© Springer Science+Business Media New York 2015
Charles M. Zaroff and Rik Carl D’Amato (eds.)The Neuropsychology of MenIssues of Diversity in Clinical Neuropsychology10.1007/978-1-4899-7615-4_6Understanding the Neuropsychology of Substance Abuse in Men
(1)
Psych Associates, 5903 Lone Oak Drive, Bethesda, MD, USA
(2)
Fielding Graduate University, Santa Barbara, Ventura, CA, USA
(3)
Developmental Neuropsychology Laboratory, Frontal Lobe Institute, Ventura, CA, USA
Keywords
SexGenderMaleNeuropsychologySubstance abuseDrug abuseStimulantOpiateCocaineAlcoholPortions of this chapter were adapted from a chapter by Horton Jr. and Horton III (2008).
Introduction
Abuse of alcohol and drugs is a very important social problem (Horton, 1993; Horton & Horton, 2005). We are seeing an increase in deaths from prescription drugs, cocaine, or heroin (CDC, 2014). Research has documented that prolonged use of alcohol and illicit drugs can cause significant residual brain damage (Goldstein & Volkow, 2011; Horton & Horton, 2005; Yucel, Lubman, Solowij, & Brewer, 2007). In this chapter we address the residual neuropsychological effects on men who have abused alcohol and other drugs.
Substance abuse problems have a long history. Human beings have used alcohol and natural substances such as peyote from cacti, and leaves from the opium plant, and other substances to change their emotions for centuries. Pharmaceutical technology has added new drugs such as Morphine, Heroin, Cocaine, Amphetamine, Lysergic Acid Diethylamide, Phencyclidine, and designer drugs such as Ecstasy with addiction potential. Research has documented that abusive use of alcohol and illicit drug use can cause significant brain damage (Allen & Landis, 1998; Goldstein & Volkow, 2011).
Overview
The fact that individuals who abuse alcohol and drugs can become brain damaged has important implications for the assessment and treatment of individual drug abusers (Horton & Horton, 2005; Spencer & Boren, 1990). Tarter and Edwards (1987) noted that little attention had been devoted to individuals with brain damage caused by substance abuse problems. Moreover, neuropsychological assessment can be used to provide a prognosis, assess potential for recovery, and provide recommendations for treatment planning and intervention. This chapter focuses on individuals with alcohol and drug abuse-caused neuropsychological deficits that are relatively enduring (Spencer & Boren, 1990) as opposed to select transient drug-related states such as intoxication and delirium. Neuropsychological effects on executive functioning, learning, memory, and perceptual and motor skills from intoxication and delirium are serious problems. For example, drunk driving and/or falls may produce life-threatening traumatic brain damage (Davis, 2011). These neuropsychological effects with intoxication and delirium are state dependent and remit after withdrawal from the abused substance or substances.
Brain Structures Related to the Addiction Processes
Human brains can include as many as 100 billion cells and function as an integrated whole through neural networks (D’Amato & Hartlage, 2008; Davis, 2011; Horton & Horton, 2005). The human brain can be subdivided structurally with different structures interacting to subserve multiple functions and behaviors and differences can be seen between male and female brains (Ruigrok et al., 2014).
Brain structures and related functions, to cite a few examples, include the hippocampus and short-term memory, the visual cortex and visual perception, and the hypothalamus and homeostasis (Horton & Wedding, 1984). Communications rely on neuronal interaction to allow for the sending and integration of information between brain regions transmitted via chemical and electrical signals. Information reception among neurons occurs at the level of the dendrites and soma. Human brains can undergo changes to the reward pathway when exposed to alcohol and psychoactive drugs such as cocaine, heroin, and marijuana. Normally, the human brain reward pathway enables positive conditioning of behaviors that precipitate the experience of pleasure. The human brain connects the behavior to the feeling, and an individual will be more likely to perform the behavior again in the future. The neurotransmitter dopamine has been identified in addiction because of its association with the reward pathway. The human brain reward pathway includes brain structures such as the ventral tegmental area, the nucleus accumbens, and the prefrontal cortex (among other brain structures) and is activated when positive reinforcement occurs with specific behaviors (e.g., see www.nida.nih.gov/pubs/Teaching/). Indeed, human beings are more likely to perform the behavior in the future if a reward follows the behavior. For example, effects of cocaine on the brain reward system can be seen as an example of how the brain reward system works. Stimulation of the nucleus accumbens or ventral tegmental area with cocaine at transmitter receptor sites activates the human brain reward pathway. Activation does not occur when cocaine is administered to receptor sites of the human brain that are not part of the brain reward system.
