NON-LESIONAL PARIETAL [dsquote]PLUS[dsquote] EPILEPSY: CLINICAL AND SURGICAL ASPECTS
Abstract number :
1.310
Submission category :
Year :
2002
Submission ID :
3576
Source :
www.aesnet.org
Presentation date :
12/7/2002 12:00:00 AM
Published date :
Dec 1, 2002, 06:00 AM
Authors :
Anthony L. Ritaccio, Manoj Raghavan, Orrin Devinsky, Werner Doyle. NYU Comprehensive Epilepsy Center, NYU School of Medicine, New York, NY
RATIONALE: Objective: To elucidate clinical, electrographic, and surgical characteristics of non-lesional localization related epilepsy with parietal foci encountered in a large surgical center.
Discrete syndromes associated with non-lesional parietal lobe epilepsy remain enigmatic due to infrequent presentation, clinical under- recognition and erroneous localization. We reviewed cases of non-lesional parietal onset within our surgical database to determine the range of presentation as determined by semiologic, electrographic, and surgical outcome analysis.
METHODS: The NYU epilepsy surgery database was queried for the years 1994-2001. Seven patients were identified posessing invasive intracranial EEG evidence of parietal onset as well as absence of a neuroanatomical correlate on MRI.
Non-invasive and invasive EEG, ictal semiology, resective strategy,pathology, and outcome was reviewed.
RESULTS: Out of the total, 5/7 were erroneously presumed extraparietal based on noninvasive ictal EEG and interpretation of clinical semiology. 2/7 had failed prior epilepsy surgery on non- parietal cortices performed years earlier. Elementary somatosensory sensations were a component of the early ictal period in 4/7. One unique patient had somatosensory [dsquote]reflex[dsquote] triggering of motor partial seizure by touching the affected limb. However, 7/7 displayed extra-parietal clinical features at onset; 7/7 frontal (unilateral or bilateral motor), 2/7 temporal (acoustic aura,language disruption), 1/7 occipital (transient amaurosis, cephalgia). 3/7 patients exhibited two discrete clinical seizure types, verified electrographically in one. Of great importance was the elaboration in 5/7 of a highly stereotyped parieto-frontal electroclinical syndrome involving simultaneous onset in parietal cortices as well as primary motor and/ or supplementary motor area (SMA), manifest by typical motor partial or SMA type clinical seizures. This finding resulted in a combined resection of both parietal and frontal tissues in 4/7. In 6/7, invasive electrodes were replaced after initial excision to obtain greater parietal coverage and potentially define the need for extension of the resection. Microscopic pathology and outcome will be discussed.
CONCLUSIONS: Our data indicate that non-lesional parietal lobe epilepsy is an infrequently encountered and cryptic entity, often masquerading as a frontal , temporal or occipital neocortical syndrome. Invasive EEG analysis has the potential for false localization of the ictal onset zone or underestimation of its extent. Due to the relative clinical silence of the parietal cortex, most seizures of parietal onset exhibit extraparietal clinical features that are a consequence of early spread. The majority of our patients elaborated a distinct syndrome characterized by a complex parietofrontal epileptogenic zone and primary motor or SMA type seizures, thereby defining a parietal [dsquote]plus[dsquote] syndrome. The concept of a pure non-lesional parietal syndrome appears artificial as our data indicate that epileptic networks are determined by neural connectivity that does not respect lobar boundaries. Anticipation of this paradigm is essential early in presurgical planning to allow for appropriate parietal area coverage.