Effect of Callosal Bisection on Ventral Hippocampal Kindling
Authors: Nomori Ya‐ suyo , Kudo Tatsuya , Ammo Kouichirou , Yagi Kazuichi 
Published: August 2009

Purpose: To examine the role of the corpus callosum (CC) in secondarily generalized convulsions originating from the hippocampus we studied ventral hippocampal kindling in cats with the CC bisected.

Methods: After approximately the anterior two thirds of the CC was bisected, electrodes were stereotaxically implanted into the ventral hippocampus (VH) and the anterior sigmoid cortex bilaterally in four adult cats. After a 2‐week recovery period, VH kindling began. The development of seizure was classified into four stages: stage 1, arrest reaction; stage 2, autonomic manifestation, facial twitching, and mastication; stage 3, contralateral head turning, circling, and convulsions of the contralateral forepaw; and stage 4, secondarily generalized convulsions. Five consecutive daily evocations of stage 4 seizures were arbitrarily designated a stable stage 4 seizure state and regarded as the completion of kindling. The results of VH kindling in nine CC‐intact cats was used as the control data.

Results: Primary site kindling: The seizure stage developed gradually from stage 1 to stage 4, which showed partial onset, bilateral and symmetrical generalized convulsions, with occasional regressions from stage 4 to earlier stages, and finally attained the stable stage 4 seizure state. The mean number (±SD) of stimulations required to attain the first seizures of stages 1, 2, 3, and 4, and the stable stage 4 (1.0±0.0, 22.5±3.5, 44.5±13.1, 58.5±6.5, and 69.3±11.3) were not significantly different from those of CC‐intact cats (1.0±0.0, 21.3±15.2, 31.3±19.3, 36.8±19.4, and 42.7±19.7), and seizure manifestations and EEG were about the same as those of the CC‐intact cats. The ratio of the total number of seizure regressions and contralateral axial rotations to the total number of stimulations after attaining the first stage 4 seizures in all CC‐bisected cats (17 of 47 and 34 of 47) were significantly greater than those in CC‐intact cats (10 of 62; p < 0.001 and 14 of 62; p < 0.001). During stage 4 seizures, latencies from stimulations to the onset of focal motor seizures were 21.3±13.6 s, which were significantly shorter (p < 0.01) than those of the control group (26.7±9.1 s), whereas latencies for generalized convulsions were not significantly different from those of CC‐intact cats. Secondary site kindling: The number of stimulations required for the first seizures of stages 1, 2, 3, and 4, and the stable stage 4 (1.0±0.0, 9.3±7.9, 36.7±17.2, 37.3±17.2, and 61.7±41.9) were not significantly different from those of control group (1.0±0.0, 5.0±3.1, 19.0±9.0, 13.0±11.3, and 20.8±9.0). The intraictal progressions to the onset of focal motor seizures and generalized convulsions (41.5±12.5 s and 67.0±17.0) in the stage 4 seizures of CC‐bisected cats were significantly slower than those of CC‐intact cats (29.6±8.6 s; p < 0.001; and 52.0±8.6 s; p < 0.01).

Conclusions: The results obtained indicate that the CC does not play a critical role in generalization and synchronization of the secondarily generalized convulsions originating from the VH. As far as the intraictal progressions of generalized convulsions are concerned, the CC may inhibit the development of limbic seizures to focal motor seizures in primary‐site kindling. Because CC bisection of cats splits generalized convulsionr to hemiconvulsions in the motor cortical kindling and transforms symmetrical generalized convulsions to asymmetrical ones in both amygdaloid and temporal cortical kindling, the CC possibly plays different roles in generalization and synchronization of seizures depending on the site kindled. Results of this work suggest that careful determination of the site of an epileptogenic focus is necessary in applying callosotomy to patients with intractable epilepsy.