Introduction 2000 1989 1990 1991 1998 2002 2005 This “white paper” on EEG biofeedback for SUD will offer an assessment of efficacy according to the guidelines jointly established by the Association for Applied Psychophysiology and Biofeedback (AAPB) and the International Society for Neurofeedback and Research (ISNR). Assessing the efficacy of neurofeedback for SUD involves several considerations. The first of these involves difficulties assessing the efficacy of any treatment method for SUD. Outcome benchmarks (i.e., total abstinence, improved function and quality of life) and time points of outcome (i.e., one year, two years post treatment) are not clearly established. Outcome assessment for treatment of SUD in itself is a complex topic well beyond the scope of this article. Because different drugs of abuse are associated with different patterns of EEG abnormality, as will be discussed in detail in this article, it is difficult to assign broad-brush EEG biofeedback solutions to SUD as a whole. Any statements of efficacy will need to describe specific EEG biofeedback protocols for specific substances of abuse. Furthermore substance abuse is often mixed substance type and comorbid conditions are common and vary from subject to subject, as will also be borne out in this article. As of yet there are no gold standard medication or other treatments for the various types of SUD and efficacy of any SUD treatment method likely falls into the “possibly effective” to “probably effective” range according to the efficacy guidelines jointly established by the AAPB and ISNR. Finally, all of the studies of EEG biofeedback in SUD to date employ EEG biofeedback as an add on to cognitive behavioral or twelve step treatment regimes, so any statements of efficacy would have to acknowledge that EEG biofeedback is not a stand alone treatment for SUD. This article is divided into several sections. In the first section after “Introduction,” we review SUD prevalence and describe qEEG changes typical for the most widespread drugs of abuse (alcohol, marijuana, heroin, cocaine, and methamphetamine). The second section describes treatment studies employing EEG biofeedback in SUD. Studies that have used the Peniston Protocol are described first, along with critical commentaries of these studies. In the second part of this section, a description of the Scott–Kaiser modification is given, along with some discussion of a rationale for why this approach may be more successful with stimulant abusers. This section also describes some current research. The third section assesses efficacy of the Peniston Protocol and the Scott–Kaiser modification. The fourth section takes a look at the clinical implications of comorbidities in neurobiofeedback treatment of alcohol and drug abuse. The fifth section discusses the clinical implications of standard cognitive-behavioral therapies in SUD treatment and reviews the rationale for the application of qEEG-guided neurofeedback intervention in SUD in conjunction with these therapies. The final section summarizes findings in qEEG and neurofeedback in SUD and additionally proposes further directions for clinical research in this area. 2000 2005a b The Journal of Neurotherapy The Journal of Applied Psychophysiology & Biofeedback 2006 2006 SUD Prevalence and qEEG Changes 2001 2003 2004 1999 2003 2004 2005 2006 2004 2006 2004 2003 2003 2004 2005 2000 2001 qEEG in Substance Use Disorders EEG in Alcoholism 1998 1997 2001a 1997 2002 2004 1999 2002 1982 2004 2001a 1998 1992 2002 2004 2006 1999 1985 1988 1993 2003a 2001a b 2002 2002 2004 1993 2002 1999 2002 2004 1996 2002 2005 2003b 2004 2004 2006 1985 1993 2003a b 2006 Therefore, qEEG alterations have been described extensively in alcoholics. Most EEG reports in alcoholic patients agree in describing alterations mainly within the beta and alpha bands. Patients with a more pronounced frontal hyperarousal have worse prognosis. Decreased power in slow bands in alcoholic patients may be an indicator of chronic brain damage, while increase in beta band may be related to various factors suggesting cortical hyperexcitability. Abnormalities in resting EEG are highly heritable traits and are often associated with a predisposition to alcoholism development. The studies on the effects of alcohol dependence on EEG coherence can be summarized as lower frontal alpha and slow-beta coherence in alcohol-dependent patients with some topographical coherence abnormality differences between alcohol-dependent males and females. EEG in Marijuana Abuse 2006 2002 2002 2002 1986 1989 1994 1976 1989 1976 1971 1973 1998 1999 2003 1971 1976 1973 1995 1994 Thus, qEEG studies on acute THC exposure reported a transient dose-dependent increase in relative power of alpha, decrease in alpha frequency, and decrease in relative power of beta at posterior EEG recording sites. Chronic marijuana abuse is known to result in a number of physiological, perceptual and cognitive effects, but persistent qEEG effects from continuing