Journal of Neurotherapy: Investigations in Neuromodulation, Neurofeedback and Applied Neuroscience EEG Biofeedback as a Treatment for Substance Use Disorders: Review, Rating of Efficacy and Recommendations for Further Research a b c Tato M. Sokhadze PhD , Rex L. Cannon MA & David L. Trudeau MD a Department of Psychiatry & Behavioral Sciences , University of Louisville School of Medicine , b University of Tennessee , Knoxville c Department of Family Medicine and Community Health , School of Health Sciences, University of Minnesota , Published online: 08 Sep 2008.

To cite this article: Tato M. Sokhadze PhD , Rex L. Cannon MA & David L. Trudeau MD (2008) EEG Biofeedback as a Treatment for Substance Use Disorders: Review, Rating of Efficacy and Recommendations for Further Research, Journal of Neurotherapy: Investigations in Neuromodulation, Neurofeedback and Applied Neuroscience, 12:1, 5-43, DOI: 10.1080/10874200802219855

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EEG Biofeedback as a Treatment for Substance Use Disorders: Review, Rating of Efficacy and Recommendations for Further Research

Tato M. Sokhadze, PhD Rex L. Cannon, MA David L. Trudeau, MD

ABSTRACT. Background. Electroencephalographic (EEG) biofeedback has been employed in substance use disorder (SUD) over the last 3 decades. SUD is a complex series of disorders with frequent comorbidities and EEG abnormalities of several types. Methods and Results. EEG biofeedback has been employed in conjunction with other thera- pies and may be useful in enhancing certain outcomes of therapy. Based on published clinical studies and employing efficacy criteria adapted by the Association for Applied Psychophysiol- ogy and Biofeedback and the International Society for Neurofeedback and Research, alpha theta training, either alone for alcoholism or in combination with beta training for stimulant and mixed substance abuse and combined with residential treatment programs, is probably efficacious. Conclusion. Considerations of further research design taking these factors into account are discussed and descriptions of contemporary research are given.

Tato M. Sokhadze is affiliated with the Department of Psychiatry & Behavioral Sciences, University of Louisville School of Medicine. Rex L. Cannon is affliated with the University of Tennessee, Knoxville. David L. Trudeau is affiliated with the Department of Family Medicine and Community Health, School of Health Sciences, University of Minnesota. Address correspondence to: Tato M. Sokhadze, PhD, Department of Psychiatry & Behavioral Sciences, University of Louisville School of Medicine, Louisville, KY 40292 (E-mail: [email protected]). Reprinted from Tato M. Sokhadze, Rex L. Cannon, and David L. Trudeau (2008). EEG Biofeedback as a Treatment for Substance Use Disorders: Review, Rating of Efficacy, and Recommendations for Further Research. Applied Psychophysiology and Biofeedback, 33(1), 1–28. This official white paper of both ISNR and AAPB is being reprinted with the kind permission of Springer Science and Business Media. This project was partially sponsored by NIDA and International Society for Neurofeedback and Research pilot research grants to Tato Sokhadze. Journal of Neurotherapy, Vol. 12(1) 2008 Copyright © 2008 ISNR. All rights reserved. doi: 10.1080/10874200802219855 5 6 JOURNAL OF NEUROTHERAPY

KEYWORDS. Alcoholism, cognitive-behavioral treatment, EEG biofeedback, ERP, neurofeedback, neurotherapy, quantitative EEG, substance use disorder

INTRODUCTION according to the guidelines jointly established by the Association for Applied Psychophy- Substance use disorders (SUDs) include siology and Biofeedback (AAPB) and the disorders related to the taking of a drug of International Society for Neurofeedback abuse (including alcohol), and represent and Research (ISNR). Assessing the efficacy the most common psychiatric conditions of neurofeedback for SUD involves several (American Psychiatric Association [APA], considerations. The first of these involves 2000) resulting in serious impairments in difficulties assessing the efficacy of any cognition and behavior. Acute and chronic treatment method for SUD. drug abuse results in significant alteration Outcome benchmarks (i.e., total absti- of the brain activity detectable with quanti- nence, improved function and quality of life) tative electroencephalography (qEEG) meth- and time points of outcome (i.e., 1 year, 2 ods. The treatment of addictive disorders by years posttreatment) are not clearly estab- electroencephalographic (EEG) biofeedback lished. Outcome assessment for treatment (or neurofeedback, as it is often called) was of SUD in itself is a complex topic well first popularized by the work of Eugene beyond the scope of this article. Because dif- Peniston (Peniston & Kulkosky, 1989, 1990, ferent drugs of abuse are associated with dif- 1991) and became popularly known as the ferent patterns of EEG abnormality, as is Peniston Protocol. This approach employed discussed in detail in this article, it is difficult independent auditory feedback of two slow to assign broad-brush EEG biofeedback brain wave frequencies, alpha (8–13 Hz) solutions to SUD as a whole. Any statements and theta (4–8 Hz) in an eyes closed con- of efficacy will need to describe specific EEG dition to produce a hypnagogic state. The biofeedback protocols for specific substances patient was taught prior to neurofeedback of abuse. Furthermore substance abuse is to use what amounts to success imagery often mixed substance type and comorbid (being sober, refusing offers of alcohol, conditions are common and vary from indi- living confidently and happy) as they drifted vidual to individual, as is also borne out in down into an alpha-theta state. Repeated this article. As of yet there are no gold stan- sessions reportedly resulted in long-term dard medication or other treatments for the abstinence and changes in personality test- various types of SUD and efficacy of any ing. Because the method seemed to work well SUD treatment method likely falls into the for alcoholics, it has been tried in individuals ‘‘possibly effective’’ to ‘‘probably effective’’ with cannabis dependence and stimulant range according to the efficacy guidelines dependence—but with limited success until jointly established by the AAPB and ISNR. the work of Scott and Kaiser (Scott, Brod, Finally, all of the studies of EEG biofeed- Sideroff, Kaiser, & Sagan, 2002; Scott & back in SUD to date employ EEG biofeed- Kaiser, 1998; Scott, Kaiser, Othmer, & back as an add on to cognitive behavioral Sideroff, 2005). They described treating or 12-step treatment regimes, so any state- stimulant abusing participants with atten- ments of efficacy would have to acknowledge tion-deficit type EEG biofeedback protocols, that EEG biofeedback is not a stand-alone followed by the Peniston Protocol, with treatment for SUD. substantial improvement in program reten- This article is divided into several sections. tion and long-term abstinence rates. This In the first section we review SUD preva- approach has become known widely as the lence and describe qEEG changes typical Scott–Kaiser modification (of the Peniston for the most widespread drugs of abuse Protocol). (alcohol, marijuana, heroin, cocaine, and This ‘‘white paper’’ on EEG biofeedback methamphetamine). The second section for SUD will offer an assessment of efficacy describes treatment studies employing EEG Scientific Articles 7 biofeedback in SUD. Studies that have used The SUD commonly referred to as ‘‘drug the Peniston Protocol are described first, addiction’’ is characterized by physiological along with critical commentaries of these dependence accompanied by the withdrawal studies. In the second part of this section, a syndrome on discontinuance of the drug description of the Scott–Kaiser modification use, psychological dependence with craving, is given, along with some discussion of a the pathological motivational state that leads rationale for why this approach may be more to the active drug-seeking behavior, and successful with stimulant abusers. This tolerance, expressed in the escalation of the section also describes some current research. dose needed to achieve a desired euphoric A third section assesses efficacy of the state. Drug addiction is a chronic, relapsing Peniston Protocol and the Scott–Kaiser mental disease that results from the pro- modification. The fourth section takes a longed effects of drugs on the brain (Dackis look at the clinical implications of comorbid- & O’Brien, 2001; Volkow, Fowler, & Wang, ities in neurobiofeedback treatment of 2003, 2004). Drug addiction can take control alcohol and drug abuse. A fifth section of the brain and behavior by activating and discusses the clinical implications of stan- reinforcing behavioral patterns that are dard cognitive–behavioral therapies (CBTs) excessively directed to compulsive drug use in SUD treatment and reviews the rationale (Di Chiara, 1999; Gerdeman, Partridge, for the application of qEEG-guided neuro- Lupica, & Lovinger, 2003). feedback intervention in SUD in conjunction From the 11 classes of substances listed in with these therapies. A final section sum- the Diagnostic and Statistical Manual of marizes findings in qEEG and neurofeed- Mental Disorders (4th ed.; DSM–IV )we back in SUD and additionally proposes discuss in our review only alcohol, cannabis further directions for clinical research in (marijuana), heroin, and such psychostimu- this area. lants as cocaine and methamphetamine. This article represents an update of earlier Addiction leads to behavioral, cognitive, reviews (Trudeau, 2000, 2005a, 2005b) of and social adverse outcomes that incur EEG biofeedback for addictive disorders substantial costs to society. In 2002, it was extended with a review on qEEG in SUD. estimated from the Substance Abuse and This review is presented as one of a series of Mental Health Service Administration articles in both the Journal of Neurotherapy (SAMHSA; 2004) that 22 million Americans and the Journal of Applied Psychophysiology have an SUD or dependence disorder, and 2 & Biofeedback describing and reviewing million of them were current cocaine users biofeedback applications for adult popula- (Vocci & Ling, 2005). In 2005, there were tions. No attempt is made to review the fields 2.4 million persons who were current cocaine of qEEG and neurobiofeedback generally users, which is more than in 2004 (see current reviews by Hammond, 2006; (SAMHSA, 2006). The number of current Kaiser, 2006), or the field of addictive disor- crack users increased from 467,000 in 2004 ders generally, although some references are to 682,000 in 2005. According to the 2004 made to specifics the authors feel are perti- revised National Survey on Drug Use and nent to a discussion of emerging concepts of Health, nearly 12 million Americans have qEEG as a sensitive tool for the brain tried methamphetamine, and 583,000 of function assessment in SUD, and EEG bio- them are chronic methamphetamine users feedback as a treatment approach for SUD. (SAMHSA, 2004). In 2005, an estimated 22.2 million persons aged 12 or older were classified with substance dependence or SUD PREVALENCE AND qEEG abuse in the past year (9.1% of the popu- CHANGES lation aged 12 or older). Of these, 3.3 million were classified with dependence on or Drug addiction can be described as a abuse of both alcohol and illicit drugs, 3.6 mental disorder with idiosyncratic beha- million were dependent on or abused illicit vioral, cognitive, and psychosocial features. drugs but not alcohol, and 15.4 million were 8 JOURNAL OF NEUROTHERAPY dependent on or abused alcohol but not 2001). Recently through intensive clinical illicit drugs. There were 18.7 million persons neurophysiological research and biological classified with dependence on or abuse of psychiatric studies many specific compo- alcohol in 2005 (7.7%). The specific illicit nents of cognitive, emotional, and beha- drugs that had the highest levels of past vioral deficits typical for SUDs have been year dependence or abuse in 2005 were identified and investigated. However, the marijuana, followed by cocaine and pain practical values of these cognitive neu- relievers. Of the 6.8 million people aged 12 roscience and applied psychophysiology or older classified with dependence on or based treatment (e.g., neurofeedback) find- abuse of illicit drugs, 4.1 million were depen- ings depend on a further integration of these dent on or abused marijuana in 2005. This methodological approaches. number represents 1.7% of the total popu- lation aged 12 or older, and 59.9% of all those classified with illicit drug dependence QEEG in SUD or abuse. Marijuana was the most commonly used illicit drug (14.6 million past month EEG in alcoholism.. Electroencephalo- users). In 2005, it was used by 74.2% of cur- graphic alterations have been described rent illicit drug users. Among current illicit extensively in alcoholic patients (Porjesz & drug users, 54.5% used only marijuana, Begleiter, 1998), but any attempt at drawing 19.6% used marijuana and another illicit a common picture from qEEG data is diffi- drug, and the remaining 25.8% used only cult because of significant methodological an illicit drug other than marijuana in the differences, such as different definitions of past month (SAMHSA, 2006). frequency bands, different filtering method- Fatal poisoning, which include overdoses ology, number of channels, reference choice, (ODs) on illicit drugs, alcohol, and medica- and so on. However, most reports of tions, is the leading cause of injury death alcoholic patients agree in describing altera- for individuals age 35 to 44 and the third tions mainly within the beta (Bauer, 1997, leading cause of injury death overall, trailing 2001b; Costa & Bauer, 1997; Rangaswamy motor vehicle accidents and firearm-related et al., 2002; Rangaswamy et al., 2004) deaths (Centers for Disease Control and Pre- and=or alpha bands (Finn & Justus, 1999). vention [CDC], 2004). Heroin-related ODs QEEG and low-resolution electromag- have increased at an alarming rate in por- netic tomography (LORETA) mapping tions of the United States and other coun- studies of detoxified alcohol-dependent tries (Darke & Hall, 2003; Landen et al., patients, as compared with normal controls, 2003), and OD has surpassed HIV infection showed an increase in absolute and relative as the primary cause of death for heroin beta power and a decrease in alpha and users. Not surprisingly, heroin is frequently delta=theta power (Saletu, Anderer, Saletu- associated with opioid-related ODs, both as Zyhlarz, Arnold, & Pascual-Marqui, 2002), a