Seizures of the posterior neocortex …

Dawn Eliashiv MD

Epilepsy & Seizures

Updated 04.27.2023
Released 02.12.2004
Expires For CME 04.27.2026

Seizures of the posterior neocortex

Author: Dawn Eliashiv MD

See Contributor Disclosures

Editor: Jerome Engel Jr MD PhD

Seizures of the posterior neocortex

In This Article

Quick Link

Introduction

Overview

Occipital and parietal lobe seizures have distinct clinical characteristics. Occipital seizures mainly present with visual symptoms, whereas parietal lobe seizures can have unusual manifestations like visuospatial difficulties or ictal pain. If medical treatment with antiseizure medications fails, seizures of the posterior neocortex can be amenable to epilepsy surgery, but success rates are lower than in other epilepsy syndromes.

Key points

	• Occipital lobe seizures present with visual symptoms, eye blinking, and nystagmus.
	• Parietal lobe seizures may present with somatosensory symptoms, ictal pain, and visuospatial abnormalities.
	• Occipital and parietal lobe seizures may propagate forward and mimic temporal and frontal lobe seizures.
	• Self-limited focal occipital childhood epilepsies (COVE syndrome: childhood occipital visual epilepsy formerly known as Gastaut syndrome and SeLEAS: self-limited epilepsy with autonomic seizures formerly known Panayiotopoulos syndrome, which has an earlier onset than COVE syndrome) present with headaches, nausea, vomiting, and visual symptoms. The ILAE Task Force has revised the nosology and definition of epilepsy syndromes with onset in childhood (78).

Historical note and terminology

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 (42). In 1879, Gowers describes visual auras in a patient with an occipital-parietal lesion (37). In the twentieth century, seizures of the posterior neocortex were further delineated (65; 90). Seizures of the posterior neocortex can generally be divided into seizures originating from the occipital or parietal lobes. Previous seizure classifications published by the International League Against Epilepsy lists occipital and parietal lobe seizures as either “simple partial” or “complex partial seizures,” dependent on the loss of consciousness or “focal seizures with elementary symptoms” and “focal seizures with experiential symptoms” (24). Focal seizures with elementary symptoms include seizures with elementary sensory experiences, eg, elementary visual hallucinations like flickering lights or primary sensory experiences like paresthesias. Focal seizures with experiential symptoms include more complex sensory experiences like formed visual hallucinations. A report of the Commission on Classification and Terminology recommended classifying seizures of the posterior cortex as “focal seizures with or without altered consciousness with occipital or parietal semiology” (08). The new classification of seizures by the International League Against Epilepsy 2017 classifies focal seizures according to whether awareness is intact or impaired (27). If associated with altered consciousness, these seizures are deemed focal unaware. Secondary generalized seizures are considered to be evolving focal to bilateral convulsive tonic-clonic. Specific syndromes are still classified as electroclinical syndromes (ie, Gastaut).

Clinical manifestations

Presentation and course

Seizure of the posterior neocortex can be recognized by the initial symptom or sign (aura). The subsequent characteristics usually reflect spread patterns, whereas initial symptoms often help identify the region of seizure origin (83). One characteristic that posterior neocortical seizures share is the tendency to have multiple spread patterns (70; 71; 90; 89; 40; 30). 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 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.

Occiptal lobe seizure spread pattern

(From: Ajmone-Marsan C, Ralston BL. The epileptic seizure. Springfield, Illinois: Charles C Thomas, 1957:214. Used with permission.)
Sensory parietal seizure spread pattern

The discharge spread from the cortical hand representation to the face and leg area. Clinically sensory symptoms often spread from the hand or arm to the face and leg following the anatomic distribution in the homunculus. (Contrib...

Occipital lobe seizures. Occipital lobe seizures can be divided into subjective and objective manifestations.

Subjective initial signs. Although visual alterations are the hallmark of occipital lobe seizures, they occur only in 47% to 85% of patients (45).

Elementary visual hallucinations. Elementary visual hallucinations occur in several forms (11; 11; 70; 71; 90; 10). Most often, visual hallucinations are multiple spots of light, steady or flashing. A white light with a greenish tinge (phosphene) is commonly described. 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. Elementary visual hallucinations are the most common aura of occipital lobe epilepsy (45).

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 (11; 11; 70; 71; 90; 10; 75; 48). Patients may not complain of visual loss unless specifically questioned (83). 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 can be prolonged and represent status epilepticus amauroticus (Ayala 1929; 75).

Complex visual hallucinations. Complex visual hallucinations are less common than elementary visual hallucinations (45). They consist of scenes or people as epileptic aura. They are thought to be associated with seizure onset in the occipital-temporoparietal junction (10). Capgras delusions involving belongings have also been rarely reported (54).

Visual illusions. Micropsia (objects appearing smaller), macropsia (objects appearing larger), metamorphopsia (distortion of images), and achromatopsia (loss of color vision) can also be clinical manifestations of seizures originating in the occipital-temporoparietal junction.

Eye movement sensations. The sensation of eye movement in the absence of detectable movement has been reported as a sign of occipital seizure origin (05; 41; 70; 71; 90). 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 (33), 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 (80; 60; 70; 71; 90). Although the literature strongly favors contralateral deviation, there are rare exceptions (70; 71; 90). Electrical stimulation studies in humans and animals have reproduced contralateral deviation.

