidents, sudden unexpected death (SUDEP), and suicides. SUDEP occurs with no apparent cause. The incidence of SUDEP is 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.

Individuals with epilepsy are at increased risk for trauma, burns, and aspiration.

Clinical

History

Taking the history: The key to diagnosis

History should be obtained from the patient, the family members, and any relevant witnesses. It is the most important part of investigating a patient’s event.

Question the patient regarding family history of seizures, febrile seizures as an infant, or prior history of traumatic or other brain insults, which may place the patient at a higher risk for seizures. If the patient has a history of seizures, include the patient's responses to previous anticonvulsants or surgery and results of previous cranial MRIs, EEGs, and EEG-video recordings.

Complex partial seizures typically last 30 seconds to 2 minutes. Longer seizures may occur when seizures become generalized with full body convulsions or transform to a state of partial status epilepticus.

Clinicians should ask detailed questions designed to extrapolate seizure-type behaviors: aura, impairment of consciousness, focal symptoms (eg, weakness, sensory changes), automatisms, and postictal behaviors.

  • Aura
    • An aura is a subjective sensation and is a simple partial seizure (ie, the initial part during which the patient is aware).
    • The type of aura is critical to identify the site of cortical onset and may be of 8 different varieties: somatosensory, visual, auditory, gustatory, olfactory, autonomic, abdominal, or psychic.
    • Typical duration is brief, rarely lasting longer than seconds.
    • Auras precede temporal lobe seizures in approximately 80% of cases.
    • The most common auras in temporal lobe seizures are abdominal (a rising epigastric sensation) and psychic aura (fear, déjà vu, jamais vu).
    • Parietal lobe seizures may begin with a contralateral sensation, usually of the positive type (electrical sensation, tingling).
    • Occipital lobe seizures may begin with contralateral visual changes, usually of the positive type, such as colored lines, spots, or shapes, or even a loss of vision. Temporal-parietal-occipital seizures may produce more formed auras.
  • Consciousness
    • Complex partial seizures, as per the ILAE, are defined by impairment in consciousness. This implies decreased responsiveness and awareness of one’s self and surroundings.
    • During a complex partial seizure, a patient is usually unresponsive and does not remember events that occurred.
    • Consciousness may not be impaired completely. Typically, patients do not respond to external stimuli but may make simple verbal responses, follow simple commands, or continue to perform simple or, less commonly, complex motor behaviors such as operating a car.
    • Impairments in consciousness should be contrasted with psychic automatisms in which the patient experiences intense feelings of strangeness.
    • Complex partial seizures are roughly equivalent to what used to be known as psychomotor seizures. In the semiologic classification, they are equivalent to automotor seizures (automatisms), whereas seizures with alteration of consciousness without motor phenomena are known as dialeptic seizures.
  • Seizure semiology: Predominant symptoms occurring during a seizure event determine seizure type. These can be assessed from direct observation or using video recordings, but this is relatively rare since most patients with epilepsy never have video recordings. Thus, in most situations, seizure semiology is based on history alone. For this reason, a purely semiologic classification has been proposed and is in use at some centers (see list below).1 Complex partial seizures of the ILAE classification can be equivalent to various categories of the semiologic classification.
    • Autonomic
    • Dialeptic
    • Simple Motor
      • Clonic
      • Tonic
      • Tonic-clonic
      • Epileptic spasm
      • Myoclonic
      • Versive
    • Complex Motor
      • Automotor
      • Hypermotor
      • Gelastic
    • Negative
      • Aphasic
      • Astatic
      • Atonic
      • Akinetic
      • Hypomotor
      • Negative myoclonic
  • Automatisms
    • Automatisms are nonpurposeful, stereotyped, and repetitive behaviors that commonly accompany complex partial seizures (they define automotor seizures in the semiologic classification). The behavior is inappropriate for the situation. Patients are usually amnestic to their automatisms. Verbal automatisms range from simple vocalizations, such as moaning, to more complex, comprehensible, stereotyped speech.
    • The most common automatisms, at least in temporal lobe epilepsy, are oral (eg, lip smacking, chewing, swallowing) and manual (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.
    • Automatisms can be more elaborate, coordinated movements involving bilateral extremities. Examples of complex motor automatisms are cycling movements of the legs and stereotyped swimming movements. Bizarre automatisms, such as alternating limb movements, right-to-left head rolling, or sexual automatisms, may occur with frontal lobe seizures.
    • Automatisms may also occur during nonepileptic states of confusion (eg, metabolic encephalopathy), after ictus, and during absence seizures, especially when prolonged.