single drug and in combination with other which is in agreement with earlier reports substances (CDC, 2004). of low-voltage fast EEG patterns, as often Many patients seeking treatment for encountered by visual EEG inspection addiction have multiple drug dependencies (Niedermeyer & Lopes da Silva, 1982). As and psychiatric comorbidities (Volkow & slow activities are considered to be inhibi- Li, 2005). Information from epidemiological tory, alpha activity may be viewed as an surveys indicates that drug addiction is a expression of normal brain functioning and common phenomenon and is associated fast beta activities as excitatory, the low- with significant effects on both morbidity voltage fast desynchronized patterns may and mortality. Large individual and societal be interpreted as hyperarousal of the central costs of drug abuse make research and nervous system (CNS) (Saletu-Zyhlarz et al., treatment of drug addiction imperative 2004). The investigations by Bauer (2001b) (French, McGeary, Chitwood, & McCoy, and Winterer et al. (1998) showed a worse 2000; Mark, Woody, Juday, & Kleber, prognosis for the patient group with a more Scientific Articles 9 pronounced frontal CNS hyperarousal. It et al., 2004) as compared to those without may be hypothesized that these hyperar- alcohol-dependent relatives. This indicates oused relapsing patients require more CNS that differences in functional brain activity sedation than abstaining ones. as measured with qEEG in alcohol- EEG maps of alcohol-dependent patients dependent patients relate not only to differ significantly from those of normal con- the impact of long-term alcohol intake but trols and patients suffering from other possibly also to genetic factors related to mental disorders and might be useful for alcohol dependence. diagnostic purposes (Pollock, Schneider, Both alcohol dependence (Schuckit & Zemansky, Gleason, & Pawluczyk, 1992; Smith, 1996) and EEG patterns (Van Saletu et al., 2002; Saletu-Zyhlarz et al., Beijsterveldt & Van Baal, 2002) are highly 2004). Decreased power in slow bands heritable. In addition, some genes coding in alcoholic patients may be an indicator for GABA receptors in the brain, which of brain atrophy and chronic brain mediate the effects of alcohol, are related damage, whereas an increase in the beta to certain EEG patterns (Porjesz et al., band may be related to various factors such 2005; Winterer, Smolka, et al., 2003). More- as medication use, family history of alcohol- over, some GABA-receptor genes that are ism, and=or hallucinations, suggesting a related to EEG patterns are also associated state of cortical hyperexcitability (Coutin- with the risk to develop alcohol dependence. Churchman, Moreno, Annez,~ & Vergara, These associations again suggest that genetic 2006). factors play a major role in the EEG differ- Abnormalities in resting EEG are often ences associated with alcohol dependence. associated with a predisposition to develop- EEG coherence analysis is a technique ment of alcoholism. Individuals with a that investigates the pairwise correlations of family history of alcoholism were found to power spectra obtained from different elec- have reduced relative and absolute alpha trodes. It measures the functional interaction power in occipital and frontal regions and between cortical areas in different frequency increased relative beta in both regions com- bands. A high level of coherence between pared with those with a negative family two EEG signals indicates a coactivation of history of alcoholism. These results suggest neuronal populations and provides infor- that resting EEG alpha abnormalities are mation on functional coupling between these associated with risk for alcoholism, although areas (Franken, Stam, Hendriks, & van den their etiological significance is unclear Brink, 2004). De Bruin et al. (2004) and De (Finn & Justus, 1999). Bruin, Stam, Bijl, Verbaten, and Kenemans Alcohol-dependent individuals have dif- (2006) investigated the pure effects of alcohol ferent synchronization of brain activity than intake on synchronization of brain activity light drinkers as reflected by differences in while minimizing the confounding influence resting EEG coherence (Kaplan, Glueck, of genetic factors related to alcohol depen- Hesselbrock, & Reed, 1985; Michael, Mirza, dence. They showed that heavily drinking Mukundan, & Channabasavanna, 1993; students with a negative family history had Winterer, Enoch, et al., 2003) and power stronger EEG synchronization at theta and (e.g., Bauer, 2001a, 2001b; Enoch, White, gamma frequencies than lightly drinking stu- Harris, Rohrbaugh, & Goldman, 2002; dents with a negative family history. This Rangaswamy et al., 2002; Saletu-Zyhlarz study suggests that, in students, heavy alco- et al., 2004). Most differences in EEG coher- hol intake has an impact on functional brain ence and power are found in the alpha and activity, even in the absence of genetic beta bands. Non-alcohol-dependent relatives factors related to alcohol dependence. of alcohol-dependent individuals also have The findings of studies on the effects of EEG differences in alpha and beta coherence alcohol dependence on EEG coherence can (Michael et al., 1993) and power (Bauer & be summarized as follows: Kaplan et al. Hesselbrock, 2002; Finn & Justus, 1999; (1985) reported lower frontal alpha and Rangaswamy et al., 2002; Rangaswamy slow-beta coherence in alcohol-dependent 10 JOURNAL OF NEUROTHERAPY male and female participants. Michael et al. 2002; Whitlow, Freedland, & Porrino, (1993) found higher central alpha and slow- 2002), providing evidence that cannabinoid beta coherence but lower parietal alpha and administration may affect the functionality slow-beta coherence in male participants of this brain area. Despite the fact that a with alcohol dependence. Winterer, Enoch, number of transient physiological, percep- et al. (2003) and Winterer, Smolka, et al. tual, and cognitive effects are known to (2003) described higher left-temporal alpha accompany acute chronic marijuana (THC) and slow-beta coherence and higher slow- exposure in humans, persistent qEEG effects beta coherence at right-temporal and frontal in humans resulting from continuing electrode pairs in alcohol-dependent male exposure to this drug have been difficult to and female participants. De Bruin et al. demonstrate (Wert & Raulin, 1986). In early (2006) showed that moderate to heavy alco- reviews of EEG and event-related potential hol consumption is associated with differ- (ERP) studies of acute and chronic THC ences in synchronization of brain activity exposure in humans (Struve, Straumanis, & during rest and mental rehearsal. Heavy Patrick, 1994; Struve, Straumanis, Patrick, drinkers displayed a loss of hemispheric & Price, 1989), it was reported that signifi- asymmetry of EEG synchronization in the cant associations between chronic exposure alpha and slow-beta band. Moderately and and clinically abnormal EEG patterns had heavily drinking men additionally showed not been demonstrated and that attempts lower fast-beta band synchronization. to use visual EEG analyses to detect transi- Therefore, qEEG alterations have been ent acute THC exposure induced EEG described extensively in alcoholics. Most alterations failed to demonstrate consistent EEG reports in alcoholic patients agree in THC–EEG effects across studies. describing alterations mainly within the beta Quantitative methods of analyzing EEG and alpha bands. Patients with a more pro- spectra from single posterior scalp deriva- nounced frontal hyperarousal have worse tions began to be applied to studies of prognosis. Decreased power in slow bands acute THC exposure. These early studies in alcoholic patients may be an indicator of reported that acute THC exposure produced chronic brain damage, whereas increases in transient increases in posterior alpha beta band may be related to various factors power, decreases in mean alpha frequency, suggesting cortical hyperexcitability. or increases in alpha synchrony (Fink, Abnormalities in resting EEG are highly Volavka, Panayiotopoulos, & Stefanis, heritable traits and are often associated with 1976; Struve et al., 1989; Tassinari, Ambro- a predisposition to alcoholism development. setto, Peraita-Adrados, & Gastaut, 1976; The studies on the effects of alcohol depen- Volavka et al., 1971; Volavka, Crown, Dorn- dence on EEG coherence can be summarized bush, Feldstein, & Fink, 1973). These studies as lower frontal alpha and slow-beta coher- found that THC produced a transient ence in alcohol-dependent patients with dose-dependent rapid onset: (a) increase in some topographical coherence abnormality relative power (amount, abundance) of differences between alcohol-dependent male alpha, (b) decrease in alpha frequency, and and female individuals. (c) decrease in relative power of beta as EEG in marijuana abuse. Several lines of measured from posterior scalp electrodes. evidence suggest that cannabis (marijuana, Later studies by Struve and colleagues tetrahydrocannabinol [THC]) may alter (Struve, Patrick, Straumanis, Fitz-Gerald, functionality of the prefrontal cortex and & Manno, 1998; Struve et al., 1999; Struve, thereby elicit impairments across several Manno, Kemp, Patrick, & Manno, 2003) domains of complex cognitive function demonstrated and replicated a significant (Egerton, Allison, Brett, & Pratt, 2006). association between chronic marijuana use Several studies in both humans and animals and topographic qEEG patterns of persistent have shown that cannabinoid exposure ‘‘alpha hyperfrontality’’ (i.e., elevations of results in alterations in prefrontal cortical alpha absolute power, relative power, and activity (Block et al., 2002; O’Leary et al., interhemispheric coherence over frontal Scientific Articles 11 cortex) as well as reductions of alpha mean qEEG finding was the elevated voltage of all frequency. These findings from chronic users nonalpha bands in THC users. are consistent with both nontopographic A third qEEG finding involved a wide- (Hockman, Perrin, & Kalant, 1971; Tassi- spread decrease in the relative power of delta nari et al., 1976; Volavka et al., 1973) and beta activity over the frontal cortical and topographic (Lukas, Mendelson, & regions in marijuana users. Benedikt, 1995; Struve et al., 1994) transient EEG in heroin addiction. Only a few EEG effects of acute THC administration. studies have investigated qEEG changes in Therefore, chronic daily THC use was found heroin addicts. Qualitative changes were to be associated with distinct topographic observed in more than 70% of heroin addicts qEEG features. Compared with nonusers, in the early abstinence (acute withdrawal) THC users had significant elevations of period; these included low-voltage back- absolute and relative power and interhemi- ground activity with diminution of alpha spheric coherence of alpha activity over the rhythm, an increase in beta activity, and a bilateral frontal cortex (referred to as ‘‘alpha large amount of low-amplitude delta and hyperfrontality’’). A second finding was theta waves in central regions (Olivennes, that the voltage (not relative power or Charles-Nicolas, & Olievenstein, 1983; coherence) of all nonalpha frequency bands Polunina & Davydov, 2004). Franken et al. was significantly elevated in THC users, (2004) found that abstinent heroin- although the voltage increase was general- dependent participants have an enhanced ized and not frontally dominant. A third fast beta power compared with healthy finding involved a widespread decrease in controls, and this finding is concordant with the relative power of delta and beta activity other EEG studies on alcohol and cocaine for cannabis users, particularly over the abusing participants (Costa & Bauer, 1997; frontal cortical regions. A fourth finding Herning, Glover, Koeppl, Phillips, & was that interhemispheric coherence of theta London, 1994; Rangaswamy et al., 2004; and possibly delta activity was also signifi- Roemer, Cornwell, Dewart, Jackson, & cantly elevated over frontal cortex for mari- Ercegovac, 1995). Spectral power and ERPs juana users. Because most studies included in heroin addicts strongly relate to absti- daily THC users and nonusers drawn from nence length (Bauer, 2001b; Polunina & an inpatient psychiatric population, the Davydov, 2004; Shufman et al., 1996). Most effects of psychiatric diagnoses or medi- studies showed considerable or even com- cation were not controlled. plete normalization of EEG spectral power Thus, qEEG studies on acute THC or magnitude of ERP components in heroin exposure reported a transient dose- ex-addicts who maintained abstinence for at dependent increase in relative power of least 3 months (Bauer, 2001a, 2002; Costa & alpha, decrease in alpha frequency, and Bauer, 1997; Papageorgiou et al., 2001; decrease in relative power of beta at Polunina & Davidov, 2004; Shufman et al., posterior EEG recording sites. Chronic 1996). marijuana abuse is known to result in a Some quantitative changes were also number of physiological, perceptual, and reported in methadone-maintenance heroin cognitive effects, but persistent qEEG effects addicts (Gritz et al., 1975), current heroin from continuing exposure to THC have addicts, and participants in heroin absti- been difficult to demonstrate. However, nence less than 80 days (Shufman et al., recent studies of Struve and his colleagues 1996). Gritz et al. demonstrated a significant have demonstrated a significant association slowing of occipital alpha rhythm peak between chronic marijuana use and frequency in 10 methadone-maintained topographic qEEG patterns of persistent patients and the same trend in 10 abstinent elevations of alpha absolute power, relative heroin-addicted participants. In one study power, and interhemispheric coherence over (Polunina & Davydov, 2004), slowing of frontal cortex, as well as reductions of slow alpha (8–10 Hz) mean frequency was alpha mean frequency. Another important significantly related to the amount of heroin 12 JOURNAL OF NEUROTHERAPY taken by these patients daily before with- characteristic for heroin withdrawal remain drawal. The prolongation of ERP compo- unclear. nent latencies in heroin addicts was also Withdrawal state in heroin addicts is reported (Papageorgiou et al., 2001), and known to elicit a strong craving for drug, these delays significantly correlated with anxiety, nervousness, deficits in inhibitory years of heroin use, rather than with absti- control, dysphoric motivational state, and nence length in the study of Bauer (1997). intrusive thoughts related to drugs (Franken, Polunina and Davydov demonstrated 