exposure to THC have been difficult to demonstrate. However, recent studies of Struve and his colleagues have demonstrated a significant association between chronic marijuana use and topographic qEEG patterns of persistent elevations of alpha absolute power, relative power, and interhemispheric coherence over frontal cortex, as well as reductions of alpha mean frequency. Another important qEEG finding was the elevated voltage of all non-alpha bands in THC users. A third qEEG finding involved a widespread decrease in the relative power of delta and beta activity over the frontal cortical regions in marijuana users. EEG in Heroin Addiction 1983 2004 2004 1997 1994b 2004 1995 1996 2001a 2004 2001b 2002 1997 2001 2004 1996 1975 1996 1975 2004 2001 1997 2004 2001a 2002 1997 2001 2004 1996 2002 1997 2002 2003 1999 2004 2000 2004 2006a 2006b 1995 2006b 2006b 2006a 2000 2007 2004 2006a b 2001a qEEG changes in heroin addicts in the acute withdrawal period have been described as low-voltage background activity with a diminution of alpha rhythm, an increase in beta activity, and a large amount of low-amplitude delta and theta waves in central regions. In general, pronounced desynchronization is characteristic for acute heroin withdrawal, but the spectral power of EEG tends to normalize almost completely after several weeks of abstinence. The most consistent changes in EEG of heroin addicts were reported in the alpha and beta frequencies, and included a deficit in alpha activity and an excess of fast beta activity in early heroin abstinence. The excess of beta appears to reverse considerably when heroin intake is stopped for several months, and therefore it may be viewed as an acute withdrawal effect. Recent studies found that the number and strength of remote functional connections among different cortical areas estimated by the index of EEG synchrony for the beta range was significantly higher in patients in acute heroin withdrawal than in healthy controls for most categories of functional connections. EEG in Cocaine Addiction 1989 2005 1969 1985 1999 1990 1998 1997 1985 1994 1996 1999 2002 1995 1985 1994b 1991 1990 1994b 1991 1996 1990 1994 1996 1995 1985 1994b 1994 1996a 1996 1995 2006 1990 1996 1995 2006 1999 2002 1999 1990 1998 1996 2002 2006 1997 2001a 1995 Therefore, acute effects of smoked crack cocaine have been shown to produce a rapid increase in absolute theta, alpha, and beta power over the prefrontal cortex, lasting up to half-an-hour after administration of the drug. The increase in theta power was reported to correlate with a positive subjective drug effect, while the increase in alpha power was reported to correlate with nervousness. qEEG measures are also sensitive to the acute and chronic effects of cocaine, as well as the effects from withdrawal and long-term abstinence from cocaine use. Some EEG characteristics observed in cocaine addicts are considered to be due to the neurotoxic effects, whereas some EEG characteristics in cocaine addicts may also indicate a predisposition toward the development of cocaine addiction. qEEG has been used more often to characterize the effects of withdrawal in cocaine-dependent patients. During protracted abstinence from cocaine qEEG effects are featured by long-lasting increases in alpha and beta bands together with reduced activity in delta and theta bands. Several recent studies employing qEEG techniques have demonstrated an association between the amount of beta activity in the spontaneous EEG and relapse in cocaine abuse. EEG in Methamphetamine Addiction 2003 2004 2003 2003 2004 2003 2004 2002 1993 1989 2002 2004 Only a few studies have examined the qEEG consequences of methamphetamine dependence. They report that methamphetamine dependent patients exhibited a significant power increase in the delta and theta bands as compared to non-drug-using control. The qEEG patterns associated with acute withdrawal and recent abstinence in methamphetamine dependence have not yet been sufficiently described. One study reported that abstinent methamphetamine dependent patients had increased EEG power in the delta and theta but not in the alpha and beta bands. In general, qEEG studies of methamphetamine addiction are in accordance with other neurocognitive studies suggesting that methamphetamine abuse is associated with psychomotor slowing and frontal executive deficits. P300 Abnormalities in Cocaine, Methamphetamine, Heroin Addiction, and Alcoholism 1994 2000 1981 1986 2004 1998 2000 1990 1996 1998 2003 1984 1990 2003 2002 2000 2005 1998 1996 2001b 2004 1970 1973 1995 1997 1997 1996 1994a 1996 1990 1994a 1993 1997 1997 1997 2000 1994 1998 In most ERP studies the P300 did not differentiate among patients characterized by histories of either cocaine, or cocaine and alcohol, or heroin dependence. Across all the patient groups, the P300 was significantly reduced in amplitude relative to P300 ERPs recorded from individuals with no history of alcohol or drug dependence. The latency of the frontal and parietal P300 was reported to be delayed, and the amplitude was reduced to novel non-targets in cocaine and alcohol-dependent subjects compared to controls in auditory and visual three-stimuli oddball tasks. Continued abstinence from heroin, cocaine, and alcohol was shown to be associated with a trend toward P300 normalization. Several studies have investigated ERP changes associated with methamphetamine abuse and dependence. In general, chronic psychoactive substance abuse and drug dependence are associated with delayed and attenuated cognitive ERP in auditory and visual oddball tasks. qEEG and ERP Abnormalities in Addiction: Psychopharmacological Effects or Trait Markers? 