Epileptic nystagmus. Nystagmus as a manifestation of epileptic discharges has been reported repeatedly (29; 05; 55; 60; 70; 71). There is disagreement, however, of the lateralizing significance of the fast and slow components (47). Lee and colleagues reviewed the literature and noted that in all 33 patients with unilateral horizontal nystagmus, the nystagmus was beating away from the side of ictal discharges (50). Monocular isolated epileptic nystagmus has been rarely described (56).

Blinking or eyelid flutter. Forced blinking or eye fluttering has been observed in up to 50% of patients with occipital lobe seizures (05; 60; 90; 04). Depth electrode studies in 24 patients have confirmed ictal blinking (mostly bilateral) as being localized to mostly occipital and occipital-temporal seizures with less frequent localization from the medial temporal and insulo-opercular (49).

Signs and symptoms of propagation. Occipital seizure foci are uniquely situated to allow multiple possible propagation patterns (01; 70; 71; 45). Occipital lobe seizures can spread above or below the sylvian fissure, medially or laterally, ipsilateral or contralateral to the side of origin.

Occiptal lobe seizure spread pattern

(From: Ajmone-Marsan C, Ralston BL. The epileptic seizure. Springfield, Illinois: Charles C Thomas, 1957:214. Used with permission.)

Several reports have noted that complex visual hallucinations usually follow elementary visual hallucination, suggesting propagation outside of the occipital lobe (55; 60; 11; 90). Complex visual hallucinations may require involvement of both limbic and neocortical structures. Propagation from the occipital lobe to medial temporal structures has been well documented (55; 60; 90). Automatisms indistinguishable from those of typical temporal lobe epilepsy occur (79; 71; 72). Suprasylvian spread results in various focal tonic and clonic motor manifestations (79; 11; 70; 71). Although contralateral propagation with lateralized clinical manifestations is theoretically possible, this has been only partially documented with intracranial recording (79).

The potential for multiple spread patterns holds true among different patients and within individual patients (79). 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.

Postictal vomiting and headaches are common with occipital lobe seizures (45; 23). Secondary generalization is frequent (61; 62; 48). Prolonged visual nonconvulsive status epilepticus has been repeatedly reported (06; 45).

Parietal lobe seizures. Similar to occipital lobe seizures, parietal lobe seizures can be divided into subjective and objective manifestations. Although certain symptoms and possibly some signs 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 (65): 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 (89; 18; 40; 72). 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 (89). 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 (77). Ictal pain is usually a sign of parietal lobe seizure origin (77). 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 has also been equated with parietal lobe seizure origin (77; 64).

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 (52). This has been documented with intracranial recording and successful surgery (77).

Vertigo. True vertigo is reportedly due to seizure activity in the temporoparietal junction. Although it is a well-established seizure symptom, epileptic vertigo is rare, and the exact neocortical representation has not been documented with precision (76). In a systematic review of epileptic vertigo and dizziness that reviewed 84 studies and 11,354 patients, localized EEG was more frequently temporal, with parietal EEG abnormalities noted only in 11.8% (82).

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 (65). A case report implicated the precuneus (57). Body image disturbances may also be seen with precuneal epilepsy (91).

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.

Proprioceptive induced seizures (motor seizures triggered by proprioceptive stimuli of extremities) are a rare manifestation of parietal lobe seizures (92).

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 (89; 02). 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 (77). Ictal hemiballism has been associated with seizure onset in the inferior parietal lobule or the parietal operculum (28).

Signs and symptoms of seizure propagation. Posterior propagation from the parietal lobe can result in a patient experiencing elementary visual hallucinations or ictal amaurosis. 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 (35; 89; 77). Inhibitory or hemiplegic seizures may occur, but it is not known whether this represents spread beyond the parietal lobe (77; 86). Inferior spread into the temporal lobe has been well documented with intracranial recording (89). It has been suggested that posterior parietal lobe seizure origin is most often associated with spread to the temporal lobes (40). Inferior parietal seizures may be associated with grimacing, expressing itself as both laughter and disgust (53).

Prognosis and complications

Prognosis, of course, depends on the underlying etiology of the seizures. The benign idiopathic occipital lobe epilepsies respond well to medications (59; 75; 26). Symptomatic occipital lobe epilepsy may respond to regular antiseizure medications, but if this is not successful, epilepsy surgery should be considered. Epilepsy surgery is less successful in the posterior neocortex than in other parts of the brain due to the large cortical surface (16). Approximately a 50% seizure-free outcome is reported in most series (70; 90; 61; 40; 72; 04; 10; 20; 16; 46; 81), although surgical success rates above 80% in occipital lobe epilepsy and above 60% in parietal lobe epilepsy have also been reported (81).

Lately, there has been discussion about whether focal childhood epilepsies such as idiopathic childhood epilepsies with occipital paroxysms cause neuropsychological impairment. A study showed that there is impaired object identification in COVE, formerly known as idiopathic childhood occipital epilepsy, possibly related to the amount of epileptiform activity (14; 66). Others found overall decreased performance in visuomotor coordination, memory, and attention in a similar patient population. Drug resistant epilepsy related to posterior cortex epilepsy in a pediatric cohort showed impairment in working memory and processing speed (73).