2003; Franken, de Haan, van der Meer, frequency shifts in the fast alpha range at Haffmans, & Hendriks, 1999; Franken the frontal and central recording sites and a et al., 2004; Stormark, Laberg, Nordby, & slowing of slow alpha mean frequency at Hugdahl, 2000). Research on functional the central, temporal, and occipital sites of connectivity in drug withdrawal states is recording in heroin abusers who used heroin restricted to a few studies on coherence of for at least 18 months. the EEG signal in abstinent heroin users In general, pronounced desynchronization (Fingelkurts et al., 2006b; Franken et al., is characteristic for acute heroin withdrawal, 2004), active heroin abusers (Fingelkurts but as mentioned previously, several studies et al., 2006a), and abstinent polysubstance (Bauer, 2001b, 2002; Costa & Bauer, 1997; abusers (Roemer et al., 1995). In a study Papageorgiou et al., 2001; Polunina & on 22 opioid-dependent patients under acute Davydov, 2004; Shufman et al., 1996) opioid influence, Fingelkurts et al. (2006a) showed that spectral power of EEG tends showed that longitudinal opioid exposure to normalize almost completely after several impairs cortical local and remote functional weeks of abstinence. The most consistent connectivity and found that local connectiv- changes in EEG of heroin addicts were ity increased, whereas the remote one reported in alpha and beta frequencies and decreased. These findings were interpreted included a deficit in alpha activity and an as specific signs of independent processing excess of fast beta activity in early heroin in the cortex of chronic heroin addicts. It abstinence. The latter abnormality appears has been suggested that such independent to reverse considerably when heroin intake processes may constitute the candidate is stopped for several months, and therefore mechanism for a well-documented pattern it may be viewed as an acute withdrawal of impairment in addicts that expresses the effect. lack of integration of different cognitive The dynamics and characteristics of functions for effective problem solving and spectral power changes within the early helps to explain the observed deficits in opiate withdrawal suggest the participation abstract concept formation, behavioral of catecholamine imbalances, especially control, and problems in the regulation of noradrenaline and perhaps to a lesser degree affect and behavior. dopamine, which are widely recognized as a Specifically, Fingelkurts et al. (2006a) main cause of opiate physical dependency found that the number and strength of symptoms (Devoto, Flore, Pira, Diana, & remote functional connections among differ- Gessa, 2002; Maldonado, 1997). Acute ent cortical areas estimated by the index of opiate administration has been shown to EEG synchrony was significantly higher in increase, whereas abstinence from chronic patients in acute heroin withdrawal than in opiate use has been shown to decrease healthy controls for most categories of func- extracellular dopamine in the nucleus accum- tional connections. Although this result was bens. In contrast, extracellular dopamine observed in the alpha as well as in the beta in the prefrontal cortex is not modified by frequency bands, it was most prominent for acute opiate use but is markedly increased the beta range. In the same patient subsam- during morphine and heroin abstinence ple under acute opioid influence the authors syndrome (Devoto et al., 2002). Relation- (Fingelkurts et al., 2006b) observed the ships between theta and beta frequencies opposite: a significant decrease in the shifts and neurotransmitter imbalances number and strength of remote functional Scientific Articles 13 connections, when compared with healthy from cocaine use (Ehlers, Wall, & Schuckit, controls. Thus, the increase of remote syn- 1989). However, some EEG characteristics chronicity among cortical areas during the observed in cocaine addicts are considered short-term withdrawal period may indicate to be due to the toxic effects of this drug the selective attentional focus on cues and on the brain, whereas some EEG characteris- memories related to drugs while ignoring tics in cocaine addicts may also indicate a neutral cues (Franken, Kroon, & Hendriks, predisposition toward the development of 2000; Sokhadze, Stewart, & Hollifield, SUD (Porjesz et al., 2005). 2007). Generally this can explain a narrow- In 1937, Hans Berger (as cited in Gloor, ing of the behavioral repertoire and compul- 1969; Herning, Jones, Hooker, Mendelson, sive drug seeking in abstinent addicted & Blackwell, 1985) was the first to study individuals (Vanderschuren & Everitt, the effects of cocaine on human EEG, 2004). Therefore, the elevated synchrony reporting an increase in activity in the beta within the beta frequency band in these stu- bandwidth. This was replicated in sub- dies (Fingelkurts et al., 2006a, 2006b) may sequent studies with a larger number of par- reflect a state of CNS activation toward ticipants (Alper, 1999; Alper, Chabot, Kim, reward-seeking behavior, with this being a Prichep, & John, 1990; Alper, Prichep, prerequisite of relapse among opiate drug Kowalik, Rosenthal, & John, 1998; Costa dependent patients (Bauer, 2001b). & Bauer, 1997; Herning et al., 1985; Noldy, QEEG changes in heroin addicts in the Santos, Politzer, Blair, & Carlen, 1994; acute withdrawal period have been described Prichep, Alper, Kowalik, & Rosenthal, as low-voltage background activity with a 1996; Prichep et al., 1999; Prichep et al., diminution of alpha rhythm, an increase in 2002; Roemer et al., 1995). Beside beta beta activity, and a large amount of low- effects, studies have reported an increase in amplitude delta and theta waves in central delta activity (Herning et al., 1985) and fron- regions. In general, pronounced desynchro- tal alpha activity (Herning, Glover, Koeppl, nization is characteristic for acute heroin et al., 1994), whereas others have reported an withdrawal, but the spectral power of EEG increase in alpha wave EEG associated with tends to normalize almost completely after bursts of cocaine-induced euphoria (Lukas, several weeks of abstinence. The most con- 1991). More recently, researchers have begun sistent changes in EEG of heroin addicts analyzing qEEG profiles of cocaine- were reported in the alpha and beta frequen- dependent patients using the spectral power cies and included a deficit in alpha activity of each primary bandwidth over the different and an excess of fast beta activity in early topographic cortical areas. Excess alpha heroin abstinence. The excess of beta activity (Alper et al., 1990; Herning, Glover, appears to reverse considerably when heroin Koeppl, et al., 1994; Lukas, 1991; Prichep intake is stopped for several months, and et al., 1996) and decreased delta activity therefore it may be viewed as an acute with- (Alper et al., 1990; Noldy et al., 1994; drawal effect. Recent studies found that the Prichep et al., 1996; Roemer et al., 1995) have number and strength of remote functional been reported, whereas others have reported connections among different cortical areas increased beta power (Herning, Glover, estimated by the index of EEG synchrony Koeppl, et al., 1994; Herning et al., 1985; for the beta range was significantly higher Noldy et al., 1994) in cocaine-dependent in patients in acute heroin withdrawal than patients, recorded in eyes closed, resting in healthy controls for most categories of conditions. The qEEG abnormalities, pri- functional connections. marily found in anterior cortical regions, EEG in cocaine addiction. Qualitative were shown to correlate with the amount EEG and qEEG measures are highly sensi- of prior cocaine use (Herning, Glover, & tive to the acute and chronic effects of Guo, 1994; Prichep et al., 1996; Roemer neurointoxication produced by such psy- et al., 1995; Venneman et al., 2006). QEEG chostimulants as cocaine, as well as effects has been used more often to characterize the from withdrawal and long-term abstinence effects of withdrawal in cocaine-dependent 14 JOURNAL OF NEUROTHERAPY patients. Several studies reported that dur- However, this sign, as well as other qEEG ing protracted abstinence from cocaine qEEG abnormal patterns, can be found in many effects are featured by long-lasting in- different psychiatric disorders, and none of creases in alpha and beta bands together with them can be considered as pathognomonic reduced activity in delta and theta bands of any specific mental or neurological (Alper et al., 1990; Prichep et al., 1996; Roemer disorder. EEG coherence in cocaine addic- et al., 1995). tion was investigated in only one study Recently Reid, Flammino, Howard, (Roemer et al., 1995). The authors reported Nilsen, and Prichep (2006) investigated globally reduced interhemispheric coherence qEEG profiles in cocaine-dependent patients in the delta and theta bands and frontally in response to an acute, single-blind, self- in the beta band. It should be noted that administered dose of smoked cocaine base participants in this study were cocaine- (50 mg) versus placebo. Cocaine produced a preferring polysubstance abusers during rapid increase in absolute theta, alpha, and abstinence and these results can hardly be beta power over the prefrontal cortex, lasting generalized to crack-cocaine-only users or up to 25 min after administration of the other categories of cocaine-dependent indivi- drug. The increase in theta power was corre- duals not enrolled in any treatment. lated with a positive subjective drug effect Therefore, acute effects of smoked crack (‘‘high’’), and the increase in alpha power cocaine have been shown to produce a rapid was correlated with nervousness. Cocaine increase in absolute theta, alpha, and beta also produced a similar increase in delta power over the prefrontal cortex, lasting up coherence over the prefrontal cortex, which to 30 min after administration of the drug. was correlated with nervousness. Placebo The increase in theta power was reported resulted only in a slight increase in alpha to correlate with a positive subjective drug power over the prefrontal cortex. These data effect, whereas the increase in alpha power demonstrate the involvement of the pre- was reported to correlate with nervousness. frontal cortex in the qEEG response to acute QEEG measures are also sensitive to the cocaine and indicate that slow wave qEEG, acute and chronic effects of cocaine as well delta and theta activity are involved in the as the effects from withdrawal and long-term processes related to experiencing rewarding abstinence from cocaine use. Some EEG properties of cocaine. characteristics observed in cocaine addicts Prichep et al. (1999) and Prichep et al. are considered to be due to the neurotoxic (2002) extended the idea of relating baseline effects, whereas some EEG characteristics EEG activity to outcome in cocaine- in cocaine addicts may also indicate a predis- dependent patients in treatment programs. position toward the development of cocaine Participants with cocaine dependence have addiction. QEEG has been used more often persistent changes in brain function assessed to characterize the effects of withdrawal in with qEEG methods, present when evaluated cocaine-dependent patients. During protrac- at baseline, 5 to 14 days after last reported ted abstinence from cocaine qEEG effects crack cocaine use, and persistent at 1- and are featured by long-lasting increases in 6-month follow-up evaluations (Alper, alpha and beta bands together with reduced 1999; Alper et al., 1990; Alper et al., 1998; activity in delta and theta bands. Several Prichep et al., 1996; Prichep et al., 2002; recent studies employing qEEG techniques Venneman et al., 2006). Several recent have demonstrated an association between studies employing qEEG techniques have the amount of beta activity in the spon- already demonstrated an association taneous EEG and relapse in cocaine abuse. between the amount of beta activity in the EEG in methamphetamine addiction. spontaneous EEG and relapse in cocaine Several studies have examined the neurobio- abuse (Bauer, 1997, 2001b). A decrease in logical consequences of methamphetamine the delta and theta bands of the EEG can dependence using qEEG methods (e.g., be regarded as a specific sign of brain Newton et al., 2003; Newton et al., 2004). dysfunction. It was found that methamphetamine Scientific Articles 15 dependent patients exhibited a significant whereas methamphetamine mobilizes and power increase in the delta and theta bands releases these monoamines from storage as compared to non-drug-using controls granules, thus producing rapid and large (Newton et al., 2003). These results are in increases in synaptic concentrations (Simon, accordance with other neurocognitive studies Dacey, Glynn, Rawson, & Ling, 2004; (Kalechstein, Newton, & Green, 2003) Simon et al., 2002). This might be respon- suggesting that methamphetamine abuse is sible for the discrepancies in observed qEEG associated with psychomotor slowing and manifestations associated with chronic frontal executive deficits. Within the methamphetamine and cocaine abuse. methamphetamine-dependent participants, Only a few studies have examined the increased theta qEEG power was found qEEG consequences of methamphetamine to correlate with response time and was dependence. They reported that methamphet- accompanied with reduced accuracy amine dependent patients exhibited a (Newton et al., 2004). To our knowledge, significant power increase in the delta and qEEG patterns associated with acute with- theta bands as compared to non-drug-using drawal and recent abstinence in metham- control. QEEG patterns associated with phetamine dependence have not yet been acute withdrawal and recent abstinence in sufficiently described. One study reported methamphetamine dependence have not yet (Newton et al., 2003) that methamphetamine been sufficiently described. One study dependent volunteers with 4 days of reported that abstinent methamphetamine abstinence had increased EEG power in the dependent patients had increased EEG delta and theta but not in the alpha and beta power in the delta and theta but not in the bands. Within the methamphetamine depen- alpha and beta bands. In general, qEEG dent group, a majority of the conventional studies of methamphetamine addiction are EEGs were abnormal (64%), compared to in accordance with other neurocognitive 18% in the nonmethamphetamine using studies, suggesting that methamphetamine group. abuse is associated with psychomotor slow- QEEG may provide a sensitive neurophy- ing and frontal executive deficits. siological outcome measure of methamphe- P300 