The term focal epilepsy is used if delineation of the epileptogenic zone in one cerebral region is possible, as evidenced by data from the history, seizure semiology, EEG, and (functional) imaging (54). The more information available in each case, the more precise the localization of the epileptogenic zone. The epileptogenic zone includes not only the ictal-onset zone that generates the patient’s typical seizures but also brain tissue that can induce seizures when the primary focus is removed (55).

Consciousness has different aspects such as perception, cognition, memory, affect, and voluntary motility (56). For practical purposes, ictal loss of consciousness is usually defined by unresponsiveness during a seizure, along with amnesia for events during the seizure and for a variable period before and after it. Consciousness may be difficult or impossible to assess during seizures in infants (48,57).

To determine unresponsiveness—the inability to respond to external stimuli—the patient is tested during and after the seizure. In some laboratories, motor response to an auditory or visual stimulus is tested (29). A patient may not respond because the patient cannot comprehend the command; even if comprehension and consciousness are intact, the motor or verbal output may be blocked. In some patients, lack of responsiveness may be the result of a peculiar motivational state (as if the person were absorbed by a hallucination) (56). During the postictal interview, the patient is asked to recall test words or items given during the seizure. Language and praxis also should be evaluated at this time to identify any deficits. Preserved responsiveness associated with automatisms is noted in complex partial seizures arising from the nondominant temporal lobe (58).

Patients with complex partial seizures with automatisms are often unaware that they have just had a seizure and cannot recall activities engaged in before the seizure onset or events that occurred during the ictus. The degree of retrograde and anterograde amnesia is variable. Postictal amnesia probably results from bilateral impairment of hippocampal function. The patient is unable to form new memories, but previously established ones are intact. Bilateral stimulation of medial temporal lobe structures or unilateral medial temporal lobe stimulation that produces afterdischarges affects the formation and retrieval of longterm memories (59, 60, 61).

Seizures arising from the frontal lobes occur in up to 30% of patients with focal epilepsy are the second most common focal type after temporal lobe seizures (72,73). In 50% of patients with frontal lobe epilepsy, seizures are accompanied by loss of consciousness (74). Seizures with loss of consciousness can arise from various locations within the frontal lobe (except from the rolandic strip) (33,42,66,68,72,75,76). Semiologic features include occurrence in clusters, occurrence many times a day, brief duration (lasting about 30 seconds with a sudden onset), and minimal postictal confusion. Bizarre attacks with prominent motor automatisms involving the lower extremities (pedaling or bicycling movements), sexual automatisms, and prominent vocalizations are common, and the seizures are remarkably stereotyped for each patient (33,42,68,77,78). Identification of seizure onset within the frontal lobe by semiology alone and differentiation of mesial temporal lobe epilepsy and frontal lobe epilepsy may be misleading and difficult (79); however, analysis of the earliest signs and symptoms, as well as their order of appearance, may allow this distinction in onset (41). Clonic seizures frequently arise from the frontal convexity, tonic seizures from the supplementary motor area, and automotor seizures from the orbitofrontal region (80). Seizures with “motor agitation” and hypermotor features are more likely to arise from the orbitofrontal and frontopolar regions (79). Up to 50% of patients develop complex partial status epilepticus (33,80,81).

The unique symptomatology of supplementary motor seizures includes an onset with abrupt tonic extension of the limbs that is often bilateral but may be asymmetric and is accompanied by nonpurposeful movements of uninvolved limbs and vocalizations (42,78,82,83). Typically, these occur out of sleep and recur many times a night. Because of their bizarre symptomatology, they are sometimes mistaken for pseudoseizures. Consciousness is often preserved in supplementary motor area seizures, and postictally baseline mentation returns quickly. Vigevano and Fusco (84) reported a familial form of supplementary motor area seizures in young children with good outcome.

Cingulate gyrus seizures, in addition to phenomena associated with supplementary motor seizures, such as asymmetric bilateral tonic posturing of the proximal limbs, may show complex behavior including oroalimentary, gestural, and sexual automatisms, mood changes, and urinary incontinence (23,85, 86, 87, 88).

Orbitofrontal seizures manifest prominent autonomic phenomena, with flushing, mydriasis, vocalizations, and automatisms. The vocalizations may consist of unintelligible screaming or loud expletives of words or short sentences. Patients also may get up and run around the room (24).

Quesney and associates (78) reported that seizures of the anterolateral dorsal convexity seizures may manifest with auras (89) such as dizziness, epigastric sensation, or fear in 50% of patients, behavioral arrest in 20%, and speech arrest in 30%. One third of the patients exhibited sniffing, chewing or swallowing, laughing, crying, hand automatisms, or kicking. A tendency to partial motor activity in the form of tonic or clonic movements contralateral to the side of the focus was also noted. Bancaud and colleagues (90) described speech arrest, visual hallucinations, illusions, and forced thinking in some patients during seizures of dorsolateral frontal origin. These patients may also show contralateral tonic eye and head deviation or asymmetric tonic posturing of the limbs before contralateral clonic activity or secondary generalization. Other patients may have autonomic symptoms such as pallor, flushing, tachycardia, mydriasis, or apnea (90).