Clinical vignette

A 54-year-old woman with a longstanding history of depression and anxiety was referred for episodes of “arm cramping” at night. She described those episodes as extremely painful, occurring frequently and with some arm shaking. She also stated that during those episodes she had a feeling such that her arm did not belong to her. The episodes started three years prior to her clinic visit. She had a history of PTSD and abuse. An MRI of her brain was normal and previous interictal EEGs were normal. Because of her long previous psychiatry history, her episodes were thought to be psychogenic. To clarify the diagnosis she was admitted for video EEG. During the first night, an episode was recorded in which the patient reported pain in her right arm. She then had dystonic posturing and severe pain in the right arm. She yelled and screamed as long as the pain lasted. She was completely conscious throughout. The EEG showed a clear rhythmic seizure discharge over the left centroparietal region. The patient became seizure free with carbamazepine.

Biological basis

Localization

By definition, seizures of the posterior neocortex originate in regions of the cerebral cortex behind the rolandic fissure, not including the posterior limits of the temporal lobe. Certain initial signs or symptoms localize the region of origin. For example, elemental visual hallucinations or ictal amaurosis localize to the occipital pole, whereas localized paresthesias would implicate the contralateral primary sensory cortex (90; 89). Visual auras of any type do not localize to a certain subregion of the occipital lobes (10). Even primary elementary hallucinations are not definitely associated with seizure onset in the mesial occipital cortex (13; 45). Bien and colleagues suggested that visual auras can also occur with anteromedial temporal lobe epilepsy (10) and are not entirely specific for occipital lobe epilepsy. Only visual field deficits seem to reliably localize to the medial occipital cortex (13).

Etiology and pathogenesis

The same principles associated with the causes of human epilepsy apply to parietal and occipital lobe seizures. These have been summarized by Engel and include nonspecific predisposing factors, specific epileptogenic disturbances, and precipitating factors (25). The causes are variable and include among others genetic disorders, postanoxic brain injury, neoplastic brain disorders, infections including neurocysticercosis, disorders of cortical development, and immune-mediated inflammatory disorders.

Pathophysiology

The underlying pathophysiology for any type of focal seizure is a disturbance of excitation and inhibition on a neuronal level that finally leads to hypersynchronization and propagation of seizure activity.

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, posttraumatic encephalomalacia, and vascular malformations are the pathological substrate for posterior neocortical seizures (20).

Differential diagnosis

Confusing conditions

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 (01; 70; 72; 90; 89; 88). The overall seizure pattern can, therefore, be misleading. Occipital lobe seizures can often masquerade as temporal lobe seizures. In a retrospective case-control series, visual symptoms were present in only 8 of 19 occipital lobe seizure patients, and occipital spikes were found in only one third (03).

Seizures originating in the parietal lobe seem to be particularly prone to be devoid of localizing information. In two studies of parietal lobe seizures, only half of the patients had clinical findings suggesting parietal lobe seizure origin (89; 18). All patients in both studies had parietal lesions on MRI that served to identify the region of seizure origin. Differential diagnosis includes nonepileptic psychogenic seizures with visual complaints or somatosensory complaints. As occipital lobe seizures are frequently followed by postictal headache, migraine is often considered an alternative diagnosis. Occipital epilepsy and migraine can be indistinguishable, unless the patient has generalized tonic-clonic convulsions or seizures with loss of consciousness (21). As pure sensory parietal seizures can present with prolonged paresthesias, those seizures are often mistaken as transient ischemic attacks. Video/EEG monitoring should be utilized to clarify the differential diagnosis.

Associated and underlying disorders

Self-limited childhood epilepsies with occipital lobe spike (COVE type and SeLEAS). Occipital lobe seizures can occur in the benign idiopathic childhood epilepsies with occipital lobe spikes (34). Two types of benign idiopathic occipital epilepsy have been described (Table 1): a syndrome with early onset (SeLEAS: formerly known as Panayiotopoulos type or benign childhood seizures susceptibility syndrome) and a late-onset form (COVE syndrome: formerly known as Gastaut type). It has been discussed whether in Panayiotopoulos type the seizures onset zone is truly in the occipital lobe or whether the epileptogenic zone is more widespread in this particular syndrome (63). Genetically, both syndromes show a complex pattern of inheritance (83).

SeLAS (self-limited epilepsy with autonomic seizures) has a mean onset age of 4.7 years. Seizures mainly consist of gaze deviation, ictal vomiting, and autonomic symptoms. Nonconvulsive prolonged episodes are common. EEG shows typical posterior paroxysmal epileptiform activity. Seizures may remit spontaneously after one to two years (26).

COVE (childhood occipital visual epilepsy) manifests between the ages of 7 and 9 years, and seizures are mainly characterized by visual hallucinations, ictal amaurosis, and postictal headaches. Status epilepticus is rare. Seizures readily respond to antiepileptic medications. MRI is normal (17).

Table 1. Clinical Characteristics of Syndromes with Occipital Lobe Seizures

Seizure syndrome	Age of onset	Seizure characteristics	Nonconvulsive status	Prognosis
SeLAS (Panayiotopoulos type)	3 to 6 years	Gaze deviation, ictal vomiting, headaches, autonomic symptoms	Common, 44% to 46%	Remits spontaneously
COVE (Gastaut type)	7 to 9 years	Visual hallucinations, amaurosis	Uncommon	Good
Symptomatic occipital lobe epilepsy	Variable, depending on etiology	Amaurosis, nystagmus, eye deviation, visual hallucinations	Variable	Depending on etiology

Symptomatic occipital lobe epilepsy. Symptomatic occipital lobe epilepsy is associated with abnormal pathology in the occipital lobes. This includes tumors, gliosis, vascular malformations, and malformations of cortical development. Age of onset and prognosis is variable due to the underlying etiology (Table 1).

