occipital epilepsy blume

doi:10.1093/brain/awh458 Brain (2005), 128, 1209–1225

Occipital epilepsy: lateral versus mesial

Warren T. Blume, Samuel Wiebe and Lisa M. Tapsell

Correspondence to: Warren T. Blume, University Hospital,

The University of Western Ontario, 339 Windermere

Road, London, Ontario, Canada N6A 5A5

E-mail: [email protected]

University Hospital, The University of Western Ontario,

London, Ontario, Canada

SummaryThis study compares ictal semiology, neurological exam-

ination and scalp EEG between lateral and mesial occi-

pital epilepsy to assess the contribution non-invasive data

make in determining the epileptogenic region within an

occipital lobe. We assessed seizure origin in 41 occipital

patients as lateral (11 patients), mesial (20) and both sur-faces (10) as indicated by subdurally recorded seizures

(nine), a lesion whose removal reduced seizure quantity

by>90% (six), or who met both criteria (26). No aspect of

semiology distinguished lateral from mesially originat-

ing occipital seizures. A pre-operative visual field deficit

appeared in eight (42%) out of 19 testable patients

with mesial originating seizures, three (30%) out of

10 patients with both surfaces epileptogenic, but noneof the 10 testable patients whose seizures arose only

from the lateral surface (P = 0.0373, lateral versus mesial

and both surfaces). Although occipital seizures appeared

on the majority of the first five scalp EEG recordings in

four (36%) out of 11 patients with laterally originating

occipital seizures compared with none of 20 patients in

whom seizures originated mesially (P = 0.0105), no other

scalp EEG feature distinguished seizures from these sur-

faces. We conclude that subdural electroencephalogra-

phy is likely to be necessary to delineate the epileptogenicregion within an occipital lobe. Nonetheless, focally ori-

ginating scalp-recorded seizures accurately lateralized the

epileptogenic zone in 20 (49%) of our 41 patients com-

pared with only one (2%) which originated contralater-

ally (P = 0.0001). This relationship held when considering

only the first five scalp EEGs: the seizures of 10 patients

(24%) appeared ipsilaterally and none contralaterally (P =

0.001). Moreover, interictal occipital (01,2) and posteriortemporal (T5, T6) spikes appeared consistently and sig-

nificantly (P < 0.001) more commonly ipsilateral to epi-

leptogenesis than contralateral using multiple methods of

analysis.

Keywords: epilepsy; occipital; semiology; EEG; location

Abbreviations: BA = Brodmann area

Received September 15, 2004. Revised January 21, 2005. Accepted January 31, 2005. Advance Access publication

March 23, 2005

IntroductionConsidering the manifestations of epileptic seizures as pro-

viding insight into the workings of the cerebral cortex, John

Hughlings Jackson (quoted by Eadie MJ and Bladin PF,

2001) wrote: ‘Cases of paralysis and convulsions may be

looked on as the results of experiments made by disease on

particular parts of the nervous system of man.’ Although

clinical–pathological associations formed the bases of his

formulations of cerebral function localization, Jackson non-

etheless realized that such correlations were inexact as: (i) the

epileptic region involved relatively normal brain adjacent to a

lesion, not the lesion itself; and (ii) ictal manifestations could

represent propagation of epileptic discharge from its origin.

Thus he indicated: ‘ . . . there will be all varieties of epilepsy,

according to the exact position of grey matter altered . . . ’.

The variability and complexity of epileptic pathophysiology

implied in these prescient statements have been borne out in

subsequent studies. Williamson (1992), reviewing frontal lobe

seizures, indicated that: ‘ . . . widely different seizure types can

originate in similar regions of the frontal lobe and . . . similar

seizure types can occur with origin in different frontal

regions . . . ’. Similarly, attempts to sub-classify temporal

lobe seizures into mesial and neocortical types on the basis

of clinical characteristics have not succeeded (Walczak,

1995). In this context, we are unaware of clinical studies

comparing mesial and lateral occipital seizures, yet this

distinction is requisite in planning surgical resection.

