Neocortical temporal lobe seizures

Fernando Cendes MD PhD (Dr. Cendes of the University of Campinas - UNICAMP has no relevant financial relationships to disclose.)
Jerome Engel Jr MD PhD, editor. (Dr. Engel of the David Geffen School of Medicine at the University of California, Los Angeles, has no relevant financial relationships to disclose.)
Originally released February 12, 2004; last updated September 10, 2016; expires September 10, 2019

Overview

Clinical expression of temporal lobe seizures depends on the location of the epileptogenic zone, type of the epileptogenic lesion, and age. Clinical and EEG manifestations are more complex in infants and children than in adults. Motor manifestations, including tonic, clonic, or complex behaviors, as well as infantile spasms, predominate in infants. Classical dyscognitive seizures with behavioral arrest and automatisms and clear lateralizing signs are rare in young children and mainly occur after 2 years of age. Lateral temporal seizures in older children and adults are characterized by auditory, somatosensory, aphasia, or psychic auras, although other ictal symptoms may occur.

Key points

 

• The most common lesions causing neocortical epilepsies are low-grade tumors, malformations of cortical development, posttraumatic, ischemic, and inflammatory-infectious scars, and cavernous angioma.

 

• Neocortical temporal lobe seizure semiology varies considerably according to the area of the temporal lobe involved.

 

• The classical lateral temporal seizures are characterized by auditory, somatosensory, aphasia, or psychic auras.

Historical note and terminology

Although nonconvulsive seizures with complex behaviors have been recognized since antiquity (Temkin 1945), their relationship to temporal lobe origin was more recently recognized, being first described in the late 1800s by Jackson (Jackson 1898; Jackson 1958). The psychic and motor characteristics of these seizures first prompted the designation of psychomotor seizures (Gibbs et al 1938; Gibbs et al 1948). With the advent of electroencephalography and the increased interest in surgical intervention, the anatomical significance of these seizures led to them being labeled temporal lobe seizures (Sutton et al 1987).

The majority of temporal lobe seizures originate in the mesial structures, primarily in the hippocampus, with the rest beginning in a variety of temporal neocortical regions. If patients with circumscribed, epileptogenic lesions other than hippocampal sclerosis are excluded, temporal seizures originating in the hippocampus and related structures are far more common than lateral neocortical seizures (Williamson et al 1997b).

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