02 May 2007
28 April 2007
Environmental Enrichment and Hebbian Pathways
Research in environmental enrichment began in 1949 with Dr. Hebb’s investigation with two groups of rats. Rats raised in his “impoverished” laboratory setting performed worse in detour and maze problems than rats raised as pets by his two daughters. While this initial investigation was very crude, it opened the door for more controlled studies in environmental enrichment and impoverishment and its impact on learning and the brain.
By 1964 Bennett et al. securely established that rats reared in an enriched environment are faster learners than their littermates raised in relative isolation. The early “enriched” environments usually were large cages that featured toys, running wheels, and other objects, and they were cohabitated by other rats. The control rats were raised in smaller cages, alone, with no objects. Rosenzweig and Bennett reviewed literature in the area in 1996, again confirming their earlier hypothesis. It was not clear then, or now, what the particular elements of the environment made it enriched, and it was not clear weather the greater physical activity of the rats in the enriched environment contributed to their higher performance in problem solving and learning.
As late as 2000 van Praag et al. in a comprehensive review could not find any isolated variables that contributed to making an environment “enriched” for animals ranging from drosophila, to rats, to humans; though they did confirm that neither observing and enriched environment without being able to participate in it (TV rat) nor social interaction alone could explain the effects of enriched environments. They did discover a confounding variable. The interaction between the environment and neural development goes both ways since neural developments effect the animal’s perception of the environment. It is not simply the environment impressing itself upon the brain. In higher animals, it is certainly possible that factors like motivation play a substantial role in the effect of an enriched environment, and the effects of voluntary physical activity are still unknown. Clearly, isolating the specific factors in an enriched environment would be greatly beneficial to the advancement of research in the area and clear up confusion.
Diamond and Hopson at the University of California (the same university that Bennet et al. made their landmark discoveries) have suggested some factors that create an enriched environment for children in their book, Magic Trees of the Mind (1999), though none of these factors have been experimentally verified. They come simply from clinical experience, surveys, and interviews (mostly anecdotal and poorly controlled).
According to Diamond and Hopson, enriched environments…
∑ Include a steady source of positive emotional support
∑ Provide a nutritious diet with enough protein, vitamins, minerals and calories
∑ Stimulate all the senses (but not all at once)
∑ Have an atmosphere free of undue pressure and stress but suffused with a degree of
pleasurable intensity
∑ Present a series of novel challenges that are neither too easy nor too difficult for the stage of development
∑ Allow for social interaction for a significant percentage of activities
∑ Promote the development of a broad range of skills and interests that are mental, aesthetic, social and emotional
∑ Give the child an opportunity to choose many of his or her own activities
∑ Give the child a change to assess the results of his or her efforts and to modify them
∑ Offer an enjoyable atmosphere that promotes exploration and the fun of learning
∑ Above all, allow the child to be an active participant rather than a passive observer.
These factors echo the observations posed in the review article. Motivation, choosing activities, being active rather than passive, social interaction, and stimulation all seem important. Nutrition is obviously important and will not be discussed further. A point that seems to be overlooked is the assessment of physical effort. Diamond and Hopson do not discus physical activity’s impact on learning.
Empirically verifying the particular factors that contribute to an enriched environment would surely be helpful. It could advise parents on weather or not to purchase Baby Einstein videos for their children, or which particular educational video would be best (though it has already been established that participation is necessary in an enriched environment. TV babies will probably do no better than TV rats). This information would be very valuable to educators, too. Arranging classrooms and curriculums may be enhanced by knowledge of enrichment’s impact on learning. Perhaps simple changes in the classroom could elicit great improvements in learning.
The best way to understand the improved performance of individuals in enhanced environments is to decipher a biological mechanism, rather than simply correlating performance and factors in an enriched environment because correlation will never be able to distinguish the interaction between the environment and neural development.
In 1949 Hebb proposed that learning and memory are based on the strengthening of synapses that occurs when pre- and postsynaptic neurons are simultaneously active. Either the pre synaptic neuron or the postsynaptic neuron (or both) changes in such a way that the activation of one cell becomes more likely to cause the other to fire. Recently, neuroscientists have amassed data showing that Hebb was somewhat correct, and the maxim “cells the fire together, wire together” has become a common colloquial term (Schwartz and Begley, 2002). This can provide the biological framework for understanding enrichment’s impact on the individual.
Dr. Kandel, the 2000 Nobel Prize winner in Physiology or Medicine, earned his share of the medal by investigating the “cells that fire together, wire together” maxim as it relates to learning in the humble Aplysia californica, the sea snail. He found that sensitized neurons had undergone long-lasting change: when excited (by touch), they discharge more neurotransmitter than do neurons that have not undergone sensitization. They also found that after periods of stimulation, certain reflex actions could be enhanced for a period of time. These stimuli modulate secondary messenger molecules like cAMP, which has been found to stimulate the formation of neural connections (Schwartz and Begley, 2002).
Enriched environments should have particular features, which can be directly linked to neural sensitization. In the case of the Aplysia, this was accomplished by simply spraying a jet of water onto its soft body tissues. Obviously different things in an enriched environment will simulate humans, but since both humans and Aplysia share similar neuronal and secondary messenger systems, it is likely that the Hebian conception of neural learning will apply to both. The task is now to demonstrate what environmental elements sensitize human neurons.
Enrichment has been linked to an increase in brain weight and dendritic branching (Pacteau et al., 1989) and improving cortical synaptic plasticity (Wainwright et al., 1993) in rats, both of which are conceptually Hebbian mechanisms. If it could be demonstrated that particular elements in an enriched environment influence these quantifiable physiological measures, then hard, empirical evidence would exist for developing enriched environments for humans.
Physiological measures of neuronal neuronal activity used on rats (which involved destruction of the animal) cannot be carried out on humans. Blood oxygen level-dependent (BOLD) functional magnetic resonance imaging (fMRI) uses alterations in brain hemodynamics to infer changes in neural activity by measuring small changes in deoxyhemoglobin within the brain’s vasculature, allowing non-invasive analysis of single-neuronal activity. The relation between fMRI and physiological measurements (such as Clark-style polographic microelectrodes inserted into the brain) is well substantiated in cats (Thompson et al., 2003), which are more closely related to humans than rats, though BOLD has not been substantiated in primates to date.
An experiment could test this by correlating specific features of the environment (for example, social interaction) to BOLD fMRI measurements and problem solving measures. It is known that the effects of an impoverished environment can be demonstrated rapidly (within a day or two) in humans, and normal humans make a rapid recovery once they are reintroduced to a normal environment (Heron 1957), so these experiments can be conducted rather safely.
An experiment is therefore proposed. A group of human subjects will be placed in environments with defined, controllable elements of enrichment for short periods of time (perhaps a day or two). They will then be compared to a group of human subjects (control 1), which were simply allowed to go about their daily lives normally with BOLD fMRI and pencil and paper problem solving tests. Another group would be placed in an impoverished environment similar to Heron’s 1957 experiment and compared in the same way. By varying the elements of enrichment, particular elements could be isolated to give an accurate picture of what really results in enrichments. Also, pedometers or heart-rate monitors could be placed on the subjects to approximate physical activity to determine if it is a variable.