Addictive drugs are psychoactive. That is, they activate portions of the human brain through specialized neurotransmitter receptor sites (Horton & Horton, 2005; Horton et al., 2001). Psychoactive drugs have the effect of facilitating relationships between intense feelings of pleasure and drug taking behavior through activation of the reward pathway. Activation can be so strong as to cause drug taking behavior to be selected over other important human behaviors (e.g., eating, child care, etc.; D’Amato, Fletcher-Janzen, & Reynolds, 2005; Davis, 2011). Alcohol and illicit drugs have the net effect of increasing firing patterns and activation of the reward pathway. The activation is associated with the reward. The effects on the reward pathway of substances of abuse are primarily responsible for the addictiveness of alcohol and psychoactive drugs. The drug (e.g., alcohol), or drugs, may also have neurotoxic effects on other human brain processes (Horton et al., 2001). For example, the abuse of cocaine disrupts the brain’s ability to utilize glucose (its metabolic activity). Glucose in the human brain provides energy that enables the brain to function (D’Amato et al., 2005; Davis, 2011). Disruption of glucose metabolism, due to abuse of cocaine, can cause disruption of specific brain functions involved in executive functioning. Similarly, another area of the brain that can be compromised by addictive drugs is the hippocampus where multiple abused substances can reduce normal short-term memory functioning (Horton & Horton, 2005; Horton & Wedding, 1984).
Gender Differences in Alcohol and Drug Abuse
It is generally agreed that the majority of studies of alcohol and drug use had been conducted among males prior to the 1970s. It might also be agreed that most individuals diagnosed with alcohol and drug abuse disorders have been males (Brady & Randall, 1999). Simply put, more is known about alcohol and drug abuse by males than by females. In contrast, evidence suggests that ovarian hormones, particularly estrogen, are influential in producing sex differences in drug abuse (Anker & Carroll, 2011). Regarding prevalence rates, males consistently report higher rates of illicit substance abuse and alcohol abuse than females. It appears that drug use is not equally distributed by gender, as males use more illicit drugs, report using drugs earlier and longer than females, and use at a higher frequency in greater amounts. Similarly, with alcohol, males drink alcohol more frequently and more often than females and have a greater number of alcohol-related health problems (Grant & Dawson, 2000). The rate of progression of addiction related problems, however, is much quicker in females than in males (Davis, 2011). Males also appear to be less vulnerable than females to the reinforcing effects of psychostimulants and opiates during the addiction process. Males also have a lower prevalence of comorbid psychiatric disorders such as depression and anxiety than women do and while women may be thought to use alcohol to self-medicate mood disturbances the same may not be true for males (Brady & Randall, 1999).
In contrast, men have a higher death rate from illicit drug use including a higher rate of death from cocaine and heroin and alcohol in combination with other drugs (Davis, 2011; Farrell & Marsden, 2008; Horton & Horton, 2005, 2008). Women are more frequently prescribed psychotropic drugs and are more likely to die from antidepressant abuse. Women also have a higher rate of use of prescription drugs such as tranquilizers, sleeping pills, and over-the-counter medications. Men are more likely to be arrested for drug-related violent crimes, and more likely to participate in drug dealing and street crimes (Brady & Randall, 1999). With respect to substance abuse treatment, however, both males and females may respond equally well (e.g., see Kosten, Gawin, Kosten, & Rousaville, 1993).
In regard to neuropsychological assessment, an authoritative review (American Academy of Neurology, 1996) has suggested that gender has consistent, but minor effects on neuropsychological assessment test results. It has been noted that males performed less well than females on tests of verbal memory but better on motor measures (American Academy of Neurology, 1996; Horton, 1979). Similarly, men evidence greater decline in neuropsychological performance then women on most neuropsychological tests in the course of normal aging. However, the review concluded, Gender effects are of modest magnitude compared to the influence of age and education on neuropsychological test performance (p. 294). At the same time, a more recent study (Ersche, Clark, London, Robbins, & Sahakian, 2005) of executive and memory functioning associated with amphetamine and opiate abuse, demonstrated paradoxical effects depending on gender. Essentially, substance abusers (i.e., amphetamine and opiate abusers) were found to be neuropsychologically impaired on measures of planning, pattern recognition, and visual paired associate learning. In addition, current amphetamine abusers were noted to display a greater degree of neuropsychological impairment than opiate abusers. Similarly, in the control group, healthy men performed better than females on visual spatial tests, consistent with previous research showing a male advantage in visual spatial task performance. Surprising, however, in the drug user groups, the pattern of results was reversed and male drug abusers showed significant neuropsychological impairments compared to both female drug abusers and the healthy male control group. Indeed, the difference in neuropsychological test results of the female controls and the female drug addicts were not statistically significant. This suggests that much additional research will be necessary in the elucidation of sex effects on neuropsychological test performance in substance abusers. There does appear to be mild confirmation that chronic drug abuse has more adverse effects on the male than female human brain (D’Amato et al., 2005; Davis, 2011).
