Kaufmann P G, Bennett P B, Farmer J C
Undersea Biomed Res. 1977 Dec;4(4):391-402.
Electroencephalographic activity of the frontal cortex, cerebellar vermis, and superior vestibular nucleus was recorded in awake rats during the high pressure nervous syndrome (HPNS) by means of permanently implanted electrodes. Power-spectrum analysis revealed a decline in the faster frequencies and an increase in the slow frequences as the seizure end-point was approached. Effects of compression to 4500 fsw varied from severe tremor and myoclonic jerks to status epilepticus, with seizures occurring at an average depth of 3560 fsw. In all animals, multifocal-spiking activity progressed in severity with increasing depth. The predominant seizure pattern observed was a spike and slow-wave pattern reminiscent of absence seizures. Initial evidence of generalized seizure activity was equally divided between the cerebellum and cortex. It is concluded that the cerebellum participates in HPNS seizures. Possible evolution of the syndrome by loss of Purkinje cell inhibitory influence on subcortical sites that modulate cortical excitability is discussed.
在清醒大鼠的高压神经综合征（HPNS）期间，通过永久植入电极记录额叶皮质、小脑蚓部和前庭上核的脑电图活动。功率谱分析显示，随着癫痫发作终点的临近，较快频率下降，较慢频率增加。压缩至4500英尺海水深度的影响从严重震颤和肌阵挛性抽搐到癫痫持续状态不等，癫痫发作平均发生在3560英尺海水深度。在所有动物中，多灶性棘波活动的严重程度随着深度增加而加重。观察到的主要癫痫发作模式是类似于失神发作的棘波和慢波模式。全身性癫痫活动的初始证据在小脑和皮质中各占一半。结论是小脑参与HPNS癫痫发作。讨论了该综合征可能因浦肯野细胞对调节皮质兴奋性的皮质下部位的抑制作用丧失而演变。