Other systemic diseases associated with occipital lobe seizures. Occipital lobe seizures occur in celiac diseases with occipital lobe calcifications (31; 09) and Sturge-Weber variant (22). Posterior reversible encephalopathy syndrome (PRES) due to hypertension or immunosuppression can be the cause of occipital lobe seizures (51).

Overlap of occipital lobe epilepsy with photosensitive genetic generalized epilepsy. Variants have been observed in patients with retinoid related orphan receptor beta genetic variants with patients exhibiting both generalized photosensitive seizures and occipital lobe seizures. The median age of onset of these patients is 3.5 years, with many suffering from intellectual disability (68). POLE (photosensitive occipital lobe epilepsy formerly known as idiopathic photosensitive occipital lobe epilepsy) is a syndrome that should be suspected in patients with seizures with occipital semiology, photosensitivity, and normal MRI (36).

No recognized diseases or syndromes are associated exclusively with parietal lobe seizures, and parietal lobe epilepsy is generally thought to be symptomatic in origin.

Diagnostic workup

If, after a thorough history and examination, focal epilepsy of any type is suspected, a high-resolution, if possible, 3T MRI should be obtained early in the course of the evaluation to search for a structural cause of the seizures. As parietal lobe seizures are difficult to diagnose and may imitate other focal epilepsies, MRI may be the only diagnostic test to suggest the parietal lobe as the site of seizure onset (67). Interictal EEG is usually performed to assess for epileptiform activity. EEG may show occipital or parietal spikes, but can be misleading and localize to the posterior temporal lobes or other cortical areas (67). Ictal EEG can show occipital or parietal rhythmic epileptiform activity.

Occiptal lobe seizures (ictal EEG)

Ictal EEG of a patient with an ongoing occipital lobe seizure. The patient was seeing flickering spots in the left visual field. (Contributed by Dr. Barbara C Jobst.)
Parietal lobe seizure (ictal EEG)

Ictal EEG of a parietal lobe seizure with the major rhythmic seizure activity ongoing over the left central region (C3). The patient had a painful seizure with dystonia of her right hand. (Contributed by Dr. Barbara C Jobst.)

Even prolonged monitoring is often not informative in patients with posterior neocortical seizure origin due to false localization on scalp EEG (11; 89; 18; 32). 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 (43).

Intractable parietal and occipital lobe epilepsy surgical treatment algorithm

Surgical treatment algorithm for intractable parietal and occipital lobe epilepsy. (From: Jobst BC. Treatment algorithms in refractory partial epilepsy. Epilepsia 2009;50(Suppl 8):51-6. Used with permission.)

Detection of a single, well-circumscribed epileptogenic lesion greatly simplifies the presurgical evaluation, and epilepsy surgery will be more successful compared to patients with nonlesional epilepsy (87). Prolonged video-EEG monitoring, ictal SPECT, FDG-PET, additional high-resolution MRI, MRI-PET fusion, magnetoencephalography, and intracranial EEG studies are essential to localize the seizure onset zone for later resection (69). Multilobar resections of the posterior neocortex also have a good success rate (74). The neuropsychological profiles of parietal and occipital lobe epilepsy are not well defined, though some studies have shown visuoconstruction and verbal and executive deficits (85).

Management

No antiseizure drugs preferentially work on the posterior neocortex. Any of the approved antiseizure medications are effective; however, not all are approved as initial therapy or monotherapy. Antiseizure medications should be chosen based on the side effect profile and comorbidities of the patient. Reproductive and psychosocial factors are other considerations.

If seizures do not respond to medical treatment, resective surgery should be considered and referral to a comprehensive surgical epilepsy center initiated even if no clear lesion on MRI can be identified (43).

Intractable parietal and occipital lobe epilepsy surgical treatment algorithm

Success rate of surgical intervention is variable (70; 89; 81). In a review and metaanalysis of 27 published case series involving occipital and posterior quadrant epilepsy surgery, an Engel class I outcome was observed in 65% of patients (38). Vagal nerve stimulation is another effective adjunctive treatment (44). Responsive neurostimulation may be another effective alternative and has been available since 2013 with a median reduction of seizures of 53% at two years (39). There are also some studies exploring the use of targeting with neurostimulation the pulvinar nucleus in patients with posterior epilepsies (15). Total and partial posterior quadrant disconnection has also been performed in select patients (58).

