Background
Broadly, seizures may be classified as either generalized or focal. The term “complex partial seizure” was originally defined by the International League Against 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 electroencephalographic (EEG) data.
On the other hand, seizures may also be described in accordance with a pure semiologic approach that uses patient symptoms alone. Thus, seizures are classified solely on the basis of their predominant symptom type (motor, sensory, etc). (See Clinical Presentation.) This approach relies on clinical data alone and underscores the importance of obtaining an accurate history.
A seizure, in and of itself, does not constitute a diagnosis of epilepsy. Recognizing a seizure is the first step in the workup for a diagnosis of possible epilepsy. A complex partial seizure is most commonly a manifestation of temporal lobe epilepsy, but the term is so broadly defined (ie, as any focal seizure with impairment of consciousness) that it is very nonspecific. For this reason, many clinicians make a point of distinguishing between temporal and extratemporal complex partial seizures.
For more information, see Epilepsy and Seizures and Simple Partial Seizures.
Pathophysiology
Single-photon emission computed tomography (SPECT) ictal studies show hypoperfusion of the bilateral frontal and parietal association cortex and hyperperfusion of the mediodorsal thalamus and rostral brainstem. Ictal effects on these structures resulting from the spread of epileptic discharges or a transsynaptic mechanism may mediate impaired consciousness during complex partial seizures.[1]
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 that include neuronal loss,[2] reorganization, neurogenesis, and altered neurotransmitter receptors.
Etiology
In the majority of cases, complex partial seizures are of unknown etiology (ie, cryptogenic). Potential causes include the following:
- Hippocampal sclerosis (mesial temporal lobe)
- Neoplasms
- Cortical malformations
- Vascular malformations
- Central nervous system (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.[3]
Epidemiology
The prevalence of epilepsy is approximately 0.5-1 case per 100 persons.[4] Complex partial seizures occur in about 35% of persons with epilepsy. Partial seizures are more common in countries where cysticercosis is prevalent.
The incidence of partial seizures in people younger than 60 years is 20 cases per 100,000 person-years. This figure rises to 80 cases per 100,000 person-years in people aged 60-80 years.
Prognosis
The mortality rate in individuals with epilepsy is 2-3 times that in the general population.[5] Most deaths are due to the underlying cause (ie, epilepsy) with the remainder due to accidents, sudden unexpected death in epilepsy (SUDEP), and suicides. SUDEP has no apparent cause. It occurs in 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.[6]
Individuals with epilepsy are at increased risk for trauma, burns, and aspiration.
Lee KH, Meador KJ, Park YD, et al. Pathophysiology of altered consciousness during seizures: subtraction SPECT study. Neurology. 2002;59(6):841-6. [Medline].
Cascino GD. Temporal Lobe Epilepsy is a progressive Neurologic Disorder: time means Neurons!. Neurology. 2009;72:1718-1719. [Medline].
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].
Annegers JF. The epidemiology of epilepsy. In: Wyllie E, ed. The Treatment of Epilepsy: Principles and Practice. Baltimore, Md: Williams & Wilkins; 1997:165-2.
Cockerell OC. The mortality of epilepsy. Curr Opin Neurol. 1996;9(2):93-6. [Medline].
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].
Luders H, Acharya J, Baugmgartner C, Benbadis S et al. Semiological seizure classification. Epilepsia. Sept 1998;39 (9):1006-13. [Medline].
Noachtar S, Peters AS. Semiology of epileptic seizures: a critical review. Epilepsy Behavior. Mary 2009;15(1):2-9. [Medline].
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].
Janszky J, Foqarasi A, Mafalova V. Unilateral hand automatisms in temporal lobe epilepsy. Seizure. 2006;15(6):393-396. [Medline].
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].
Loddenkemper T, Kotagal P. Lateralizing sings during seizures in focal epilepsy. Epilepsy and Behavior. 2005;7:1-17. [Medline].
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].
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].
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].
Arunkumar G, Morris H. Epilepsy update: new medical and surgical treatment options. Cleve Clin J Med. 1998;65(10):527-32, 534-7. [Medline].
Browne TR. Pharmacokinetics of antiepileptic drugs. Neurology. 1998;51(5 suppl 4):S2-7. [Medline].
Consensus Committee. Consensus statements: medical management of epilepsy. Neurology. 1998;51(5 suppl 4):S39-43. [Medline].
Feely M. Fortnightly review: drug treatment of epilepsy. BMJ. 1999;318(7176):106-9. [Medline].
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].
French JA, Pedley TA. Clinical practice. Initial management of epilepsy. N Engl J Med. Jul 10 2008;359(2):166-76. [Medline].
Koepp MJ, Woermann FG. Imaging structure and function in refractory focal epilepsy. Lancet Neurol. 2005;4(1):42-53. [Medline].
Levy RH, Mattson RH, Meldrum BS. Antiepileptic Drugs. 4th ed. New York, NY: Raven; 1995.
Mattson RH. Medical management of epilepsy in adults. Neurology. 1998;51(5 suppl 4):S15-20. [Medline].
Pellock JM. Treatment of seizures and epilepsy in children and adolescents. Neurology. 1998;51(5 Suppl 4):S8-14. [Medline].
Schlienger RG, Shear NH. Antiepileptic drug hypersensitivity syndrome. Epilepsia. 1998;39(suppl 7):S3-7. [Medline].
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].
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].
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].
Morrell MJ. Guidelines for the care of women with epilepsy. Neurology. 1998;51(5 suppl 4):S21-7. [Medline].
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].
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].
Benbadis SR. Epileptic Seizures and Syndromes. Neurologic Clinics. May 2001;19 (2):[Medline].
Benbadis SR, Tatum WO. Advances in the Treatment of Epilepsy. American Family Physician. July 2001;64 (1):91-98. [Medline].