A plausible hypothesis would be that elements in the enriched environment that causes “arousal,” would provide stimulation for the Hebbian pathway (which can be monitored using BOLD fMRI) and result in better problem solving scores. Schwartz and Begley suggested this “arousal hypothesis” in 2002. A contrary finding would be if no evidence for the Hebbian pathways was found, or if the neuronal activity was highly irregular in different individuals.
References:
Bennett, E. L., Diamond, M. C., Krech, D. and Rosenzweig, M. R. (1964) Chemical and Anatomical Plasticity in the Brain. Science. 146: 610-619
Diamond, M. C. and Hopson, J. L. (1999) Magic Trees of the Mind: How to Nurture Your Child's Intelligence, Creativity, and Healthy Emotions from Birth Through Adolescence. New York. Penguin.
Hebb, D. O. (1949) The Organization of Behavior. New York. Wiley.
Heron, W. (1957, January) Pathology of Boredom. Scientific American. 52-56
Pacteau, C., Einon, D. and Sinden, J. (1989) Early Rearing Environment and Dorsal Hippocampal Ibotenic Acid Lesions: Long-Term Influences on Spatial Learning and Alteration in the Rat. Behavioral Brain Research. 34: 79-96
Rozenzweig, M. R. and Bennett, E. L. (1996) Psychobiology of plasticity: effects of training and experience on brain and behavior. Behavioral Brain Research. 78: 57-65
Schwartz, J. M. and Begley, S. (2002) The Mind and the Brain: Neuroplasticity and the Power of Mental Force. New York. HarperCollins.
Thompson, J. K., Peterson, M. R. and Freeman, R. D. (2003) Single-Neuron Activity and Tissue Oxygenation in the Cerebral Cortex. Science. 299: 1070-1072
Van Praag, H., Kempermann, G. and Gage, F. H. (2000) Neural Consequences of Environmental Enrichment. Nature Reviews Neuroscience. 1:191-198
Wainwright, P. E. et al. (1993) Effects of Environmental Enrichment on Cortical Depth and Morris-maze Performance in B6D2F2 Mice Exposed Prenatally to Ethanol. Neurobehavioral Toxicology and Teratology. 15: 11-20
By 1964 Bennett et al. securely established that rats reared in an enriched environment are faster learners than their littermates raised in relative isolation. The early “enriched” environments usually were large cages that featured toys, running wheels, and other objects, and they were cohabitated by other rats. The control rats were raised in smaller cages, alone, with no objects. Rosenzweig and Bennett reviewed literature in the area in 1996, again confirming their earlier hypothesis. It was not clear then, or now, what the particular elements of the environment made it enriched, and it was not clear weather the greater physical activity of the rats in the enriched environment contributed to their higher performance in problem solving and learning.
As late as 2000 van Praag et al. in a comprehensive review could not find any isolated variables that contributed to making an environment “enriched” for animals ranging from drosophila, to rats, to humans; though they did confirm that neither observing and enriched environment without being able to participate in it (TV rat) nor social interaction alone could explain the effects of enriched environments. They did discover a confounding variable. The interaction between the environment and neural development goes both ways since neural developments effect the animal’s perception of the environment. It is not simply the environment impressing itself upon the brain. In higher animals, it is certainly possible that factors like motivation play a substantial role in the effect of an enriched environment, and the effects of voluntary physical activity are still unknown. Clearly, isolating the specific factors in an enriched environment would be greatly beneficial to the advancement of research in the area and clear up confusion.
Diamond and Hopson at the University of California (the same university that Bennet et al. made their landmark discoveries) have suggested some factors that create an enriched environment for children in their book, Magic Trees of the Mind (1999), though none of these factors have been experimentally verified. They come simply from clinical experience, surveys, and interviews (mostly anecdotal and poorly controlled).
According to Diamond and Hopson, enriched environments…
∑ Include a steady source of positive emotional support
∑ Provide a nutritious diet with enough protein, vitamins, minerals and calories
∑ Stimulate all the senses (but not all at once)
∑ Have an atmosphere free of undue pressure and stress but suffused with a degree of
pleasurable intensity
∑ Present a series of novel challenges that are neither too easy nor too difficult for the stage of development
∑ Allow for social interaction for a significant percentage of activities
∑ Promote the development of a broad range of skills and interests that are mental, aesthetic, social and emotional
∑ Give the child an opportunity to choose many of his or her own activities
∑ Give the child a change to assess the results of his or her efforts and to modify them
∑ Offer an enjoyable atmosphere that promotes exploration and the fun of learning
∑ Above all, allow the child to be an active participant rather than a passive observer.
These factors echo the observations posed in the review article. Motivation, choosing activities, being active rather than passive, social interaction, and stimulation all seem important. Nutrition is obviously important and will not be discussed further. A point that seems to be overlooked is the assessment of physical effort. Diamond and Hopson do not discus physical activity’s impact on learning.
Empirically verifying the particular factors that contribute to an enriched environment would surely be helpful. It could advise parents on weather or not to purchase Baby Einstein videos for their children, or which particular educational video would be best (though it has already been established that participation is necessary in an enriched environment. TV babies will probably do no better than TV rats). This information would be very valuable to educators, too. Arranging classrooms and curriculums may be enhanced by knowledge of enrichment’s impact on learning. Perhaps simple changes in the classroom could elicit great improvements in learning.
The best way to understand the improved performance of individuals in enhanced environments is to decipher a biological mechanism, rather than simply correlating performance and factors in an enriched environment because correlation will never be able to distinguish the interaction between the environment and neural development.
In 1949 Hebb proposed that learning and memory are based on the strengthening of synapses that occurs when pre- and postsynaptic neurons are simultaneously active. Either the pre synaptic neuron or the postsynaptic neuron (or both) changes in such a way that the activation of one cell becomes more likely to cause the other to fire. Recently, neuroscientists have amassed data showing that Hebb was somewhat correct, and the maxim “cells the fire together, wire together” has become a common colloquial term (Schwartz and Begley, 2002). This can provide the biological framework for understanding enrichment’s impact on the individual.
Dr. Kandel, the 2000 Nobel Prize winner in Physiology or Medicine, earned his share of the medal by investigating the “cells that fire together, wire together” maxim as it relates to learning in the humble Aplysia californica, the sea snail. He found that sensitized neurons had undergone long-lasting change: when excited (by touch), they discharge more neurotransmitter than do neurons that have not undergone sensitization. They also found that after periods of stimulation, certain reflex actions could be enhanced for a period of time. These stimuli modulate secondary messenger molecules like cAMP, which has been found to stimulate the formation of neural connections (Schwartz and Begley, 2002).