Media

References

01: Ajmone-Marsan C, Ralston BL. The epileptic seizure: its functional morphology and diagnostic significance. Springfield, Illinois: Charles C Thomas, 1957:211-5.
02: Akimura T, Fujii M, Ideguchi M, Yoshikawa K, Suzuki M. Ictal onset and spreading of seizures of parietal lobe origin. Neurol Med Chir (Tokyo) 2003;43(11):534-40. PMID 14705319
03: Appel S, Sharan AD, Tracy JI, Evans J, Sperling MR. A comparison of occipital and temporal lobe epilepsies. Acta Neurol Scand 2015;132(4):284-90. PMID 25809072
04: Aykut-Bingol C, Bronen RA, Kim JH, Spencer DD, Spencer SS. Surgical outcome in occipital lobe epilepsy: implications for pathophysiology. Ann Neurol 1998;44(1):60-9. PMID 9667593
05: Bancaud J, Talairach J, Bonis A, et al. Les epilepsies occipitales. In: La Stéréo-électroencéphalographie dans l’Épilepsie. Masson: Paris, 1965:93-103.
06: Barry E, Sussman NM, Bosley TM, Harner RN. Ictal blindness and status epilepticus amauroticus. Epilepsia 1985;26(6):577-84. PMID 4076063
07: Battino D, Tomson T. Management of epilepsy during pregnancy. Drugs 2007;67(18):2727-46. PMID 18062721
08: Berg A, Berkovic SF, Brodie MJ, et al. Revised terminology and concepts for organization of seizures and epilepsies: report of the ILAE commission on Classification and Terminology, 2005-2009. Epilepsia 2010;51(4):676-85. PMID 20196795
09: Bernasconi A, Bernasconi N, Andermann F, et al. Celiac disease, bilateral occipital calcifications and intractable epilepsy: mechanisms of seizure origin. Epilepsia 1998;39(3):300-6. PMID 9578049
10: Bien CG, Benninger FO, Urbach H, Schramm J, Kurthen M, Elger CE. Localizing value of epileptic visual auras. Brain 2000;123(Pt 2):244-53. PMID 10648433
11: Blume WT. Occipital lobe epilepsies. In: Luders H, editor. Epilepsy surgery. New York: Raven Press Ltd, 1991:167-71.
12: Blume WT, Whiting SE, Girvin JP. Epilepsy surgery in the posterior cortex. Ann Neurol 1991;29:638-45. PMID 1892366
13: Blume WT, Wiebe S, Tapsell LM. Occipital epilepsy: lateral versus mesial. Brain 2005;128(Pt 5):1209-25. PMID 15788545
14: Brancati C, Barba C, Metitieri T, et al. Impaired object identification in idiopathic childhood occipital epilepsy. Epilepsia 2012;53(4): 686-94. PMID 22352401
15: Burdette D, Mirro EA, Lawrence M, Patra SE. Brain-responsive corticothalamic stimulation in the pulvinar nucleus for the treatment of regional neocortical epilepsy: A case series. Epilepsia Open 2021;6(3):611-7. PMID 34268893
16: Caicoya AG, Macarron J, Albisua J, Serratosa JM. Tailored resections in occipital lobe epilepsy surgery guided by monitoring with subdural electrodes: characteristics and outcome. Epilepsy Res 2007;77(1):1-10. PMID 17923392
17: Caraballo RH, Cersosimo RO, Fejerman N. Childhood occipital epilepsy of Gastaut: a study of 33 patients. Epilepsia 2008;49(2):288-97. PMID 17888075
18: Cascino GD, Hulihan JF, Sharbrough FW, Kelly PJ. Parietal lobe lesional epilepsy: electroclinical correlation and operative outcome. Epilepsia 1993;34(3):522-7. PMID 8504784
19: Cedzich C, Taniguchi M, Schafer S, Schramm J. Somatosensory evoked potential phase reversal and direct motor cortex stimulation during surgery in and around the central region. Neurosurgery 1996;38(5):962-70. PMID 8727822
20: Dalmagro CL, Bianchin MM, Velasco TR, et al. Clinical features of patients with posterior cortex epilepsies and predictors of surgical outcome. Epilepsia 2005;46(9):1442-9. PMID 16146440
21: Davies PT, Panayiotopoulos CP. Migraine triggered seizures and epilepsy triggered headache and migraine attacks: a need for re-assessment. J Headache Pain 2011;12(3):287-8. PMID 21516466
22: DeMarco P, Lorenzin G. Growing bilateral occipital calcifications and epilepsy. Brain Dev 1990;12(3):342-4. PMID 2403206
23: Ekstein D, Schachter SC. Postictal headache. Epilepsy Behav 2010;19(2):151-5. PMID 20829119
24: Engel J Jr. Report of the ILAE classification core group. Epilepsia 2006;47(9):1558-68. PMID 16981873
25: Engel J Jr. Causes of human epilepsy. In: Engel J Jr, editor. Seizures and epilepsy. 2nd edition. New York: Oxford University Press, 2013:157-90.
26: Ferrie C, Caraballo R, Covanis A, et al. Panayiotopoulos syndrome: a consensus view. Dev Med Child Neurol 2006;48(3):236-40. PMID 16483404
27: Fisher RS. The new classification of seizures by the International League Against Epilepsy 2017. Curr Neurol Neurosci Rep 2017;17(6):48. PMID 28425015
28: Fluchere F, McGonigal A, Villeneuve N, Chauvel P, Bartolomei F. Ictal “hemiballic-like” movement: lateralizing and localizing value. Epilepsia 2012;53(2):e41-5. PMID 22191383
29: Foerster O, Penfield W. The structural basis of traumatic epilepsy and results of radical operations. Brain 1930;53:99-119.
30: Fogarasi A, Boesebeck F, Tuxhorn I. A detailed analysis of symptomatic posterior cortex seizure semiology in children younger than seven years. Epilepsia 2003;44(1):89-96. PMID 12581235
31: Fois A, Vascotto M, Di Bartolo RM, Di Marco V. Celiac disease and epilepsy in pediatric patients. Childs Nerv Syst 1994;10(7):450-4. PMID 7842435
32: Foldvary N, Klem G, Hammel J, Bingaman W, Najm I, Luders H. The localizing value of ictal EEG in focal epilepsy. Neurology 2001;57(11):2022-8. PMID 11739820
33: Galimberti CA, Versino M, Sartori I, Manni R, Martelli A, Tartara A. Epileptic skew deviation. Neurology 1998;50(5):1469-72. PMID 9596010