Abnormalities in cocaine, methamphet- tamine abuse-related persistent alterations amine, heroin addiction, and alcoholism. in neurocognitive functions (Newton et al., The P300 component of the ERP, occurring 2004). In a study by Simon et al. (2002), 300- to 600-msec poststimulus, is the most when performance of patients with SUD widely used ERP in psychiatry and other was compared to their matched nonusing clinical applications (Polich & Herbst, 2000; control groups, both methamphetamine Polich, Pollock, & Bloom, 1994; Pritchard, and cocaine abusers were impaired on cogni- 1981, 1986; Pritchard, Sokhadze, & tive measures but the type and degree of Houlihan, 2004). The amplitude of the P300 impairments were somewhat different. Some reflects the allocation of attentional of these differences between methamphet- resources, whereas the latency is considered amine and cocaine effects on cognitive func- to reflect stimulus evaluation and classi- tions and electrophysiological alterations can fication time (Katayama & Polich, 1998; be explained by differential pharmacoki- Polich & Herbst, 2000). The P300 is usually netics of these two drugs, as cocaine is obtained in an oddball paradigm, wherein rapidly metabolized with an elimination two stimuli are presented in a random order, half-life of several hours, whereas metham- one of them frequent (standard) and another phetamine is eliminated more slowly, with one rare (target; Polich, 1990). A modifi- an elimination half-life averaging 12 hr cation of the oddball task has been used (Cook et al., 1993; Jeffcoat, Perez-Reyes, where a third, also rare stimulus (distracter), Hill, Sadler, & Cook, 1989). Moreover, is presented along with standard and target cocaine differs from methamphetamine in stimuli. It was reported that these infrequent that cocaine inhibits the reuptake of distracters elicit a frontocentral P300, so dopamine, serotonin, and norepinephrine, called P3a, whereas the rare targets elicit a 16 JOURNAL OF NEUROTHERAPY parietal P300, so called P3b (Katayama & abstinence), in 18 current heroin users and Polich, 1996, 1998). The P3a is recorded at in 20 matched healthy participants. Absti- the anterior scalp locations and has been nent heroin addicts exhibited a significant interpreted as reflecting frontal lobe activity reduction of the P300 amplitude at the (Gaeta, Friedman, & Hunt, 2003; Knight, central frontal region, relative to the other 1984). Though the P300 response in general two groups. is thought to represent ‘‘context updating= The results of early work examining the closure,’’ in a three-stimuli oddball task the effect of cannabis use and THC administra- P3a is interpreted as ‘‘orienting,’’ and the tion on visual and auditory ERPs have been P3b is viewed as an index of the ability to inconclusive (Rodin, Domino, & Porzak, maintain sustained attention to target 1970; Roth, Galanter, Weingartner, (Na¨a¨ta¨nen, 1990). The anterior P3a indexes Vaughan, & Wyatt, 1973). Later studies of the contextual salience of the rare stimuli, Patrick et al. (1995) and Patrick, Straumanis, whereas the posterior P3b is indexing Struve, Fitz-Gerald, and Manno (1997) task-relevance of the stimuli (Gaeta et al., could not find P300 latency differences in 2003). audio and visual oddball tasks between A robust finding in ERP studies on THC users without psychiatric problems alcoholism is that alcoholics as well as and controls. Although THC users displayed individuals at high risk to develop alcohol- reduced auditory and visual P300 amplitudes ism have been shown to have a low P300 in this study, when age differences between amplitude in various task paradigms (Cohen, THC users and controls were removed, all Ji, Chorlian, Begleiter, & Porjesz, 2002; significant P300 amplitude differences were Hada, Porjesz, Begleiter, & Polich, 2000; removed as well. Porjesz & Begleiter, 1998; Porjesz et al., Acute and chronic use of cocaine exerts 2005). Kouri, Lukas, and Mendelson (1996) neuropharmacological effects on amplitude examined the P300 component in patients and latency of both anterior and posterior who were dually dependent on cocaine and P300 ERP components (Biggins, MacKay, heroin. The results showed no P300 ampli- Clark, & Fein, 1997; Fein, Biggins, & tude differences between the patients and MacKay, 1996; Herning, Glover, & Guo, healthy non-drug-dependent volunteers 1994; Kouiri et al., 1996; Polich, 1990). when patients presented for detoxification. Longer P300 (P3b) latency without abnor- However, after the course of detoxification, malities in amplitude was reported in several the P300 amplitude was significantly smaller studies on cocaine withdrawal (Herning, in the cocaine- and heroin-dependent group Glover, & Guo, 1994; Lucas, 1993). Noldy than in the nondependent control group. In and Carlen (1997) demonstrated effects of a study by Bauer (2001a), the P300 did not cocaine withdrawal on the latency of the differentiate among patients characterized P300 in an auditory oddball task. In by histories of either cocaine, or cocaine cocaine-dependent patients, P3a amplitude and alcohol, or heroin dependence. Across decrements over frontal areas are persistent all the patient groups, the P300 was signifi- even after long periods of abstinence (Bauer, cantly reduced in amplitude relative to the 1997). The latency of the P3a was delayed P300 ERPs recorded from individuals with and the amplitude was reduced to novel non- no history of alcohol or drug dependence. targets in cocaine and alcohol-dependent This study also demonstrated that continued participants compared to controls (Biggins abstinence from heroin and from cocaine et al., 1997; Hada et al., 2000) in auditory and alcohol is also associated with a trend and visual three-stimuli oddball tasks. toward normalization of the P300. In a Several studies have investigated ERP recent study of Papageorgiou et al. (2004), changes associated with methamphetamine the P300 component was evaluated during abuse and dependence. The P300 component the anticipatory period of a short memory of the auditory ERP was reported to show a task in 20 patients characterized by a past prolonged latency in the oddball task in history of heroin dependence (6 months methamphetamine dependent participants Scientific Articles 17 with a history of psychosis, compared to 1997; O’Connor et al., 1994), and bipolar normal controls (Iwanami et al., 1998; or major affective disorder (Friedman & Iwanami, Suga, Kaneko, Sugiyama, & Squires-Wheeler, 1994). Reduced P300 Nakatani, 1994). In particular, the patients amplitude related to prefrontal brain dys- with methamphetamine dependence showed function may suggest that a deficit in reduced P3a amplitude in the reading task inhibitory control is an underlying and delayed P3b latency with normal P3b mechanism shared by different psycho- amplitude in the auditory oddball task. This pathologies (Bauer & Hesselbrock, 1999; was interpreted as indicating a prolonged Clark, Parker, & Lynch, 1999; Tarter et al., central noradrenergic dysfunction because 2003). According to Bauer (2002), certain of earlier methamphetamine use. ERP and qEEG abnormalities and impaired In most ERP studies the P300 did not functioning on complex cognitive tests in differentiate among patients characterized patients formerly dependent on cocaine by histories of cocaine, or cocaine and might not be proximately caused by drug use alcohol, or heroin dependence. Across all per se but be more related to comorbid the patient groups, the P300 was significantly alcohol use or another psychiatric condition. reduced in amplitude relative to P300 Taken together, the findings converge on the ERPs recorded from individuals with no conclusion that there exists an inherited history of alcohol or drug dependence. The predisposition for an externalizing psycho- latency of the frontal and parietal P300 pathology that includes ADHD, conduct was reported to be delayed, and the disorder, and substance abuse. Posttraumatic amplitude was reduced to novel nontargets stress disorder (PTSD) seems to heighten in cocaine and alcohol-dependent partic- the risk for addiction as well. Thus, the ipants compared to controls in auditory reviewed findings support the hypothesis and visual three-stimuli oddball tasks. Con- that addicted participants may manifest a tinued abstinence from heroin, cocaine, P300 amplitude reduction and qEEG and alcohol was shown to be associated abnormalities as a trait reflecting the with a trend toward P300 normalization. CNS disinhibition, which may be a predis- Several studies have investigated ERP posing factor for addiction liability, resis- changes associated with methamphetamine tance to drug habit extinction, and relapse abuse and dependence. In general, chronic vulnerability. psychoactive substance abuse and drug Heritability and neurotransmitter consid- dependence are associated with delayed and erations in SUDs. There has been a consist- attenuated cognitive ERP in auditory and ent drift in addiction research between the visual oddball tasks. psychosocial, cognitive, and behavioral qEEG and ERP abnormalities in addiction: aspects of addiction and the biological and psychopharmacological effects or trait genetic emphasis. In much of the present Markers?. Whether qEEG alterations and data relating to genetics and animal P300 decrements found in most of SUD models (Blum et al., 2006; Porjesz et al., are only a coincident ‘‘marker’’ of vulner- 2005; Ryabinin & Weitemier, 2006; ability or make a direct etiologic con- Samochowiec et al., 2006), studies suggest tribution to risk for substance dependence that a genetic predisposition for SUD is an is stillunknown (Bauer & Hesselbrock, accepted concept. Much of the genetic 2001; Carlson, Iacono, & McGue, 2002; research addresses the influence of alleles O’Connor, Bauer, Tasman, & Hesselbrock, thought responsible in coding for genes 1994; Polich et al., 1994; Porjesz & Begleiter, that express phenotypic neurotransmitter 1998). The P300 reduction and abnormal production and distribution; mainly involv- qEEG patterns are seen in mental disorders ing endorphins, dopamine and serotonin. that often are comorbid with substance These neurotransmitters, dopamine in abuse, such as conduct disorder (Bauer & particular, are also suspect in other Hesselbrock, 1999, 2001), attention deficit appetitive and mood disorders and psycho- hyperactivity disorder (ADHD; Bauer, pathologies, of particular note, Reward 18 JOURNAL OF NEUROTHERAPY

Deprivation Syndrome. Reward Deprivation STUDIES OF EEG BIOFEEDBACK IN Syndrome is described as a dysfunction in SUBSTANCE ABUSE TREATMENT the Brain Reward Cascade and proposes that abnormal craving behavior is a conse- The Peniston Protocol (Alpha-Theta quence of defects in the DRD2 and D1, Feedback) D3, D4 and D5 dopaminergic receptor genes. Early studies of Kamiya (e.g., Nowlis & Kenneth Blum and colleagues (Blum et al., Kamiya, 1970) on self-regulation of alpha 1990; Blum et al., 1993) described this syn- rhythm elicited substantial interest in the drome and identified the D2 dopamine potential clinical applications of alpha bio- receptor gene as a possible candidate for feedback for SUD treatment. There were susceptibility to alcoholism in severe alco- reported several uncontrolled case studies holics (Blum et al., 1993) and proposed this and conceptual reviews on alpha EEG train- gene’s association with dopamine production ing for alcohol (DeGood & Valle, 1978; and distribution may produce a sevenfold Denney, Stelson, & Hardt, 1991; Jones & increase in the likelihood of developing Holmes, 1976; Passini et al., 1977; Tarbox, alcohol use problems (Uhl, Blum, Noble, & 1983; Watson, Herder, & Passini, 1978) and Smith, 1993). This DRD2 dopamine recep- drug abuse treatment (Brinkman, 1978; tor gene and polymorphisms within its Goldberg, Greenwood, & Taintor, 1976, genetic coding specific to addiction remain 1977; Lamontagne, Beausejour, Annable, & unclear because of its involvement in Tetreault, 1977; Sim, 1976), but the impact other disorders, including obesity (Blum of alpha biofeedback training as a SUD ther- et al., 2006), Tourette’s syndrome (Comings apy was not significant. et al., 1991) pathological aggression and vio- The bulk of the literature to date regard- lence, PTSD (Comings, Muhleman, & ing EEG biofeedback of addictive disorders Gysin, 1996) and schizoid–avoidant disorder is focused on alpha-theta biofeedback. The (Chen et al., 2005). SUD were classified as technique involves the simultaneous a subtype of Reward Deprivation Syndrome measurement of occipital alpha (8–13 Hz) and treatment regimens for these disorders and theta (4–8 Hz) and feedback by separate have been classified as inadequate (Blum auditory tones for each frequency represent- et al., 2007) and research continues in devel- ing amplitudes greater than preset thresh- oping possible genetic interventions that may olds. The participant is encouraged to relax produce dopamine and other neurotransmit- and to increase the amount of time the signal ter regulation in substance induced rapid is heard, that is, to increase the amount of dopamine increase in limbic regions (Blum time that the amplitude of each defined et al., 2007). bandwidth exceeds the threshold. A variety It is clear that heritability plays an impor- of equipment and software has been used tant role in addictive disorders, however, to acquire, process, and filter these signals, to what extent environment, perception and and there are differences in technique synaptic permanency and plasticity influence inherent with equipment and software. the course of genetic adaptation or maladap- Alpha-theta feedback training was first tive traits requires further investigation. Sug- employed and described by Elmer Green gested neuroanatomical substrates involved and colleagues (Green, Green, & Walters, in SUD implicate mesolimbic and dien- 1974) at the Menninger Clinic. This method cephalon regions, including the substantia was based on Green’s observations of single nigra, reticular formation, medial forebrain lead EEG during meditative states in prac- bundle, nucleus accumbens, septum pedicu- ticed meditators, during which increased lum, olfactory tubercule, and hippocampus theta amplitude was observed following an and suggest that any concentration of alco- initial increased alpha amplitude, then a hol exposure to these regions would make drop off of alpha amplitude (theta=alpha alcohol use virtually unavoidable (Myers & crossover). When the feedback of the alpha Privette, 1989). and theta signal was applied to participants, Scientific Articles 19 states of profound