Enriched environments should have particular features, which can be directly linked to neural sensitization. In the case of the Aplysia, this was accomplished by simply spraying a jet of water onto its soft body tissues. Obviously different things in an enriched environment will simulate humans, but since both humans and Aplysia share similar neuronal and secondary messenger systems, it is likely that the Hebian conception of neural learning will apply to both. The task is now to demonstrate what environmental elements sensitize human neurons.
Enrichment has been linked to an increase in brain weight and dendritic branching (Pacteau et al., 1989) and improving cortical synaptic plasticity (Wainwright et al., 1993) in rats, both of which are conceptually Hebbian mechanisms. If it could be demonstrated that particular elements in an enriched environment influence these quantifiable physiological measures, then hard, empirical evidence would exist for developing enriched environments for humans.
Physiological measures of neuronal neuronal activity used on rats (which involved destruction of the animal) cannot be carried out on humans. Blood oxygen level-dependent (BOLD) functional magnetic resonance imaging (fMRI) uses alterations in brain hemodynamics to infer changes in neural activity by measuring small changes in deoxyhemoglobin within the brain’s vasculature, allowing non-invasive analysis of single-neuronal activity. The relation between fMRI and physiological measurements (such as Clark-style polographic microelectrodes inserted into the brain) is well substantiated in cats (Thompson et al., 2003), which are more closely related to humans than rats, though BOLD has not been substantiated in primates to date.
An experiment could test this by correlating specific features of the environment (for example, social interaction) to BOLD fMRI measurements and problem solving measures. It is known that the effects of an impoverished environment can be demonstrated rapidly (within a day or two) in humans, and normal humans make a rapid recovery once they are reintroduced to a normal environment (Heron 1957), so these experiments can be conducted rather safely.
An experiment is therefore proposed. A group of human subjects will be placed in environments with defined, controllable elements of enrichment for short periods of time (perhaps a day or two). They will then be compared to a group of human subjects (control 1), which were simply allowed to go about their daily lives normally with BOLD fMRI and pencil and paper problem solving tests. Another group would be placed in an impoverished environment similar to Heron’s 1957 experiment and compared in the same way. By varying the elements of enrichment, particular elements could be isolated to give an accurate picture of what really results in enrichments. Also, pedometers or heart-rate monitors could be placed on the subjects to approximate physical activity to determine if it is a variable.
A plausible hypothesis would be that elements in the enriched environment that causes “arousal,” would provide stimulation for the Hebbian pathway (which can be monitored using BOLD fMRI) and result in better problem solving scores. Schwartz and Begley suggested this “arousal hypothesis” in 2002. A contrary finding would be if no evidence for the Hebbian pathways was found, or if the neuronal activity was highly irregular in different individuals.
References:
Bennett, E. L., Diamond, M. C., Krech, D. and Rosenzweig, M. R. (1964) Chemical and Anatomical Plasticity in the Brain. Science. 146: 610-619
Diamond, M. C. and Hopson, J. L. (1999) Magic Trees of the Mind: How to Nurture Your Child's Intelligence, Creativity, and Healthy Emotions from Birth Through Adolescence. New York. Penguin.
Hebb, D. O. (1949) The Organization of Behavior. New York. Wiley.
Heron, W. (1957, January) Pathology of Boredom. Scientific American. 52-56
Pacteau, C., Einon, D. and Sinden, J. (1989) Early Rearing Environment and Dorsal Hippocampal Ibotenic Acid Lesions: Long-Term Influences on Spatial Learning and Alteration in the Rat. Behavioral Brain Research. 34: 79-96
Rozenzweig, M. R. and Bennett, E. L. (1996) Psychobiology of plasticity: effects of training and experience on brain and behavior. Behavioral Brain Research. 78: 57-65
Schwartz, J. M. and Begley, S. (2002) The Mind and the Brain: Neuroplasticity and the Power of Mental Force. New York. HarperCollins.
Thompson, J. K., Peterson, M. R. and Freeman, R. D. (2003) Single-Neuron Activity and Tissue Oxygenation in the Cerebral Cortex. Science. 299: 1070-1072
Van Praag, H., Kempermann, G. and Gage, F. H. (2000) Neural Consequences of Environmental Enrichment. Nature Reviews Neuroscience. 1:191-198
Wainwright, P. E. et al. (1993) Effects of Environmental Enrichment on Cortical Depth and Morris-maze Performance in B6D2F2 Mice Exposed Prenatally to Ethanol. Neurobehavioral Toxicology and Teratology. 15: 11-20
27 April 2007
Baptizing in Beer
"Since as we have learned from your report, it sometimes happens because of the scarcity of water, that infants of your lands are baptized in beer, we reply to you in the tenor of those present that, since according to evangelical doctrine it is necessary "to be reborn from water and the Holy Ghost" (John III:5) they are not to be considered rightly baptized who are baptized in beer."
-Cum sicut ex, Pope Gregory IX to Archbishop Sigurd of Norway, 13c
I find it funny that beer was more available than water in Norway in the 13th century.
-Cum sicut ex, Pope Gregory IX to Archbishop Sigurd of Norway, 13c
I find it funny that beer was more available than water in Norway in the 13th century.
22 April 2007
Post-traumatic Stress Disorder and Substance Abuse
Post-traumatic stress disorder (PTSD) is a major anxiety disorder with a community-based prevalence of 8% of adults in the Unites States. It is common among survivors of rape, military combat and captivity, and ethnically or politically motivated internment and genocide (DSM-IV-TR, p 466).
Though such figures imply no causality, 35% percent of men with PTSD demonstrate substance abuse/dependency compared to 15% of men without PTSD, and 28% of women with PTSD demonstrate substance abuse/dependency compared to 14% without PTSD (Kessler, 1995). There is a certainly a correlation between PTSD and substance abuse that is significant and worth investigating.
There is a significant statistical association between substance-related and other psychiatric disorders in the general, and 16 clinical populations (indicated by odds ratio greater than one) suggest that these disorders may be casually related to one another (Hubbard and Martin, 2001, p. 5; DSM-IV-TR # 309.81). Substance abuse has an odds ratio of approximately three (Hasin and Nunes, 1998, p. 1-30; DSM-IV-TR p. 465).
Two major survey studies indicate that PTSD is frequently co-morbid with substance abuse and dependency. The National Vietnam Veteran Readjustment Study (NVVRS) showed that veterans with PTSD also met the criteria for substance abuse (20%) and dependency (75%), which is considerably higher than the typical population or even the typical Vietnam veteran population (Kulka et al., 1990). Furthermore, the NVVRS showed that veterans exposed to high war zone stress had twice the rate of PTSD (Jordan et al., 1991). The Center for Disease Control also conducted a study that showed 39% of Vietnam veterans with PTSD were also substance abusers/dependent (Heath Status of Vietnam Veterans, 1989).
PTSD is not just “combat fatigue” or “shell-shock.” It is observed in different types of people, all of which have been exposed to trauma, but its manifestations are significantly different in children, who will not be considered further in this discussion. It is found with great frequency among women, usually victims of sexual assault (Breslau et al., 1991). These women also frequently demonstrate co-morbid substance abuse/dependency.
