ACKNOWLEDGEMENTS AND DISCLOSURES

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HISTORICAL NOTE AND NOMENCLATURE

Some signs and symptoms associated with posterior neocortical seizure origin such as paresthesias and elementary visual hallucinations have been recognized as epileptic phenomena since antiquity. In fact, the original "aura" description was probably a somatosensory aura consisting of a localized "cold breeze" (Temkin 1945). Although many other premonitory signs were recognized by the ancients, it was not until the latter half of the nineteenth century that Jackson started to add some anatomical perspective to these signal symptoms and signs ( Jackson 1958). The localizing significance of these initial seizure manifestations was greatly refined during the middle of the twentieth century by both the French and Montreal schools (Penfield and Jasper 1954; Ohtsu et al 2003). The explosive growth of epilepsy centers and epilepsy surgery programs during the past 20 years has further added to our knowledge about seizures in general and our understanding of posterior neocortical seizures in particular.

CLINICAL MANIFESTATIONS

One characteristic that posterior neocortical seizures share is the tendency to have multiple spread patterns (Salanova et al 1992; 1993; Williamson et al 1992a; 1992b; 1995; Ho et al 1994; Fogarasi et al 2003). This can occur among different patients or among different seizures in the same patient. Therefore, patients with this type of seizure origin can present with stereotyped but very different-appearing clinical seizures depending on direction of seizure spread, or, conversely, individual patients can have seizures that are not stereotyped from one to another, strongly suggesting multifocality. For the purposes of description, posterior neocortical seizures are usually divided into 2 categories: those that begin in the occipital lobes and those that begin in the parietal lobes.

Occipital lobe seizures. All seizures can be defined by subjective features (symptoms) and objective features (signs). They can be defined further by the initial symptom or sign (signal finding, aura) and the subsequent characteristics, with the latter usually reflecting spread patterns, whereas initial findings often help identify the region of seizure origin (Taylor et al 2003).

Subjective initial signs.

Elementary visual hallucinations. Elementary visual hallucinations can occur in several forms (Blume1991; Blume et al 1991; Salanova et al 1992; 1993; Williamson et al 1992a). Most often, these visual hallucinations are a spot of light, steady or flashing. A white light with a greenish tinge (phosphene) is commonly described. However, descriptions of multicolored or monochromatic light have been reported as well. The visual hallucinations can be central or lateralized. When lateralized, they occur contralateral to the seizure focus. If they appear in the upper quadrant, the seizure discharge is below the calcarine fissure. Symptoms in the inferior quadrant have an analogous anatomical relationship. The visual hallucination may move horizontally, usually from the side contralateral to the seizure focus. This is the most common symptom of occipital seizure origin and has been recognized as a seizure warning since antiquity (Temkin 1945).

Ictal amaurosis. Visual loss at seizure onset is almost as common a symptom of occipital lobe seizure onset as elementary visual hallucinations, but it is not as widely recognized (Blume 1991; Blume et al 1991; Salanova et al 1992; 1993; Williamson et al 1992a; Shahar and Barak 2003). Patients may not complain of visual loss unless specifically questioned (Taylor et al 2003). Visual loss is usually bilateral, but homonymous hemianopsia contralateral to the seizure discharge can occur. It may be possible that the patient often does not perceive hemi-field deficits. Ictal amaurosis usually consists of a blackout, but whiteouts or diffuse perceptions of color can occur. Ictal amaurosis may present as a prolonged seizure state in status epilepticus amauroticus (Ayala 1929; Shahar and Barak 2003).

Eye movement sensations. The sensation of eye movement in the absence of detectable movement has been reported as a sign of occipital seizure origin (Bancaud et al 1965; Holtzman 1977; Salanova et al 1992; 1993; Williamson et al 1992a). Sometimes this symptom is described as a sensation of the eyes being pulled back in the head. Although this might actually be occurring, detection would require direct examination during the symptom.

Diplopia. Diplopia has rarely been reported as an epileptic manifestation (Galimberti et al 1998), but the localizing value is not known.

Objective initial signs.

Eye deviation. Early deviation of the eyes with or without head deviation is frequently reported in seizures beginning in the occipital lobe (Takeda et al 1970; Munari et al 1984; Salanova et al 1992; 1993; Williamson et al 1992a). Although the literature strongly favors contralateral deviation, there are rare exceptions (Salanova et al 1992; 1993; Williamson et al 1992a). Electrical stimulation studies in humans and animals have reproduced contralateral deviation.

