Lesion Correlates for Major Disorders of Consciousness

These lesion correlates are best approached as strong general tendencies with clinical/predictive validity but not invariance, for there are exceptions.

Coma 1. Major lesions of mesodiencephalic areas or diffuse axonal injury.

2. Severe toxic-metabolic or neuromodulatory disturbances.

PVS 1. Initial stage of recovery from coma from brain injury, from above etiologies.

2. Lesser lesions of mesodiencephalic and reticular areas, typically sparing some pontine, midbrain, or other mesodiencephalic regions.

AKM 1. A secondary stage of recovery from Coma ^ PVS ^ AKM, especially from posterior intralaminar thalamic (ILN) lesions.

2. Bilateral cingulate lesions.

3. Extensive lesion of periaqueductal gray (PAG) or VTA lesions.

4. Extensive bilateral lesions of the basal ganglia (BG), especially nucleus accumbens and globus pallidus, more rarely bilateral caudate.

5. On rare occasions, medial forebrain bundle, other RAS areas.

HKM 1. Extensive bilateral lesions of posterior heteromodal cortical fields, typically from bilateral middle cerebralatery (MCA) infarctions.

Delirium 1. Serious toxic-metabolic disturbances or major disruption of neuromodulatory systems, particularly DA, ACh, but on occasion NE, very occasionally 5-HT.

2. Major lesions of right parietal or right prefrontal areas, right basal ganglia, thalamic, or reticular regions. Less frequently, left-hemisphere lesions of same regions.

3. Classically associated with Alzheimer's disease (AD) and superimposed but relatively more modest toxic metabolic or neuromodulatory disturbances. (AD, along with several other neurodegenerative disorders, appears to substantially lower thresholds for delirium from a host of factors—see chapter on neurodegenerative disorders).

In lesion studies, one must note that lesions necessary for serious impairment of consciousness in the adult may be somewhat different from lesions potentially interfering with the development of consciousness in the young, and neurodevelopmental dimensions of this problem are very poorly understood. Despite these complexities, lesion correlates suggest a fairly delimited, mostly midline set of structures that appear to be essential, with more dorsal and lateral structures enabling cognitive extensions of a core consciousness. This is consistent with other lines of evidence that midline and ventral structures in the brain provide the more primitive, affective, and integrative functions. Evidence from several lines of investigation suggests that the most critical components in descending order are:

1. The multicomponent distributed reticular systems previously outlined (the RAS broadly defined),

2. Several mesodiencephalic regions sitting above and in communication with those systems, including midbrain superior colliculus (SC) and cuneiform nucleus (CUN), the intralaminar thalamic nuclei, and the nRt (reticular nucleus of the thalamus), which jointly comprise the dorsal systems of the ERTAS or the extended reticular thalamic activating system (some schemes label both SC and CUN as "midbrain reticular formation" and therefore part of the ERTAS concept);

3. Regions of paleocortex, particularly anterior cingulate;

4. Heteromodal regions in posterior cortex, perhaps particularly right-hemisphere parietal regions, particularly inferior areas;

Regions for which there is incomplete evidence would include the cerebellum (particularly midline regions such as the vermis/fastigal nucleus that have largely reticular connectivities), primary somatosensory cortex, insula, and several other paralimbic regions. It seems likely that cerebellar vermis and paralimbic insula contribute more to core consciousness, while contributions of idiotypic somatosensory regions (S1 and S2) are more likely "extended" and cognitive. However, the matter is still largely undecided, with no conclusive empirical evidence yet available. Extensive bilateral damage to dorsolateral prefrontal cortices, essential for working memory and the executive aspects of attentional function and gaze control, produces a severely disorganized state, akin to a chronic delirium (see clinical case discussion). It is an open point whether this is a disorder of core or extended consciousness. Extensive bilateral lesions of these basic regions cause one of the disorders outlined in Table 3.1. Regions of other brain areas (particularly of widespread unimodal and idiotypic neocortical regions) can and do produce serious affective, behavioral, and cognitive changes but probably not disturbances of primary or core consciousness.

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