Localization and the temporal lobe

Complex partial seizures can arise from any location but most commonly arise from the temporal lobe (60%). Temporal lobe seizures have highly specific behaviors as compared with extratemporal seizures.

Complex partial seizures of temporal lobe origin often begin with a motionless stare followed by oral or manual automatisms. 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.

Temporal lobe type seizures (temporal lobe epilepsy) require a treatment approach emphasizing early surgical referral. Careful notation of seizure aura, seizure semiology, and postictal phenomena can give highly sensitive localizable signs and further provide high presurgical value in these cases.

  • Lateralizing signs with corresponding sensitivities2
    • Contralateral
      • Unilateral sensory aura (89%)
      • Hemifield visual/sensory aura (100%)
      • Motor version (100%)
      • Clonic activity (83%)
      • Tonic activity (100%)
      • Figure 4 sign (89%)
      • Unilateral dystonic posturing (100%)
      • Postictal palsy (93%)
    • Ipsilateral
      • Postictal nose wiping (92%)
    • Nondominant lobe
      • Ictal spitting (75%)
      • Ictal vomiting (81%)
      • Ictal speech (83%)
    • Dominant lobe
      • Ictal aphasia/dysphasia (100%)

Physical

The vast majority of patients with focal epilepsies and complex partial seizures have normal neurologic examination.

Physical examination is directed to elucidate focal cortical neurologic findings, such as aphasia, unilateral neglect, apraxia, or unilateral signs.

Causes

The cause of complex partial seizures is most often unknown (cryptogenic). Causes include the following:

  • Hippocampal sclerosis (mesial temporal lobe)
  • Neoplasms
  • Cortical malformations
  • Vascular malformations
  • Stroke
  • 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.

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

References

  1. Luders H, Acharya J, Baugmgartner C, Benbadis S et al. Semiological seizure classification. Epilepsia. Sept 1998;39 (9):1006-13. [Medline].

  2. Loddenkemper T, Kotagal P. Lateralizing sings during seizures in focal epilepsy. Epilepsy and Behavior. 2005;7:1-17. [Medline].

  3. American Academy of Neurology. Practice parameter: a guideline for discontinuing antiepileptic drugs in seizure-free patients--summary statement. Report of the Quality Standards Subcommittee of the American Academy of Neurology. Neurology. Aug 1996;47(2):600-2. [Medline].

  4. Annegers JF. The epidemiology of epilepsy. In: Wyllie E, ed. The Treatment of Epilepsy: Principles and Practice. Baltimore, Md: Williams & Wilkins; 1997:165-2.

  5. Artama M, Auvinen A, Raudaskoski T, et al. Antiepileptic drug use of women with epilepsy and congenital malformations in offspring. Neurology. 2005;64(11):1874-8. [Medline].

  6. Arunkumar G, Morris H. Epilepsy update: new medical and surgical treatment options. Cleve Clin J Med. 1998;65(10):527-32, 534-7. [Medline].

  7. Benbadis SR. Epileptic Seizures and Syndromes. Neurologic Clinics. May 2001;19 (2):[Medline].

  8. Benbadis SR, Tatum WO. Advances in the Treatment of Epilepsy. American Family Physician. July 2001;64 (1):91-98. [Medline].

  9. Browne TR. Pharmacokinetics of antiepileptic drugs. Neurology. 1998;51(5 suppl 4):S2-7. [Medline].

  10. Cascino GD. Temporal Lobe Epilepsy is a progressive Neurologic Disorder: time means Neurons!. Neurology. 2009;72:1718-1719. [Medline].

  11. Chang BS, Lowenstein DH. Epilepsy. N Engl J Med. Sep 25 2003;349(13):1257-66. [Medline].

  12. Cockerell OC. The mortality of epilepsy. Curr Opin Neurol. 1996;9(2):93-6. [Medline].

  13. Consensus Committee. Consensus statements: medical management of epilepsy. Neurology. 1998;51(5 suppl 4):S39-43. [Medline].

  14. Feely M. Fortnightly review: drug treatment of epilepsy. BMJ. 1999;318(7176):106-9. [Medline].

  15. French J, Smith M, Faught E, Brown L. Practice advisory: The use of felbamate in the treatment of patients with intractable epilepsy: report of the Quality Standards Subcommittee of the American Academy of Neurology and the American Epilepsy Society. Neurology. May 12 1999;52(8):1540-5. [Medline].

