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hyperactive (e.g., studies done in public or tertiary facilities as opposed to private-practice settings).
Diagnostic, selectional, and situational factors that explicitly or implicitly facilitate the inclusion of aggressive children in a so-called "hyperactive" sample will also facilitate the conclusion that hyperactive children tend to abuse drugs. Factors biased against the inclusion of aggressive children will have the opposite effect. To reduce the danger of such discrepant and confusing effects, we have suggested that children who are hyperactive and aggressive be diagnostically and prognostically separated from children who are exclusively hyperactive (Langhorne and Loney 1979).
Among the other predictors of behavioral outcomes among so-called hyperkinetic children are the social or environmental correlates of aggression: social class, family composition, parenting style, urban residence, etc. While individual aggressive characteristics, such as rebelliousness, determine a youngster's susceptibility to illegal drug use, many of these socioecological antecedents of aggression also influence the availability of illegal substances. It is our feeling that the interaction of susceptibility and availability explains why exclusively hyperactive (nonaggressive) youngsters do not abuse drugs. Although they may be susceptible to drug use because of their immaturity and restlessness, many are also socially awkward and rejected children to whom drugs are less available because of their isolation from the peer settings in which much early drug use is initiated (Jessor and Jessor 1977).
in our theory, childhood aggression and childhood hyperactivity are assumed to have different antecedents and different consequents both at referral and at followup. If valid, this theory also explains why treatment with central nervous system stimulants does not lead to improved adolescent behavior and reduced delinquency (Weiss et al. 1975). Although drug treatment reduces childhood inattention and hyperactivity, behavior outcome and subsequent delinquency are determined instead by childhood aggression and by its ecological antecedents-which are not affected by drug treatment. Thus, drug treatment for childhood hyperactivity is ineffective in reducing adolescent symptomatology because childhood hyperactivity is not the first link in a chain leading to teenage delinquency and deviant behavior (Milich and Loney 1979).
A complete theory of substance abuse will ultimately describe the multivariate interaction of enduring personal factors or traits, such as aggression (Eron 1978; Olweus 1978; Robins 1978), with situational factors, such as parental modeling, peer pressure, substance availability, and treatment history. A good theory will encompass and estimate the effects of such individual factors as age, sex, and race; such geographical factors as region and community; and such temporal factors as year or era--all of which have been little studied among hyperkinetic children. In so doing, an adequate theory will locate drug attitudes and use within a matrix of health-threatening and norm-violating behaviors.
In addition to the likelihood that stimulant medication fails to decrease the risk of delinquency in general among hyperkinetic children, concern has been expressed about the possibility that treatment with stimulant drugs further increases the risk that hyperkinetic children will abuse drugs--either pharmacologically (by initiating a dependency that
children continue on their own) or psychologically (by creating a predisposition toward chemical solutions for complex problems). Because ethical and practical considerations preclude random assignment of children to long-term treatment groups, investigators interested in the safety and efficacy of treatment with stimulants have usually had to rely on naturally occurring diagnostic and treatment groups. Therefore, the great majority of early followup studies (e.g., Laufer 1971; Mendelson et al. 1971; Minde et al. 1971; Weiss et al. 1971) were carried out on samples of previously medicated youngsters, without control groups or systematic comparison data. There are some recent data (Beck et al. 1975; Denhoff and Stern 1979; Henker et al., in press) comparing substance use among previously medicated hyperactive children and nonhyperactive (and, of course, nonmedicated) agemates. Although few group differences were found in these data, it is unclear to what degree a negative effect of hyperactivity (or of behavior problems in general) might have been canceled out by a positive effect of medication. Or perhaps a positive effect associated with hyperactivity was canceled out by a negative effect of medication. Hechtman et al. (in press) found no greater substance abuse among essentially untreated hyperactive youngsters and their nonhyperactive classmates. Blouin et al. (1978) compared treated and untreated youngsters within a hyperactive sample and found no statistically significant (p < .05) differences between the groups in their use of hard liquor, beer, wine, or marijuana.
