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Cortical changes in epilepsia partialis continua.

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Cortical Changes
in Epilepsia Partialis
Luis Garcia-Butiuel. MD
In a recent paper describing unilateral cerebral damage in a
case of epilepsia partialis continua (Ann Neurol 1:195,
13771, Knopman and his associates concluded that the
cortical changes in the left hemisphere were a result of the
continued epileptic accivity arising from that hemisphere.
They ascribed the damage in the left hemisphere to the
increased but unfulfilled metabolic demands placed upon it
by its sustained excitation. The lesions that they found,
however, involved the cortex of virtually the entire left
hemisphere. If such lesions had originated from seizure
activity, one would have to postulate propagation of the
discharge to the entire ipsilateral cortex while the contralateral hemisphere remained seizure free.
Evidence from both electrical [21 and metabolic studies
[ 11 indicates that focal cortical discharges follow corticofugal
pathways to subcortical nuclei, and thence to the contralateral
homotopic cortex. Corticocortical spread may play a role in
the Jacksonian march of a focal motor seizure, for instance,
but it is doubtful that the march would progress to the
ipsilateral cortex of the parietal and temporal lobes without
first spreading to the subcortical structures and across the
The widespread cortical changes confined to one hemisphere would be easier to explain as a combination of
systemic metabolic problems, which the patient was known
to have, and unequal perfusion of the two hemispheres,
which could have occurred even in the absence of any
obvious vascular lesions. The seizures would thus be the
result, rather than the cause, ofthe observed cortical lesions.
1. Collins RC, Kennedy C, Sokoloff L, et al: Metabolic anatomy of
focal motor seizures. Arch Neurol 33:536-542, 1976
2. Wilder BJ, Schmidt RP: Propagation of epileptic discharge from
chronic neocortical foci in monkey. Epilepsia 6:297-309, 1965
From the Veterans Administration Hospital, Portland, OR 97207.
Alexander G. Reeves, MD, George Margolis, MD,
and David Knopman, M D
D r Garcia-Bunuel’s points are pertinent, and we considered
them in analyzing our patient.
Multifocal cortical involvement by seizure discharge occurs in epilepsia partialis continua (EPC)[I]. I t would be
expected that the cortical or subcortical epileptic threshold
would be diffusely lowered by systemic metabolic abnormalities known to be associated with EPC,and multifocal
seizure activicy might chen be even more likely to occur.
Currently there is no good explanation for the ipsilateral
origin and containment of seizure discharge in EPC associated with syscemic metabolic abnormality.
The experimental evidence marshalled by Dr GarciaBunuel concerns seizure activity induced by focal irritative
lesions or stimulation in otherwise normal animals, that is,
those without metabolic abnormality. Also, the experimental animals were not being treated with anticonvulsant medications, which would be expected to modify the spread of
seizure activity. Experimental primate and recent clinical
studies suggest that secondary generalization of seizure
accivity occurs primarily via the forebrain commissures and
secondarily by more resistant brainstem pathways [ 2 ] . O u r
experience suggests that, at least in some patients, subcortical generalization is more easily blocked by anticonvulsant
medication than is commissural corticocortical spread [Z].
Following anterior corpus callosum section, generalization of left focal frontal seizure activity was retarded for
some months in a recent patient in our series of forebrain
commissurotomies. Clinical generalizacion again occurred
in parallel with the electroencephalographic observation of
spread of seizure activity from the frontal region posteriorly
to the parietooccipital and temporal scalp leads and then to
the opposite parietotemporal and frontal leads. The patient
was taking anticonvulsant medications throughout. These
observacions suggest chat seizure activity can progressively
involve larger areas of ipsilateral cortex under special circumstances, whether che spread be corticocortical or from
cortex to subcortical regions and back to cortex.
D r Garcia-Bunuel’s alternative explanation for our patient’s cortical damage is difficult to support. Midway in her
final stay, brain scan flow studies and carotid system arteriography did not demonstrate evidence of decreased
cerebral perfusion. Also, we are unfamiliar with any systemic metabolic abnormality, with the possible exception of
hypoglycemia (which our patient did not have) that could, in
the absence of seizure activity, produce such a severe unilateral anoxic-ischemic change.
1. Thomas JE, Reagon TJ, Klass D: Epilepsia partialis continua.
Arch Neural 34:266-275, 1977
2. Wilson DH, Reeves AG, Gazzaniga M, et al: Forebrain commissurotomy for the control of intractable seizures. Neurology
(Minneap) 27:708-715, 1977
From the Section of Neurology, Dartmouth-Hitchcock Medical
Center, Hanover, NH 03755.
544 Annals of Neurology Vol 2 N o 6 December 1977
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change, cortical, partialis, epilepsies, continue
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