The likelihood and extent of cognitive impairment from excessive use of alcohol may reflect an interaction between drinking history, constitution and environm ental factors (eg. beverage type, drinking pattern, diet, inborn metabolic or endocrine abnorm ality, age related diseases, etc). These influences can confound NP investigation and lead to spurious
distinctions between different types of ARBD (L ishm an 1990; Hall 1989; Butters & G ranholm 1987; G oldstein 1987, citing T arter, H egedus, Van Thiel, Schade & Starzi 1984, Tarter, Hegedus, Van Thiel, Schade, Pollit- Heyl & Gavaler 1984, Blass & Gibson 1977). Although the ABS and WKS can dev elo p in parallel as the res u lt of either alcohol n eurotoxicity or thiam ine deficiency m echanism s (Butters & G ranholm 1987), the severity of deficits could be represented on a continuum rath e r than as discrete syndrom es (W ilkinson 1987, citing R yback 1971, Ryan & Butters 1980; Ron 1987; Bow den 1990). L ishm an (1990) suggested excessive drinkers may be d ifferen tially su sceptible to one or the o th er m ec h an ism and those vulnerable to both would be more likely to develop chronic WKS. B ow den (1990, citing H arper 1979, 1983, H arp er et al 1986, Torvik, L indboe & R ogde 1982) considered the acute and chronic form s of the WKS to be partly reversible, have highly variable or asym ptom atic signs and sy m p to m s and w as m ore c o m m o n than p re v io u s ly b e liev ed . He s u p p o rte d the n o tio n that a lc o h o l in som e w ay p re v e n te d adeq u ate thiam ine m etabolism and that exclusion of classic cases of W KS merely confounded investigation which proposed different types of ARBD.
F a c t o r s A f f e c t i n g C o g n i t i v e P e r f o r m a n c e
Family History of Alcoholism
A part from genetic influence such as that asso ciated with the drinking status o f b io lo g ical fathers at tim e of co n ce p tio n (G ran t 1987, citing H e n n ec k e 1984, E lm asian , N e v ille, W oods, S c h u c k it & B lo o m 1982, Schuckit 1984), impaired brain function has been associated with adverse in d iv id u al and family b ackgrounds (G rant 1987, citing T arter, H egedus, G oldstein, Shelly & A lterm an 1984, Ervin, Little, Streissguth and Beck 1984). H ow ever, results have been equivocal and there have been no system atic NP perform ance differences that could be attributed solely to a fa m ily h isto ry of a lc o h o lis m for e ith e r a lc o h o lic or n o n a lc o h o lic offspring (G rant 1987). On the other hand, adverse living conditions and
experiences associated with growing up in a family where members abuse alcohol could be sufficient to account for variation in cognitive deficits between both dependent and nondependent drinkers (Grant 1987, citing Alterman & Tarter 1985). Thus, care in establishing relevant individual and family background variables may be more important than genetic considerations in predicting NP performance.
Aboriginals generally interpreted the right to vote at federal elections in 1962 as their right to drink, with a subsequent rise in alcohol related problems and offences noted the following year (Brady 1990a, citing Sansom 1980, Nathan & Japanangka 1983, Myers 1986). Within 20 years 80% of aboriginal families in NSW were reported to be affected by alcohol (Hunt 1981). However, as most of the patients in the present study were old enough to have missed the influence of an early family history of alcoholism, no attempt was made to measure this factor in the present study.
Neuromedical Risk
Premorbid and concurrent neuromedical risk factors can account for NP deficits in those who misuse alcohol and are usually controlled for in any systematic study of drinking history and NP performance. Moreover, a number of medical disorders which can interact with drinking pattern to produce poor cognitive function have been found to be more prevalent among alcoholics (Grant, Adams & Reed 1984). Several neuromedical risk factors are usually considered in the selection and matching of suitable comparison groups or the multivariate analysis of excessive drinking and NP performance (Grant 1987, citing Adams & Grant 1986):
Head Injury: (Golden, Moses, Coffman, M iller & Strider 1983; Walsh
C hildhood L earning D isorders: (R hodes and Ja sin sk i 1990; G rant 1987, citing De O baldia & P arsons 1984; G rant 1987; Parsons 1986, citing De O baldia, Parsons, Y ohm an 1983).
W ith d ra w a l S y m p to m s: (M iller and Saucedo 1983, citing L usins et al 1980, F lem in g & G u th rie 1980, E ck a rd t, P a rk e r, N o b le, F eld m an & G ottschalk 1978 & 1980, G uthrie 1980, Jones 1971, R ada et al 1977; Grant 1987, citing L oberg 1986; L oberg & M iller 1986; G oldstein, Tarter, Shelly, A lterm an and P etraru lo 1983; G oldstein 1987).
Vascular D isorders: (F u n k en stein 1988; G rant 1987, citin g H illborn & K aste 1981, T aylor & C om bs-O rm e 1985; A lbert 1988c; M azzucchi, M utti, P o letti, R av an etti, N o v arin i & P arm a 1986, citin g G au tier 1983; Juveia
1 9 9 2 ).
Liver Disease: (G oldstein 1987, citing T arter, S tarzi et al 1984; C larke & Saunders 1988; H unt 1981; G rant 1987, citing Sm ith & Sm ith 1977, Lee, M öller, H ardt, H aubek & Jensen 1979, K roll, S ieg el, O 'N eill & Edw ards 1980, G ilberstadt et al 1980, T arter 1985; Irw in et al 1989; R ichardson et al 1991; Batey, Burns, Benson & Byth 1992).
N u tritio n a l D eficiency: (L ezak 1983; A lb ert 1988b; L ezak 1983, citing G uthrie & E llio tt 1980; M iller and Saucedo 1983, citing G uthrie 1980, Flem ing & G u th rie 1980; L oberg and M iller 1986; G rant 1987, citing G rant, A dam s & R eed 1979, S h erlo ck 1984; B o w d en 1990; K lekam p, R ied el, H a rp er & K re tsch m a n n 1987; R ied e l, K lek am p , H arp er, and K retsch m an n 1989).
Other Drugs: (Joynt & Shoulson 1985; A lbert 1988b, citing D rachm an & L e a v itt 1974, S u m m ers 1978; G ra n t 1987, c itin g G ra n t, H eato n , M cSw eeny, A dam s & Tim m s 1982, P rig atan o , P arso n s, W right, Levin &