Schraeder P L, Celesia G G
Arch Neurol. 1977 Nov;34(11):677-82. doi: 10.1001/archneur.1977.00500230047007.
Epileptogenic foci were produced by application of penicillin to the auditory cortex of cats. A gradual modification of the evoked potentials to clicks and of the recovery cycle to paired clicks was noted following the application of penicillin. With the onset of interictal spikes, responses were initially depressed. The depression gradually changed till every click triggered a reflex epileptogenic spike. Areas surrounding the primary focus and areas at the mirror focus had depressed evoked potentials, while at the primary focus a click elicited reflex spikes. Progressive recruitment of cortical regions farther away from the primary focus was noted with increased epileptogenicity. The recovery cycle was also affected with prolongation of the absolute refractory period. These complex modifications of sensory input were closely related to the intensity of the epileptogenic disturbance, the distance of the area processing the information from the primary epileptogenic focus, and the time of arrival of the signal to be processed in relation to the interictal and ictal discharges.
通过向猫的听觉皮层注射青霉素来产生致痫灶。注射青霉素后，可观察到对点击声诱发的电位以及对成对点击声的恢复周期逐渐发生改变。随着发作间期棘波的出现，反应最初受到抑制。这种抑制逐渐变化，直到每次点击都引发反射性致痫棘波。主病灶周围区域和镜像病灶区域的诱发电位受到抑制，而在主病灶处，点击声会引发反射性棘波。随着致痫性增加，可观察到离主病灶更远的皮质区域逐渐被募集。恢复周期也受到影响，绝对不应期延长。感觉输入的这些复杂改变与致痫干扰的强度、处理信息区域与原发性致痫灶的距离以及待处理信号相对于发作间期和发作期放电的到达时间密切相关。
