Damage of the neocortex that disconnects this structure from subcortical networks creates a condition in which behavioral routines that depend on the neocortex can no longer be modified. For example, paired lesions of the anterior and posterior ocular pathways of the neocortex by damage of the frontal eye fields and superior colliculi eliminate all visually guided saccadic eye movements (Figure 1), while sparing the vestibuloocular reflex and optokinetic nystagmus, two reflexes mediated by subcortical networks (Schiller and Tehovnik 2015). Significantly, following such damage these reflexes can no longer be modified, even though saccadic eye movements can still be generated, while performing the reflexes. This underscores how dependent subcortical mechanisms are on the neocortex for altering behavior (Hebb 1949), even though it has been found that reflexes based on eye blink conditioning that utilize robust but simplistic stimuli (electric shock, loud tones, or bright visual stimuli) can still be associated in the absence of the neocortex (Swain, Thompson et al. 2011), which could be referred to as ‘blind’ perception or sensation subthreshold to consciousness (Graziano et al. 2016; Tehovnik et al. 2021). Nevertheless, Pavlov (1929) observed that most classically conditioned reflexes in his dogs were abolished following neocortical removal. In short, any behavior that depends on the high-resolution computations of the neocortex—such as language or complex movement sequences—can never be modified following neocortical ablation (Kimura 1993; Vanderwolf 2006).

Hence, the neocortex is the command and control center of the brain by way of learning, and it makes sense that when the neocortex is disconnected from subcortical networks by damage of the pons and midbrain all consciousness is extinguished (Levy et al. 1987; Monti et al. 2010; Owen 2008; Owen et al. 2006; Plum and Posner 1980; Schiff, Llinas et al 2002; also see Arnts et al. 2020 on hydrocephalic patients).

Figure 1: Head-fixed rhesus monkeys were required to grasp food items positioned in a board spanning 60 by 60 degrees of visual angle (panel A), as their saccadic eye movements were measured. Normal subjects had no difficulty obtaining the food items and generating saccadic eye movements toward the targets (fixation location specified by the distribution of the dots, panel B). Following bilateral lesions of either the frontal eye fields or superior colliculus, subjects still grasped the food items and made saccades toward the targets (panels C, D, E, and F). In the absence of both the frontal eye fields and superior colliculi, the subjects could still grasp the food items, but they failed to generate visually guided saccades thereby fixing the eyes in central orbit (panels G and H). In primates, the frontal eye fields are located anterior to the forelimb representation of the motor cortex, and the superior colliculi receive projections from the entire neocortex but especially from the striate and extrastriate visual areas. The frontal eye field and superior colliculi represent the two neocortical channels that interconnect the neocortex and brain stem for the mediation of visually guided saccades (Schiller and Tehovnik 2015). From figure 15-14 of Schiller and Tehovnik (2015).