Complex Partial Seizures
- Author: Elizabeth Carroll, DO; Chief Editor: Selim R Benbadis, MD more...
A complex partial seizure starts focally within the brain and causes impairment of consciousness. In most patients, complex partial seizures represent underlying temporal lobe epilepsy. See the image below.
Essential update: FDA approves vigabatrin for adjunctive treatment of complex partial seizures in children
In October 2013, the FDA approved vigabatrin (Sabril) as add-on therapy for children aged 10 years and older with complex partial seizures that are refractory to several other treatments. Vigabatrin should be used in such cases only if the possible treatment benefit outweighs the risk for vision loss associated with the drug.
Vigabatrin is already approved as adjunctive therapy, but not first-line treatment, for adults with refractory complex partial seizures and for infants from 1 month to 2 years of age with infantile spasms for whom the possible benefit outweighs the potential risk for vision loss. Vigabatrin is available through a restricted program under a risk evaluation and mitigation strategy, the SHARE Program.
Signs and symptoms
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.
Typically of brief duration, rarely lasting longer than seconds
Eight different varieties are recognized: somatosensory, visual, auditory, gustatory, olfactory, autonomic, abdominal, and psychic
Auras precede temporal lobe seizures in approximately 80% of cases; the most common are abdominal (a rising epigastric sensation) and psychic (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 (eg, colored lines, spots, or shapes) or a loss of vision
Temporal-parietal-occipital seizures may produce more formed auras
Usually, during a complex partial seizure, the patient is unresponsive and does not remember events that occurred
Although patients typically do not respond to external stimuli, they may make simple verbal responses; follow simple commands; or continue to perform simple or, less commonly, complex motor behaviors (eg, operating a car)
Automatisms are nonpurposeful, stereotyped, and repetitive behaviors that commonly accompany complex partial seizures
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 also be more elaborate, coordinated movements involving bilateral extremities (eg, cycling movements of the legs, stereotyped swimming movements)
Bizarre automatisms (eg, alternating limb movements, right-to-left head rolling, sexual automatisms) may occur with frontal lobe seizures
Seizure features by site of origin
Temporal lobe seizures 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
In temporal lobe seizures, lateralizing signs with corresponding sensitivities include the following[4, 5] :
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%)
See Clinical Presentation for more detail.
Laboratory studies aim to rule out potential causes or, more often, triggers for seizures. Routine workup for all patients should include EEG and MRI of the brain; most of the time, the results will be normal. A patient with seizures that are difficult to control should be reassessed for a possible alternative diagnosis or temporal lobe epilepsy, using prolonged EEG-video monitoring to record patient events. Lumbar puncture may be indicated for a patient with new-onset seizure when an acute inflammatory or infectious process is being considered, but it is not indicated in patients with chronic epilepsy.
Concentrations of antiepileptic drugs, if being used
Consider a urine drug screen
Used to exclude an obvious structural lesion as the cause [6, 7]
Should include contrast with gadolinium to allow assessment of possible neoplastic and vascular etiologies
MRI with temporal cuts measures hippocampal volumes in assessment for temporal lobe epilepsy
Increased signal on fluid-attenuation inversion recovery (FLAIR) T2-weighted MRI can detect sclerosis of the mesial temporal lobe in 80-90% of cases
EEG within 24 hours is more sensitive for diagnosing epileptiform abnormalities than later EEG is (51% sensitivity vs 34%), but it is often impractical
Epileptiform discharges, when present, help localize the seizure focus
A negative interictal EEG does not exclude a diagnosis of epilepsy
If the waking EEG is negative, a sleep-deprived EEG may demonstrate epileptiform abnormalities
See Workup for more detail.
Treatment of complex partial seizures may involve pharmacologic therapy and, in certain cases, epilepsy surgery.[8, 9, 10, 11, 12, 13, 14, 15, 16, 17] Special considerations apply to women with childbearing potential.
Treatment with antiepileptic medication should always be initiated once a diagnosis of epilepsy is made
All current antiepileptic drugs (AEDs), with the exception of ethosuximide, can be used in the treatment of complex partial seizures
The best-tolerated AED should be selected for the patient on the basis of side effects and drug interactions
Monotherapy is always initially preferred over polytherapy for treating seizures
High dosages of a single agent may be required to achieve seizure control before adding a second agent
Women of childbearing age should be educated regarding the drug interactions between AEDs and contraceptive therapy
Women who become pregnant and have a history of seizures should be continued on current AED therapy that controls seizures and should not be switched to a secondary agent simply because of pregnancy
Epilepsy surgery is indicated for patients who have frequent, disabling seizures despite adequate trials of 2 or more anticonvulsants
Video EEG should be used before surgical referral to qualify events, assess severity, and aid in localization
Surgical procedures include temporal lobectomy, extratemporal resections, corpus callosotomy, placement of a vagus nerve stimulator, hemispherectomy, and multiple subpial transection
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.
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.
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, reorganization, neurogenesis, and altered neurotransmitter receptors.
In the majority of cases, complex partial seizures are of unknown etiology (ie, cryptogenic). Potential causes include the following:
Hippocampal sclerosis (mesial temporal lobe)
Central nervous system (CNS) infections
Immune-mediated CNS inflammation
Hypoxic-ischemic brain injury
Febrile seizures, especially complex, are associated with an increased risk of later development of complex partial seizures and epilepsy.
The prevalence of epilepsy is approximately 0.5-1 case per 100 persons. 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.
The mortality rate in individuals with epilepsy is 2-3 times that in the general population. 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.
Individuals with epilepsy are at increased risk for trauma, burns, and aspiration.
Jeffrey S. FDA Okays Vigabatrin as Add-on for Seizures in Children. Available at http://www.medscape.com/viewarticle/813666. Accessed: November 2, 2013.
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. 1999 May 12. 52(8):1540-5. [Medline].
French JA, Pedley TA. Clinical practice. Initial management of epilepsy. N Engl J Med. 2008 Jul 10. 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].
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. 1987 Jan. 21(1):22-31. [Medline].
Annegers JF. The epidemiology of epilepsy. 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. 1982 Jun. 23(3):343-50. [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. 2006 Aug 8. 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. 1991 Jul. 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. 1996 Aug. 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].