[Cognitive dysfunction following anterior communicating artery aneurysm rupture. Comparison with alcoholic Korsakoff...

The present study aims to compare neuropsychological performance of patients following anterior communicating artery aneurysm rupture (ACoA) with that of patients with alcoholic Korsakoff syndrome (AKS). Fifteen ACoA patients and ten age-and education-matched AKS patients were included in the study. All the patients were tested at least one year post onset of their illness at a stable condition. The WAIS and forward digit span scores of AKS were also matched to ACoA, and simple attention and general intelligence were well preserved both in ACoA and AKS. Frontal function as measured by the Wisconsin card sorting test (Keio version) (KWCST) was equivalently impaired in the two groups. Anterograde memory as measured by Wechsler memory scale subtests, serial seven word learning test, Rey auditory verbal learning test, and logical memorizing test (Luria's paired word-picture association), was more severely impaired in AKS than ACoA in contrast to the comparable attention, intelligence, and frontal function: (1) memory tasks with low correlations to KWCST (serial word learning tasks and paired verbal associates), reflecting primary simple serial memorizing, and (2) memory tasks with high correlations to KWCST (logical memory and logical memorizing), reflecting higher and complicated strategic mnemonic activities. However, the correlations between these anterograde memory subtests and KWCST were substantially equivalent in ACoA and AKS. This suggests that the differences in anterograde amnesia demonstrated in ACoA and AKS may be of quantitative, not of qualitative property. The extent of deficits in semantic encoding as measured by Wickens' release from proactive interference paradigm (PI release) was also milder in ACoA than AKS. Both AKS and ACoA failed to show PI release in contrast to normal PI release demonstrated in age-matched ten healthy subjects. PI release in ACoA, however, was in between AKS and healthy subjects. The results were interpreted in the light of a recently postulated hypothesis that a combination of frontal lobe damage and memory impairment is crucial for causing a deficit in semantic encoding. The extent of damage in the memory circuit in ACoA may be variable, which may result in milder degree of anterograde amnesia and semantic encoding than AKS in the present study.