34: Gastaut H. A new type of epilepsy: benign partial epilepsy of childhood with occipital spike-waves. Clin Electroencephalogr 1982;13:13-22. PMID 6802526
35: Geier S, Bancaud J, Talairach J, Bonis A, Hossard-Bouchaud H, Enjelvin M. Ictal tonic postural changes and automatisms of the upper limb during epileptic parietal lobe discharges. Epilepsia 1977;18:517-24. PMID 590226
36: Gomez-Porro P, Aledo-Serrano A, Toledano R, García-Morales I, Gil-Nagel A. Genetic (idiopathic) generalized epilepsy with occipital semiology. Epileptic Disord 2018;20(5):434-9. PMID 30361187
37: Gowers WR. Cases of cerebral tumour illustrating diagnosis and localisation. Lancet 1879;1:363-5.
38: Harward SC, Chen W, Rolston JD, Haglund MM, Englot DJ. Seizure outcomes in occipital lobe and posterior quadrant epilepsy surgery: a systematic review and meta-analysis. Neurosurgery 2018;82(3):350-8. PMID 28419330
39: Heck CN, King-Stephens D, Massey AD, et al. Two-year seizure reduction in adults with medically intractable partial onset epilepsy treated with responsive neurostimulation: final results of the RNS System Pivotal trial. Epilepsia 2014;55(3):432-41. PMID 24621228
40: Ho SS, Berkovic SF, Newton MR, Austin MC, McKay WJ, Bladin PF. Parietal lobe epilepsy: clinical features and seizure localization by ictal SPECT. Neurology 1994;44:2277-84. PMID 7991112
41: Holtzman RN. Sensations of ocular movement in seizures originating in occipital lobe. Neurology 1977;27:554-6. PMID 405625
42: Jackson JH. Selected writings of John Hughlings Jackson Volumes 1 and 2. Taylor J, editor. London, England: Staples Press, 1958.
43: Jobst BC. Treatment algorithms in refractory partial epilepsy. Epilepsia 2009;50 Suppl 8: 51-6. PMID 19702734
44: Jobst BC. Brain stimulation for surgical epilepsy. Epilepsy Res 2010;89(1):154-61. PMID 19766458
45: Jobst BC, Roberts DW, Williamson PD. Occipital lobe nonconvulsive status epilepticus. In: Kaplan PW, Drislane F, editors. Nonconvulsive status epilepticus. New York: Demos Medical Publishing, 2008.
46: Jobst BC, Williamson PD, Thadani VM, et al. Surgical treatment of occipital lobe epilepsy. Are there any predictors of a good outcome. Epilepsia 2007;0 Suppl 0:2.074.
47: Kaplan PW, Tusa RJ. Neurophysiologic and clinical correlations of epileptic nystagmus. Neurology 1993;43(12):2508-14. PMID 8255448
48: Kun Lee S, Young Lee S, Kim DW, Soo Lee D, Chung CK. Occipital lobe epilepsy: clinical characteristics, surgical outcome, and role of diagnostic modalities. Epilepsia 2005;46(5):688-95. PMID 15857434
49: Lagarde S, Dirani M, Trebuchon A, et al. Ictal blinking in focal seizures: insights from SEEG recordings. Seizure 2020;81:21-8. PMID 32688170
50: Lee SU, Suh HI, Choi JY, Huh K, Kim HJ, Kim JS. Epileptic nystagmus: a case report and systematic review. Epilepsy Behav Case Rep 2014;2:156-60. PMID 25667896
51: Lee VH, Wijdicks EF, Manno EM, Rabinstein AA. Clinical spectrum of reversible posterior leukoencephalopathy syndrome. Arch Neurol 2008;65(2):205-10. PMID 18268188
52: Leiguarda R, Starkstein S, Nogues M, Berthier M, Arbelaiz R. Paroxysmal alien hand syndrome. J Neurol Neurosurg Psychiatry 1993;56(7):788-92. PMID 8331355
53: Lentoiu C, Oane I, Barborica A, et al. Motor and emotional facial features in parietal lobe seizures: an ictal functional connectivity study using SEEG. Epileptic Disord 2022;24(5):838-46. PMID 35811434
54: Lilly B, Maynard E, Melvin K, Holroyd S. “Capgras” delusions involving belongings not people and evolving visual hallucinations associated with occipital lobe seizures. Case Rep Psychiatry 2018;2018:1459869. PMID 29707400
55: Ludwig BI, Marsan CA. Clinical ictal patterns in epileptic patients with occipital electroencephalographic foci. Neurology 1975;25:463-71. PMID 1169704
56: Ma Y, Wang J, Li D, Lang S. Two types of isolated epileptic nystagmus: case report. Int J Clin Exp Med 2015;8(8):13500-7. PMID 26550287
57: Mailo J, Tang-Wai R. Insight into the precuneus: a novel seizure semiology in a child with epilepsy arising from the right posterior precuneus. Epileptic Disord 2015;17(3):321-7. PMID 26235442
58: Markosian C, Dodson V, Zhang HJ, Mahalingam RS, Geller EB, Tomycz LD. Total and partial posterior quadrant disconnection for medically refractory epilepsy: A systematic review. Seizure 2021;91:66-71. PMID 34102378
59: Mennink S, van Nieuwenhuizen O, Jennekens-Schinkel A, van der Schouw YT, van der Meij W, van Huffelen AC. Early prediction of seizure remission in children with occipital lobe epilepsy. Eur J Paediatr Neurol 2003;7(4):161-5. PMID 12865055
60: Munari C, Bonis A, Kochen S, et al. Eye movements and occipital seizures in man. Acta Neurochir 1984;33([Suppl] (Wien)):47-52.
61: Palmini A, Andermann F, Dubeau F, et al. Occipitotemporal epilepsies: evaluation of selected patients requiring depth electrodes studies and rationale for surgical approaches. Epilepsia 1993;34(1):84-96. PMID 8422868
62: Panayiotopoulos CP. Visual phenomena and headache in occipital epilepsy: a review, a systematic study and differentiation from migraine. Epileptic Disord 1999;1(4):205-16. PMID 10937155
63: Panayiotopoulos CP, Michael M, Sanders S, Valeta T, Koutroumanidis M. Benign childhood focal epilepsies: assessment of established and newly recognized syndromes. Brain 2008;131(Pt 9):2264-86. PMID 18718967
