Stress, Trauma and Substance Use

Brian E Bride, Samuel A MacMaster

• Publisher: Routledge
• Year: 2013
• ISBN:
  9781317997641
• Edition: 1
• Topic: Medicina
• Subtopic: Teoría, práctica y referencia médicas

The editors of Stress, Trauma, and Substance Use have gathered a collection of innovative chapters written by cutting edge researchers that depict both the breadth of the relationships between stress, trauma, and substance use, as well as how closely these phenomena are all too often linked.

Individually, the chapters in this volume present innovative conceptual models, original research findings, and recommendations to service providers that are applicable to a diverse body of individuals affected by a wide variety of stressful and/or traumatic experiences, such as HIV/AIDS, incarceration, homelessness, sexual assault, and other forms of trauma and violence in addition to substance use. Taken as a whole, the content of this text provides a window into the true nature of the multi-layered and interconnected relationship between stress, trauma, and substance use. The untangling of these relationships holds great promise for continued research that develops a better understanding of these phenomena and ultimately improves the lives of individuals touched by these experiences.

This book was previously published as a special issue of Stress, Trauma, and Crisis: An International Journal.

1
An Integrated Sensory-linguistic Approach for Drug Addiction: A Synthesis of the Literature and New Directions for Treatment Research

HOLLY C. MATTO
University at Albany, State University of New York, USA

Introduction

This article synthesizes contemporary neuroscience research on stress vulnerability and its effects on information processing, and is presented as the scientific basis for a new approach to drug-addiction treatment for chronic substance-dependent persons. Research shows that deficits in representational integration, resulting from differences in the way information is processed under extreme stress conditions, requires multi-moclal treatment strategies that can accommodate the special learning needs of clients with chronic substance dependency. One new treatment approach, an integrated sensory-linguistic model based on dual representation theory, is introduced. This treatment model encourages clients to take hold of the sensory and emotional elements related to the addiction process through in vivo visual processing experiences that are integrated with cognitive-behavioral techniques, rather than leaving this material vulnerable to implicit activation by environmental triggers. The treatment model's direct linkage to this contemporary body of scientific research is explicated. The paper concludes by outlining important new opportunities for research on stress vulnerability and addiction.

Literature Review

Animal studies have shown that drug-seeking behavior is precipitated by five factors: 1) conditioned stimuli; 2) stress; 3) withdrawal; 4) drug injection; and 5) electrical brain stimulation (Spanagel, 2003, p. 297). Presented is a review of the literature on the factors specific to a stress vulnerability model of chronic drug addiction—conditioned stimuli, neural stress trajectory, and withdrawal.

Conditioned Stimuli

Research studies examining conditioned stimuli and cue reactivity have shown that desire to drink severity and physiological reactivity are strongly associated with relapse rate (Cooney, Litt, Morse, Bauer, & Gaupp, 1997); and drug cravings have been found to be strongly associated with drag cue reactivity from conditioned stimuli (Glautier & Drummond, 1994), suggesting the need for treatment approaches to focus on coping with cravings and managing cue reactivity in order to decrease the risk of relapse. Negative mood states have been found to significantly increase craving for drugs/alcohol (Litt, Cooney, Kadden, & Gaupp, 1990; Quigley & Marlatt, 1999; Robbins, Ehrman, Childress, Cornish, & O'Brien, 2000), which, in turn, increase relapse potential. Along these lines, Cooney et al. (1997) state a need for developing "treatment methods that help [cue] reactors reduce their responsiveness to negative mood states and to stimuli in the environment" (p. 249), indicating the importance of attending to both internal (physiological and psychological) and external (context-dependent) cues for treatment focus. Thus, attention to the specific internal as well as environmental cues that leave an addicted person with marked vulnerability to relapse is a salient component of any treatment program for addicted persons struggling in the early stages of recovery.

Neural Stress Trajectory and Withdrawal

Neuroscientists specializing in drug addiction have found that cravings result from an increasingly hyperaroused neural system that, with progressed substance use, enhances the urge to use and produces strong motivation to initiate drug-seeking behavior (Koob & Le Moal, 1996; Robinson & Berridge, 1993). "A second and potentially independent pathway may induce alcohol craving and relapse by negative motivational states, including conditioned withdrawal and stress. This pathway seems to involve the glutamatergic system and the corticotropin-releasing hormone (CRH)-system. Chronic alcohol intake leads to compensatory changes within these systems. During withdrawal and abstinence, increased glutamatergic excitatory neurotransmission as well as increased CRH release lead to a state of hyperexcitability that becomes manifest as craving, anxiety, seizures, and autonomic dysregulation" (Spanagel, 2003, p. 298).