relaxation and reverie as manifested by EEG (Twemlow, Sizemore, were reported to occur. The method was seen & Bowen, 1977). These initial studies as useful in augmenting psychotherapy and advanced the utility of biofeedback induced promoting individual insight. It could be theta states in promoting insight and seen as a use of brain wave signal feedback attitude change in alcoholics, with the to enable a participant to maintain a parti- assumptions that biofeedback-induced theta cular state of consciousness similar to a states are associated with heightened aware- meditative or hypnotic relaxed state over a ness and suggestibility, and that this heigh- 30- or 40-min feedback session. tened awareness and suggestibility would Goslinga (1975) gave the first description enhance recovery. Outcome data regarding of the use of alpha-theta feedback in a abstinence were not reported. SUD treatment program. This integrated In the first reported randomized and con- program started in 1973 at the Topeka VA trolled study of alcoholics treated with and included group and individual therapies. alpha-theta EEG biofeedback, Peniston and Daily 20-min EEG biofeedback sessions Kulkosky (1989) described positive outcome (integrated with EMG biofeedback and tem- results. Their participants were male inpa- perature control biofeedback) were conduc- tients in a VA hospital treatment program, ted over 6 weeks, resulting in free, loose all with established chronic alcoholism associations, heightened sensitivity, and and multiple past failed treatments. Follow- increased suggestibility. Patients discussed ing a temperature biofeedback pretraining their insights and experiences associated with phase, Peniston’s experimental participants biofeedback in therapy groups several times (n ¼ 10) completed fifteen 30-min sessions a week, augmenting expressive psycho- of eyes closed occipital alpha-theta biofeed- therapy. The first published clinical reports back. Compared to a traditionally treated of efficacy of alpha-theta training at the alcoholic control group (n ¼ 10), and Topeka VA were by Twemlow and Bowen nonalcoholic controls (n ¼ 10), alcoholics (1976), who explored the impact of alpha- receiving brainwave biofeedback showed theta training on psychodynamic issues in significant increases in percentages of EEG 67 nonpsychotic chronic male alcoholics in recorded in the alpha and theta rhythms, an inpatient treatment program. In this non- and increased alpha rhythm amplitudes controlled study, they found that ‘‘religious- (single lead measurements at international ness’’ as a predictor of ‘‘self-actualization’’ site O1). The experimentally treated may have increased as a result of imagery participants showed reductions in Beck experienced in theta states. This was seen Depression Inventory scores compared to as positive to the program goal of augment- the control groups. Control participants ing Alcoholics Anonymous as a recovery who received standard treatment alone philosophy. The high suggestibility of the showed increased levels of circulating beta- method was acknowledged; ‘‘treatments such endorphin, an index of stress, whereas the as brainwave training, which utilize abstract, EEG biofeedback group did not. Thirteen- ill understood techniques are potential month follow-up data indicated significantly repositories of magical projection and more sustained prevention of relapse in fantasy and would logically be more accept- alcoholics who completed alpha-theta brain- able to alcoholics who are able to have wave training as compared to the control ‘faith’ (devoutly or moderately religious)’’ alcoholics, defining successful relapse pre- (Twemlow & Bowen, 1977, pp. 591–598). vention as ‘‘not using alcohol for more In another uncontrolled study at the Topeka than 6 contiguous days’’ during the follow- VA, 21 alcoholics were reported to exhibit up period. In a further report on the same within and across session increases in control and experimental participants, Penis- raw theta amplitudes at occipital areas ton and Kulkosky (1990) described substan- bilaterally measured by single lead EEG tial changes in personality test results in during the course of alpha-theta training, the experimental group as compared to the becoming more able to achieve deep states controls. The experimental group showed 20 JOURNAL OF NEUROTHERAPY improvement in psychological adjustment on a deeply relaxed state where hypnagogic 13 scales of the Millon Clinical Multiaxial reverie is present, this may simply represent Inventory compared to the traditionally drowsiness; Niedermeyer 1999.) Following treated alcoholics who improved on only 2 the session, with the participant in a relaxed scales and became worse on 1 scale. On the and suggestible state, a therapy session is 16-PF personality inventory, the neurofeed- conducted between the participant and back training group demonstrated improve- therapist where the contents of the imagery ment on 7 scales, compared to only 1 scale experienced is explored and ‘‘abreactive’’ among the traditional treatment group. This experiences are explored (Peniston & small n study employed controls and blind Kulkosky, 1989, 1990, 1991). outcome evaluation, with actual outcome Saxby and Peniston (1995) reported on figures of 80% positive outcome versus 14 chronically alcohol dependent and 20% in the traditional treatment control depressed outpatients using this same proto- condition at 4-year follow-up. col of alpha-theta brainwave biofeedback. The protocol described by Peniston at the Following treatment, participants showed Fort Lyons VA just cited is similar to that substantial decreases in depression and initially employed by Twemlow and col- psychopathology as measured by standard leagues at the Topeka VA and Elmer Green instruments. The 21-month follow-up data at the Menninger Clinic, with two additions— indicated sustained abstinence from alcohol temperature training and script. Peniston confirmed by collateral report. These male introduced temperature biofeedback train- and female outpatients received twenty ing as a preconditioning relaxation exercise, 40-min sessions of feedback. along with an induction script to be read at Bodenhamer-Davis and Calloway (2004) the start of each session. This protocol reported a clinical trial with 16 chemically (described as follows) has become known dependent outpatients, 10 of whom were as the Peniston Protocol and has become probationers classified as high risk for rearr- the focus of research in subsequent studies. est. Participants completed an average of 31 Participants are first taught deep relaxation alpha-theta biofeedback sessions. Psycho- by skin temperature biofeedback, for a mini- metrics demonstrated improvements in per- mum of five sessions, that additionally sonality and mood. Follow-up at 74 to 98 incorporates autogenic phrases. Peniston months indicated 81.3% of the treatment also used the criteria of obtaining a tempera- participants were abstinent. Rearrest rates ture of 94 before moving on to EEG bio- and probation revocations for the probation feedback. Participants then are instructed treatment group were lower than those for a in EEG biofeedback and in an eyes closed probation comparison group (40% vs. 79%). and relaxed condition, receive auditory sig- Fahrion (1995) gave a preliminary report nals from an EEG apparatus using an inter- (n ¼ 119) on a large randomized study of national site O1 single electrode. A standard alpha-theta training for addiction in the induction script employing suggestions to Kansas Prison System using group-training relax and ‘‘sink down’’ into reverie is read. equipment. A report of the completed When alpha (8–12 Hz) brainwaves exceed a study (n ¼ 520; Fahrion, 2002) showed preset threshold, a pleasant tone is heard, little difference between the two groups and by learning to voluntarily produce this overall at 2-year outcome. But when results tone, the participant becomes progressively were analyzed for age, race, and drug of relaxed. When theta brainwaves (4–8 Hz) choice, neurofeedback emerged as a more are produced at a sufficiently high ampli- efficacious treatment for younger and tude, a second tone is heard, and the partici- non-White and nonstimulant abusing pant becomes more relaxed and, according participants. Of interest, this protocol was to Peniston, enters a hypnagogic state of free not effective for cocaine abusers. (Stimulant reverie and high suggestibility. (Although abusers are discussed later in this article theta increase and alpha decrease are under the Scott–Kaiser modification of the thought by Peniston to be associated with Peniston protocol.) Scientific Articles 21

The issue of alpha-theta biofeedback in showed that alpha-theta training results in culturally sensitive groups that have not an increase of theta=alpha ratios, as com- responded to traditional modes of addiction pared to a control condition. In an in-depth treatment (such as confrontational group critical analysis that examines inconsistencies therapies) has been considered in an open reported in the original Peniston papers, case series reported by Kelly (1997). This Graap and Freides (1998) raised serious 3-year follow-up study presented the treat- issues about the reporting of original sam- ment outcomes of 19 Dine’ (Navajo) clients. ples and procedures in these studies. In their Four (21%) participants achieved ‘‘sustained analyses the results may have been as much full remission,’’ 12 (63%) achieved ‘‘sus- because of the intense therapies accompany- tained partial remission,’’ and 3 (16%) ing the biofeedback as the biofeedback itself. remained ‘‘dependent.’’ The majority of The participants may have been comorbid participants also showed a significant for a number of conditions, which were increase in ‘‘level of functioning.’’ not clearly reported, particularly PTSD, Schneider et al. (1993) used slow cortical which may have been the focus of the potential biofeedback to treat 10 unmedi- treatment. In his reply to these criticisms, cated alcoholic patients in four neurofeed- Peniston (1998) acknowledged that it back sessions after hospitalization. Seven ‘‘remains unknown whether the temperature patients participated in a fifth session an training, the visualizations, the ATBWNT average of 4 months later. Six of these 7 (alpha-theta brain wave neurotherapy), the patients had not had a relapse at the fol- therapist, the placebo, or the Hawthorne low-up. These results are similar to those effects are responsible for the beneficial reported for alpha-theta training. results’’ (pp. 273–275). The criticism raised Several other studies using the Peniston here by Graap and Friedes (1998) regarding protocol and its modifications reported Peniston’s articles could also be applied to cases with positive clinical effects (Burkett, earlier replication studies. Neither Peniston’s Cummins, Dickson, & Skolnick, 2003; studies nor the replication studies provide DeBeus, Prinzel, Ryder-Cook, & Allen, sufficient detail regarding the specifics of 2002; Fahrion, Walters, Coyne, & Allen, the types of equipment used for alpha-theta 1992; Finkelberg et al., 1996; Skok, Shubina, feedback, including filtering methods for Finkelberg, Shtark, & Jafarova, 1997). These the EEG signal or other technical infor- studies suggest that an applied psychophy- mation, to permit exact reproduction of the siological approach based on an alpha-theta feedback protocols with other equipment. biofeedback protocol is a valuable alterna- Outcome criteria also vary in the replication tive to conventional substance abuse treat- studies, with varying measures of abstinence ment (Walters, 1998). Nevertheless, most of and improvement. An exception to these these results were reported at the society concerns is the report of Scott et al. (2005), meetings, and only few of these studies were which is discussed later in greater detail. published in mainstream peer-reviewed jour- It should be noted that psychostimulant nals other than the Journal of Neurotherapy. (cocaine, methamphetamine) addictions A critical analysis of the Peniston Protocol may require approaches and neurofeedback is discussed at length in the previous reviews protocols other than alpha=theta training. (Trudeau, 2000, 2005a, 2005b). Several con- Persons who are cocaine dependent are trolled studies of the Peniston protocol for cortically underaroused during protracted addictions, completed by Lowe (1999), abstinence (Roemer et al., 1995). QEEG Moore and Trudeau (1998), and Taub and changes, such as a decrease in high beta Rosenfeld (1994), suggest that alpha-theta (18–26 Hz) power are typical for withdrawal training for addictions may be nonspecific from cocaine (Noldy et al., 1994). Cocaine in terms of effect when compared to abusers who are still taking this drug often suggestion, sham or controlled treatment, show low amounts of delta and excess or meditational techniques. By contrast, amounts of alpha and beta activity (Alper, Egner, Strawson, and Gruzelier (2002) 1999; Prichep et al., 1999), whereas chronic 22 JOURNAL OF NEUROTHERAPY methamphetamine abusers usually exhibit Kulkosky, 1990). Their experimental partic- excessive delta and theta activity (Newton ipants underwent an average of 13 SMR- et al., 2003). Thus, cocaine and methamphet- beta (12–18 Hz) neurofeedback training amine users may warrant a different EEG sessions followed by 30 alpha-theta sessions biofeedback protocol, at least at the begin- during the first 45 days of treatment. Treat- ning stages of neurofeedback therapy. ment retention was significantly better in the EEG biofeedback group and was associated with the initial SMR-beta train- The Scott-Kaiser Modification of the ing. A subsequently published article Peniston Protocol (Scott et al., 2005) reported on an expanded series of 121 inpatient drug program partic- Scott and Kaiser (1998) described combin- ipants randomized to condition, followed ing a protocol for attentional training (beta up at 1 year. Participants were tested and and=or sensorimotor rhythm [SMR] aug- controlled for the presence of attentional mentation with theta suppression) with the and cognitive deficits, personality states, Peniston protocol (alpha-theta training) in and traits. The experimental group showed a population of participants with mixed sub- normalization of attentional variables stance abuse, rich in stimulant abusers. The following the SMR-Beta portion of the beta protocol is similar to that used in neurofeedback, whereas the control group ADHD (Kaiser & Othmer, 2000) and was showed no improvement. Experimental par- used until measures of attention