This naturalistic study of the effects of self-reported sobriety or continued drinking over a mean retest interval of 22 months identified memory and gait and balance as components of our test battery for which significant improvement was detected in self-proclaimed abstaining alcoholics relative to controls. By contrast, self-proclaimed abstaining alcoholics did not manifest greater improvement relative to controls on standardized measures of intelligence. A modest increase in lateral ventricular volume in the abstaining alcoholics was comparable to that seen in the controls, whereas relapsing alcoholics showed significant greater lateral ventricular enlargement than either abstaining alcoholics or controls. While the changes in fourth ventricles did not differ between groups, the profile of change, with Relapsers showing increased volume relative to both controls and Abstainers, was similar to that observed for lateral ventricles.
This sample of previously treated alcohol dependent individuals is consistent with other samples in demonstrating considerable individual variation in vulnerability to the effects of alcoholism on cognitive performance. The fact that Relapsers manifest unimpaired memory at baseline compared with Abstainers suggests another dimension along which samples of people who have consumed large amounts of alcohol over their life differ: level of impairment ranges from notable to none. Lack of detected impairment may be more common in non-treatment seeking alcoholics than treatment-seeking ones (Fein and Landman, 2005
). Further, studies with larger samples have shown that familial alcoholism, antisocial personality, and physical well-being, all perhaps phenotypes for a more basic genetic trait, as well as age and education, can all predict level of neuropsychological deficits (Grant et al., 1984
; Tarter and Edwards, 1986
; Parsons, 1987b
; Bates et al., 2002
; Bates et al., 2005
). Our study, however, does not have the power (cf, Bates et al., 2004
) to determine whether such variables contributed to the Relapsers’ initial superior performance.
Most (8 of 10) of the Abstainers were initially tested within only 2 months of sobriety, whereas most (3 of 5) of the Relapsers were tested after more than 6 months of sobriety. Across the entire sample, alcoholics who had been sober longer at study entry tended to perform better on the memory tests, and this higher baseline may have also contributed to lack of change among the Relapsers. Sobriety at baseline, however, was not associated with baseline ventricular volume, but did predict subsequent change – longer sober showed more enlargement, an effect that may have been driven by one participant, sober for over 2 years at study entry, who relapsed during the follow-up period.
While the 5 Relapsers were high performers at study entry, 4 of them showed reduction on the General Memory Index at retesting. This reduction in memory performance among the Relapsers is difficult to interpret, especially as they differed widely in length of sobriety at first assessment, were retested at varying intervals and had consumed highly variable amounts of alcohol between assessments. The extent to which lower memory performance of the 10 Abstainers at study entry was due to innate differences from the Relapsers or recency of testing since attaining sobriety is unknown. However, 9 of the Abstainers showed memory improvement at retest that was on average greater than that seen in controls. This suggests that sobriety enhanced the normal practice effect on self-cuing and active retrieval needed to perform various memory tasks, an effect particularly evident for Story Recall.
The amount and direction of change in overall memory performance as indexed by the WMS-R across all alcoholic subjects was related to amount of change in the lateral ventricular volume. Our measure of lateral ventricular volume might be taken as an approximation of the integrity of adjacent structures and regions invoked in the WMS-R battery (cf, Symonds et al., 1999
). These include frontal lobe systems, used for strategic executive function, such as self-cueing and semantic organization (Incisa della Rocchetta and Milner, 1993
; Fletcher et al., 1998
; Savage et al., 2001
), and medial temporal lobe structures used for nonstrategic declarative memory (Zola-Morgan and Squire, 1992
; Corkin et al., 1997
). Importantly, associations were not present between change in memory and change in the fourth ventricle, a CSF-filled space adjacent to the cerebellum.
The alcoholics in this study (both Relapsers and Abstainers) also showed evidence for improvement in ataxia over time relative to the controls. However, improvement in ataxia was modestly associated with decreases in volume of the fourth ventricle, specifically in Abstainers, but showed no association with change in volume of the lateral ventricles. The proximity of the fourth ventricle to the cerebellum makes it a proxy measure for this complex structure (cf, Symonds et al., 1999
), the integrity of which is associated with static balance and gait (Sullivan et al., 2000a
; Sullivan et al., 2006
). The lack of association between change in either behavioral measure and either ventricular volume among the controls may reflect a limited range of age-related change occurring over one year among controls compared to greater recovery, or exacerbation-related change occurring among the alcoholics.
This report is limited by its small sample size, varying lengths of sobriety at study entry, and reliance on self-reported estimates of drinking that varied across subjects in quantity, recency, and duration. Despite these limitations, this naturalistic study provides support for the concept that fluctuations in the volumes of CSF-filled space may provide a proxy measure for structural brain changes associated with cognitive and motor processes that are amenable to recovery with sobriety. The results need to be evaluated in a larger sample, matched on length of sobriety at baseline, and with expanded assessments of regional brain change.