Approximately 40% to 80% of patients with temporal lobe epilepsy have seizures with stereotyped automatisms of the
mouth and hands and other motor manifestations (excluding focal clonic activity and version) that suggest a temporal lobe origin (29, 30, 31, 32,38, 39, 40). Secondary generalization occurs in approximately 60% of temporal lobe seizures (91,92). Postictally, gradual recovery follows several minutes of confusion; however, patients may carry out automatic behavior, such as getting up, walking about, or running, of which they have no memory. Attempts to restrain them may only aggravate matters. Violence, invariably nondirected, may be seen during this period (93,94). The patient is usually amnestic for the seizure but may be able to recall the aura. A few patients may exhibit retrograde amnesia for several minutes before the seizure. In young children, partial seizures of temporal lobe onset are characterized predominantly by behavioral arrest with unresponsiveness (48,57,95); automatisms are usually oroalimentary, whereas discrete manual and gestural automatisms tend to occur in children older than age 5 or 6 years (96, 97, 98). In younger children, symmetric motor phenomena of the limbs, postures similar to frontal lobe seizures in adults, and head nodding as in infantile spasms were typical (96). Because it is impossible to test for consciousness in infants, focal seizures with impairment of consciousness may manifest as hypomotor seizures, a bland form of complex partial seizure with none or only few automatisms (99). In very young infants, these may also occasionally be accompanied by central apnea (100).

A few well-documented cases of complex partial seizures arising from the parietal lobes have been reported (101, 102, 103). Like seizures of occipital lobe onset, partial seizures from the parietal lobe manifest loss of consciousness and automatisms when they spread to involve the temporal lobe. Initial sensorimotor phenomena may point to onset in the parietal lobe, as do vestibular hallucinations such as vertigo, described in seizures beginning near the angular gyrus. Language dysfunction may occur in seizures arising from the dominant hemisphere. Also described in parietal lobe complex partial seizures have been auras including epigastric sensations, formed visual hallucinations, behavioral arrest, and panic attacks (18,27,103, 104, 105, 106). In a study of patients with parietal lobe epilepsy as evidenced by ictal single-photon-emission computed tomography (SPECT) (7 of 14 patients with focal seizures with impairment of consciousness) (101), 6 had prominent staring and relative immobility (dileptic), and one patient had hypermotor features.

A limiting factor in many studies of seizure symptomatology is that relatively few reported patients with extratemporal complex partial seizures become seizure free after cortical resection. This casts some doubt on the localization of the epileptic focus (42,78,100, 107,108).

The following features suggest the occipital lobe as the origin of a complex partial seizure: (a) Visual auras, usually of elementary sensations such as white or colored flashing lights, are often in the part of the visual field corresponding to the focus (20, 109,110); the visual phenomena may remain stationary or move across the visual field. (b) Ictal blindness in the form of a whiteout or blackout may be reported (111). (c) Version of the eyes and head to the opposite side is common and is a reliable lateralizing sign (65,112); patients may report a sensation of eye pulling to the opposite side even in the absence of eye deviation (20,113). (d) Rapid, forced blinking and oculoclonic activity also may be seen (114). Other symptoms may result from spread to the temporal or parietal lobes (19,53,103,115). Suprasylvian spread to the mesial or parietal cortex produces symptomatology similar to that in supplementary motor seizures, whereas spread to the lateral parietal convexity gives rise to sensorimotor phenomena. Spread to the lateral temporal cortex followed by involvement of the mesial structures may produce formed visual hallucinations followed by automatisms and loss of consciousness. Direct spread to the mesial temporal cortex may mimic mesial temporal epilepsy. The visual auras may be the only clue to recognizing the occipital lobe onset of these seizures; however, the patient may not recall them because of retrograde amnesia, if the aura was fleeting, or if the seizure is no longer preceded by the aura as it was in the past (110).

In a study of 42 patients with occipital lobe epilepsy, 73% experienced visual auras (116) frequently followed by loss of consciousness possibly as a consequence of ictal spread into the frontotemporal region. Vomiting is more common in benign than in symptomatic occipital lobe seizures and may also represent ictal spread to the temporal lobes (89,117).

Auras have been reported in 20% to 93% of patients with temporal lobe seizures (26,29,31,118, 119, 120, 121) and in approximately 50% to 67% of seizures arising from the frontal lobe (78, 79, 80, 81, 82, 83, 84, 85, 86, 87, 88, 89, 90, 91, 92, 93, 94, 95, 96, 97, 98, 99, 100, 101, 102, 103, 104, 105, 106, 107, 108, 109, 110, 111, 112, 113, 114, 115, 116, 117, 118, 119). The auras may be similar in both groups. In the Cleveland Clinic series of patients with documented temporal lobe epilepsy (seizure free after temporal lobectomy), only 28% of seizures recorded in the laboratory were accompanied by a definite aura (40). Some patients who experience an aura cannot recall it after a focal seizure with impairment of consciousness. This is frequently
observed during video-electroencephalography monitoring in which the patient may press a buzzer alarm at the onset of the seizure but cannot recall doing so subsequently (P. Kotagal, personal observation). Young children with auras (who are unable to verbalize them) may run to their mothers and cling to them (122).