64: Pazarci NK, Bebek N, Baykan B, Gurses C, Gokyigit A. Reappraisal of pain as a rare symptom of seizures. Epilepsy Behav 2016;55:101-7. PMID 26773678
65: Penfield W, Jasper H. Epilepsy and the functional anatomy of the human brain. Boston: Little, Brown & Co, 1954.
66: Polat M, Gokben S, Tosun A, Serdaroglu G, Tekgul H. Neurocognitive evaluation in children with occipital lobe epilepsy. Seizure 2012;21(4):241-4. PMID 22265577
67: Ristic AJ, Alexopoulos AV, So N, Wong C, Najm IM. Parietal lobe epilepsy: the great imitator among focal epilepsies. Epileptic Disord 2012;14(1): 22-31. PMID 22426412
68: Sadleir LG, de Valles-Ibáñez G, King C, et al. Inherited RORB pathogenic variants: overlap of photosensitive genetic generalized and occipital lobe epilepsy. Epilepsia 2020;61(4):e23-9. PMID 32162308
69: Salamon N, Kung J, Shaw SJ, et al. FDG-PET/MRI coregistration improves detection of cortical dysplasia in patients with epilepsy. Neurology 2008;71(20):1594-1601. PMID 19001249
70: Salanova V, Andermann F, Olivier A, Rasmussen T, Quesney LF. Occipital lobe epilepsy: electroclinical manifestations, electrocorticography, cortical stimulation and outcome in 42 patients treated between 1930 and 1991. Surgery of occipital lobe epilepsy. Brain 1992;115(Pt 6):1655-80. PMID 1486456
71: Salanova V, Andermann F, Rasmussen TB. Occipital lobe epilepsy. In: Wyllie E, editor. The treatment of epilepsy: principles and practices. Philadelphia: Lea & Febiger, 1993:533-40.
72: Salanova V, Andermann F, Rasmussen T, Olivier A, Quesney LF. Parietal lobe epilepsy. Clinical manifestations and outcome in 82 patients treated surgically between 1929 and 1988. Brain 1995;118(Pt 3):607-27. PMID 7600082
73: Santos LE, de Angelis G, Velasco TR, Thome U, et al. The intellectual profile of pediatric patients with posterior cortex epilepsy. Epilepsy Behav 2021;125:108447. PMID 34839240
74: Sarkis RA, Jehi L, Najm IM, Kotagal P, Bingaman WE. Seizure outcomes following multilobar epilepsy surgery. Epilepsia 2012;53(1):44-50. PMID 21955142
75: Shahar E, Barak S. Favorable outcome of epileptic blindness in children. J Child Neurol 2003;18(1):12-6. PMID 12661932
76: Siegel AM. Parietal lobe epilepsy. Adv Neurol 2003;93:335-45. PMID 12894418
77: Siegel AM, Williamson PD, Roberts DW, Thadani VM, Darcey TM. Localized pain associated with seizures originating in the parietal lobe. Epilepsia 1999;40(7):845-55. PMID 10403207
78: Specchio N, Wirrell EC, Scheffer IE, et al. International League Against Epilepsy classification and definition of epilepsy syndromes with onset in childhood: Position paper by the ILAE Task Force on Nosology and Definitions. Epilepsia 2022;63(6):1398-442. PMID 35503717
79: Stewart LF, Dreifuss FE. "Centrencephalic" seizure discharges in focal hemispheral lesions. Arch Neurol 1967;17(1):60-8. PMID 6026173
80: Takeda A, Bancaud J, Talairach J, Bonis A, Bordas-Ferrer M. Concerning epileptic attacks of occipital origin. Electroencephalogr Clin Neurophysiol 1970;28(6):647-8. PMID 4192863
81: Tandon N, Alexopoulos AV, Warbel A, Najm IM, Bingaman WE. Occipital epilepsy: spatial categorization and surgical management. J Neurosurg 2009;110(2):306-18. PMID 19046038
82: Tarnutzer AA, Lee SH, Robinson KA, Kaplan PW, Newman-Toker DE. Clinical and electrographic findings in epileptic vertigo and dizziness: a systematic review. Neurology 2015;84(15):1595-1604. PMID 25795644
83: Taylor I, Scheffer IE, Berkovic SF. Occipital epilepsies: identification of specific and newly recognized syndromes. Brain 2003;126(Pt 4):753-69. PMID 12615636
84: Tellez-Zenteno JF, Hernández-Ronquillo L. A review of the epidemiology of temporal lobe epilepsy. Epilepsy Res Treat 2012;2012:630853. PMID 22957234
85: Traianou A, Patrikelis P, Kosmidis MH, Kimiskidis VΚ, Gatzonis S. The neuropsychological profile of parietal and occipital lobe epilepsy. Epilepsy Behav 2019;94:137-43. PMID 30909077
86: Umeoka S, Baba K, Terada K, et al. Bilateral symmetric tonic posturing suggesting propagation to the supplementary motor area in a patient with precuneate cortical dysplasia. Epileptic Disord 2007;9(4):443-8. PMID 18077232
87: Urbach H, Binder D, von Lehe M, et al. Correlation of MRI and histopathology in epileptogenic parietal and occipital lobe lesions. Seizure 2007;16(7):608-14. PMID 17560810
88: Williamson PD. Parietal lobe epilepsy. In: Oxbury T, Polkey C, Duchowny M, editors. Intractable focal epilepsy. London: Harcourt Brace & Co. Ltd., 1999.
89: Williamson PD, Boon PA, Thadani VM, et al. Parietal lobe epilepsy: diagnostic considerations and results of surgery. Ann Neurol 1992b;31:193-201. PMID 1575458
90: Williamson PD, Thadani VM, Darcey TM, et al. Occipital lobe epilepsy: clinical characteristics, seizure spread patterns and results of surgery. Ann Neurol 1992a;31:3-13. PMID 1543348
91: Yang Y, Wang H, Zhou W, Qian T, Sun W, Zhao G. Electroclinical characteristics of seizures arising from the precuneuis based on stereoencephalography (SEEG). BMC Neurol 2018;18(1):110. PMID 30103717
92: Zheng Y, Ming WJ, Zheng Z, et al. Pearls & oy-sters: parietal lobe epilepsy in disguise: motor attacks induced by proprioceptive triggers. Neurology 2022;98(12):509-13. PMID 35101912