normalized, ticipants demonstrated significant changes and then the standard Peniston protocol (p < .05) beyond the control participants without temperature training was applied on 5 of the 10 scales of the Minnesota (Scott et al., 2002). The study group is sub- Multiphasic Personality Inventory-2. stantially different than that reported in Participants in the experimental group either the Peniston or replication studies. were also more likely to stay in treatment The rationale is based in part on reports of longer and more likely to complete treatment substantial alteration of qEEG seen in stimu- as compared to the control group. Finally, lant abusers associated with early treatment the 1-year sustained abstinence levels were failure (Prichep et al., 1996; Prichep significantly higher for the experimental et al., 2002) likely associated with marked group as compared to the control group. frontal neurotoxicity and alterations in The approach of beta training in conjunc- dopamine receptor mechanisms (Alper, tion with alpha-theta training has been 1999). In addition, preexisting ADHD is applied successfully in a treatment program associated with stimulant preference in aimed at homeless crack cocaine abusers in adult substance abusers and is independent Houston, as reported by Burkett et al. of stimulant associated qEEG changes. (2003), with impressive results. Two hundred These findings of chronic EEG abnormality seventy male addicts received 30 sessions of a and high incidence of preexisting ADHD in protocol similar to the Scott-Kaiser modifi- stimulant abusers suggest they may be less cation. One-year follow-up evaluations of able to engage in the hypnagogic and auto- 94 treatment completers indicated that suggestive Peniston protocol (Trudeau, 95.7% of participants were maintaining a Thuras, & Stockley, 1999). Furthermore, regular residence; 93.6% were employed=in eyes-closed alpha feedback as a starting school or training, and 88.3% had no sub- protocol may be deleterious in stimulant sequent arrests. Self-report depression scores abusers because the most common EEG dropped by 50% and self-report anxiety abnormality in crack cocaine addicts is scores by 66%. Furthermore, 53.2% excess frontal alpha (Prichep et al., 2002). reported no alcohol or drug use 12 months In their initial report, Scott and Kaiser after biofeedback, and 23.4% used drugs or (1998) described substantial improvement alcohol only one to three times after their in measures of attention and also of person- stay. This was a substantial improvement ality (similar to those reported by Peniston & from the expected 30% or less expected Scientific Articles 23 recovery in this group. The remaining 23.4% specific neurophysiological operant learning reported using drugs or alcohol more than 20 (LORETA Neurofeedback; Cannon et al., times over the year. Urinalysis results corro- 2007; Cannon, Lubar, Gerke, & Thornton, borated self-reports of drug use. The treat- 2006; Congedo, 2003; Congedo, Lubar, & ment program saw substantial changes in Joffe, 2004), and finally, they want to utilize length of stay and completion. After the both the assessment and neurophysiological introduction of the neurofeedback to the data for development of statistical models mission regimen, length of stay tripled, for possible diagnostic and predictive pur- beginning at 30 days on average and culmi- poses and to provide a means for a neuro- nating at 100 days after the addition of neu- physiological measure of treatment efficacy. rotherapy. In a later study the authors Research indicates that substance abusers reported follow-up results on 87 participants have elevated beta activity in an EEG resting after completion of neurofeedback training state as compared with normative groups (Burkett, Cummins, Dickson, & Skolnick, (Rangaswany et al., 2002) and elevated alpha 2005). The follow-up measures of drug activity after administering a mood-altering screens, length of residence, and self- substance (Cohen, Porjesz, & Begleiter, reported depression scores showed signifi- 1993; Kaplan et al., 1985, 1988). It is sug- cant improvement. It should be noted that gested that many of the neurophysiological this study had limitations, because neuro- markers may provide information about feedback was positioned only as an adjunct the state of the individual prior to the devel- therapy to all other faith-based treatments opment of an addictive disorder and that for crack cocaine abusing homeless persons these brain functions are under genetic con- enrolled in this residential shelter mission trol (Porjesz et al., 2002; Porjesz et al., and was an uncontrolled study. Yet the 2005; Tapert et al., 2004). Kaplan et al. improvement in program retention is impres- (1985) reported lower frontal alpha and sive and may well be related to the improved slow-beta coherence in alcohol-dependent outcome. male and female participants. Michael et al. (1993) found higher central alpha and slow- beta coherence but lower parietal alpha and Continuing Research: Self-Perception slow-beta coherence in male participants and Experimental Schemata in the with alcohol dependence; contrarily, other Addicted Brain findings suggest that morphine, alcohol, and marijuana show increased alpha 2 power Rex Cannon, Joel Lubar, and Deborah in the spectral EEG and relate this to the Baldwin of the Brain Research and Neuro- euphoric state produced by the drug (Lukas, psychology Laboratory at University of 1991, 1993; Lukas et al., 1989, 1995). Tennessee at Knoxville are performing Winterer, Enoch, et al. (2003) and Winterer, research with three goals in mind: First, they Smolka, et al. (2003) described higher left- wish to attempt to reconcile and integrate temporal alpha and slow-beta coherence data from all disciplines involved in and higher slow-beta coherence at right-tem- addiction research to develop a novel poral and frontal electrode pairs in alcohol- approach for neurophysiological study dependent male and female participants. pertaining to SUDs and conceivably deter- De Bruin et al. (2004) showed that moderate mine and describe EEG source generators to heavy alcohol consumption is associated that are instrumental in the processes of with differences in synchronization of brain self-perception and experiential schemata activity during rest and mental rehearsal. utilizing a recently developed assessment Heavy drinkers displayed a loss of hemi- instrument. Second, they want to utilize spheric asymmetry of EEG synchronization this information to develop an integrative in the alpha and low-beta band. Moderately treatment model for addictive disorders and heavily drinking male participants based on this research, involving novel additionally showed lower fast-beta band group-processing methods and spatial synchronization. Decision-making processes 24 JOURNAL OF NEUROTHERAPY and the ability to form a resistance to drugs uninhibited association of all current interac- (i.e., the ability to say no) involve numerous tions and situations with past events. brain regions, including the insular, somato- Opposite to what often is implied, these sensory, orbitofrontal, anterior cingulate, features may not originate from the conse- and dorsolateral prefrontal cortices, as well quences of substance abuse but from earlier as the amygdala, hippocampus, and thalamic periods in development (Vos, 1989), and in nuclei (Bechara, 2005). the perspective of this research these features This research considers the integration of and others have an etiology in specific the features of addicted persons as reported neurophysiological regions that are the in earlier studies, case reports and theoretical direct result of dendritic pruning that occurs concepts as vital in understanding behavioral in early development that continues on into manifestations of the suspected neural path- adolescence and, unless intervention or ways that are premised to be involved in the awareness of these schemata are achieved, development of SUD. Some of the funda- they remain problematic into adulthood. mental descriptions of addicted individuals To date, studies identifying such schematic portray them as passive with dependent source generators and their relationship strivings, emotionally immature, abounding with SUDs using qEEG and standardized with fears of responsibility or independent LORETA are scant. This research is designed action and ultimately, infantile inadequate to assess the neural activation patterns personalities (Coodley, 1961), as well as emo- relative to schemata regarding the self in tionally, socially, and educationally under- recovering addicts and identify possible developed (Meyerstein, 1964), and immature generators in the cortex as compared to and regressive (Dorsey, 1961; Gerard & controls. In this research, it is hypothesized Kornetsky, 1955; Hill, 1962). These indivi- that there is dendritic pruning early in duals are reported to struggle with affirming developmental phases that contribute to positive thoughts of self-esteem, tendencies frequency specific activity in neuronal to undervalue themselves and be self- populations in the ventromedial portions of deprecating, and exhibit difficulty adjusting the prefrontal cortex and limbic regions. to others and these tendencies are veiled Furthermore, it is proposed that these by overt behavioral patterns, including neural pathways hinder the integration of physical or verbal abuse. affect, cognition, reward, and decision- Individuals with SUD present with a making processes and adversely influence vast number of paradoxical characteristics, the perception of self and self in relation to including an overwhelming sense of experience and the development of adaptive inadequacy disguised by an apparent schemata and personality characteristics. overwhelming sense of confidence. Similarly, an apparent abundance of anger and aggression utilized as a disguise for a paral- Integration of Cognitive Neuroscience yzing sense of fear, more specifically, Approaches in Assessment of Functional fear of people, economic insecurity, rejec- Outcomes of Neurofeedback and Behavioral- tion, and alienation, which paradoxically Therapy-Based Interventions in SUD are exacerbated by the continued use of the substance. One of the more profound Sokhadze, Stewart, and Hollifield (2007) idiosyncratic characteristics of this popu- in their conceptual review proposed an inte- lation is the tendency to ruminate and associ- grated approach to assessment and treat- ate past events, perceptions, and the ment utilizing cognitive neuroscience associated emotions with both present and methods (e.g., qEEG, ERP), conventional future. The perception of experience is often psychotherapeutic treatment, and neurofeed- clouded by the personalization of events back therapy to assess the recovery of cogni- (real or imagined) and reinforced with a tive and emotional functions affected deliberate, ambiguous effort to avoid recon- by chronic psychostimulant drug abuse co- ciling this confound, which reinforces an occurring with PTSD. Cognitive neuroscience Scientific Articles 25 methodologies used for assessment of the (MET) in an outpatient population. The outcome effects of psychotherapy and purpose of this research is also to character- neurofeedback interventions for comorbid ize changes in cognitive functioning associa- disorders have significant potential for ted with the success rate of three arms for additionally identifying neurophysiological cocaine addiction treatment (MET, NFB, and clinical markers of treatment progress combined MET þ NFB). Prior, during, (Sokhadze, 2005). These outcome markers and subsequent to the aforementioned bio- may provide useful information for planning behavioral therapies, individual differences bio-behavioral interventions in this form of in qEEG and dense-array ERP are being dual diagnosis. assessed during cognitive tasks containing Angela Stotts and colleagues (Stotts, drug-related and generally affective cues, Potts, Ingersoll, George, & Martin, 2006) and during cognitive tasks aimed to test at the University of Texas at Houston, in cortical inhibitory capacity, selective atten- collaboration with researchers at Rice Uni- tion, response error processing, and cortical versity, used motivational interviewing (MI) functional connectivity. Preliminary data with personalized feedback, particularly from this study were presented at the 2007 employing the ERP markers of deficiencies annual meeting of ISNR (Sokhadze, in selective attention task produced by Tasman, Stewart, Singh, & Hollifield, 2007) cocaine abuse in crack addicts. In a random- and are being prepared for publication. ized, controlled pilot study these authors (Sokhadze, Martin, Stotts, & Potts, 2004; Sokhadze, Potts, Martin, & Stotts, 2005; Stotts et al., 2006) evaluated the feasibility EFFICACY OF ALPHA-THETA and preliminary efficacy of a brief MI inter- TRAINING vention using EEG=ERP graphical feedback for crack cocaine abusers. Treatment-seeking The Guidelines for Evaluation of Clinical cocaine abusers (N ¼ 31) were randomly Efficacy of Psychophysiological Interven- assigned to a two-session MI intervention tions (LaVaque et al., 2002), which have or a general educational drug counseling been accepted by AAPB and ISNR, specify (control) condition. All participants received five types of classification for the effective- EEG assessments based on dense-array ERP ness of biofeedback procedures, ranging tests in a selective attention task at intake from ‘‘not empirically supported’’ to ‘‘effi- and post-treatment. Results indicated that cacious and specific.’’ The requirements for the MI intervention was feasible and the sub- each classification level are summarized in jective impact of the EEG=ERP feedback brief next. A more complete description was positive. Significant group differences may be found in LaVaque et al. (2002). in percentage of cocaine positive urine screens across the study were found, favoring the MI group—84.9% for the control group Criteria for Levels of Evidence of Efficacy and 62.6% in the MI group. In a current study at the University of Level 1: Not empirically supported. This Louisville, Tato Sokhadze and his colleagues classification is assigned to those treatments are utilizing dense-array qEEG=ERP vari- that have only been described and supported ables and measures of behavioral perform- by anecdotal reports and=or case studies in ance on mental tasks (reaction time, nonpeer reviewed journals. accuracy) to explore the cognitive functions Level 2: Possibly efficacious. This classi- in patients with cocaine abuse=dependence fication is considered appropriate for those diagnosis and the recovery of these treatments that have been investigated in functions during bio-behavioral intervention at least one study that had sufficient based on an integrated neurofeedback statistical power and well-identified outcome (NFB) approach (Scott-Kaiser protocol) measures but lacked randomized assignment and motivational enhancement therapy to a control condition internal to the study. 26 JOURNAL OF NEUROTHERAPY