Penfield and Rasmussen (1950) obtained only gross light,

shadows and colours when electrically stimulating the

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occipital lobe and only occipital lobe stimulation produced

such unformed (unstructured) visual phenomena. Similarly,

Penfield (1954) described occipital seizures as consisting

of unstructured visual phenomena, although some of his

case reports describe generalized motor seizures as well.

He further indicated considerable overlap of visual phenom-

ena between mesial and lateral occipital attacks; but only that

lateral occipital ictal visual phenomena were more apt to be

twinkling and bilateral than were mesial ones.

As the stages of sequential visual processing are unequally

represented on the mesial and lateral occipital surfaces, we

postulated that surface-specific ictal semiology would emerge.

In humans, the primary visual cortex [V1 or Brodmann area

17 (BA17)] lies mainly on the mesial aspect of the occipital

lobe (Truex and Carpenter, 1969). As the initial cortical area

of visual perception, stimuli recorded by the retina are

processed at V1 to provide information of features such as

precise retinal locus, spatial contrast, and orientation (Inouye,

1909; Hubel and Wiesel, 1979). Stimulation of the primary

visual cortex elicits simple phenomena such as flashes of light

[Forster (1929), cited by Brodal, 1981].

The first order visual association areas, particularly V4 and

V5, lie in the prestriate cortex (BA 18, 19) that surrounds the

primary visual cortex on the mesial surface and occupies all

the lateral occipital surface anterior to a rudiment of V1

(Gloor, 1997; Truex and Carpenter, 1969). V4, inhabiting

the caudal fusiform and adjacent lingual gyrus, constitutes

the principal origin of the ventral stream of visual process-

ing providing inputs into the inferotemporal-occipital cortex

whose neurons are sensitive to form, pattern and colour

(Desimone and Ungerleider, 1989); this was subsequently

confirmed by human PET studies (Haxby et al., 1991).

The prestriate area also contains V5, probably at the region

of confluence of the occipital-parietal-temporal lobes. V5 is

a corresponding relay of the dorsal stream of visual pro-

cessing concerned mainly with object localization and eye-

hand coordination (Goodale and Milner, 1992). The prestriate

cortex also contains multiple retinotopic maps of the con-

tralateral visual field, each with a distinct functional role

(Zeki, 1976), but such maps lack the discrete and orderly

properties of the striate cortex (Kandel and Wurtz, 2000).

Thus, both V4 and V5 of the prestriate cortex convey stimuli

into higher-order visual processing areas in the occipital-

temporal lobe (ventral stream) and the parietal lobe (dorsal

stream). As V4 and V5 function as relays to the two streams

of higher-order visual processing, it is not surprising that

stimulation of the prestriate region by Forster (1929) elicited

more complex visual sensations such as animals, people and

various objects. Additionally, ocular deviation can be

obtained by stimulating the prestriate area (BA 18, 19),

but not the striate area (BA 17) (Truex and Carpenter,

1969). As a higher proportion of the mesial occipital region

is occupied by the striate cortex than is the lateral surface and

because of the considerable striate epileptogenicity (Ebersole

and Chatt, 1986), we postulated that, compared with

lateral originating seizures, mesial ictal phenomena would

be: (i) more often unformed (unstructured); (ii) more

commonly localized focally in the visual field; and (iii)

less often associated with ocular deviation. Decisions sur-

rounding sites of invasive recording for possible surgical

management are determined by the relative localizing values

of ictal semiology, neurological examination, interictal and

ictal EEG, and neuroimaging. Thus, we compare ictal semi-

ology and scalp EEG findings in proven lateral occipital

seizure disorders to those of mesial occipital epilepsy. The

lateralizing value of occipital interictal and ictal epileptiform

potentials is also assessed as previous studies (Williamson

et al., 1992; Salanova et al., 1993) concluded that scalp EEG

fails to distinguish left from right occipital epileptogenesis.

MethodFocal occipital epilepsy was clinically suspected from: (i) ictal semi-

ology (Penfield, 1954; Williamson et al., 1992; Blume and Wiebe,

2000); (ii) scalp interictal and ictal EEG (Blume and Wiebe, 2000),

and (iii) any occipital cortical lesion on MRI. Medical intractability

was determined by the hospital’s epilepsy programme and referral

physicians on the bases of seizure incidence and severity, and

response to appropriate focal epilepsy management.