Another design has involved the comparison of hyperactive and nonhyperactive individuals within larger groups of psychoeducational, psychiatric, or neurological referrals. Two such studies (Blouin et al. 1978; Schuckit et al. 1978) have yielded numerically intriguing but statistically insignificant differences in substance use associated with hyperactivity--even though aggressive youngsters were not specifically excluded. Likewise, two studies of hyperkinetic children (Cantwell 1972; Morrison and Stewart 1971) that are widely cited as supporting the link between hyperactivity and subsequent alcohol use and antisocial behavior are difficult to interpret because childhood hyperactivity and childhood aggression are not separated. More of Goodwin et al.'s (1975) alcoholic adoptees recalled being hyperactive as children than did nonalcoholic controls, but they also recalled being more aggressive and shyer. Among an adolescent group being treated for drug abuse, Schuckit et al. (1978) found that hyperkinetic/antisocial subjects were significantly more likely than nonhyperkinetic subjects to have been warned by a physician that drugs had damaged their health. That finding is difficult to interpret, however, because more of the hyperkinetic subjects probably had contact with physicians, who may be prone to attribute symptoms among hyperkinetic youngsters to drug abuse (Topaz 1971) when in fact the symptoms predated the use of illegal drugs.
Among drug-treated hyperactive children, good treatment response appears to be associated with less use of alcohol (Blouin et al. 1978) and of drugs (Kramer and Loney 1978) at five-year followup. Much further work is obviously going to be required, particularly to separate and specify the effects on adolescent drug use of: (1) behavior and learning problems in general (by comparing hyperactive children with randomly selected or normal children); (2) hyperkinesis per se (by comparing hyperkinetic children with other children having behavior and learning problems); (3) the diagnosis or label "hyperkinetic" (by comparing diagnosed hyperkinetic children with undiagnosed hyperkinetic children); (4) drug treatment for hyperkinesis (by comparing medicated
hyperkinetic children with nonmedicated hyperkinetic children); and (5) pharmacological response to that treatment (by comparing medicated hyperkinetic children who responded well with medicated hyperkinetic children who did not). Meanwhile, it appears that the risk of substance use among hyperactive youngsters may be neither great nor increased by early drug treatment.
Although our theory is derived from examination of an "abnormal" sample, it can be removed from a medical context by considering hyperactivity and aggression as psychological traits rather than as psychiatric disorders. There is, in fact, considerable doubt that childhood hyperactivity is an authentic medical syndrome (Langhorne et al. 1976; Ross and Ross 1976; Sandberg et al. 1978). A medical syndrome should ideally have a specific etiology, a particular pattern of symptoms, a predictable response to treatment, and a uniform course and outcome. Certainly hyperactive children are noted for their interindividual heterogeneity and their cross-situational variability, and questions of etiology and diagnosis remain unanswered. In psychological terms, then, individual susceptibility to subsequent drug use is associated with childhood aggression. It is not associated with childhood hyperactivity, either directly or indirectly (through the effect of hyperactivity on aggression). Such translation from psychiatric categorization to psychological quantification places these findings regarding the predictors of substance use among hyperactive children into a comparable framework as studies of predictors of substance use among children in general (Jones 1968; Lettieri 1975). However, one genuinely special population consists of children who have been treated with stimulant drugs. Within that population, two special subpopulations are those children whose clinical response has been positive (i.e., who have shown symptom reduction) and those children whose clinical response has not been positive. So far, it is not clear that drug treatment per se modifies children's attitudes in such a way that the probability of subsequent drug use is affected either positively or negatively. But our theory, and the findings from which it is derived, suggest that positive drug response may reduce the probability of subsequent drug abuse by decreasing children's irritability, touchiness, and sullenness, and by increasing their frustration tolerance. If so, this would be an effect of medication upon the early temperamental/emotional aspects of aggressive behavior. Medication does not appear to have direct effects on any overtly behavioral aspects of aggression except for substance use.
Reinforcement and the
William E. McAuliffe, Ph.D.