Clearly the relationship between substance abuse/dependency and PTSD is important and impacts a broad community, making it a highly relevant topic for development. Furthermore, because of PTSD’s symptoms, conventional substance abuse/dependency programs my not work as well as they would on a person without PTSD. Therefore treatment strategies are greatly impacted, and the entire approach of treatment is positioned differently. Unlike a typical co-morbid situation, where both problems can be treated independently, co-morbid PTSD and substance/abuse must be approached uniquely.
It is important to realize that there is no drug preference for those who meet PTSD criteria. One investigator hypothesized that a special relationship existed between narcotic use and PTSD since the dominant theory of the relationship between PTSD and substance abuse/dependency is the self-medication hypothesis. In testing his narcotic preference hypothesis, the investigator found that there was no particular drug preference for PTSD substance abusers. In fact there was marked variability, some preferring marijuana, others alcohol and others still preferring narcotics, hallucinogens and other drugs (Robins, 1975). This suggests that the self-medication hypothesis may not be as useful as thought since drugs that would assuage anxiety and other unpleasant PTSD symptoms (narcotics) should be preferred over drugs which wont be as useful.
Indeed, the relationship between PSTD and substance/abuse dependency is unclear. As mentioned earlier, the dominant hypothesis is the self-medication hypothesis. Essentially, this hypothesis states that PTSD is a primary disorder and that drugs are taken to assuage the uncomfortable anxiety-related symptoms of the psychiatric disorder (Khantzian, 1985) (Lehman et al., 1989). Substance abuse among trauma survivors may represent attempts at avoidance of negative memories and affective responses (Follette, 1998). Sometimes this is called “tension-reduction.” A particular investigator emphasized the importance of the euphoria produced by many drugs such as cocaine, opiates, marijuana, and, to a lesser degree, alcohol. Since a distinguishing (and sometimes anguishing) feature of PSTD is flat affect, these drugs may play a role in helping the PTSD afflicted individual restore feeling and fight numbness (Kosten and Krystal, 1988). One investigator said, “PTSD patients with pronounced avoidance/numbing symptoms may rely more on drug abuse to induce sensations that are otherwise blunted” (McFall et al., 1992, p 361). There is clearly some evidence for the self-medication model, and it is the most common understanding among contemporary psychiatrists.
Other investigators demonstrate that drug use prior to the development of PTSD predict drug abuse/dependency following the development of PTSD more readily than the self-medication hypothesis, which stipulates that PTSD must be primary (Helzer, 1984). This realization seriously undermines the self-medication hypothesis. Also, it has been found that to have significant success in treating PTSD and co-morbid substance abuse/dependency; both PTSD and the substance abuse must be individually treated (Volpiceli, 1987). This may seem obvious, but if PTSD is truly a primary disorder, and is successfully treated, the substance abuse/dependency should clear up. Though it is possible that those with PTSD are simply developing an addiction to the drug. This could explain why they continue to abuse despite successful PTSD treatment. The primary/secondary relationship between PTSD and substance abuse/dependency is unclear (Minkoff, 1989), but successful treatment approaches always tackle both problems together.
There are several treatment approaches for those with co-morbid PTSD and substance abuse/dependency. The most successful ones often take a broad approach targeting both PTSD and substance abuse/dependency by utilizing cognitive-behavior therapies, group therapies and self-help programs.
There tends to be a general recommendation against the use of drugs when treating co-morbid PTSD and substance abuse/dependency (Schnitt 1984), though there are several drugs that can be effectively prescribed for treating PTSD. This is because there is addiction potential with many drugs used to treat PTSD, and substance abusing PTSD patients are more likely to abuse a drug than a typical PTSD patient. Preferred drugs for treatment have minimal addiction potential. The most recommend drugs are the SSRIs: fluoxetine and sertraline (Hubbard and Martin, 2001, p26) (Asnis et al., 2004) because of lack of addiction potential (it is actually difficult to keep people on these drugs), good effectiveness and ease of administration (Taylor and Gorman, 1992). Also they are preferred because of lack of toxicity in case of overdose (Hubbard and Martin, 2001, p. 27). Higher does doses of these drugs may be required in alcohol abusing/dependency individuals due to hepatic injury resulting in elevated hepatic enzymes (Mason, 1996).
Neuroleptics like chlorpromazine and olanzepine are also used to treat anxiety associated with PTSD (Hubbard and Martin, 2001, p 28), but less frequently. Chlorpromazine has anxiety-inducing withdrawal symptoms and other negative side effects, and olanzepine has sedative effects, which lends the drug to possible abuse. For opioid dependence: methadone, buprenorphine, and l-alpha-acetylmethodol (LAAM) are used (Hubbary and Martin, 2001, p. 28) and may be helpful in PTSD patients with narcotics dependence. The new MDMA experimental therapy (Mithoefer, 2006) is vigorously not recommended due to addiction potential in PTSD patients with existing substance use problems.
There are drawbacks to drug therapies in general. To begin with, they all approach the PTSD as primary and drug abuse/dependency as secondary, as suggested by the self-medication model while it has been demonstrated that the primary/secondary relationship is unclear. They also completely overlook the entire substance use problem, which is best approached first (Follette, 1998, p. 231). The use of these drugs will also make it difficult for patients to enter 12-step programs like AA and NA, which have been found to be helpful (Hubbard and Martin, 2001, p. 29), because these programs aim for complete sobriety. There is still a dearth of information bearing directly on the functions of alcohol and drug ingestion in relation to PTSD; few studies have attempted to test the self-medication hypothesis directly (Follette et al., 1998, p. 229). It is known however that treating the drug use problem first, followed by PTSD treatments, is more effective than treating PTSD first, followed by drug treatments, or, by simultaneous treatment (Follette et al., 1998, p. 231).
There are alternative theories about the relationship of PTSD and drug abuse/dependency. According to classical conditioning theories of relapse, stimuli that reliably precede administration of alcohol or drugs may come to elicit a variety of possible substance-related conditioned responses (“cravings”). Exposure to these “triggers” and the conditioned emotional and physical response increased the likelihood of substance consumption. Because substance abusing/dependent individuals with PTSD often drink or use drugs in the presence of traumatic reminders, memories, or PTSD symptoms, these trauma-related stimuli may also come to elicit urges to drink or use substances (Rohsenow et al., 1990). Some researchers have investigated this hypothesis in women with some success (Peirce et al., 1996), but it is a fairly unexplored hypothesis that has yielded little in the way of successful treatment strategies.
Another simpler hypothesis is that since anxiety is increased as a symptom of PTSD, that people with normal levels of anxiety sensitivity begin to consume alcohol and other drugs to reduce the anxiety. High anxiety sensitivity has been linked to higher levels of alcohol consumption (Stewart et al., 1995) in people without PTSD, so it is plausible that normal levels of anxiety producing stimuli in an otherwise normal person with PTSD may drive them to substance abuse/dependence. This theory is appealingly simple, and it informs us as to why reducing anxiety-causing fixtures in a PTSD patient’s life can help prevent relapse.