Strip or grid subdural recordings or both were made when non-

invasive data did not adequately determine the principal epilepto-

genic region. Informed consent for telemetred recordings, invasive

recordings and any subsequent operation was obtained. Subdural

grid and strip electrodes consisted of 3 mm stainless steel disks

imbedded in silicon. Subdural strips were placed through burrholes

or by craniotomy for grid placement. All subdurally recorded

patients had bilateral mesial and lateral occipital coverage and

mesial temporal coverage. Most had lateral temporal electrodes

as well. Thus, multiple surface bilateral occipital subdural electro-

encephalography was performed in 35 out of 41 patients: 26 out of

32 with focal occipital neuroimaging lesions and nine without.

Ictal semiology was obtained by descriptions from the patient and

witness, and those of hospital personnel during seizures recorded by

the Epilepsy Unit. Specific aspects included: (i) location of formed

and unformed visual phenomena (Blume et al., 2001b); (ii) dyscog-

nitive (complex partial) components; and (iii) motor phenomena

including ocular and cephalic versive, tonic, clonic and tonic–

clonic features. Neurological examination features principally

sought included visual fields, motor deficits and congenital derma-

tological abnormalities.

Ictal and interictal epileptiform and non-epileptiform occipital,

temporal and diffuse scalp EEG patterns were visually assessed from

16–18 channel out-patient and telemetered recordings comparing

mesially versus laterally originating occipital seizures as indicated

below. Each EEG feature was analysed in four ways, i.e. whether a

phenomenon appeared on: (i) any of the first five scalp recordings;

(ii) a majority of the first five scalp recordings; (iii) any of the scalp

recordings; and (iv) a majority of all the recordings.

We studied the following scalp EEG phenomena: (i) alpha sym-

metry; (ii) delta presence and location; (iii) occipital, temporal and

parietal spikes; (iv) bisynchronous epileptiform activity including

spike-waves; and (v) location of clinical and sub-clinical electro-

graphic seizures, including the proportion with ambiguous origin.

We selected consecutive candidates for epilepsy surgery in whom

at least the majority of clinical seizures arose from an occipital lobe.

Thus, we included patients whose subdurally recorded seizures arose

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from a single occipital lobe (nine patients), those with an occipital

lesion whose removal reduced seizure quantity by >90% (six

patients), or who met both criteria (26 patients). Anterior limits

of the occipital lobe were determined on the lateral surface by

the upper end of the parietal occipital fissure and the preoccipital

notch (Leavens, 1991). The mesial occipital surface was defined as

the cuneus and the lingual gyrus, each extending to the anterior

limits as above defined. Therefore, the inferior limit of the mesial

surface was considered the collateral sulcus and its anterior limit the

parietal-occipital fissure and a line extending from it inferiorly to

the pre-occipital notch. Its superior limit was the border between the

mesial surface and the lateral convexity (Truex and Carpenter,

1969). The remainder of the occipital lobe was considered ‘lateral’

for the purpose of this study. Anatomical borders were applied to

both electrographic and imaging data. The epileptogenic surface was

identified as lateral, mesial or both based on subdural seizure origin,

location of an epileptogenic lesion or both. Lateral or mesial was

identified if all seizures arose from a single surface and any epilep-

togenic lesion resided there (Fig. 1). Both surfaces were considered

epileptogenic within an occipital lobe if: (i) seizure origins varied

between mesial and lateral surfaces or onset appeared on both sur-

faces; (ii) a relevant lesion involved both surfaces; or (iii) a lesion

occupied mostly one aspect while seizures arose from the other.

Excluded were occipital seizure patients with a more active extraoc-

cipital epileptogenic zone defined by scalp, invasive EEG, or both.

Forty-one patients satisfied these criteria.

Prior to invasive recordings (subdurals in 35 patients: electrocor-

ticography in six patients), five patients had 1–5 outpatient and

telemetered EEGs, 16 patients had 6–10 recordings, 15 patients

had 11–20 recordings, and five patients had >20 recordings.

ResultsSeizures originated on the mesial surface in 20 patients, the

lateral surface in 11, and on both surfaces in 10 patients.