Level 3: Probably efficacious. Treatment can be classified as Level 3—probably approaches that have been evaluated and efficacious—when combined with an shown to produce beneficial effects in mul- inpatient rehabilitative treatment modality tiple observational studies, clinical studies, in participants with long-standing alcohol wait-list control studies, and within-subject dependency. This classification is based and between-subject replication studies merit on the original randomized and controlled this classification. study of the Peniston Protocol (Peniston & Level 4: Efficacious. To be considered effi- Kulkosky, 1989, 1990, 1991) and multiple cacious, a treatment must meet the following observational and uncontrolled studies criteria: that preceded (Twemlow & Bowen, 1977; Twemlow et al., 1977) and followed these 1. In a comparison with a no-treatment studies (Bodenhamer-Davis & Calloway, control group, alternative treatment 2004; Burkett et al., 2003; DeBeus et al., group, or sham (placebo) control utilizing 2002; Fahrion, 1995; Fahrion et al., 1992; randomized assignment, the investiga- Finkelberg et al., 1996; Saxby & Peniston, tional treatment is shown to be statisti- 1995; Skok et al., 1997). Using these criteria cally significantly superior to the control and based on reported studies to date the condition or the investigational treatment Scott-Kaiser modification of the Peniston is equivalent to a treatment of established Protocol can also be classified as probably efficacious (Level 3) when combined with efficacy in a study with sufficient power residential rehabilitation modalities in to detect moderate differences. stimulant abusers. This rating is based on 2. Studies have been conducted with a popu- one controlled study of 121 participants lation treated for a specific problem, from in which Peniston’s outcomes of both whom inclusion criteria are delineated in psychometric improvement and abstinence a reliable, operationally defined manner. improvement were replicated (Scott et al., 3. The study used valid and clearly specified 2005) and one observational study of 71 outcome measures related to the problem participants (Burkett et al., 2003.) being treated. Alpha-theta training protocols do not 4. Data are subjected to appropriated data completely meet the criteria for the Level 4 analysis. ‘‘efficacious’’ classification. Although there 5. Diagnostic and treatment variables and are sufficient studies that show statistically procedures are clearly defined in a man- significant superiority of randomly assigned ner that permits replication of the study treatment groups to no-treatment control by independent researchers. groups, and studies have been conducted 6. Superiority or equivalence of the investi- with populations treated for a specific prob- gational treatment have been shown in at lem, from whom inclusion criteria are least two independent studies (LaVaque delineated in a reliable, operationally et al., 2002). defined manner, and the studies cited use valid and clearly specified outcome measures Level 5: Efficacious and specific. To meet related to the problem being treated with the criteria for this classification, the treat- data subjected to appropriate data analysis, ment needs to be demonstrated to be statisti- there remains the shortcoming cited by cally superior to a credible sham therapy, Graap and Freides (1998) for the initial pill, or bona fide treatment in at least two reports of Peniston and Kulkosky (1989, independent studies. 1990, 1991). We recall the qualifying limita- tions of LaVaque et al. (2002), who stated that ‘‘the diagnostic and treatment variables Criteria Overview and procedures are not clearly defined in a manner that permits replication of the study Using these criteria and based on the by independent researchers’’ (p. 280). How- studies reported to date alpha-theta training ever the Scott et al. (2005) report does Scientific Articles 27 appear to clearly delineate treatment 1993). Independent of other psychiatric variables and procedures. One other comorbidity, ADHD alone significantly independent study showing the superiority increases the risk for SUD (Biederman et al., of modified alpha-theta training to control 1995). Associated social and behavioral condition would meet the stated criteria for problems may make individuals with a Level 4 efficacious classification. comorbid SUD and ADHD treatment resis- To be considered Level 5 (‘‘efficacious and tant (Wilens, Biederman, & Mick, 1998). specific’’), modified alpha-theta training In male participants ages 16 to 23, the would need to be shown to be superior to presence of childhood ADHD and conduct sham or bona fide treatment. It has not been disorder is associated with nonalcohol demonstrated that the Peniston type SUD (Gittelman, Mannuzza, Shenker, & alpha-theta feedback is more efficacious Bonagura, 1985; Mannuzza, Klein, Konig, than sham treatment (Lowe, 1999; Moore & Giampino, 1989). In summary childhood & Trudeau, 1998; Trudeau, 2000, 2005a, ADHD associated with conduct disorder in 2005b) or alternative treatment that involves male individuals is an antecedent for adult meditation (Taub & Rosenfeld, 1994). nonalcohol SUD and anti-social personality disorder (Wender, 1995). The incidence of ADHD in clinical SUD populations has CLINICAL CONSIDERATIONS: been studied and may be as high as 50% COMORBIDITIES OF SUD AND for adults (Downey, Stelson, Pomerleau, & IMPLICATIONS FOR Giordani, 1997) and adolescents (Horner & INDIVIDUALIZED (QEEG-GUIDED) Scheibe, 1997). Adult residual ADHD is NEUROFEEDBACK especially associated with cocaine abuse and other stimulant abuse (Levin & Kleber, There are several conditions commonly 1995). Monastra et al. (2005) in a white associated with addictive disorders that have paper review of ADHD, cite positive known neurophysiological aberrations. The treatment outcomes of just under 80% in co-occurrence of alcohol and other SUDs treatment of ADHD with neurofeedback. with other psychiatric disorders has been Rates of PTSD occurring in persons widely recognized. Co-occurrence of SUD primarily identified with or in treatment for and other psychiatric diagnosis (e.g., PTSD, substance abuse vary from 43% (Breslau, antisocial personality disorder, ADHD, Davis, Andreski, & Peterson, 1991) up to unipolar depression etc.) is highly prevalent 59% (Triffleman, Carroll, & Kellogg, 1999). (Drake & Wallach, 2000; Evans & Sullivan, In a general population study, Cottler et al. 1995; Grant et al., 2004; Jacobsen, (1992) reported that cocaine abusers were Southwick, & Kosten, 2001). Persons with three times more likely to meet diagnostic co-occurring other mental disorders and criteria for PTSD compared to individuals SUD have a more persistent illness course without a SUD. Kalechstein et al. (2000) and are more refractive to treatment than found that methamphetamine-dependent those without dual diagnoses (Brown, individuals are at greater risk to experience Recupero, & Stout, 1995; O’Brien et al., particular psychiatric symptoms. There was 2004; Schubiner et al., 2000; Swartz & reported a significant Dependence Gender Lurigio, 1999). Depression occurs in effect, with methamphetamine-dependent approximately 30% of chronic alcoholics female participants reporting significantly (Regier et al., 1990). In treatment settings, more overall posttraumatic stress symp- these depressed patients can present tomatology compared to female participants particular challenges to the clinician, as they reporting no dependence, whereas male may not respond as well to treatment as participants significantly differed only with other patients; may have greater relapse, respect to depression. Peniston and Kulk- attrition, and readmission rates; and may osky (1991) reported effective treatment of manifest symptoms that are more severe, PTSD using a protocol similar to the one chronic, and refractory in nature (Sheehan, they employed for alcoholics. 28 JOURNAL OF NEUROTHERAPY

Hughes and John (1999) reviewed the presented. Basically, this technique involves applicability of qEEG findings in SUD. the use of qEEG to identify patterns of They noted that in numerous qEEG studies EEG that deviate from standardized there is a consensus of increased beta relative norms and individualized EEG biofeedback power in alcoholism and increased alpha in protocols to correct them (Romano-Micha, cannabis and crack cocaine users. They 2003). DeBeus et al. (2002) are presently concluded that the evidence provided by stu- conducting a randomized controlled study dies to date is insufficient to recommend of neurotherapy for SUD that examines the qEEG as a routine clinical assessment difference between a qEEG-based treatment, tool in SUD, although it may be useful in a research-based (Scott-Peniston) treatment, differential diagnosis in difficult cases. and a wait-list control for chemically depen- A number of specific qEEG abnormalities dent outpatients. Preliminary results are have been described as specific to suspected promising. Although historically alpha-theta neurotoxicities associated with chronic training has been the accepted approach in stimulant abuse. These studies (Alper et al., treating chemical dependency, this study 1990; Noldy et al., 1994; Prichep et al., suggests qEEG-based training is a viable 1996; Roemer et al., 1995; Trudeau, Thuras, alternative, demonstrating similar outcomes & Stockley, 1999) based on reasonably for personality change and abstinence rates. uniform abstinence times and employing Future directions include determination different EEG technology and analytical of those likely to benefit from one of the approaches, have produced remarkably simi- particular treatments or a combination of lar findings of alpha relative amplitude the two and analysis of long-term abstinence excess with delta relative amplitude deficit rates. Gurnee (2004) presented data on a that is striking. Excess alpha amplitude with series of 100 sequential participants with slowing of alpha frequency associated with SUD who were treated by qEEG-based chronic cannabis abuse has been reported neurotherapy, with marked heterogeneity of (Struve et al., 1998). As noted, Scott and qEEG subtypes and corresponding symptom Kaiser (1998) described combining a proto- complexes. In this clinically derived scheme, col for attentional training (beta reward) qEEGs that deviate from normative data- with alpha-theta training in a population of bases, mainly with excess alpha amplitude, participants whose primary drugs of abuse are associated more often with depression were stimulants and who had features of and ADD. Those with deficient alpha ampli- ADHD. tude are associated with anxiety, insomnia, It may make good sense clinically to and alcohol=drug abuse. Beta excess ampli- consider specific neurotherapy treatment of tude is associated with anxiety, insomnia, these disorders either in place of or preceding and alcohol=drug abuse. Central abnormali- alpha-theta therapy, similar to the ties are interpreted as mesial frontal dysfunc- Scott-Kaiser approach. Second, applicable tion and are associated with anxiety, neurotherapy approaches are attractive rumination, and obsessive compulsive symp- alternative therapies for coexisting or under- toms. The therapeutic approach is to base lying conditions in SUD clients who neurotherapy on correcting identified qEEG have high-risk behaviors for medication abnormalities, that is, train beta excess treatment, such as overdosing, abuse, or amplitude down when present, while moni- poor compliance. Although there are no toring symptoms. published systematic studies of neurotherapy Tentative findings suggest that qEEG treatment of co-occurring depression, trau- variables may be used to predict those alco- matic brain injury (TBI), ADHD, PTSD, holics and drug abusers most at risk for or drug neurotoxicity on the course and relapse. Winterer et al. (1998) were able to outcome of addictive disorders, several predict relapse among chronic alcoholics recent reports of neurotherapy for addictions with 83 to 85% success, significantly outper- based on qEEG findings, which in turn forming prediction from clinical variables. may be related to comorbidities, have been Although they found more desynchronized Scientific Articles 29