Epileptic nystagmus. Nystagmus as a manifestation of epileptic discharges has been reported repeatedly (Foerster and Penfield 1930; Bancaud et al 1965; Ludwig and Marsan 1975; Munari et al 1984; Salanova et al 1992; 1993). There is disagreement, however, of the lateralizing significance of the fast and slow components.

Blinking or eyelid flutter. Blinking is often seen at the beginning of seizures, but when it has a forced or fluttering appearance, occipital lobe seizure origin should be suspected (Bancaud et al 1965; Munari et al 1984; Williamson et al 1992a).

Diplopia. As noted previously, doubling of vision has been reported, but whether there is actual objective evidence of oculomotor imbalance is unknown (Galimberti et al 1998).

Signs and symptoms of propagation. Occipital seizure foci are uniquely situated to allow multiple possible propagation patterns (Ajmone-Marsan and Ralston 1957; Stewart and Dreifuss 1967; Salanova et al 1992; 1993). Occipital lobe seizures can spread above or below the sylvian fissure, medially or laterally, ipsilateral or contralateral to the side of origin. Several reports have noted that complex visual hallucinations usually follow elementary visual hallucination, suggesting propagation outside of the occipital lobe (Gowers 1885; Russell and Whitty 1955; Huott et al 1974; Ludwig and Marsan 1975; Munari et al 1984; Blume et al 1991; Williamson et al 1992a). Complex visual hallucinations may require involvement of both limbic and neocortical structures (Gloor et al 1982). Propagation from the occipital lobe to medial temporal structures has been well documented (Ludwig et al 1975; Munari et al 1984; Williamson et al 1992a). Automatisms indistinguishable from those of typical temporal lobe epilepsy can occur (Stewart and Dreifuss 1967; Salanova et al 1993; 1995). Suprasylvian spread results in various focal tonic and clonic motor manifestations (Stewart and Dreifuss 1967; Blume 1991; Salanova et al 1992; 1993). Although contralateral propagation with lateralized clinical manifestations is theoretically possible, this has been only partially documented with intracranial recording (Stewart and Dreifuss 1967).

The potential for multiple spread patterns holds true among different patients and within individual patients (Stewart and Dreifuss 1967). Patients with occipital lobe seizure origin, therefore, do not present with any specific seizure pattern, and some may have several different seizure types, suggesting multifocal disease.

In conclusion, occipital lobe seizures are rare, constituting only 1% of the large nontumoral Montreal series (Rasmussen 1975; Salanova et al 1992). Because of the variable spread patterns, there is no specific seizure type, making clinical localization difficult. Careful attention to early symptoms and signs can help identify most, but not all, occipital lobe seizures.

Parietal lobe seizures. Like occipital lobe seizures, parietal lobe seizures can be divided into subjective and objective manifestations. Although there are certain symptoms and possibly some signs that help identify parietal lobe origin, much of the parietal lobe is silent with respect to clinical seizure manifestations. In addition, some aspects of seizure-induced parietal lobe dysfunction might not be apparent without specific testing, ie, testing of various cortical somatosensory functions.

An example of this is found in the classic monograph Epilepsy and the Functional Anatomy of the Human Brain (Penfield and Jasper 1954): Patient J. St. had a seizure limited to the parietal lobe recorded during corticography under local anesthesia. Two-point discrimination was impaired during the seizure but returned to normal after the seizure. Such a serendipitous observation would rarely be possible. It would also require that the seizure remain limited to the parietal lobe, which is often not the case.

Subjective manifestations.

Paresthesias. Paresthesias are usually contralateral to the side of seizure onset (Williamson et al 1987; 1992b; Cascino et al 1993; Ho et al 1994; Salanova et al 1995). They consist of localized numbness or a "pins and needles" sensation. Unpleasant crawling sensations have also been described. When localized at onset, they may remain localized or they may exhibit a march similar to focal clonic motor seizures (Jacksonian march). Ipsilateral or bilateral paresthesias suggest involvement of secondary parietal sensory systems (Williamson et al 1992b). Contralateral paresthesias are the most common subjective manifestation of parietal lobe seizure origin, but they probably occur in less than half of the patients with this type of seizure disorder.

