Clinical Textbook of Addictive Disorders 3rd ed - R. Frances, S. Miller, A. Mack (Guilford, 2005) WW

3. Psychological Evaluation 41neuropsychological tests but should also attempt to determine from other psychometricinstruments (as well as from biomedical or laboratory tests) the possibleetiological basis for the manifest disturbances.Approximately 75% of individuals with alcohol dependence demonstratesome form of CNS disturbance, as measured by neuropsychological tests (Tarter& Edwards, 1985). Emerging findings also suggest that other forms of substanceabuse are frequently associated with deficits on neuropsychological tests. Generallyspeaking, chronic alcohol abuse can cause both cognitive and physicaldamage to the brain that is typically expressed as visuomotor deficits, while verbalability remains essentially intact. Impairments have also been frequentlyobserved on tasks measuring abstract thinking and memory capacity, as well ason tests measuring visuospatial processes (Tarter & Ryan, 1983). These deficitsappear to be most pronounced in individuals who are in less than optimalhealth, or who have experienced the cumulative effects of multiple CNS insults(Grant, Adams, & Reed, 1979). With respect to biomedical factors, a low-gradechronic hepatic encephalopathy may contribute substantially to the cognitivedeficits found in cirrhotic alcoholics. This neuropsychiatric disturbance has acomplex etiology. For example, the encephalopathy, revealed as poor performanceon cognitive tests, is caused to large degree by the liver’s failure tocatabolize circulating neurotoxins (Tarter, Edwards, & Van Thiel, 1986). Furthermore,it should be noted that a hepatic encephalopathy may have a varietyof other etiological determinants (Tarter et al., 1986). In effect, the manifestcognitive deficits have a multifactorial etiology.Neuropsychological deficits associated with alcoholism are well documented.Indeed, two syndromes of cognitive disorder have been described. Adementia has been observed that is distinguishable according to both neuroanatomicaland cognitive manifestations from the more florid amnestic orKorsakoff’s syndrome (Wilkinson & Carlen, 1980). A number of other neurologicalconditions have also been described, although their neuropsychologicalmanifestations have not yet been studied.Less is known regarding neuropsychological sequelae following other typesof substance abuse. Evidence has been presented indicating that the chronic useof phencyclidine (PCP), inhalants, benzodiazepines, heroin, cocaine, andamphetamines may be associated with neuropsychological impairments in someindividuals (Parsons & Farr, 1981). One major methodological problem in thisarea of study is that it is not possible to ascertain the specific effects of a certaindrug on CNS functioning, because polydrug abuse is the typical pattern of consumption.Also, the frequency and quantity of drug use are extremely variable;hence, determining a dose–effect relationship is difficult, if not impossible.These qualifications notwithstanding, the available evidence indicates that, asa group, substance abusers perform deficiently on certain neuropsychologicaltests indexing CNS integrity. As is the case among individuals with alcoholdependence, poor neuropsychological test performance has a multifactorial eti-