(less alpha and theta and more beta activity) Kumar, 1998) and PTSD (Graap, Ready, over frontal areas in alcoholics in general, Freides, Daniels, & Baltzell, 1997; Huang- those individuals who relapsed displayed Storms, Bodenhamer-Davis, Davis, & Dunn, even more of this activity. Bauer (2001b) 2006). Alpha-theta feedback has been des- obtained EEG data on alcohol, cocaine, or cibed as efficacious in postcombat PTSD opioid dependent patients after 1 to 5 (Peniston & Kulkosky, 1991, Peniston, months of sobriety. Those who had relapsed Marriman, Deming, & Kulkosky, 1993). 6 months later were also characterized However, additional research needs to be by increased beta (19.5–39.8 Hz) activity completed to determine the clinical outcome relative to those maintaining abstinence. and efficacy of bio-behavioral treatment Relative beta power was superior to severity based on brain wave self-regulation in addic- of the alcoholism, depression level, antisocial tion disorders that are comorbid with personality disorder, childhood conduct various anxiety disorders and PTSD. problems, family history, or age as predic- tors and was unaffected by the substance of abuse. The EEG differences between CLINICAL CONSIDERATIONS: relapse-prone and abstinence-prone groups COGNITIVE-BEHAVIORAL were found to be related to the interaction AND NEUROFEEDBACK TREATMENT of two premorbid factors: childhood conduct IN SUDs disorder and paternal alcoholism. These findings receive further support from Bauer Because of its chronic nature, long-term (1993) and Prichep et al. (1996, 1999), who treatment for SUD is usually necessary also found that beta activity was predictive (Crits-Christoph et al., 1997, 1999). Effective of treatment failure. They found two clusters agonist and antagonist pharmacotherapies among cocaine addicts: One had more severe as well as symptomatic treatments exist for damage (alpha) and tended to remain in opioid dependence, but neither agonists nor treatment. Those with less severe alpha antagonists have been approved as uniquely excess and more beta activity tended to effective for treatment of stimulant abuse or leave treatment. They also discovered that dependence (Grabowski, Shearer, Merrill, & dropouts could not be determined from the Negus, 2004). There is no current evidence presence of anxiety or depression or demo- supporting the clinical use of carbamazepine graphic variables. (Tegretol), antidepressants, dopamine Treatment of patients with substance agonists (drugs commonly used to treat abuse disorder by neurofeedback may Parkinson’s and Restless Leg Syndrome), become more complicated when patients disulfiram (Antabuse), mazindol (an experi- present various psychiatric conditions. When mental anorectic), phenytoin (Dilantin), addiction is comorbid with ADHD, it is nimodipine (Nimotop), lithium, and other suggested that SMR (or beta increase, theta pharmacological agents in the treatment decrease) training should be conducted to of cocaine dependence (de Lima, de Oliveira address the related ADHD disorder first Soares, Reisser, & Farrell, 2002; Venneman (Biederman et al., 1997). Applicability of et al., 2006). Because no proven effective neurofeedback methods to treat anxiety pharmacological interventions are available and affective disorders is reviewed by for cocaine addiction or for methampheta- Hammond (2006). Peniston and Kulkosky mine addiction, treatment of stimulant (1990) described personality normalization addiction has to rely on existing CBTs in alcoholics treated with EEG biofeedback. or CBT combined with other biobehavi- Alpha-theta feedback has also been reported oral approaches (Van den Brink & van Ree, as efficacious in alcoholics with depressive 2003). symptoms (Saxby & Peniston, 1995). There According to Volkow et al. (2004), are only a few case studies on the efficacy successful strategies for behavioral treatment of neurofeedback for treating generalized in drug addiction may include (a) interven- anxiety disorder (Vanathy, Sharma, & tions aimed to decrease the reward value of 30 JOURNAL OF NEUROTHERAPY the drug and simultaneously increase values IV–TR, APA, 2000) or is not driven by of natural reinforcement, (b) approaches self-medication strategies, the simultaneous aimed to change stereotype conditioned treatment of both psychiatric conditions drug-seeking behaviors, and (c) methods to may be required. In this situation, treatment train and strengthen frontal inhibitory could be guided by the two following control. Because stressful events can result concepts: First, behavioral interventions to in relapse to drug taking behavior (Koob & activate and strengthen circuits involved in Le Moal, 2001), an adjunct treatment strat- inhibitory control, such as bio-behavioral egy is to interfere with the neurobiological self-regulation training, may increase suc- responses to stress (Goeders, 2003; Koob & cessful abstinence from drug taking. Second, Le Moal, 2001). Treatment of comorbid considering the important role of cognitive mental conditions may also require the con- and emotional processes involved in the pre- current treatment of drug addiction. In some disposition for drug abuse, the development cases, however, comorbid drug addiction of nonpharmacological interventions (e.g., may result from attempts to alleviate the psy- CBT, stress management, neurofeedback) is chiatric disorder through self-medication a feasible strategy. (i.e., co-occurring cocaine use and ADHD and=or heroin addiction co-occurring with PTSD). In other cases, severity of a psychi- DIRECTIONS FOR FURTHER atric disorder symptom may increase as RESEARCH a result of drug abuse (Volkow et al., 2003, 2004). Specific patterns of qEEG abnormality In patients with drug abuse arising from an associated with specific substance use attempt to self-medicate (Khantzian, 1985, toxicity such as those found in stimulant 1997), treatment of the comorbid mental dis- abuse or alcohol abuse or with comorbidities order may help prevent abuse. For instance, such as ADHD (Chabot & Serfontein, 1996), treatment of the preexisting condition of PTSD (Huang-Storms et al., 2006) or TBI ADHD may prevent cocaine abuse (Biederman (Thatcher, Walker, Gerson, & Geisler, et al., 1997; Biederman et al., 1995). In some 1989) suggest underlying brain pathologies cases though the persistent qEEG abnormali- that might be amenable to EEG biofeedback ties associated with chronic SUD may happen that is tailored to the person. These to be independent from ADHD clinical status approaches would likely be individualized (Trudeau et al., 1999). The co-occurrence of rather than protocol based and would be ADHD and SUD has received considerable used independently or in conjunction with attention in the recent clinical and scientific classic alpha-theta training. By way of literature (Davids et al., 2005). These two disor- example, these could include protocols spe- ders are often linked to one another. Because cific to the qEEG abnormality, such as fron- the core symptoms of ADHD may be tal delta reward to correct the frontal delta mimicked by the effects of psychoactive drugs, deficit in cocaine abuse that Alper (1999) it is difficult to diagnose one disorder in the hypothesized may be related to cocaine sen- presence of the other (Davids et al., 2005). sitization and changes in dopamine trans- ADHD has been found to be associated with mission. To our knowledge this has never an earlier onset of SUD (Horner & Scheibe, been studied and is clearly a research (not a 1997). It is generally assumed that untreated clinical) recommendation. QEEG patterns ADHD is a risk factor for SUD develop- and abnormalities depend significantly on ment (Biederman, Wilens, Mick, Faraone, & whether the participant is still currently Spenser, 1998; Biederman et al., 1997; using, the chronicity of use, and the current Mannuzza et al., 1989, 1998; Trudeau, 2005a, stage of withdrawal or protracted absti- 2005b). nence. A neurofeedback protocol selected In a case of comorbidity in which the use for an individual client with SUD should of drugs antecedes a mental disease (e.g., be directly related to the level of current substance-induced anxiety disorder; DSM– substance use or abstinence, especially in Scientific Articles 31 such classes of drugs as heroin, where the and reported. Finally, studies need to adhere withdrawal syndrome results in substantial to clearly defined outcome measures that physiological manifestations including tran- have established reliability and validity. sient qEEG changes. Other important recommendations for Even though there are no reported system- future development of the field are listed atic studies of EEG biofeedback treatment of next: commonly occurring comorbidities of SUD, it makes sense that clinical EEG biofeedback 1. The availability of an increased number treatment study protocols consider the pres- of channels for EEG and ERP recording ence of ADHD, TBI, depression, and drug (e.g., higher spatial sampling rate) makes associated neurotoxicity. This approach it possible to better localize the source may improve outcome, especially in conven- of brain activity. More focused research tional treatment resistant participants. of this type seems warranted. Unfortunately, only a few large-scale stu- 2. There are several specific functional dies of neurofeedback in addictive disorders have been reported in the literature. Most, diagnostic tools from the cognitive if not all of the recommendations previously neuroscience arsenal that are very specific made regarding further research (Trudeau, for testing addictive disorders. Those that 2000, 2005b) have yet to be implemented. may be especially valuable include cue These recommendations are summarized reactivity tests using qEEG and ERP as follows. measures. Cue reactivity is a very sensate First, studies require external, systematic test of motivational relevance of drug- replicability of brain wave feedback methods related items (Carter & Tiffany, 1999) and results in diverse populations that that can be detected using EEG methods. include various control and alternative treat- 3. In addition to using more traditional neu- ment conditions wherein the groups are rocognitive tests (TOVA, IVAþ , etc.) matched on key dimensions. Second, details that are commonly included in neurofeed- need to be given regarding the equipment back research (e.g., in particular in studies that was used and the associated technical on effectiveness of neurotherapy in specifications (e.g., details about amplifi- ADHD treatment), there may be value cation, filtering, spectral extraction, window- in incorporating standardized tests with ing, and other pertinent information) needed EEG=ERP recording to assess executive by neurofeedback specialists for replication functions in addicts. Tests that warrant and comparison. Third, the essential compo- mention are the Continuous Performance nents and durations for brain wave feedback Test (Go–NoGo task), Stroop test, required for therapeutic advantage need Eriksen flanker test, and so on. Some of to be stated, including double-blinded these tests are sufficiently sensitive for studies that control for all other possible assessing recovery of cortical inhibition therapeutic effects. Fourth, open clinical function commonly known to be trials that investigate efficacy of the types of protocols used for ADHD, PTSD, impaired in patients with SUD. depression, and TBI remediation with SUD 4. Testing emotional reactivity and responsive- participants comorbid for those conditions ness in addiction is another important need to be reported. Fifth, open clinical domain where qEEG and ERP methods trials that assess the efficacy of EEG biofeed- may help to obtain more effective evaluation back in addressing the specific qEEG of the affective state of recovering addicts. changes of chronic alcohol, heroin, cannabis, and stimulant abuse need to be reported. In future neurofeedback treatment for Sixth, the physiological and psychological SUD, attempts should be made to integrate processes of the therapeutic effects of EEG neurotherapy with other well-known behav- biofeedback, including studies of qEEG ioral interventions for drug abuse, such as and ERP changes, need to be investigated CBT and MET (Miller & Rollnick, 2002). 32 JOURNAL OF NEUROTHERAPY

As a population, drug addicts are very memory, and overall behavioral perfor- difficult to treat, characterized by a low mance. More research is needed also to relate motivation to change their drug habit and cognitive functionality measures to clinical a reluctance to enter inpatient treatment. outcome (e.g., relapse rate, drug screens, CBT and MET are powerful psychothera- psychiatric status, etc.). Such qEEG=ERP peutic interventions that can help to bring studies may facilitate the translation of about rapid commitment to change addictive clinical neurophysiology research data into behaviors. These behavioral therapies are routine practical tools for assessment of especially useful for enhancing compliance functional recovery both in alcoholism and with drug-dependent individuals and addiction treatment clinics. We believe that facilitating their neurofeedback treatment administration of some of already-described engagement. qEEG assessments at the pretreatment Neurofeedback may be among the most baseline might provide useful predictors promising biofeedback modalities for the of clinical outcome and relapse risk. Incor- treatment of adolescents with addictive poration of cognitive tests with EEG and disorders because of the neuroplasticity ERP (e.g., P300) measures into cognitive- potential of the adolescent brain. Although behavioral and neurofeedback-based inter- there is little work available on the preven- ventions may have significant potential for tion and treatment of SUD in adolescents identifying whether certain qEEG=ERP utilizing neurotherapy, there is no reason measures can be used as psychophysiological to suspect that the approaches used in markers of treatment progress (and=or adults would not be applicable in SUD relapse vulnerability) and may provide useful adolescents (Trudeau, 2005b). EEG biofeed- information in planning cognitive-behavioral back treatment of ADHD may be im- and neurotherapy treatment when substance portant in prevention for children and abuse is comorbid with a mental disorder. adolescents at risk for developing SUD. It With the advances made in the last several may be possible that EEG biofeedback ther- years, we hope that continued interest apy of childhood ADHD may result in a will be generated to further study brain- decrease in later life SUD (Wilens et al., wave biofeedback treatment of addictive 1998). This remains speculative, as there disorders. Effectiveness in certain ‘‘hard-to- have been no reported studies of the effects treat’’ populations (conventional treatment of neurofeedback treatment on prevention resistant alcoholics, crack cocaine addicts, of SUD to date. cognitively impaired substance abusers) is There are several important applications promising. The prospect of an effective of the neurofeedback protocols for enhance- medication free, neurophysiologic, and self- ment of cognitive performance in healthy actualizing treatment for a substance-based, participants (reviewed in Vernon, 2005). This brain-impaired, and self-defeating disorder promising new line of neurofeedback-based such as SUD is attractive. cognitive neuroscience research (Barnea, Rassis, & Zaidel, 2005; Egner & Gruzelier, 2001, 2003, 2004a, 2004b; Egner, Zech, & Gruzelier, 2004; Vernon et al., 2003) has REFERENCES significant potential to elucidate neurobiolo- gical mechanisms explaining how neurofeed- Alper, K. R. (1999). The EEG and cocaine sensitiza- back training may alter and enhance tion. Journal of Neuropsychiatry and Clinical cognition and behavioral performance in Neuroscience, 11, 209–221. patients with SUD as well. Alper, K. R., Chabot, R. J., Kim, A. H., Prichep, L. S, & John, E. R. (1990). Quantitative EEG correlates Drugs of abuse can impair cognitive, of crack cocaine dependence. Psychiatry Research, emotional, and motivational processes. More 35, 95–106. qEEG and cognitive ERP research is needed Alper, K. R., Prichep, L. S., Kowalik, S., Rosenthal, to characterize the chronic and residual M. S, & John, E. R. (1998). Persistent QEEG effects of drugs on attention, emotion, abnormality in crack cocaine users at 6 months Scientific Articles 33

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