  16. French JA, Pedley TA. Clinical practice. Initial management of epilepsy. N Engl J Med. Jul 10 2008;359(2):166-76. [Medline].

  17. Harden CL, Pennell PB, Hauser WA. Practice Parameter Update: Management Issues for women with epilepsy – focus on pregnancy (an evidence-based review): Vitamin K, folic acid, blood levels, and breastfeeding. Neurology. July 2009;73 (2):142-149. [Medline].

  18. Horvath R, Kalmar Z, Feher N, Fogarasi A, Gyimesi C, Janszky J. Brain lateralization and seizure semiology: ictal clinical lateralizing signs. Ideggyogy Sz. Jully 2008;61 (7-8):231-237. [Medline].

  19. Janszky J, Foqarasi A, Mafalova V. Unilateral hand automatisms in temporal lobe epilepsy. Seizure. 2006;15(6):393-396. [Medline].

  20. King MA, Newton MR, Jackson GD, et al. Epileptology of the first-seizure presentation: a clinical, electroencephalographic, and magnetic resonance imaging study of 300 consecutive patients. Lancet. 1998;352(9133):1007-11. [Medline].

  21. Knake S, Triantafyllou C, Wald LL, et al. 3T phased array MRI improves the presurgical evaluation in focal epilepsies: a prospective study. Neurology. 2005;65(7):1026-1031. [Medline].

  22. Koepp MJ, Woermann FG. Imaging structure and function in refractory focal epilepsy. Lancet Neurol. 2005;4(1):42-53. [Medline].

  23. Kotagal P, Arunkumar G, Hammel J, Mascha E. Complex partial seizures of frontal lobe onset statistical analysis of ictal semiology. Seizure. 2003;12(5):268-81. [Medline].

  24. Lee KH, Meador KJ, Park YD, et al. Pathophysiology of altered consciousness during seizures: subtraction SPECT study. Neurology. 2002;59(6):841-6. [Medline].

  25. Leestma JE, Walczak T, Hughes JR, et al. A prospective study on sudden unexpected death in epilepsy. Ann Neurol. 1989;26(2):195-203. [Medline].

  26. Levy RH, Mattson RH, Meldrum BS. Antiepileptic Drugs. 4th ed. New York, NY: Raven; 1995.

  27. Mattson RH. Medical management of epilepsy in adults. Neurology. 1998;51(5 suppl 4):S15-20. [Medline].

  28. Meador KJ, Baker GA, Finnell RH, et al. In utero antiepileptic drug exposure: fetal death and malformations. Neurology. Aug 8 2006;67(3):407-12. [Medline].

  29. Morrell MJ. Guidelines for the care of women with epilepsy. Neurology. 1998;51(5 suppl 4):S21-7. [Medline].

  30. Noachtar S, Peters AS. Semiology of epileptic seizures: a critical review. Epilepsy Behavior. Mary 2009;15(1):2-9. [Medline].

  31. Pazzaglia P, D'Alessandro R, Lozito A, Lugaresi E. Classification of partial epilepsies according to the symptomatology of seizures: practical value and prognostic implications. Epilepsia. Jun 1982;23(3):343-50. [Medline].

  32. Pellock JM. Treatment of seizures and epilepsy in children and adolescents. Neurology. 1998;51(5 Suppl 4):S8-14. [Medline].

  33. Pellock JM, Willmore LJ. A rational guide to routine blood monitoring in patients receiving antiepileptic drugs [editorial]. Neurology. Jul 1991;41(7):961-4. [Medline].

  34. Rocca WA, Sharbrough FW, Hauser WA, et al. Risk factors for complex partial seizures: a population-based case-control study. Ann Neurol. Jan 1987;21(1):22-31. [Medline].

  35. Schlienger RG, Shear NH. Antiepileptic drug hypersensitivity syndrome. Epilepsia. 1998;39(suppl 7):S3-7. [Medline].

  36. Shorvon S. Handbook of Epilepsy. Second. Malden, Massachusetts: Blackwell Publishing Ltd; 2005.

  37. Wylie E, Ajay G. Treatment of epilepsy: Principles and Practice. Fourth. New York, New York: Lippincott, Williams and Wilkins; 2005.

Further Reading

Keywords

complex partial seizures, seizure treatment, epilepsy, seizure causes, attacks, complex partial status epilepticus, sudden unexpected death in epilepsy, SUDEP

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, 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.

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: eMedicine Salary Employment

 
 
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