Contributors

All contributors' financial relationships have been reviewed and mitigated to ensure that this and every other article is free from commercial bias.

Author

Dawn Eliashiv MD

Dr. Eliashiv of the David Geffen School of Medicine at the University of California, Los Angeles, received honorariums from Eisai, Medtronic Inc., Neuropace, and UCB for consulting work.
See Profile

Editor

Jerome Engel Jr MD PhD

Dr. Engel of the David Geffen School of Medicine at the University of California, Los Angeles, has no relevant financial relationships to disclose.
See Profile

Former Authors

Peter D Williamson MD (original author) and Barbara C Jobst MD

This is an article preview.
Start a Free Account
to access the full version.

Nearly 3,000 illustrations, including video clips of neurologic disorders.
Every article is reviewed by our esteemed Editorial Board for accuracy and currency.
Full spectrum of neurology in 1,200 comprehensive articles.
Listen to MedLink on the go with Audio versions of each article.

Questions or Comment?

MedLink®, LLC

3525 Del Mar Heights Rd, Ste 304
San Diego, CA 92130-2122

Toll Free (U.S. + Canada): 800-452-2400

US Number: +1-619-640-4660

Support: service@medlink.com

Editor: editor@medlink.com

ISSN: 2831-9125

Seizures of the posterior neocortex

Associated Disorders

Neoplasms
Posttraumatic encephalomalacia
Vascular malformations

Differential Diagnosis

frontal lobe seizures
lateral temporal seizures
mesial temporal seizures
panic attacks
nonepileptic psychogenic seizures
- migraine
- transient ischemic attacks

Also Relevant

Epilepsy
Epilepsy surgery in adults
Focal sensory seizures with experiential symptoms
Idiopathic childhood occipital epilepsy of Gastaut
Panayiotopoulos syndrome
- Photosensitive occipital lobe epilepsy

Clinical Categories

Epilepsy & Seizures

Patient Handouts

Seizure first aid

Web References

Guidelines

Seizures of the posterior neocortex

Introduction

Overview

Key points

Historical note and terminology

Clinical manifestations

Presentation and course

Prognosis and complications

Clinical vignette

Biological basis

Localization

Etiology and pathogenesis

Pathophysiology

Epidemiology

Prevention

Differential diagnosis

Confusing conditions

Associated and underlying disorders

Table 1. Clinical Characteristics of Syndromes with Occipital Lobe Seizures

Diagnostic workup

Management

Special considerations

Pregnancy

Anesthesia

Media

References

Contributors

Author

Editor

Former Authors

Patient Profile

This is an article preview. Start a Free Account to access the full version.

Questions or Comment?

Also in This Category

Anti-LGI1 encephalitis

Self-limited (familial) neonatal epilepsy

Epilepsy with auditory features

Alcohol withdrawal seizures

Epileptic lesions due to malformation of cortical development

Epileptic spasms

Sleep and epilepsy

Neocortical temporal lobe seizures

This is an article preview.
Start a Free Account
to access the full version.