The theory summarized here emerged from systematic empirical research and critical reexamination of prior literature concerning opiate addiction (McAuliffe and Gordon 1974, 1975, 1979; McAuliffe 1975a,b, 1979; Gordon 1979). This effort has resulted in the firm establishment of euphoric effects as one of the several major sources of reinforcement deriving directly from opiates even in chronic addiction (McAuliffe and Gordon 1974, 1975), and clarification of the conditions under which euphoric effects are available even to many first-time users of opiates (McAuliffe 1975a). Prior to these investigations, most social scientists accorded a relatively restricted role to euphoria (e.g., Lindesmith 1947), and this view also found considerable acceptance among physical and medical scientists. Euphoric effects sometimes reported or assumed in the medical literatures were often considered atypical. Now, with such fundamental issues behind us, it is possible to use a reinforcement theory to organize and interpret many of the more detailed empirical phenomena of opiate abuse, where that theory has available to it for explanatory purposes the full range of effects produced by opiate drugs. The present digest reflects the current stage of development of such a theory. (For a full statement, see McAuliffe and Gordon 1979.)
A BRIEF OVERVIEW
THE CAUSE OF ADDICTION
According to our theory, opiate addiction is caused by the extremely potent reinforcing effects of opiate drugs. These effects consist of euphoria (including the impact effect or "rush"), reduction of withdrawal, and miscellaneous psychotherapeutic and analgesic properties,
which combine independently to produce a complex schedule of reinforcement for taking opiates. Opiate use, consequently, is an operantly conditioned response whose tendency becomes stronger as a function of the quality, number, and size of the reinforcements that follow it. Addiction, in our theory, refers to the strength of the drug-taking response and is thus a continuous variable, rather than a qualitatively different state. Addiction begins to grow with the first reinforced opiate-taking response. When the opiate-taking response has become powerful enough, as the result of sufficient reinforcement, the user experiences an increased desire or "craving" for opiate effects.
Craving may, however, be contingent upon the presence of discriminative stimuli that signal to the user that reinforcement for taking opiates is indeed possible; for example, that he or she is not under opiate blocking by antagonists such as naloxone at the time. An experiment by Mirin et al. (1976, figure 3) found that addicts' self-reported intensity of craving rose rapidly when heroin was readily available, fell rapidly under methadone detoxification, and remained low when heroin was again made available while the subjects were on a blocking regimen receiving naltrexone.
A more meaningful definition of "addiction." in common parlance, persons are said to be "addicted" when they have become physically dependent or at least seem unable to refrain from using a drug. We regard these events as merely signalling that a sufficient history of reinforcement has probably been acquired to impel a high rate of use. In the case of strong physical dependence, the user is confronted with the necessity of responding at a minimal rate (which happens to be also a high rate) if immediate use for whatever reason is to continue at all and if a negative reinforcer is to be successfully avoided. In our theory, there is no single point at which an individual suddenly becomes "addicted." Instead, the individual's addiction develops insidiously and varies continuously, so that what others seemingly mean when they label someone an "addict" is merely a person with a strong addiction (i.e., a history of reinforced drug taking sufficient to outweigh the more acceptable reinforcers of life, such as are associated with one's job, family, friends, sex life, and respectability).
Physical dependence on opiates is neither a necessary nor a sufficient condition for the development of addiction. Physical dependence simply sets the stage for experiencing withdrawal distress, reduction of which constitutes one of the drug's powerful reinforcing effects. Other effects (principally euphoria, but including secondary social gains, and relief of pain, anxiety, and fatigue) can themselves produce or contribute to addiction. Most, if not all, street addicts are reinforced in the early stages of heroin use by effects other than withdrawal, and their drug-taking response at that stage must be strong . enough so that it occurs every day for a few weeks in order for them to develop physical dependence. Since contemporary opiate abusers know about physical dependence and usually prefer to avoid it, their daily use prior to dependence must reflect the existence of an addiction of some strength. We have interviewed heroin users who had never been dependent but who were either adamant about wanting to continue heroin use despite the risks and severe social pressures or convinced that they could not stop even though they wanted to. We and other researchers (Lindesmith 1947; Robins 1974a) have also interviewed persons who had used opiates compulsively on a daily basis for many months without ever interrupting long enough to experience withdrawal sickness.