Most recent developments in treatment combine some form of exposure therapy for PTSD with an empirically supported treatment for substance use disorder (Coffey, 2005).
It is vital to begin substance use treatments before the treatment of concurrent PTSD (Follette et al., 1998, p. 231), which seems to undermine the belief that PTSD is a primary diagnoses. Too many problems are encountered during PTSD treatments with substance abusers/dependents unless initial efforts towards sobriety are made. Practitioners have difficulty engaging the patient, drug therapies will probably not be adhered to, and exploration of trauma-related issues may be harmful to the patient who is currently abusing a substance (Reilly, 1994).
A general treatment strategy outlined by Follette et al. (1998, p. 237-243) would include using assessment to direct the treatment process, and assessment should be ongoing. The patient needs to be monitored carefully to detect any trends or events that are creating anxiety or possibly triggering the PTSD symptoms. A therapeutic relationship must be forged between the therapist, the client and any other groups helping the client. People with PTSD often have interpersonal difficulties associated with flat affect and other symptoms of PTSD, so the confrontational style of many self-help groups, particularly those of the 12-step variety, may be problematic. In this case, the therapist should direct the patient into the most appropriate groups, since AA and NA have been found to be helpful (Hubbard and Martin, 2001, p. 29). The next step in the treatment plan is to build motivation and set goals. This may involve different interviewing techniques, and Miller and Rollnick’s method (1991) is recommended by Follette et al (1998). It is based on providing helpful extended discussion of motivation enhancement methods based on five broad principles: (1) express empathy, (2) develop discrepancy (amplify in the client’s mind the discrepancy between current behavior and future goals), (3) avoid argumentation, (4) roll with resistance, and (5) support self-efficacy. Once the interviewing process has been completed, managing exposure to alcohol, drugs, and cues has to be undertaken. This may involve modifying the social environment. Often the spouse can be of great help in this process (Kosten, 1987). Finally implementing relapse prevention methods and training skills for risky situations must be undertaken. A summary of steps for therapy recommendations was published by Follette et al. (1998) on pages 246 and 247.
In conclusion, PTSD co-morbid with substance abuse/dependency is a relevant, but treatable problem. Its etiology and causes are largely unexplained, and the working hypotheses are inadequate, but some effective treatment therapies have emerged empirically. The future holds hope of finding even more effective, specific, treatment approaches, and hopefully a better understanding of the relationship of PTSD and substance abuse/dependency.
References
American Psychiatric Association (2000) Diagnostic and Statistical Manual of Mental
Disorders, Forth Edition, Text Revision. Washington, D.C. American Psychiatric Association.
American Psychiatric Association Task Force on Treatments of Psychiatric Disorders
(1989) A Task Force Report of the American Psychiatric Association. Washington, D.C., American Psychiatric Association.
Asnis GM, Kohn SR, Henderson M, Brown NL. (2004) SSRIs versus Non-SSRIs in Post-
traumatic Stress Disorder: An Update with Recommendations. Drugs. 64(4):383-404
Breslau, N., Davis, G.C., Peterson, E.L., and Schultz, L. (1997) Psychiatric Sequelae of
Posttraumatic Stress Disorder in Women. Archives of General Psychiatry, 54, 81-87
Briere, J. (1992) Child abuse trauma: Theory and Treatment of the Lasting Effects.
Newbury Park, CA. Sage Press.
Coffey, S. F., Schumacher, J. A., Brimo, M. L. and Brady, K. T. (2005) Exposure
Therapy for Substance Abusers with PTSD. Behavior Modification, 29:1, 10-38
Hasin, D. S. and Nunes, E. V. (1998) Comorbidity of Alcohol, Drug, and Psychiatric
Disorders: Epidemiology. Dual Diagnoses in Treatment. New York: Marcel Dekker, Inc.
Health Status of Vietnam Veterans. (1989) Volume IV Psychological and
Neuropsychological Evaluation. US Department of Health and Human Services Public Health Service, Center for Disease Control, Atlanta Georgia, pg 62 in Kofoed, L., Friedman, M. J. and Peck, R. (1993) Alcoholism and Drug Abuse in Patients with PTSD. Psychiatric Quarterly. 64:2 151-171
Helzer, J. E. (1984) The Impact of Combat on Later Alcohol Use by Vietnam Veterans.
Journal of Psychoactive Drugs. 16(2):183-191 in Kofoed, L., Friedman, M. J. and Peck, R. (1993) Alcoholism and Drug Abuse in Patients with PTSD. Psychiatric Quarterly. 64:2 151-171
Hubbard, J. R. and Martin, P, R. (eds.) (2001) Substance Abuse in the Mentally and
Physically Disabled. New York. Marcel Dekker, Inc.
Jordan, B. K., Schlenger, W. E., Hough, R. et al. (1991) Lifetime and Current Prevalence
of Specific Psychiatric Disorders Among Vietnam Veterans and Controls. Archives of General Psychiatry 48:207-215 in Kofoed, L., Friedman, M. J. and Peck, R. (1993) Alcoholism and Drug Abuse in Patients with PTSD. Psychiatric Quarterly. 64:2 151-171
Follette, V. M., Ruzek, J. I. and Abueg, R. F. (1998) Cognitive-behavioral therapies for
trauma. New York. Guilford Press.
Kessler, R. C., Sonnega, A., Bromet, E., Hughes, M. and Nelson, C. B. (1995)
Posttraumatic Stress Disorder in the National Comorbidity Survey. Archives of General Psychiatry, 52, 1048-1060
Khantzian, E. J. (1985) The Self-Medication Hypothesis of Addictive Disorders: Focus
on Heroin and Cocaine Dependence. The American Journal of Psychiatry 142:1259-1264
Kosten, T. R. and Krystal, J (1988) Biological Mechanisms in Post Traumatic Stress
Disorder Relevance for Substance Abuse. Recent Developments in Alcoholism 6:49-68
Kulka, R. A., Schlenger, W.E., Fairbank, J. A. et al. (1990) Trauma and the Vietnam War
Generation. New York. Bruner-Mazel 117-126 in Kofoed, L., Friedman, M. J. and Peck, R. (1993) Alcoholism and Drug Abuse in Patients with PTSD. Psychiatric Quarterly. 64:2 151-171
Lehman, A.F., Myers, P. and Corty, E. (1989) Assessment and Classification of Patients
with Psychiatric and Substance Abuse Syndromes. Hospital and Community Psychiatry 40:1019-1025
Mason, B. J. (1996) Dosing Issues in the Pharmacotherapy of Alcoholism. Alcohol
Clinical Experience Research 20:10A-16A
McFall, M. E., Mackay, P. W. and Donovan, D. M. (1992) Combat-related Posttraumatic
Stress Disorder and Severity of substance abuse in Vietnam Veterans. Journal of Studies on Alcohol 53, 357-363
Miller, W. R. and Rollnick, S. (1991) Motivational Interviewing: Preparing People to
Change Addictive Behavior. New York. Guilford Press.