Assessment Issues in Psychoactive Substance Abuse
Age, gender, education, and ethnicity differences are potential assessment confounds in the research (Davis & D’Amato, 2014; Horton et al., 2001; Reed & Grant, 1990). A large number of neuropsychological tests are correlated with age, gender, education, and ethnicity (Heaton, Miller, Taylor, & Grant, 2004). While the availability of more accurate and comprehensive age, education, gender, and ethnicity norms for a number of neuropsychological tests may help to address this problem area (Davis & D’Amato, 2014; Heaton et al., 2004), others have averred that there are potential problems using age and education norms (Davis, 2011; Reitan & Wolfson, 2005). The issue of use of multiple substances of abuse by individuals who abuse alcohol and other drugs is another major assessment confound (Reed & Grant, 1990). The majority of substance users abuse alcohol as well as other psychoactive drugs. In reality, the daily consumption of addictive substances by an alcohol and drug abuser is primarily determined by alcohol and psychoactive drug availability. In research as well as in practice, the amount of alcohol and psychoactive drugs taken by alcohol and drug abusers is also a potential assessment confound (Horton et al., 2001; Reed & Grant, 1990). Objective methods for hair and blood analysis are complicated and expensive. Self-reports concerning substance use from alcohol and drug addicts are solicited after the ingestion of the substance of abuse has occurred. Also, substance abusers’ recall of amounts of alcohol and drugs abused can be impaired by their acquired memory deficits as well as by use of the drugs themselves.
Furthermore, another potential assessment confound is that the mode of consumption can mediate the effects of the abused drugs (Reed & Grant, 1990). Intake of various psychoactive drugs through either needle injection, orally, or nasally can cause different effects of the drugs on the human brain (Horton et al., 2001). Drug effects that depend on the mode of consumption include immediate action of the drug, and the amount of the drug, and how quickly the drug enters the blood stream, among others. The mode of consumption mediates expected residual neuropsychological impairment. More possible confounds include premorbid and concurrent medical risk factors (Reed & Grant, 1990). Multiple premorbid and concurrent risk factors can influence a person’s susceptibility to developing neuropsychological deficits after alcohol and drug abuse. These can include Learning Disabilities (LD) and Attention Deficit Hyperactivity Disorder (ADHD), genetic and metabolic disorders, and early brain injuries, and can compromise various body organ systems (i.e., liver, kidney, etc.), causing organ dysfunction, which can have secondary negative effects on brain functioning (Tarter & Edwards, 1987). Psychiatric conditions can also occur along with a drug addiction, a lack of certain nutrients, exposure to neurotoxic substances during child development, and in some cases subsequent brain dysfunction (Davis, 2011; Tarter & Edwards, 1987).
Neuropsychological Assessment
Clinical neuropsychological tests (D’Amato & Hartlage, 2008; Reitan & Wolfson, 1993) can discriminate individuals with brain damage from normal individuals (D’Amato et al., 2005; Horton & Horton, 2005, 2008). Neurotoxic disorders (i.e., caused by alcohol and certain psychoactive drugs) and brain injuries are examples of neuropsychological impairing conditions where clinical neuropsychological evaluation is the best method for assessing executive functioning, memory, attention, and perceptual-motor deficits (Horton & Wedding, 1984). Clinical neuropsychological screening tests have been empirically validated by numerous researchers (Davis, 2011; McCaffrey, Krahula, Heimberg, Keller, & Purcell, 1988; Mezzich & Moses, 1980; Reitan, 1973). Effective substance abuse neuropsychological screening measures have been identified (i.e., Trail Making Test [TMT], Symbol Digit Modalities Test [SDMT], Bender Gestalt Test [BGT], Hooper Visual Organization Test [HVOT], Canter Background Interference Procedure [CBIP], Benton Visual Retention Test [BVRT], etc.). The most widely used neuropsychological screening measure has been the TMT (Davis, 2011; Horton, 1979; Horton & Wedding, 1984; Mezzich & Moses, 1980).
