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1.  Consciousness and epilepsy: why are patients with absence seizures absent? 
Progress in brain research  2005;150:271-286.
Epileptic seizures cause dynamic, reversible changes in brain function and are often associated with loss of consciousness. Of all seizure types, absence seizures lead to the most selective deficits in consciousness, with relatively little motor or other manifestations. Impaired consciousness in absence seizures is not monolithic, but varies in severity between patients and even between episodes in the same patient. In addition, some aspects of consciousness may be more severely involved than other aspects. The mechanisms for this variability are not known. Here we review the literature on human absence seizures and discuss a hypothesis for why effects on consciousness may be variable. Based on behavioral studies, electrophysiology, and recent neuroimaging and molecular investigations, we propose absence seizures impair focal, not generalized brain functions. Imapired consciousness in absence seizures may be caused by focal disruption of information processing in specific corticothalamic networks, while other networks are spared. Deficits in selective and varying cognitive functions may lead to impairment in different aspects of consciousness. Further investigations of the relationship between behavior and altered network function in absence seizures may improve our understanding of both normal and impaired consciousness.
doi:10.1016/S0079-6123(05)50020-7
PMCID: PMC3153469  PMID: 16186030
2.  Posterior Cingulate, Precuneal & Retrosplenial Cortices: Cytology & Components of the Neural Network Correlates of Consciousness* 
Progress in brain research  2005;150:205-217.
Neuronal aggregates involved in conscious awareness are not evenly distributed throughout the CNS but are comprised of key components referred to as the neural network correlates of consciousness (NNCC). A critical node in this network is the retrosplenial, posterior cingulate, and precuneal cortices (RSC/PCC/PrCC). The cytological and neurochemical composition of this region is reviewed in relation to the Brodmann map. This region has the highest level of brain glucose metabolism and cytochrome c oxidase activity. Monkey studies suggest that the anterior thalamic projection likely drives RSC and PCC metabolism and that the midbrain projection to the anteroventral thalamic nucleus is a key coupling site between the brainstem system for arousal and cortical systems for cognitive processing and awareness. The pivotal role of RSC/PCC/PrCC in consciousness is demonstrated with posterior cingulate epilepsy cases, midcingulate lesions that de-afferent this region and are associated with unilateral sensory neglect, observations from stroke and vegetative state patients, alterations in blood flow during sleep, and the actions of anesthetics. Since this region is critically involved in self reflection, it is not surprising that it is similarly a site for the NNCC. Interestingly, information processing during complex cognitive tasks and during aversive sensations such as pain induces efforts to terminate self reflection and result in decreased processing in PCC/PrCC. Finally, anatomical relations between the neural correlates of mind and NNCC in the cingulate gyrus do not appear to overlap and suggests that mental function and conscious awareness may be mediated by two neural networks.
doi:10.1016/S0079-6123(05)50015-3
PMCID: PMC2679949  PMID: 16186025
cingulate gyrus; medial parietal cortex; metabolism; anesthetics; sleep; anterior thalamus

Results 1-2 (2)