2001 2002 1994 1994 1998 1999 2001 1997 1994 1994 1999 1999 2003 2002 Heritability and Neurotransmitter Considerations in Substance Use Disorders 2006 2005 2006 2006 2006 1990 1993 1996 1993 1993 2006 1991 1996 2005 2007 2007 1989 Studies of EEG Biofeedback in Substance Abuse Treatment The Peniston Protocol (Alpha-Theta Feedback) 1970 1978 1991 1976 1977 1983 1978 1978 1976 1977 1977 1976 The bulk of the literature to date regarding EEG biofeedback of addictive disorders is focused on alpha-theta biofeedback. The technique involves the simultaneous measurement of occipital alpha (8–13 Hz) and theta (4–8 Hz) and feedback by separate auditory tones for each frequency representing amplitudes greater than pre set thresholds. The subject is encouraged to relax and to increase the amount of time the signal is heard, that is to say, to increase the amount of time that the amplitude of each defined bandwidth exceeds the threshold. A variety of equipment and software has been used to acquire, process, and filter these signals, and there are differences in technique inherent with equipment and software. 1974 1975 1976 1977 1977 1989 n n n 1990 1999 1989 1990 1991 1995 2004 1995 n n 2002 1997 1993 2003 2002 1992 1996 1997 1998 The Journal of Neurotherapy 2000 2005a b 1999 1998 1994 2002 1998 1998 1998 2005 1995 1994 1999 1999 2003 The Scott–Kaiser Modification of the Peniston Protocol 1998 2000 2002 1996 2002 1999 1999 2002 1998 1990 2005 p 2003 2005 Continuing Research Self-Perception and Experimental Schemata in the Addicted Brain 2006 2007 2003 2004 2002 1993 1985  2002 2005 2004 1985 1993 1989 1995 2003a b 2004 2005 1961 1964 1961 1955 1962 1989 To date, studies identifying such schematic source generators and their relationship with SUD using qEEG and standardized low-resolution electromagnetic tomography (sLORETA) are scant. This research is designed to assess the neural activation patterns relative to schemata regarding the self in recovering addicts and identify possible generators in the cortex as compared to controls. In this research, it is hypothesized that there is dendritic pruning early in developmental phases that contribute to frequency specific activity in neuronal populations in the ventromedial portions of the prefrontal cortex and limbic regions. Furthermore, it is proposed that these neural pathways hinder the integration of affect, cognition, reward and decision-making processes and adversely influence the perception of self and self in relation to experience and the development of adaptive schemata and personality characteristics. Integration of Cognitive Neuroscience Approaches in Assessment of Functional Outcomes of Neurofeedback and Behavioral Therapy Based Interventions in SUD 2007a 2005 2006 2006 2004 2005 N 2007b Efficacy of Alpha Theta Training 2002 2002 Criteria for Levels of Evidence of Efficacy Level 1: Not empirically supported Level 2: Possibly efficacious Level 3: Probably efficacious Level 4: Efficacious In a comparison with a no-treatment control group, alternative treatment group, or sham (placebo) control utilizing randomized assignment, the investigational treatment is shown to be statistically significantly superior to the control condition or the investigational treatment is equivalent to a treatment of established efficacy in a study with sufficient power to detect moderate differences; The studies have been conducted with a population treated for a specific problem, from whom inclusion criteria are delineated in a reliable, operationally defined manner; The study used valid and clearly specified outcome measures related to the problem being treated; The data are subjected to appropriate data analysis; The diagnostic and treatment variables and procedures are clearly defined in a manner that permits replication of the study by independent researchers, and 2002 Level 5: Efficacious and Specific 1989 1990 1991 1977 1977 2002 2003 1992 1996 1997 2004 1995 1995 2005 2003 1998 1989 1990 1991 2002 2005 2000 2005a b 1999 1998 1994 Clinical Considerations: Comorbidities of SUD and Implications for Individualized (qEEG-Guided) Neurofeedback 2000 1995 2004 2001 1995 2004 2000 1999 1990 1993 1995 1998 1985 1989 1995 1997 1997 1995 2005 1991 1999 1992 2000 1991 1999 1990 1994 1996 1995 1999 1998 1998 2003 2002 2004 1998 2001 1993 1996 1997 2006 1990 1995 1998 2006 1997 1991 1993 Clinical Considerations: Cognitive-Behavioral and Neurofeedback Treatment in Substance Use Disorders 1997 1999 2004 2002 2006 2003 2004 2001 2003 2001 2003 2004 1985 1997 1995 1997 1999 2005 2005 1997 1997 1998 1998 2005a b 2000 Directions for Further Research  1996 2006 1989 1999 Even though there are no reported systematic studies of EEG biofeedback treatment of commonly occurring comorbidities of SUD, it makes sense that clinical EEG biofeedback treatment study protocols consider the presence of ADHD, TBI, depression, and drug-associated neurotoxicity. This approach may improve outcome, especially in conventional treatment resistant participants. 