Ictal pain. Ictal pain is rare, and when it occurs in isolation misdiagnosis is common (Siegel et al 1999). A recent study of ictal pain found that it is usually a sign of parietal lobe seizure origin (Siegel et al 1999). The pain usually consists of a burning, unpleasant dysesthesia with lateralization and distribution characteristics similar to those described for paresthesias. Severe, cramping, lateralized abdominal pain recently has also been equated with parietal lobe seizure origin (Siegel et al 1999). Head pain may also be associated with parietal lobe seizure origin, but this needs additional verification.

Visual distortions. A distortion of objects or body parts is a rare seizure symptom of presumed parietal lobe origin, but this has yet to be documented.

Alien hand (La main etrangere). The sensation that a body part, usually a hand, does not belong to the person is another rare parietal lobe seizure symptom (Leiguarda et al 1993). This has been documented with intracranial recording and successful surgery (Siegel et al 1999).

Vertigo. True vertigo is reportedly due to seizure activity in the temporo-parietal junction. Although a well-established seizure symptom, epileptic vertigo is rare, and the exact neocortical representation has not been documented with precision (Fried et al 1995).

Gustatory hallucinations. Gustatory hallucinations are well-described seizure symptoms, but their localizing significance is not precise. They can be elicited by stimulating the anterior temporal structures, the parietal operculum, and the anterior insula (Hausser-Hauw and Bancaud 1987).

Sensations of movement. During vertiginous seizures, the environment may appear to move. In addition, the sensation of body part movement without observable movement has been reported as a symptom of parietal lobe seizure activity (Penfield and Jasper 1954).

Disorders of reading and language. The wide variety of reading, writing, and speech disorders associated with structural damage of the language-dominant parietal lobe might occur transiently as ictal symptoms during limited parietal lobe seizures but, other than nonspecific dysphasic disorders, these have not been selectively demonstrated.

Objective disorders. The parietal lobes are generally associated with processing sensory information and, as such, would not be expected to produce much in the form of objective ictal behavior (Williamson et al 1992b; Akimura et al 2003). Exceptions might be demonstrable disorders of language mentioned previously or curious reactions to unpleasant stimuli, such as severe pain. Inhibitory motor or paralytic seizures can be associated with parietal lobe seizure origin (Siegel et al 1999).

Signs and symptoms of seizure propagation. Posterior propagation from the parietal lobe can result in a patient experiencing elementary visual hallucinations or ictal amaurosis (Williamson 1987). Anterior spread can produce focal clonic motor activity. Asymmetrical tonic motor activity is often seen with seizures of parietal lobe origin during which there is intracranial recording evidence for and against spread to the supplementary motor area (Geier et al 1977; Williamson et al 1992b; Siegel et al 1999). Inhibitory or hemiplegic seizures may occur, but it is not known whether this represents spread beyond the parietal lobe (Siegel et al 1999). Inferior spread into the temporal lobe has been well documented with intracranial recording (Williamson et al 1992b). It has been suggested that posterior parietal lobe seizure origin is most often associated with spread to the temporal lobes, producing "psychoparetic" seizures (Ho et al 1994). Parietal lobe seizures resembling panic attacks probably also reflect temporal lobe seizure spread (Alemayehu et al 1995; Sazgar et al 2003).

LOCALIZATION

PATHOPHYSIOLOGY
The tendency toward multiple spread patterns, although not unique, is characteristic of seizures of the posterior neocortex. The same is not true of mesial temporal lobe seizures or most frontal neocortical seizures. The pathophysiology of this characteristic, although not known, almost certainly reflects the rich connectivity of these regions. Disorders of neural development, neoplasms, hamartomas, and vascular malformations all can cause seizures in the posterior neocortex, as they can elsewhere in the forebrain.

DIFFERENTIAL DIAGNOSIS

Because seizures originating in the posterior neocortex can have multiple spread patterns, they can mimic other types of seizures such as lateral temporal, mesial temporal, or frontal lobe seizures (Ajmone-Marsan and Ralston 1957; Salanova et al 1992; 1995; Williamson et al 1992a; 1992b; Williamson 1999). The overall seizure pattern can, therefore, be very misleading. Careful attention to the initial seizure characteristics will help correctly identify most seizures, but there will be exceptions. Seizures originating in the parietal lobe seem to be particularly prone to be devoid of localizing information. In 2 of the more recent studies of parietal lobe seizures, only half of the patients had clinical findings suggesting parietal lobe seizure origin (Williamson et al 1992b; Cascino et al 1993). All patients in both studies had parietal lesions on MRI that served to identify the region of seizure origin. Parietal lobe seizures masquerading as panic attacks have been reported (Alemayehu et al 1995), but this ictal manifestation may be more often associated with right temporal lobe seizure origin (Sazgar et al 2003). Exact localization of seizure origin only matters when surgical intervention is being considered. When the MRI is normal in a patient with medically intractable epilepsy, parietal lobe seizure origin can easily be missed during the presurgical evaluation. An ictal SPECT may be the only means of correctly localizing these patients (Ho et al 1994), but its reliability in this situation has not been thoroughly tested.