Ictal semiology, age of onset, pathologyNo aspect of ictal semiology (Tables 1 and 2) distinguished

laterally from mesially originating occipital seizures. A pre-

operative visual field defect appeared in eight (42%) of the

19 testable patients with mesially originating seizures, three

(30%) of the 10 patients with both surfaces epileptogenic, but

none of the 10 testable patients whose seizures arose only

from the lateral surface (P = 0.0265, lateral versus mesial;

P = 0.0373, lateral versus mesial and both; Table 3).

Age of current seizure onset did not significantly differ

among the groups (Table 4) nor did type of pathology

(Table 5).

Ictal semiology and epileptogenic areas of individual

patients appear in the Appendix.

EEG analyses: mesial versus lateralWith a single exception, none of the studied scalp EEG fea-

tures (Table 6) distinguished lateral versus mesial occipital

epileptogenesis when analysed according to the presence of

a phenomenon on any, or a majority, of the first five or all pre-

invasive scalp recordings. The single exception was that

occipital seizures appeared in a majority of the first five

scalp EEG recordings in four (36%) out of 11 patients

with laterally originating occipital seizures compared with

none of 20 patients in whom the seizures originated mesially

(P = 0.0105).

EEG: ipsilateral versus contralateralOccipital seizures appeared ipsilateral to the side of ulti-

mately established epileptogenesis in the first five records

1

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7

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(A)

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Fig. 1 Continued on next page.

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1

2

3

4

5

6

7

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10

(B)

1

2

3

4

5

6

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9

10

(C)

Fig. 1 Representation of subdurally recorded EEGs of patient whose occipital seizures arose simultaneously from both mesial and lateralsurfaces. Depicts a limited sample of multiple left mesial and lateral electrode positions. First four channels represent a vertically orientatedmesial line extending from just above the calcarine cortex downwards; the bottom six lines depict an obliquely-placed electrode extendingfrom the junction of the mesial and lateral surfaces (channel 5) around to the convexity in a posterior to anterior direction on the occipitallobe convexity (channels 6–10). (A) Widely synchronous interictal spikes involving principally the lateral surface but clearly present onmesial derivations as well. (B) Clinical seizure begins as high frequency waves in principally the lateral surface (channels 6–9) andevolving instantly to a more restricted portion of the mesial surface (channels 3,4). (C) Seizure now involves principally the mesial surface(channels 3,4) but involves both surfaces in a widespread fashion. Settings: 50 mV/mm; 30 mm/sec.




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of 10 (24%) of these 41 patients and none appeared contralat-

erally (P = 0.001) (Table 7). Considering all pre-invasive

EEGs among these 41 patients, ipsilaterally originating occi-

pital seizures appeared in 20 (49%) compared with one (2%)

contralaterally (P = 0.0001).

All four methods of scalp EEG analysis disclosed that

occipital (01, 02) and posterior temporal (T5, T6) spikes

each appeared more commonly ipsilateral to epileptogenesis

than contralateral (Table 7). Anterior temporal spikes

appeared contralateral to occipital epileptogenesis in 11 out of

41 patients (27%) but in fewer patients than ipsilateral ones.

Surgical follow-upAs the focus of this study was not surgical effectiveness, its

follow-up was only assessed retrospectively from material

available on hospital charts. Of the 32 patients for whom

adequate (>2 years) follow-up was obtained, seven (22%)

were seizure-free on one or more antiepileptic medications,

14 (44%) were improved and 11 (34%) were not helped.

Effectiveness did not significantly vary among the epilepto-

genic areas.

DiscussionAlthough the array of visual, dyscognitive and motor attacks

matched those of other substantial series, the incidences of

these ictal phenomena differed somewhat, possibly reflecting

referral patterns or seizure definitions. Unformed visual

Table 1 Seizure semiology and surface ofoccipital seizure origin

Lateral Mesial Both Total

Number of patients 11 20 10 41Visual aura 10 15 10 35Visual unformed 9 13 9 31Visual formed 5 8 6 19Never visual 1 5 0 6Autonomic 3 4 3 10Abdominal cephalic 1 6 4 11Unilateral somatosensory 2 2 0 4Bilateral somatosensory 3 3 0 6Dyscognitive 9 17 6 32Never aura 0 2 0 2Unilateral motor 8 10 5 23Bilateral motor 10 16 8 34Any motor 10 17 10 37Versive contralateral 2 8 3 13Versive ipsilateral 0 1 0 1

All relationships in this table are statistically non-significant.