The Halstead-Reitan Neuropsychological Test Battery (HRNTB) is the best validated set of neuropsychological assessment procedures currently available (D’Amato & Hartlage, 2008; Halstead, 1947; Horton & Wedding, 1984; Reitan & Davison, 1974). The HRNTB was empirically validated as a battery to be sensitive to the effects of brain damage early on (Halstead, 1947). The test measures from Halstead’s (1947) neuropsychology laboratory at the University of Chicago Medical School are the Category Test—a measure of visual abstraction and concept information; the Tactual Performance Test—a measure of psychomotor/tactual perceptual-problem solving; the Speech Sound Perception Test—a measure of the ability to perceive speech sounds; the Rhythm Test—a measure of the ability to discriminate rhythms; and the Finger Tapping test—a measure of motor speed. A number of measures were added to the HRNTB by Reitan (Reitan & Davison, 1974) at his neuropsychology laboratory at the University of Indiana Medical School, including the Reitan-Indiana Aphasia Screening Test—a measure of language functioning; the Reitan-Klove sensory perceptual examination—a measure of sensory perception functioning; the TMT; intelligence testing; academic achievement testing; and personality testing. Also, the HRNTB is frequently supplemented with additional measures of language, memory, and attention functioning depending on the needs of the patient (D’Amato et al., 2005; Davis, 2011). Many research studies have comprehensively assessed alcohol and drug abusers with the HRNTB. In a landmark study, that used the HRNTB with drug and alcohol abusers, found alcoholics were significantly impaired on the HRNTB, with respect to the level of performance while drug addicts, considered as a heterogeneous group, were not. Alcoholics have shown neuropsychological difficulties with visual abstraction, set shifting, and visual spatial skills (Benedict & Horton, 1992). A subset of HRNTB measures has been found to be sensitive to adaptive abilities of alcoholics (Horton & Anilane, 1986; Schau & O’Leary, 1977). Specific patterns of neuropsychological impairment for drug addicts have been noted on measures of fine motor speed, auditory rhythm pattern recognition, visual abstraction, and set shifting abilities (Horton & Horton, 2005, 2008). Brief selective reviews of the residual neuropsychological impairment that follows abuse of specific psychoactive drugs in males are presented below.
Marijuana/Cannabis
The early work in the 1970s looking at neuropsychological impairments among marijuana abusers (Carlin & Trupin, 1977; Grant, Rochford, Fleming, & Stunkard, 1973; Mendelson & Meyer, 1972) did not find any residual deficits, leading one to believe that perhaps cannabis does not have a permanent deleterious effect on the cerebrum. But this has been challenged. Research over that past 40 years (e.g., Meier et al. 2012; Page, Fletcher, & True, 1988; Schwartz, Gruenewald, Klitzner, & Fedio, 1989), using more controlled studies, found that unquestionably after marijuana abuse memory and concentration functions were impaired. Just why the earlier studies failed to find this impairment is open to question, but one could question the samples and measures used. More recently, deficits in executive functioning, in addition to memory impairments have been found related to cannabis abuse (Bolla, Eldreth, Matochik, & Cadet, 2005; Horton & Horton, 2008; Horton & Roberts, 2001; Pope & Yurgelun-Todd, 1996).
To clearly answer this question, Grant, Gonzales, Carey, Natarajan, and Wolfson (2003) conducted a large meta-analytic study, synthesizing the empirical research on the residual effects of cannabis use among adults. Of 1014 studies they looked at, they retained only 15, eliminating the others because of various methodological flaws. Within these 15 studies, they looked at the performance of the 704 cannabis users and 484 non-users, and they found clear neuropsychological impairments only for learning and short-term memory. The deficits were sufficiently minor, leading the authors to conclude that the therapeutic effects of cannabis may outweigh the deleterious neuropsychological effects. This meta-analysis was limited to data from adults; children, with their developing brains, may be more vulnerable to the effects of cannabis. Although there was, unfortunately, nothing noted on the direct effects on children, Goldschmidt, Day, and Richardson (2000) and Fried and Smith (2001) found that prenatal exposure to marijuana resulted in neuropsychological deficits in offspring as children. Clearly, more research must be conducted in this area if clear conclusions are to be reached—indeed, given that states have legalized the use of this drug—and current issues, such as driving and reporting to work under the influence of the drug have been reported in the public press (National Institute on Drug Abuse, 2012).
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