ATTENTION, CONSCIOUSNESS, SLEEP AND WAKEFULNESS 

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AFTER BILAT HYPOTHALAMIC LESIONS 

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fig. 6. Cat with transection at the pontobulbar junction shows partially activated EEG (A), loss 

 of activation and replacement with spindle bursts after caudal hypothalamic lesion <B), and ipsi- 

 lateral loss of spindle bursts in the right hemisphere of the cortex following lesions to the right tha- 

 lamic regions (centromedian, mti .il.unin.u and ventral nuclei 1 which previously gave bursts syn- 

 chronized with those of the cortex. [From I.inclslev et nl . (163).] 



with slow waves and spindle hursts. When a lesion 

 was made so as to transect the ARAS bilaterally in 

 the region of the posterior hypothalamus, periodic 

 and prominent spindle bursts appeared in all cortical 

 regions. These spindle bursts occurred simultaneously 

 in the cortex and in certain nuclei of the thalamus. 

 They were observed primarily in the centromedian 

 nucleus, in the lateral intralaminar nuclei, and in the 

 lateral parts of the ventralis lateralis and ventralis 

 anterior. Unilateral decortication abolished the 

 spindle bursts in the ipsilateral thalamic regions 

 previously showing them, but synchronous spindle 

 bursts remained in contralateral thalamus and cortex. 

 Similarly, as shown in figure 6C, lesions restricted to 

 the thalamic nuclei showing spindle bursts abolished 

 the synchronized cortical bursts on die ipsilateral 

 side but did not interfere with the simultaneous 

 bursts in the thalamus and cortex of the opposite side. 

 Thus, there is evidence that unspecific nuclei of the 

 thalamus, even though they may not have direct 

 connections with the cortex, nevertheless maintain a 

 temporal synchrony with it. 



It is of interest that these nuclei showing spindle 



bursts in synchrony with the cortex were also part of 

 the complex of nuclei shown b\ Morison & Dempse) 

 (179), Starzl & Magoun (222 1 and Starzl & Whitlock 

 (223) to produce widespread cortical recruiting re- 

 sponses. It is further of interest that nuclei of the 

 ventral complex, especially ventralis anterior, were 

 involved in the corticothalamic spindle bursts, for 

 several studies seem to indicate that the nucleus 

 ventralis anterior may be a common point of egress 

 for impulses from the unspecific nuclei ( [42, 223, 228). 

 More recently Eidelberg et al. (69) concluded that 

 the nucleus ventralis anterior serves as a relay sta- 

 tion for the nonspecific thalamic projections, since 

 lesions in no other part of the thalamus, or the septum, 

 blocked recruiting responses as did lesions in the 

 ventralis anterior. Chow et al. (48), concerned with 

 more massive lesions in the rostral thalamus, found 

 that barbiturate bursts and recruiting responses were 

 degraded by anterior thalamic lesions. Although 

 some temporary behavioral changes were noted, 

 none persisted beyond 2 to 8 weeks, and cats with 

 rostral thalamic lesions could learn a visual form 

 discrimination, suggesting that there was no marked 