Table 5 Pathology* and epileptogenic surface

Lateral Mesial Both

Number of patients 11 20 10Dysplasia 2 2 1Ischaemia/ulegyria 0 3 2Ganglioglioma 1 3 0Arteriovenous malformation 1 1 2

*Four most common pathological findings. Others are: astro-cytoma (three patients); dysembryoblastic neuroepithelial tumour(two); traumatic scar (two); non-specific gliosis (two); chronicencephalitis (one); meningeal angiomatosis (one); normal (eight);unavailable (four).

Table 3 Visual fields

Lateral Mesial Both

Number of patients 11 20 10Normal 10 11 7Quadrantopia/hemianopia 0 8 3Untestable (optic atrophy) 1 1 0

P = 0.0265 (10 lateral versus 19 mesial testable patients).P = 0.0373 [lateral versus mesial and both (39 testable patients)].

Table 2 Unformed visual ictal phenomena

Lateral Mesial Both

Number of patients 11 20 10Contralateral 4 9 8Bilateral 6 5 6Ipsilateral 0 0 0

P = 0.4908 (not significant).

Table 4 Age of current seizure onset (years)

Lateral Mesial Both

Number of patients 11 20 10Mean 10.7 11.5 13Median 12 8 10.5

ANOVA P value = 0.8580 (not significant).

Table 6 EEG items present on any of first five scalpEEGs (31 patients)*

Lateral Mesial

Number of patients 11 20Ipsilateral alpha reduction 6 (55) 9 (45)Ipsilateral posterior delta 6 (55) 7 (35)Bilateral posterior delta 1 (9) 4 (20)Ipsilateral occipital spikes 6 (55) 8 (40)Contralateral occipital spikes 1 (9) 3 (15)Ipsilateral posterior temporal spikes 6 (55) 11 (55)Contralateral posterior temporal spikes 0 (0) 2 (10)Ipsilateral anterior temporal spikes 2 (18) 8 (40)Contralateral anterior temporal spikes 1 (9) 4 (20)Ipsilateral parietal spikes 7 (64) 6 (30)Contralateral parietal spikes 0 (0) 1 (5)Bisynchronous spikes 3 (27) 8 (40)Ambiguous seizure origin 2 (18) 10 (50)Seizure ipsilateral occipital 5 (45) 3 (15)Seizure contralateral occipital 0 (0) 0 (0)Any ipsilateral anterior temporal abnormality 3 (27) 9 (45)Any contralateral temporal abnormality 1 (9) 4 (20)

*Percentages given in parentheses. The incidence of none of thesefeatures differs significantly between mesial and lateral occipitalepileptogenesis.




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phenomena appeared in 31 out of 41 (76%) of our patients,

15 out of 25 (60%) of the Williamson et al. (1992) series and

26 out of 55 (47%) of the patients studied by Ludwig and

Ajmone Marsan (1975). Formed visual phenomena were

recorded in 19 (46%) of our patients compared with three

(12%) and eight (14%) of these other series, respectively.

Dyscognitive or temporal lobe-like attacks occurred in 32

(78%) of this series—more than the 44% of the Williamson

series and 29% of the study by Ludwig and Ajmone Marsan.

Various types of motor seizures occurred in 91% of the Lud-

wig and Ajmone Marsan series and 37 (90%) of our series,

but only 12% of the Williamson series.

Physiological and anatomical factors may be invoked to

explain the inability of ictal semiological and scalp EEG

features to distinguish lateral from mesial occipital epilepsy.

We first describe properties facilitating mesial occipital to

lateral occipital–temporal propagation, then components

mediating lateral to mesial occipital spread.

