Prolonged "postictal" aphasia: Demonstration of persistent ictal activity with intracranial electrodes
Lawrence J. Hirsch, MD;,
Ronald G. Emerson, MD; and
Timothy A. Pedley, MD
From the Comprehensive Epilepsy Center, Columbia University College of Physicians & Surgeons, New York–Presbyterian Hospital, Columbia Campus, New York.
Address correspondence and reprint requests to Dr. L.J. Hirsch, Comprehensive Epilepsy Center, Columbia University College of Physicians & Surgeons, New York–Presbyterian Hospital, Columbia Campus, 710 West 168th Street, New York, NY 10032; e-mail: LJH3{at}columbia.edu
We present a case of a 40-year-old woman with recurrent episodesof prolonged postictal aphasia lasting for days to weeks. Althoughthere was no scalp EEG correlate, intracranial recordings demonstratedongoing ictal activity, predominantly in the posterior lefttemporal lobe, during several days of her typical "postictal"aphasia.
A 40 year-old woman with no risk factors for epilepsy had intractablecomplex partial and secondarily generalized seizures since age15 years. These were often followed by postictal aphasia thatlasted for days to weeks. Despite MRI evidence of mesial temporalsclerosis, an earlier left anterior temporal lobectomy helpedonly transiently. During an evaluation for additional epilepsysurgery, left hemisphere subdural grid and strip electrodeswere inserted ( figure, A). She had a typical complex partialseizure with secondary generalization. Electrical onset wasin the anterior superior temporal gyrus (electrodes LT2 to 4).IV lorazepam was administered within 2 minutes and quickly terminatedclinical seizure activity. However, intracranial recordingsdemonstrated ongoing ictal activity throughout the left temporallobe. Additional IV lorazepam and fosphenytoin were given, andno further clinical seizures occurred. She became alert buthad severe deficits in naming, repetition, comprehension, andreading, similar to prior episodes, as well as right agraphesthesiaand hemianopia. Subdural electrodes demonstrated ongoing ictalactivity (rhythmic theta and alpha) in the basal and posterolateraltemporal neocortex (highlighted areas in the figure, A), occasionallyspreading more superiorly.
Figure. (A) A map of the intracranial electrodes, seizure onset zone, and the most commonly involved area of sustained electrical discharge during aphasia. (B, C) Second postictal day, severe persistent aphasia. (B) No scalp EEG correlate (bottom 3 channels) to frequent bursts of polyspikes in the basal and lateral left temporal lobe on subdural recordings. (C) Rare time of subtle scalp EEG correlate: low-voltage pseudoperiodic sharp waves on scalp EEG (bottom 3 channels) correlating with high voltage bursts of polyspikes in the basal and lateral left temporal lobes, with some suprasylvian extension (G38, G46). LF = lateral frontal 8 contact strip; MT = mid-temporal 8 contact strip; PT = post-temporal 8 contact strip; SF = subfrontal 6 contact strip; LT = lateral temporal 6 contacts strip; G = grids (6 x 8 and 2 x 8, continuous numbering).
Inferior and anterior temporal lobe scalp electrodes (F9, T9,P9, AT1, and Fp1) were added. Over the next several days, intracranialictal activity gradually fragmented, but bursts of spikes andpolyspikes continued to occur every 1 to 3 seconds in the samearea. Her aphasia remained severe. Simultaneous recordings fromproximate scalp electrodes did not reflect ictal activity throughoutmost of postictal days 2 through 6. Two samples taken 48 hoursafter her convulsion are shown in the figure, B andC. FigureBshows typical activity during this period, with no scalp EEGcorrelate. FigureC is an example from the rare times when asubtle scalp EEG correlate could be seen, consisting of low-voltagepseudoperiodic discharges; this was most evident when subduralrecordings showed spread to suprasylvian electrodes (G38, G46).
No further clinical seizures occurred. The patient was treatedwith high doses of four anticonvulsant medications. Her hemianopiaand agraphesthesia on the right resolved in less than 1 week.The aphasia improved slowly 7 to 10 days after her convulsionas the intracranial EEG discharges gradually subsided. Comprehensionand naming deficits were the last to improve. She then underwentresection of the anterior superior temporal gyrus, where allrecorded seizures had originated. Mild to moderate anomia persistedpostoperatively.
We describe a woman with recurrent episodes of secondarily generalizedseizures followed by days to weeks of aphasia that eventuallyimproved. Although scalp EEG did not reveal ictal activity,intracranial electrodes demonstrated that this "postictal" aphasiawas correlated with an ongoing ictal discharge.
This is certainly not the first report of prolonged aphasiafrom epileptiform activity,1,2 nor of a prolonged postictaldeficit. However, we are unaware of another report of an isolatedclinical seizure followed by a prolonged postictal deficit (aphasiain this patient) without a scalp EEG correlate that proved tobe due to ongoing ictal activity utilizing intracranial recordings.It is not surprising that this can occur, as there are documentedcases of cognitive impairment during highly focal intracranialelectrical activity, including discharges that could not bedetected at the scalp.3,4 We believe it is important to considerthe possibility that prolonged "postictal" deficits may be dueto ongoing ictal discharges, as additional anticonvulsant medicationmay be indicated.
There were rare periods in this case when there were subtlepseudoperiodic discharges on the scalp EEG during ongoing ictalactivity intracranially, and persistent aphasia. This supportsthe view that in some instances, periodic lateralized epileptiformdischarges (PLED) on the scalp EEG are actually ictal.5 It ispossible that functional imaging with PET or SPECT can helpmake this differentiation, as focal increased blood flow ormetabolism during a prolonged postictal deficit or during PLEDmay suggest an ictal state.6 This was not performed in our patient.
We conclude that prolonged "postictal" deficits may sometimesbe due to ongoing ictal activity that is not evident on scalpEEG.
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Received March 13, 2000.
Accepted in final form August 31, 2000.
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Case history.
