Brain Advance Access originally published online on March 23, 2005
Brain 2005 128(5):1209-1225; doi:10.1093/brain/awh458
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Occipital epilepsy: lateral versus mesial
University Hospital, The University of Western Ontario, London, Ontario, Canada
Correspondence to: Warren T. Blume, University Hospital, The University of Western Ontario, 339 Windermere Road, London, Ontario, Canada N6A 5A5 E-mail: warren.blume{at}lhsc.on.ca
Received September 15, 2004. Revised January 21, 2005. Accepted January 31, 2005.
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This study compares ictal semiology, neurological examination and scalp EEG between lateral and mesial occipital 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 surfaces (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 originating 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 none of 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 surfaces. We conclude that subdural electroencephalography is likely to be necessary to delineate the epileptogenic region within an occipital lobe. Nonetheless, focally originating scalp-recorded seizures accurately lateralized the epileptogenic zone in 20 (49%) of our 41 patients compared with only one (2%) which originated contralaterally (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 posterior temporal (T5, T6) spikes appeared consistently and significantly (P < 0.001) more commonly ipsilateral to epileptogenesis than contralateral using multiple methods of analysis.
Key Words: epilepsy; occipital; semiology; EEG; location
Abbreviations: BA = Brodmann area
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Introduction |
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Considering the manifestations of epileptic seizures as providing 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 nonetheless 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 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 phenomena 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 [Förster (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 processing 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 processing concerned mainly with object localization and eye-hand coordination (Goodale and Milner, 1992). The prestriate cortex also contains multiple retinotopic maps of the contralateral 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 Förster (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 surrounding 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 semiology 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.
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Focal occipital epilepsy was clinically suspected from: (i) ictal semiology (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 epileptogenic 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 electroencephalography 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) dyscognitive (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 dermatological 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 symmetry; (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 electrographic 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 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 epileptogenic 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 surfaces; (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 extraoccipital epileptogenic zone defined by scalp, invasive EEG, or both. Forty-one patients satisfied these criteria.
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Prior to invasive recordings (subdurals in 35 patients: electrocorticography 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.
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Seizures 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, pathology
No aspect of ictal semiology (Tables 1 and 2) distinguished laterally from mesially originating occipital seizures. A preoperative 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).
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Age of current seizure onset did not significantly differ among the groups (Table 4) nor did type of pathology (Table 5).
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Ictal semiology and epileptogenic areas of individual patients appear in the Appendix.
EEG analyses: mesial versus lateral
With a single exception, none of the studied scalp EEG features (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).
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EEG: ipsilateral versus contralateral
Occipital seizures appeared ipsilateral to the side of ultimately established epileptogenesis in the first five records of 10 (24%) of these 41 patients and none appeared contralaterally (P = 0.001) (Table 7). Considering all pre-invasive EEGs among these 41 patients, ipsilaterally originating occipital seizures appeared in 20 (49%) compared with one (2%) contralaterally (P = 0.0001).
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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-up
As 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 epileptogenic areas.
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Discussion |
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Although 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 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 Ludwig 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]deoxyglucose 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 activity spread extensively to adjacent neocortex and limbic structures. 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 cortex 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 participation 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 phenomena 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 temporal 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 epileptic 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 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 underlie 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 originating attacks.
Although no aspect of scalp EEG distinguished mesial from lateral occipital epileptogenesis (Table 6), interictal and ictal epileptiform abnormalities correlated highly with ictal lateralization (Table 7). EEG provided similar lateralizing help in temporal lobe epilepsy (Blume et al., 1993a, 2001a).
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Acknowledgements |
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Cortical 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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