Minkoff, K. (1989) An Integrated Treatment Model for Dual Diagnoses of Psychosis and
Addiction. Hospital and Community Psychiatry 40:1031-1036.
Mithoefer, M. C. (2006) Phase II clinical trial testing the safety and efficacy of
3,4methylenedioxymethamphetamine (MDMA)-assisted psychotherapy in subjects with chronic posttraumatic stress disorder. FDA Study # 63-384. Multidisciplinary Association for Psychedelic Studies. Accessed 17 April 2007 http://www.maps.org/mdma/protocol/index.html
Peirce, J. M., Brown, J. M., Long, P. J. Nixon, S. J., Borrell, G. K. and Holloway, F. A.
(1996) Comorbidity and Subjective reactivity to meaningful cues in Female Methadone Maintenance Patients. Paper presented at annual meeting of the Association for Advancement of Behavior Therapy, New York. (Reported in Follette et al., 1998.)
Reilly, P. M., Clark, H. W., Shopshire, M. S., Lewis, E. W. and Sorensen, D. J. (1994)
Anger Management and Temper Control: Critical Components of Posttraumatic Stress Disorder and Substance Abuse Treatment. Journal of Psychoactive Drugs 26, 401-407
Robins, L. N., Helzer, J. E., Davis, D. H. (1975) Narcotics Use in Southeast Asia and
Afterwards. Archives of General Psychiatry 32:955-961 in Kofoed, L., Friedman, M. J. and Peck, R. (1993) Alcoholism and Drug Abuse in Patients with PTSD. Psychiatric Quarterly. 64:2 151-171
Roshenow, D. J., Childress, A. R., Monti, P. M., Niaura, R. S. and Abrams, D. B. (1990)
Cue Reactivity in Addictive behaviors: Theoretical and Treatment Implications. International Journal of Addictions, 25, 957-993 (in Follette et al., 1998, p 229)
Schnitt J. M. and Nocks, J. J. (1984) Alcoholism Treatment of Vietnam Veterans with
Post Traumatic Stress Disorder. Journal of Substance Abuse Treatment. 1:179-189
Stewart, S. H. and Zeitlin, S. B. (1995) Anxiety Sensitivity and Alcohol Use Motives.
Journal of Anxiety Disorders, 9, 229-240
Taylor, L. and Gorman, J. (1992) Theoretical and Therapeutic Considerations for the
Anxiety Disorders. Psychiatric Quarterly. 63:319-342
Volpicelli, J. R. (1987) Uncontrollable Events and Alcohol Drinking. British Journal of
Addiction. 82:381-392
Though such figures imply no causality, 35% percent of men with PTSD demonstrate substance abuse/dependency compared to 15% of men without PTSD, and 28% of women with PTSD demonstrate substance abuse/dependency compared to 14% without PTSD (Kessler, 1995). There is a certainly a correlation between PTSD and substance abuse that is significant and worth investigating.
There is a significant statistical association between substance-related and other psychiatric disorders in the general, and 16 clinical populations (indicated by odds ratio greater than one) suggest that these disorders may be casually related to one another (Hubbard and Martin, 2001, p. 5; DSM-IV-TR # 309.81). Substance abuse has an odds ratio of approximately three (Hasin and Nunes, 1998, p. 1-30; DSM-IV-TR p. 465).
Two major survey studies indicate that PTSD is frequently co-morbid with substance abuse and dependency. The National Vietnam Veteran Readjustment Study (NVVRS) showed that veterans with PTSD also met the criteria for substance abuse (20%) and dependency (75%), which is considerably higher than the typical population or even the typical Vietnam veteran population (Kulka et al., 1990). Furthermore, the NVVRS showed that veterans exposed to high war zone stress had twice the rate of PTSD (Jordan et al., 1991). The Center for Disease Control also conducted a study that showed 39% of Vietnam veterans with PTSD were also substance abusers/dependent (Heath Status of Vietnam Veterans, 1989).
PTSD is not just “combat fatigue” or “shell-shock.” It is observed in different types of people, all of which have been exposed to trauma, but its manifestations are significantly different in children, who will not be considered further in this discussion. It is found with great frequency among women, usually victims of sexual assault (Breslau et al., 1991). These women also frequently demonstrate co-morbid substance abuse/dependency.
Clearly the relationship between substance abuse/dependency and PTSD is important and impacts a broad community, making it a highly relevant topic for development. Furthermore, because of PTSD’s symptoms, conventional substance abuse/dependency programs my not work as well as they would on a person without PTSD. Therefore treatment strategies are greatly impacted, and the entire approach of treatment is positioned differently. Unlike a typical co-morbid situation, where both problems can be treated independently, co-morbid PTSD and substance/abuse must be approached uniquely.
It is important to realize that there is no drug preference for those who meet PTSD criteria. One investigator hypothesized that a special relationship existed between narcotic use and PTSD since the dominant theory of the relationship between PTSD and substance abuse/dependency is the self-medication hypothesis. In testing his narcotic preference hypothesis, the investigator found that there was no particular drug preference for PTSD substance abusers. In fact there was marked variability, some preferring marijuana, others alcohol and others still preferring narcotics, hallucinogens and other drugs (Robins, 1975). This suggests that the self-medication hypothesis may not be as useful as thought since drugs that would assuage anxiety and other unpleasant PTSD symptoms (narcotics) should be preferred over drugs which wont be as useful.
Indeed, the relationship between PSTD and substance/abuse dependency is unclear. As mentioned earlier, the dominant hypothesis is the self-medication hypothesis. Essentially, this hypothesis states that PTSD is a primary disorder and that drugs are taken to assuage the uncomfortable anxiety-related symptoms of the psychiatric disorder (Khantzian, 1985) (Lehman et al., 1989). Substance abuse among trauma survivors may represent attempts at avoidance of negative memories and affective responses (Follette, 1998). Sometimes this is called “tension-reduction.” A particular investigator emphasized the importance of the euphoria produced by many drugs such as cocaine, opiates, marijuana, and, to a lesser degree, alcohol. Since a distinguishing (and sometimes anguishing) feature of PSTD is flat affect, these drugs may play a role in helping the PTSD afflicted individual restore feeling and fight numbness (Kosten and Krystal, 1988). One investigator said, “PTSD patients with pronounced avoidance/numbing symptoms may rely more on drug abuse to induce sensations that are otherwise blunted” (McFall et al., 1992, p 361). There is clearly some evidence for the self-medication model, and it is the most common understanding among contemporary psychiatrists.