DIAGNOSTIC WORKUP

The extent of the diagnostic workup will vary, depending on the questions being asked. If, after a thorough history and examination, focal epilepsy of any type is suspected, a high-resolution MRI should be obtained early in the course of the evaluation to search for a structural cause of the seizures. Finding such lesions can influence management for obvious reasons. Routine EEGs and even prolonged monitoring is often not informative and can be misleading in patients with posterior neocortical seizure origin (Blume et al 1991; Williamson et al 1992b; Cascino et al 1993; Foldvary et al 2001). If a detected structural lesion is considered benign, or if the MRI is normal, further diagnostic workup is not required, and medical management should be initiated or continued. If medications fail to control seizures and surgical intervention is being considered, the diagnostic evaluation becomes more extensive. Detection of a single, well-circumscribed epileptogenic lesion greatly simplifies the presurgical evaluation, but seizures should be recorded to establish a causative relationship. In the absence of a detectable lesion, the presurgical evaluation becomes much more difficult. A detailed description of this type of evaluation is beyond the scope of this discussion. Suffice it to say, much will depend on the experience and facilities of the center doing the evaluation.

SYNDROMES AND DISEASES IN WHICH THE SEIZURE TYPE OCCURS

PROGNOSIS AND COMPLICATIONS

When epileptogenic lesions are present, the prognosis is, to some extent, related to the lesion. Recurrent occipital lobe seizures in the form of nonconvulsive status epilepticus can lead to permanent blindness (Ayala 1929). Surgery can produce excellent results in terms of seizure control, but postoperative neurologic deficits cannot always be avoided (Williamson et al 1992a; 1992b). The prognosis of benign idiopathic childhood epilepsy with occipital spikes is usually good with medical treatment alone (Mennink et al 2003; Shahar and Barak 2003).

MANAGEMENT

There are no antiepileptic drugs that work preferentially on the posterior neocortex. For focal seizures in general, phenytoin and carbamazepine are probably the preferred antiepileptics among the older drugs. New antiepileptic drugs will undoubtedly prove beneficial, but specificity or superiority is not known. In patients with detectable epileptogenic lesions, surgery aimed at removing the lesion and the epileptogenic zone can be very helpful. Although postoperative neurologic deficits will occur in some patients, occasionally they can be avoided.

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ILAE
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ABBREVIATIONS
MRI: Magnetic resonance imaging
SPECT: Single photon emitted computed tomography
AED: antiepileptic drug

SUBTOPICS
Occipital lobe seizures
Parietal lobe seizures

MAJOR KEYWORD DESCRIPTORS
clinically silent seizures
epileptogenic lesions
ictal amaurosis
ictal pain
neocortical
objective clinical characteristics
painful seizures
seizure spread patterns
seizures
somatosensory seizures
subjective clinical characteristics
visual disturbances

MINOR KEYWORD DESCRIPTORS
altered consciousness
epilepsy surgery
medical intractability

AGE OF PRESENTATION
02-05 years
06-12 years
13-18 years
19-44 years
45-64 years
64+ years

AGE OF TYPICAL PRESENTATION
02-05 years
06-12 years
12-18 years

GLOSSARY
Seizures of the posterior neocortex are a heterogeneous group of seizures that originate in the occipital and parietal lobes. They are characterized by multiple different spread patterns. There are multiple causes. They can often, but not always, be correctly identified by early symptoms and signs.

PERMUTED TOPIC, SYNONYMS, VARIANTS
Seizures of the posterior neocortex
posterior neocortex, Seizures of the
neocortex, Seizures of the posterior
seizures, Occipital lobe
seizures, Parietal lobe

RELATED SUMMARIES
Epilepsy
Idiopathic photosensitive occipital lobe epilepsy
Surgical treatment of seizures originating outside the temporal lobe

DIFFERENTIAL DIAGNOSIS
frontal lobe seizures
lateral temporal seizures
medically intractable epilepsy
mesial temporal seizures
panic attacks

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