2000 2005b Studies require external, systematic replicability of brain wave feedback methods and results in diverse populations that include various control and alternative treatment conditions wherein the groups are matched on key dimensions. Details need to be given regarding the equipment that was used and the associated technical specifications (e.g., details about amplification, filtering, spectral extraction, windowing, and other pertinent information) needed by neurofeedback specialists for replication and comparison. The essential components and durations for brain wave feedback required for therapeutic advantage need to be stated, including double-blinded studies that control for all other possible therapeutic effects. Open clinical trials that investigate efficacy of the types of protocols used for ADHD, PTSD, depression, and TBI remediation with SUD subjects comorbid for those conditions need to be reported. Open clinical trials that assess the efficacy of EEG biofeedback in addressing the specific qEEG changes of chronic alcohol, heroin, cannabis and stimulant abuse need to be reported. The physiological and psychological processes of the therapeutic effects of EEG biofeedback, including studies of qEEG and ERP changes, need to be investigated and reported. Studies need to adhere to clearly defined outcome measures that have established reliability and validity. The availability of an increased number of channels for EEG and ERP recording (e.g., higher spatial sampling rate) makes it possible to better localize the source of brain activity. More focused research of this type seems warranted. 1999 In addition to using more traditional neurocognitive tests (TOVA, IVA+, etc.) that are commonly included in neurofeedback research (e.g., in particular in studies on effectiveness of neurotherapy in ADHD treatment) there may be value in incorporating standardized tests with EEG/ERP recording to assess executive functions in addicts. Tests that warrant mention are the Continuous Performance Test (Go-NoGo task), Stroop test, Eriksen flanker test, etc. Some of these tests are sufficiently sensitive for assessing recovery of cortical inhibition function commonly known to be impaired in patients with SUD. Testing emotional reactivity and responsiveness in addiction is another important domain where qEEG and ERP methods may help to obtain more effective evaluation of the affective state of recovering addicts. 2002 2005b 1998 2005 2005 2001 2003 2004a b 2004 2003 Drugs of abuse can impair cognitive, emotional and motivational processes. More qEEG and cognitive ERP research is needed to characterize the chronic and residual effects of drugs on attention, emotion, memory, and overall behavioral performance. More research is needed also to relate cognitive functionality measures to clinical outcome (e.g., relapse rate, drug screens, psychiatric status, etc.). Such qEEG/ERP studies may facilitate the translation of clinical neurophysiology research data into routine practical tools for assessment of functional recovery both in alcoholism and addiction treatment clinics. We believe that administration of some of above described qEEG assessments at the pre-treatment baseline might provide useful predictors of clinical outcome and relapse risk. Incorporation of cognitive tests with EEG and ERP (e.g., P300) measures into cognitive-behavioral and neurofeedback based interventions may have significant potential for identifying whether certain qEEG/ERP measures can be used as psychophysiological markers of treatment progress (and/or relapse vulnerability), and also may provide useful information in planning cognitive-behavioral and neurotherapy treatment when substance abuse is comorbid with a mental disorder. With the advances made in the last several years, it is hoped that continued interest will be generated to further study brainwave biofeedback treatment of addictive disorders. Effectiveness in certain “hard to treat” populations (conventional treatment resistant alcoholics, crack cocaine addicts, cognitively impaired substance abusers) is promising. The prospect of an effective medication free, neurophysiologic, and self-actualizing treatment for a substance based, brain impaired, and self-defeating disorder such as SUD is attractive.