Abstract
ALTHOUGH the pathogenesis and pathophysiology of idiopathic narcolepsy remain obscure, it is known that symptomatic forms may follow head injury, cerebral arteriosclerosis, encephalitis lethargica, and intracranial tumors involving the posterior portion of the hypothalamus. Ranson 1 in 1939 produced somnolence in monkeys with lesions limited to the subthalamus and hypothalamus. It remained, however, for the recent studies of Magoun and his co-workers 2 clearly to show that afferent stimulation of the ascending activating system of the brain stem underlies wakefulness, while absence of this influence results in sleep. An arousal reaction, or state of wakefulness, was produced by stimulation of the dorsal portion of the hypothalamus, the subthalamus, the related medial bulbar reticular formation, or the tegmentum of the pons and midbrain. Lesions of the ventral portion of the diencephalon and the tegmentum of the midbrain, within the area of distribution of the ascending reticular activating system, produced recurrent electroencephalographic
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