In vivo mammillary body volume deficits in amnesic and nonamnesic alcoholics

Citation
Ev. Sullivan et al., In vivo mammillary body volume deficits in amnesic and nonamnesic alcoholics, ALC CLIN EX, 23(10), 1999, pp. 1629-1636
Citations number
54
Categorie Soggetti
Clinical Psycology & Psychiatry","Neurosciences & Behavoir
Journal title
ALCOHOLISM-CLINICAL AND EXPERIMENTAL RESEARCH
ISSN journal
01456008 → ACNP
Volume
23
Issue
10
Year of publication
1999
Pages
1629 - 1636
Database
ISI
SICI code
0145-6008(199910)23:10<1629:IVMBVD>2.0.ZU;2-D
Abstract
Background: Neuropathological studies use the presence of mammillary body ( MB) pathology as a cardinal, diagnostic feature of Wernicke's encephalopath y (WE) in neuropsychiatric diseases, most notably alcoholism. Although Kors akoffs Syndrome (KS), which is marked behaviorally by dense global amnesia, is a typical sequela of WE, it remains controversial whether these two con ditions necessarily co-occur and whether MB pathology is therefore a diagno stic requisite for KS. Methods: We investigated these issues by examining, in vivo, 24 nonamnesic alcoholics (ALC), 5 amnesic alcoholics (KS), and 51 normal controls with th ree-dimensional MRI and memory testing. MB volume was determined from succe ssive, 1 mm thick slices. Results: The ALC group had significantly smaller MB volumes bilaterally (me an = 54.5 +/- 22.0 mm(3)) than controls (mean = 66.3 +/- 17.1 mm(3)), and t he KS group had even smaller MB volumes than the ALC group (mean = 20.7 +/- 14.8 mm(3)). Only 2 ALC patients met historical clinical criteria for past WE, and their MB volumes were well within range of the remaining 22 ALC pa tients. Although all five KS patients met historical clinical criteria for WE, three KS did not have accompanying dementia and had the same degree of MB volume loss as the ALC; the remaining two KS had accompanying dementia a nd MB volumes half the volume of the ALC group and of KS patients without d ementia. Conclusions: These findings provide volumetric in vivo evidence that: (1) M B volume deficits do occur in alcoholics without amnesia, although these de ficits are not present in all such alcoholics; (2) greater MB volume defici ts are present in alcoholics with clinically detectable amnesia or dementia ; (3) MB shrinkage is related to severity of cognitive and memory dysfuncti on, which suggests a continuum of MB pathology in chronic alcoholism to KS; and (4) the presence of WE in all of the KS patients and in the two ALC pa tients with the greatest long-term declarative memory deficit supports the possibility of an additional and unique pathology distinguishing nonamnesic and amnesic alcoholism.