Sleep Induced by Subthalamic Lesions with the Hypothalamus Intact

Abstract

The sleep-producing effect of hypothalamic lesions has been convincingly demonstrated (Ranson 1 ). There are, however, still many unsolved problems which bear upon the central mechanism of the sleep-waking process. Supporting the view, notably that of Kleit-man, 2 that sleep primarily depends upon a reduction of afferent impulses, Bremer 3 demonstrated that a transection of the brain stem behind the 3rd nuclei produces in the electrocorticogram and in the behavior of the eyeballs signs characteristic of sleep. Extensive bilateral thalamic lesions which destroyed the chief endings of the centripetal pathways from the spinal cord and rhombencephalon (Ranson) failed, however, to abolish the normal waking state. This indicates that centripetal systems outside the dorsal thalamus play an important part in maintaining the waking state. Thalamic lesions extending more ventrally than those of Ranson, reaching beyond the dorsal thalamus, but remaining outside the hypothalamus, were produced by Spiegel and Inaba, 4 who observed prolonged sleep following such lesions. The region ventrally adjacent to the thalamus, the so-called subthalamus, contains important fiber connections with the hypothalamus (Woollard, 5 and Papez 6 ). It therefore seemed pertinent to investigate whether lesions of the subthalamus, sparing the hypothalamus, would interfere with the normal sleep-waking rhythm. By means of the Horsley-Clarke stereotaxic apparatus the thalamus was pierced on both sides and bilateral circumscribed lesions were placed in the subthalamus. In control experiments lesions were confined to the thalamus or the hypothalamus. Experiments in all were made on 25 cats. Regardless of the anesthetic used (ether or nembutal), the cats with subthalamic lesions exhibited sleep (average duration 4 days). There was usually first deep sleep from which the animals could not be awakened and then somnolence associated with catatonia.