Studying penicillin-induced seizures with [14C]deoxygluc-

ose autoradiography in the rat occipital cortex, Collins and

Caston (1979) found that relatively mild (15–25 units) mesial

foci spread readily to the lateral occipital region and vice

versa. Stronger foci (80 units) involved most of the occipital

lobe ipsilateral to injection and contralaterally; seizure activ-

ity spread extensively to adjacent neocortex and limbic struc-

tures. Cain (1982) readily produced kindling of deep layers of

rat occipital cortex, but rarely when stimulating superficial

layers. Using microinjections of penicillin into each of the

several layers of visual cortex, Ebersole and Chatt (1986) also

found layer 4 to be the most epileptogenic. Layer 4 apparently

serves as a pacemaker for epileptogenesis in other visual

cortical areas particularly to layers 3, then 2. The pyramidal

neurons of layers 2 and 3 have abundant axonal connections

to other cortical areas both ipsilaterally and contralaterally.

Abundant multisynaptic projections from the occipital cor-

tex to lateral and mesial temporal structures exist (Jones and

Powell, 1970; Turner et al., 1980). Thus, occipital-originating

seizures may readily spread to the ipsilateral and even the

contralateral temporal lobe as disclosed by both intracranial

(Olivier et al., 1982; Salanova et al., 1992; Williamson et al.,

1992; Palmini et al., 1993; Fava and Blume, 2002) and scalp

EEG (Ludwig and Ajmone Marsan, 1975). Penfield and Perot

(1963) elicited experiential (structured) visual phenomena by

electrical stimulation of various temporal neocortical sites as

did Gloor et al. (1982) by amygdala electrical stimulation.

These anatomical and physiological relationships indicate

that experiential visual and dyscognitive ictal phenomena

could represent seizures arising at any point along this

striate cortex–amygdala axis and thus fail, as in this series,

to distinguish a lateral occipital from a mesial occipital

seizure origin. Visual experiential phenomena—seizure-

related or spontaneously occurring—may require participa-

tion of both neocortical and limbic structures (Blume et al.,

1993b).

Although processing of unformed (unstructured) visual

phenomena occurs in primary visual cortex (V1 or BA 17)

(Hubel and Wiesel, 1959, 1962), such simple visual phenom-

ena have been evoked by stimulation of both primary visual

(striate) and extra-striate and prestriate (BA 18 and 19)

cortices by Penfield (1954). Although the occipital to tem-

poral neocortex pathway was recognized earlier (see above),

reciprocal connections have more recently been demonstrated

between temporal neocortex and the primary visual cortex

(Felleman and Van Essen, 1991; Kastner and Ungerleider,

2000; Albright and Stoner, 2002).

Epileptogenic properties of primary visual cortex (see

above) apparently invite propagation of epileptic discharge

from other parts of the occipital cortex. Jasper (1969)

indicated that an area of propagation would sustain an epi-

leptic discharge if inhibition were relatively weak, as in layer

4 of visual cortex (Ebersole and Chatt, 1986), or if it received

‘sufficient excitatory drive’. Enhanced synaptic efficiency

with high frequency action potentials of epileptic discharges

(Lisman, 1997) would promote the latter. Similarly, Chervin

et al. (1988), studying epileptic propagation in bicuculline-

treated neocortical slices, indicated that relative efficacy of

horizontal excitatory projections influenced the direction of

propagation. Such effects would augment the tendency of a

lateral occipital originating seizure to propagate ‘backward’

to the primary visual cortex and contribute further to the

Table 7 Lateralizing value of scalp EEG features (41 patients)

EEG feature First five scalp EEG recordings All pre-invasive recordings

Any Majority Any Majority

IPSI CONTRA IPSI CONTRA IPSI CONTRA IPSI CONTRA

Occipital seizure 10 0 4 0 20 1 4 0(0.0010) (N.S.) (0.0001) (N.S.)

Occipital (01,02) spikes 19 4 15 1 22 7 17 1(0.0004) (0.0001) (0.001) (0.0001)

Posterior temporal 22 2 14 0 24 3 16 1(T5,T6) spikes (0.0001) (0.0001) (0.0001) (0.0001)Anterior temporal spikes 12 5 3 1 25 11 3 2(M1,2; F7,8;T3,4) (N.S.) (N.S.) (0.0035) (N.S.)

