This article includes discussion of frontal lobe seizures, complex partial seizures of frontal lobe origin, focal dyscognitive seizures of frontal lobe origin, frontal lobe epilepsy, neocortical epilepsy, and seizures of the anterior neocortex. The foregoing terms may include synonyms, similar disorders, variations in usage, and abbreviations.
Frontal lobe seizures can have bizarre manifestations; however, they are easily recognizable if the clinician is well aware of the clinical presentation. Frontal lobe seizures are typically brief, nocturnal, and without loss of consciousness. Focal clonic seizures, asymmetric tonic seizures, hyperkinetic seizures, absence type seizures, and masticatory seizures originate in different subregions of the frontal lobes. Treatment includes medical as well as surgical options.
• Focal clonic seizures originate in the primary motor area; asymmetric tonic seizures involve the supplementary motor area; and prefrontal seizures often manifest as hyperactive seizures.
• Frontal lobe seizures may have bizarre manifestations with hyperactive behavior and preserved consciousness.
• Frontal lobe seizures can be misdiagnosed as psychiatric disease or sleep disorders.
• Frontal lobe seizures are brief and nocturnal and occur in clusters.
Historical note and terminology
The first detailed description of focal clonic seizures, a type of seizure originating in the posterior frontal lobes, was published by JF Bravais in 1827 (Bravais 1827). Hughlings Jackson, in 1867, related clonic seizures to electric discharges in the contralateral prerolandic region (Taylor 1958). He described seizures with a “march of spasm” and wrote: “We may first see movement of the index-finger, then of the hand, then the whole arm, then of the face, leg, then of bilateral muscles” (Loiseau 1992). The Commission on Classification and Terminology of the International League Against Epilepsy still classified these seizures as “Jacksonian seizures” in 1989 (Anonymous 1989). In later classifications by the International League Against Epilepsy, those seizures are listed as “focal clonic seizure (without spread)” and “Jacksonian march seizures (with local spread)” (Engel 2006a; Engel 2006b). They are also referred to as “focal motor seizures with elementary clonic motor signs” (Engel 2006a; Engel 2006b), “clonic seizures” (Luders et al 1998), “simple motor seizures,” or “somatomotor seizures.” If they involve the entire hemibody they are termed “hemiclonic seizures” (Engel 2006a). If focal clonic seizures persist for a prolonged time the term “epilepsia partialis continua” is applied (Engel 2006b).
Penfield and Welch performed stimulation experiments of the human and monkey cortex. They defined the supplementary motor area (Brodmann area 6) as a region of the brain that mediates speech and behavioral arrest, vocalization, and asymmetric contralateral posturing when stimulated (Penfield 1951). They described supplementary motor area seizures as seizures with speech arrest, unilateral arm posturing, and head or eye deviation, later referred to as "fencing posture" (Penfield and Welch 1949; Penfield and Jasper 1954). In a detailed study of pharmacologically induced seizures, Ajmone-Marsan created the term "M2e" to describe tonic abduction and external rotation of the shoulder with flexion of the elbow with or without head turning. He described supplementary motor involvement if M2e posturing occurred without loss of consciousness and without progression into a secondarily generalized tonic-clonic seizure (Ajmone-Marsan and Ralston 1957). With the introduction of intracranial long-term EEG recordings, supplementary motor area seizures again became the focus of scientific interest in the late 1980s and early 1990s and were described in greater detail (Dinner et al 1987; Morris et al 1987; Morris et al 1988; Fried et al 1991; Tuxhorn et al 1992; Lim et al 1994; Connolly et al 1995; Roberts et al 1995; Baumgartner et al 1996; Janszky and Jokeit 2000; Fogarasi et al 2001). The terms “adversive seizure” and “supplementary sensorimotor seizures” were also used to describe supplementary motor area seizures (Ajmone-Marsan and Ralston 1957; Aghakhani et al 2004). They were also listed as “focal (asymmetrical) tonic seizures” by previous publications (Engel 2006a; Engel 2006b).
Complex partial seizures of frontal lobe origin with bizarre automatisms were initially recognized by Tharp, who described 3 patients that were misdiagnosed as having psychogenic attacks (Tharp 1972). Using stereoencephalography, Geier, Bancaud, and Talairach defined frontal lobe automatisms further (Geier et al 1976; Geier et al 1977), and detailed descriptions of complex partial seizures of frontal lobe origin followed (Williamson et al 1985b; Waterman et al 1987). The term "hypermotor seizure" was proposed for this type of seizure (Luders et al 1998). These seizures are also termed "frontal lobe seizures with hypermotor automatisms," "frontal lobe seizures with frenetic automatisms," "complex partial seizures frontal lobe type," "frontal lobe seizures with agitated behavior," or "seizures with hyperactive automatisms" (Williamson and Jobst 2000). They were also termed “hyperkinetic seizures” or “focal motor seizures with hyperkinetic automatisms” in some classification publications (Engel 2006a; Engel 2006b).
In the latest report of the International League Against Epilepsy (ILAE) on revised terminology and concepts for organization of seizures and epilepsy, frontal lobe seizures are classified as “focal seizures” with further descriptors such as “with or without impairment of consciousness” or “with or without observable motor components” (Berg 2010).
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