According to this view, alcoholics who are susceptible to alcohol toxicity but not to thiamine deficiency may develop permanent or transient cognitive deficits associated with cortical shrinkage. Those alcoholics who are susceptible to thiamine deficiency alone will develop a mild or transient Korsakoff state with anterograde amnesia as a salient feature. Alcoholics with dual vulnerability, suffering from a combination of alcohol neurotoxicity and thiamine deficiency, will experience widespread damage to large regions of the cerebral cortex as well as to structures deep within the brain. Consequently, these people will exhibit severe anterograde amnesia and other cognitive impairments. The following discussion of theoretical models that have been proposed to explain cognitive deficits primarily will consider those people mentioned in the first group—those with alcohol problems whose cognitive impairments most likely are related to cortical brain changes and who exhibit no clinical signs of anterograde amnesia.