N.S. = not significant. Any/majority = feature appeared on any/majority of such recordings. IPSI/CONTRA = feature ipsilateral/contralateral to epileptogenesis. Parentheses = two-sided P values IPSI versus CONTRA.




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similarity of occipital epileptic semiology between lateral and

mesial occipital origins. That Bien et al. (2000) reported

visual aura from extra-occipital as well as occipital sources

may also reflect these propagation mechanisms.

This facilitated intra-occipital ictal propagation may under-

lie the similar motor semiology of lateral and mesial occipital

epileptogenesis: equal access to supra-Sylvian or to brainstem

motor regions may be available for lateral or mesial origin-

ating attacks.

Although no aspect of scalp EEG distinguished mesial from

lateral occipital epileptogenesis (Table 6), interictal and ictal

epileptiform abnormalities correlated highly with ictal later-

alization (Table 7). EEG provided similar lateralizing help in

temporal lobe epilepsy (Blume et al., 1993a, 2001a).

AcknowledgementsCortical resective surgery was performed by Dr. John Girvin

and Dr. Andrew Parrent. Mrs Maria Raffa carefully typed the

manuscript and helped to create the Appendix.

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Appendix

Patient No. Patient Ictal Semeiology Epileptogenic Area(s)

LATERAL01 A A-G Multicoloured flashing lights right upper quadrant. Right arm

numbness and jerking. Impaired awareness and dysphasia.GTC.

02 AK Visual blurring or dimming diffusely. Bright lights in all fieldsor objects very bright. Horizontal black and white stripes incentre of visual field. Diffuse numbness, loss of awareness.GTC.

03 DC Objects frozen in position like looking through a window,diffuse; head leftward and GTC. Diffuse numbness. Staring.

04 DS No visual aura. Cephalic sensation; stares, right or both eyelidstwitch, hyperventilates, clonic rightward conjugate eyedeviation, talks nonsense with normal words; face flushed.

05 JC Bilateral blurred vision beginning at periphery of fields andmoving towards centre; flickering lights at centre of field;stares, looks around, confused or may fall atonically.Left limb or bilateral numbness and jerking.




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06 NL Diffuse black vision and staring with diffuse tremor; epigastricsensations; automatisms of right hand; head rightward or rightlimbs tonic; GTC.

07 PMc Difficulty focusing and concentrating; right manualautomatisms; walks about. Tonic seizure, right limbs; GTC.

08 RH Right upper quadrant flashing lights; bilateral retroorbitalheadache with face flushed. Right homonymous hemianopiaand GTC.

09 TC Sudden complete bilateral visual loss (90% of seizures), orcomplete bilateral blurring, or objects enlarge and contract;(10%) stares, looks around, fear; (rare) tonic left face, arm inflexion, rarely both legs or GTC.

10 WA Pulsating light in right upper quadrant with scotoma;difficulty understanding what he is seeing; dysphasia;(rarely) GTC.




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11 WV Vision diffusely black; restless, flexes left leg; left handautomatisms. Dots, left visual field, vision ‘‘spinning’’;right hand automatisms, left arm tonically flexed; righttonic-clonic, face flushed. Sees circles, limbs stiff.

MESIAL12 CB White circles, coloured circles, lights, all right upper visual

field; rightward head deviation. Epigastric sensation, fear, righthemifield images slanted, head leftward. Loss of awareness,oroalimentary automatisms, bimanual automatisms; armsflexed. GTC (rare). Diffuse sensation (rare).

13 DC Flashing white lights, right upper visual field; lights spread tocentre; split in two phenomena which revolve about each other.Darkening of vision; mumbling, left hand automatisms. Headleftward, diffuse rigidity in flexion. Undescribable diffusesensation; GTC. GTC without warning.

14 DL Whirling, shimmering visual phenomenon left upper quadrant;spatial disorientation. Sees school scene or self brushing teeth or‘‘smurfs’’ in different episodes.




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15 DMac Nausea; confused, talks nonsense; oroalimentary automatisms.GTC.

16 DR Unpleasant fearful diffuse sensation; moans, oroalimentaryautomatisms, left or right hand automatisms. Flashing lightsthen darkness left visual field. Right hemiclonic; GTC.