Other investigators demonstrate that drug use prior to the development of PTSD predict drug abuse/dependency following the development of PTSD more readily than the self-medication hypothesis, which stipulates that PTSD must be primary (Helzer, 1984). This realization seriously undermines the self-medication hypothesis. Also, it has been found that to have significant success in treating PTSD and co-morbid substance abuse/dependency; both PTSD and the substance abuse must be individually treated (Volpiceli, 1987). This may seem obvious, but if PTSD is truly a primary disorder, and is successfully treated, the substance abuse/dependency should clear up. Though it is possible that those with PTSD are simply developing an addiction to the drug. This could explain why they continue to abuse despite successful PTSD treatment. The primary/secondary relationship between PTSD and substance abuse/dependency is unclear (Minkoff, 1989), but successful treatment approaches always tackle both problems together.
There are several treatment approaches for those with co-morbid PTSD and substance abuse/dependency. The most successful ones often take a broad approach targeting both PTSD and substance abuse/dependency by utilizing cognitive-behavior therapies, group therapies and self-help programs.
There tends to be a general recommendation against the use of drugs when treating co-morbid PTSD and substance abuse/dependency (Schnitt 1984), though there are several drugs that can be effectively prescribed for treating PTSD. This is because there is addiction potential with many drugs used to treat PTSD, and substance abusing PTSD patients are more likely to abuse a drug than a typical PTSD patient. Preferred drugs for treatment have minimal addiction potential. The most recommend drugs are the SSRIs: fluoxetine and sertraline (Hubbard and Martin, 2001, p26) (Asnis et al., 2004) because of lack of addiction potential (it is actually difficult to keep people on these drugs), good effectiveness and ease of administration (Taylor and Gorman, 1992). Also they are preferred because of lack of toxicity in case of overdose (Hubbard and Martin, 2001, p. 27). Higher does doses of these drugs may be required in alcohol abusing/dependency individuals due to hepatic injury resulting in elevated hepatic enzymes (Mason, 1996).
Neuroleptics like chlorpromazine and olanzepine are also used to treat anxiety associated with PTSD (Hubbard and Martin, 2001, p 28), but less frequently. Chlorpromazine has anxiety-inducing withdrawal symptoms and other negative side effects, and olanzepine has sedative effects, which lends the drug to possible abuse. For opioid dependence: methadone, buprenorphine, and l-alpha-acetylmethodol (LAAM) are used (Hubbary and Martin, 2001, p. 28) and may be helpful in PTSD patients with narcotics dependence. The new MDMA experimental therapy (Mithoefer, 2006) is vigorously not recommended due to addiction potential in PTSD patients with existing substance use problems.
There are drawbacks to drug therapies in general. To begin with, they all approach the PTSD as primary and drug abuse/dependency as secondary, as suggested by the self-medication model while it has been demonstrated that the primary/secondary relationship is unclear. They also completely overlook the entire substance use problem, which is best approached first (Follette, 1998, p. 231). The use of these drugs will also make it difficult for patients to enter 12-step programs like AA and NA, which have been found to be helpful (Hubbard and Martin, 2001, p. 29), because these programs aim for complete sobriety. There is still a dearth of information bearing directly on the functions of alcohol and drug ingestion in relation to PTSD; few studies have attempted to test the self-medication hypothesis directly (Follette et al., 1998, p. 229). It is known however that treating the drug use problem first, followed by PTSD treatments, is more effective than treating PTSD first, followed by drug treatments, or, by simultaneous treatment (Follette et al., 1998, p. 231).
There are alternative theories about the relationship of PTSD and drug abuse/dependency. According to classical conditioning theories of relapse, stimuli that reliably precede administration of alcohol or drugs may come to elicit a variety of possible substance-related conditioned responses (“cravings”). Exposure to these “triggers” and the conditioned emotional and physical response increased the likelihood of substance consumption. Because substance abusing/dependent individuals with PTSD often drink or use drugs in the presence of traumatic reminders, memories, or PTSD symptoms, these trauma-related stimuli may also come to elicit urges to drink or use substances (Rohsenow et al., 1990). Some researchers have investigated this hypothesis in women with some success (Peirce et al., 1996), but it is a fairly unexplored hypothesis that has yielded little in the way of successful treatment strategies.
Another simpler hypothesis is that since anxiety is increased as a symptom of PTSD, that people with normal levels of anxiety sensitivity begin to consume alcohol and other drugs to reduce the anxiety. High anxiety sensitivity has been linked to higher levels of alcohol consumption (Stewart et al., 1995) in people without PTSD, so it is plausible that normal levels of anxiety producing stimuli in an otherwise normal person with PTSD may drive them to substance abuse/dependence. This theory is appealingly simple, and it informs us as to why reducing anxiety-causing fixtures in a PTSD patient’s life can help prevent relapse.
Most recent developments in treatment combine some form of exposure therapy for PTSD with an empirically supported treatment for substance use disorder (Coffey, 2005).
It is vital to begin substance use treatments before the treatment of concurrent PTSD (Follette et al., 1998, p. 231), which seems to undermine the belief that PTSD is a primary diagnoses. Too many problems are encountered during PTSD treatments with substance abusers/dependents unless initial efforts towards sobriety are made. Practitioners have difficulty engaging the patient, drug therapies will probably not be adhered to, and exploration of trauma-related issues may be harmful to the patient who is currently abusing a substance (Reilly, 1994).
A general treatment strategy outlined by Follette et al. (1998, p. 237-243) would include using assessment to direct the treatment process, and assessment should be ongoing. The patient needs to be monitored carefully to detect any trends or events that are creating anxiety or possibly triggering the PTSD symptoms. A therapeutic relationship must be forged between the therapist, the client and any other groups helping the client. People with PTSD often have interpersonal difficulties associated with flat affect and other symptoms of PTSD, so the confrontational style of many self-help groups, particularly those of the 12-step variety, may be problematic. In this case, the therapist should direct the patient into the most appropriate groups, since AA and NA have been found to be helpful (Hubbard and Martin, 2001, p. 29). The next step in the treatment plan is to build motivation and set goals. This may involve different interviewing techniques, and Miller and Rollnick’s method (1991) is recommended by Follette et al (1998). It is based on providing helpful extended discussion of motivation enhancement methods based on five broad principles: (1) express empathy, (2) develop discrepancy (amplify in the client’s mind the discrepancy between current behavior and future goals), (3) avoid argumentation, (4) roll with resistance, and (5) support self-efficacy. Once the interviewing process has been completed, managing exposure to alcohol, drugs, and cues has to be undertaken. This may involve modifying the social environment. Often the spouse can be of great help in this process (Kosten, 1987). Finally implementing relapse prevention methods and training skills for risky situations must be undertaken. A summary of steps for therapy recommendations was published by Follette et al. (1998) on pages 246 and 247.
In conclusion, PTSD co-morbid with substance abuse/dependency is a relevant, but treatable problem. Its etiology and causes are largely unexplained, and the working hypotheses are inadequate, but some effective treatment therapies have emerged empirically. The future holds hope of finding even more effective, specific, treatment approaches, and hopefully a better understanding of the relationship of PTSD and substance abuse/dependency.
References
American Psychiatric Association (2000) Diagnostic and Statistical Manual of Mental
Disorders, Forth Edition, Text Revision. Washington, D.C. American Psychiatric Association.
American Psychiatric Association Task Force on Treatments of Psychiatric Disorders
(1989) A Task Force Report of the American Psychiatric Association. Washington, D.C., American Psychiatric Association.
Asnis GM, Kohn SR, Henderson M, Brown NL. (2004) SSRIs versus Non-SSRIs in Post-
traumatic Stress Disorder: An Update with Recommendations. Drugs. 64(4):383-404
Breslau, N., Davis, G.C., Peterson, E.L., and Schultz, L. (1997) Psychiatric Sequelae of
Posttraumatic Stress Disorder in Women. Archives of General Psychiatry, 54, 81-87
Briere, J. (1992) Child abuse trauma: Theory and Treatment of the Lasting Effects.
Newbury Park, CA. Sage Press.
Coffey, S. F., Schumacher, J. A., Brimo, M. L. and Brady, K. T. (2005) Exposure
Therapy for Substance Abusers with PTSD. Behavior Modification, 29:1, 10-38
Hasin, D. S. and Nunes, E. V. (1998) Comorbidity of Alcohol, Drug, and Psychiatric
Disorders: Epidemiology. Dual Diagnoses in Treatment. New York: Marcel Dekker, Inc.
Health Status of Vietnam Veterans. (1989) Volume IV Psychological and
Neuropsychological Evaluation. US Department of Health and Human Services Public Health Service, Center for Disease Control, Atlanta Georgia, pg 62 in Kofoed, L., Friedman, M. J. and Peck, R. (1993) Alcoholism and Drug Abuse in Patients with PTSD. Psychiatric Quarterly. 64:2 151-171
Helzer, J. E. (1984) The Impact of Combat on Later Alcohol Use by Vietnam Veterans.
Journal of Psychoactive Drugs. 16(2):183-191 in Kofoed, L., Friedman, M. J. and Peck, R. (1993) Alcoholism and Drug Abuse in Patients with PTSD. Psychiatric Quarterly. 64:2 151-171
Hubbard, J. R. and Martin, P, R. (eds.) (2001) Substance Abuse in the Mentally and
Physically Disabled. New York. Marcel Dekker, Inc.
Jordan, B. K., Schlenger, W. E., Hough, R. et al. (1991) Lifetime and Current Prevalence
of Specific Psychiatric Disorders Among Vietnam Veterans and Controls. Archives of General Psychiatry 48:207-215 in Kofoed, L., Friedman, M. J. and Peck, R. (1993) Alcoholism and Drug Abuse in Patients with PTSD. Psychiatric Quarterly. 64:2 151-171
Follette, V. M., Ruzek, J. I. and Abueg, R. F. (1998) Cognitive-behavioral therapies for
trauma. New York. Guilford Press.
Kessler, R. C., Sonnega, A., Bromet, E., Hughes, M. and Nelson, C. B. (1995)
Posttraumatic Stress Disorder in the National Comorbidity Survey. Archives of General Psychiatry, 52, 1048-1060
Khantzian, E. J. (1985) The Self-Medication Hypothesis of Addictive Disorders: Focus
on Heroin and Cocaine Dependence. The American Journal of Psychiatry 142:1259-1264
Kosten, T. R. and Krystal, J (1988) Biological Mechanisms in Post Traumatic Stress
Disorder Relevance for Substance Abuse. Recent Developments in Alcoholism 6:49-68
Kulka, R. A., Schlenger, W.E., Fairbank, J. A. et al. (1990) Trauma and the Vietnam War
Generation. New York. Bruner-Mazel 117-126 in Kofoed, L., Friedman, M. J. and Peck, R. (1993) Alcoholism and Drug Abuse in Patients with PTSD. Psychiatric Quarterly. 64:2 151-171
Lehman, A.F., Myers, P. and Corty, E. (1989) Assessment and Classification of Patients
with Psychiatric and Substance Abuse Syndromes. Hospital and Community Psychiatry 40:1019-1025
Mason, B. J. (1996) Dosing Issues in the Pharmacotherapy of Alcoholism. Alcohol
Clinical Experience Research 20:10A-16A
McFall, M. E., Mackay, P. W. and Donovan, D. M. (1992) Combat-related Posttraumatic
Stress Disorder and Severity of substance abuse in Vietnam Veterans. Journal of Studies on Alcohol 53, 357-363
Miller, W. R. and Rollnick, S. (1991) Motivational Interviewing: Preparing People to
Change Addictive Behavior. New York. Guilford Press.
Minkoff, K. (1989) An Integrated Treatment Model for Dual Diagnoses of Psychosis and
Addiction. Hospital and Community Psychiatry 40:1031-1036.
Mithoefer, M. C. (2006) Phase II clinical trial testing the safety and efficacy of
3,4methylenedioxymethamphetamine (MDMA)-assisted psychotherapy in subjects with chronic posttraumatic stress disorder. FDA Study # 63-384. Multidisciplinary Association for Psychedelic Studies. Accessed 17 April 2007 http://www.maps.org/mdma/protocol/index.html
Peirce, J. M., Brown, J. M., Long, P. J. Nixon, S. J., Borrell, G. K. and Holloway, F. A.
(1996) Comorbidity and Subjective reactivity to meaningful cues in Female Methadone Maintenance Patients. Paper presented at annual meeting of the Association for Advancement of Behavior Therapy, New York. (Reported in Follette et al., 1998.)
Reilly, P. M., Clark, H. W., Shopshire, M. S., Lewis, E. W. and Sorensen, D. J. (1994)
Anger Management and Temper Control: Critical Components of Posttraumatic Stress Disorder and Substance Abuse Treatment. Journal of Psychoactive Drugs 26, 401-407
Robins, L. N., Helzer, J. E., Davis, D. H. (1975) Narcotics Use in Southeast Asia and
Afterwards. Archives of General Psychiatry 32:955-961 in Kofoed, L., Friedman, M. J. and Peck, R. (1993) Alcoholism and Drug Abuse in Patients with PTSD. Psychiatric Quarterly. 64:2 151-171
Roshenow, D. J., Childress, A. R., Monti, P. M., Niaura, R. S. and Abrams, D. B. (1990)
Cue Reactivity in Addictive behaviors: Theoretical and Treatment Implications. International Journal of Addictions, 25, 957-993 (in Follette et al., 1998, p 229)
Schnitt J. M. and Nocks, J. J. (1984) Alcoholism Treatment of Vietnam Veterans with
Post Traumatic Stress Disorder. Journal of Substance Abuse Treatment. 1:179-189
Stewart, S. H. and Zeitlin, S. B. (1995) Anxiety Sensitivity and Alcohol Use Motives.
Journal of Anxiety Disorders, 9, 229-240
Taylor, L. and Gorman, J. (1992) Theoretical and Therapeutic Considerations for the
Anxiety Disorders. Psychiatric Quarterly. 63:319-342
Volpicelli, J. R. (1987) Uncontrollable Events and Alcohol Drinking. British Journal of
Addiction. 82:381-392
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