17 GS-J Flashing white lights in peripheral portion of right field;rightward ocular and cephalic deviation; GTC.

18 HW Coloured monsters. Cephalic sensation; merging of colouredobjects; a desk appears; micropsia, macropsia; completeloss of vision.

19 JB No visual aura; sick sensation; left arm automatisms; eyesclosed, neck flexed; bilateral tonic, left leg jerking.




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20 JF Visual blurring diffusely; head leftward, arms tonic, eyesupwards. Designs or ‘‘word-like figures’’ in a ‘‘French-likescript’’. Diffuse blackening of vision; sounds distant; all limbsstiffen, leftward ocular and cephalic deviation; bimanualautomatisms.

21 JL White or coloured flashing lights, right upper visual fieldproximally; eyes left. GTC.

22 JS Bilateral black and white spots peripherally moving to centre;loss of awareness, blinking, eyes left; myoclonic movementsof arms, left leg. Fear, sensation of someone sneaking upbehind her.

23 JW Walls converging; stares, gaze leftward, confused;oroalimentary automatisms. GTC.

24 KH Confused, automatisms. Diffuse loss of vision; fearfulabdominal sensation; oroalimentary and bimanual automatisms;left arm numb and tonic, eyes left.




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25 LS Intermixed colours especially blue and purple like a blob of oilon water in right lower quadrant; sour taste, abdominalsensation; impaired awareness, dysphasia; right sided motor;GTC. Cephalic sensation, vision darkened. Pencil outline of aface and threatening voices. Father standing in right lowerquadrant.

26 MD Flashing lights right visual field. Old cars and old fashionobjects. Stares, fear without visual aura; abdominal sensation,oroalimentary automatisms; eyes right; blinks. GTC.

27 MH No visual aura. Stares, bimanual automatisms. Atonic dropattacks.

28 ML Ictus emeticus. Stares; bimanual and oroalimentaryautomatisms.

29 NK Sees colours in all fields or left field. Abdominal sensation;bimanual automatisms; atonic fall. GTC.




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30 SS Rightward head and eye deviation. Peripheral blurred anddistorted vision bilaterally and changing colours in centre.Colour alteration and darkening diffusely. Diffuse tingling, leftarm numbness and left shoulder clonus. ‘‘CPS’’. GTC.

31 TE Macropsia, jamais vu. Anxiety, disoriented, bimanualautomatisms, oroalimentary automatisms, mute.

BOTH32 CC Blurred vision diffusely; epigastric sensation; eyes fluttering.

GTC.

33 EMc Flickering colours right field and diffusely. Stares, automatisms.Head and eyes right; GTC.




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34 JMc Light flashes right upper quadrant. Familiar scene rightcentrally. Anxiety, fear, staring, oroalimentary automatisms.GTC.

35 KMac Blurring and flickering in right field proximally; right clonicocular deviation. Loss of awareness, automatisms.

36 LG GTC. Loss of vision diffusely, atonic falls. Vertiginous visualsensation, feels hot or cold.




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37 MA Multicoloured stripes, left field or bilateral; blinks; diplopia,floor slanted; loss of vision; nausea; unresponsive,impaired awareness. GTC.

38 SE Flashing yellow and red balls of lights, right lower field,enlarging gradually, face flushed; GTC.

39 SF Flashing lights, left field; white flashing circles in centre of field;head, eyes, body leftward; abdominal sensation, loss ofawareness, oroalimentary automatisms.




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40 ST Blurred vision bilaterally or left field; head, eyes left;oroalimentary automatisms, unresponsive; GTC.

41 YD Flashing lights left upper field; GTC. Yellow and white dotsdiffusely. Vision tunnel-like. Visual scenes of past life.Distortion or blurring in left field and diffusely. Abdominalsensation, vacant sensation. Left sided numbness.

Semiology: Commas (,) separate simultaneous components. Semicolons (;) distinguish sequential features. Full stop (.) separatecomplete seizures. GTC = generalized tonic-clonic; Epileptogenic areas: Based on subdurally recorded clinically typical seizures; except forPatient No. 3 where area combines recorded seizures and a lesion; and Patients 8, 10, 14, 20, 35, and 38 which describe epileptogeniclesions only.




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