This stress trajectory initially develops in the hypothalamic-pituitary-adrenal (HPA) axis which, when activated, releases corticotropin-releasing hormone (CRH) and, ultimately, glucocorticoid hormones (Cortisol), leading to heightened vulnerability to drug-seeking behaviors. Recent animal studies have found that drug-seeking behavior can be reduced by blocking CRH levels using a CRH antagonist and by controlling the stress hormone corticosterone (Cortisol in humans; Marinelli & Piazza, 2003), demonstrating that "CRHR1 activation contributes to foot-shock stress-induced reinstatement of alcohol seeking via its action on extrahypothalamic sites" (Spanagel, 2003, p. 305).

Other studies that have examined disruption in this fear-stress system suggest that when glutamate levels are significantly increased in the amygdala, resulting from engagement with drug-related stimuli, the neural circuitry becomes hyperaroused (Quertemont, de Neuville, & De Witte, 1998), indicating that substance-related conditioned stimuli create a biological stress reaction that can motivate behavior to alleviate the negative state. Prolonged substance use that produces chronic stress on the biological system, such as repeated drug use—withdrawal cycles that create patterned and persistent system dysregulation, heightens reactivity to conditioned stimuli and increases the risk of relapse. This neurophysiological dysregulation provides a biological understanding for why stress and concomitant problematic affect are two of the most significant predictors of substance abuse relapse (Brewer, Catalano, Haggerty, Gainey, & Fleming, 1998); with some researchers indicating problematic affect/emotions account for 35% of relapse episodes (Quigley & Marlatt, 1999). The next section on information processing further explains the impact of this neural stress trajectory on learning, memory and behavior for persons with chronic drug addiction.

Information Processing

In addition to the direct impact of stress on biological arousal and craving reactivity, research shows stress related to substance use and withdrawal profoundly disrupts the body's natural ability to modulate subsequent stress response (leading to heightened and persistent excitation), and that this directly influences information (representations originating from interaction with stimuli; Massaro & Cowan, 1993) processing (flow of information through a system; Massaro & Cowan, 1993) which, then, influences learning and memory.

A recent study by Saal, Dong, Bonci, and Malenk (2003) found exposure to stress itself (without concomitant exposure to drugs) induced long-term potentiation (LTP) (synaptic mechanism responsible for associational learning that strengthens future learned response to an activating stimulus; Teyler & DiScenna, 1987), similar to LTP induction caused by addictive drugs alone (i.e., alcohol, nicotine, cocaine, amphetamine, morphine). These results show that the stress trajectory and its conditioning properties mimicked the drug trajectory and its conditioning properties, and suggests that stress alone may create vulnerability to past addiction reminders and may motivate drug seeking behaviors. These researchers suggest that a priming effect (where previously-learned material increases the efficiency in responding to similar information in the future) is evidenced; whereby, stress itself mimics the pathway of previous drug-use experiences and, therefore, contributes to heightened drug-seeking motivation.

Schacter, Chiu, and Ochsner (1993) and Squire, Knowlton, and Musen (1993) work indicates that "perceptual priming" works independent of declarative (conscious processing) memory, and that such stimuli can have a long-term effect on behavior. In addition, the distinct perceptual features of the stimuli (e.g., image, sound, tone, etc.) will influence the reinstatement process between the new stimuli and previous stimuli experience. Taken together, these findings indicate that chronic substance dependent persons who experience extreme stress independent of and/or related to their addiction may have addiction reminders (e.g., conditioned stimuli) stored as learned responses that are not consciously processed (i.e., non-declarative memories) that become vulnerable to activation at this implicit or non-declarative level.

Further, strong emotional arousal that occurs during stress-induced experiences has been shown to strengthen the implicated neural circuitry and, therefore, enhance memory encoding of the stress experience, creating a strong learned response—a phenomenon Daniel Schacter (20Q1) calls "persistence." As such, emotionally intense substance-related experiences (associated with withdrawal, risky drug-seeking behaviors, etc.) are likely to strengthen biologically wired non-declarative memories of these experiences. The brain's natural response to this neural excitation that occurs at the time of a significant stress experience is the release of gamma-aminobutyric acid (GABA), a synaptic inhibitor that dampens the excitatory response in the amygdala. However, conditioned stimuli associated with strong emotional arousal derived from previous learning associations and developed over time (conditioned responses that become automatic) can negate GABAs inhibitory effects and maintain anxiety. Specifically, the stress hormone Cortisol has been found to limit GABA's ability to inhibit glutamate's excitatory response (LeDoux, 2002; Spanagel, 2003), suggesting that increased stress, which increases the release of Cortisol and weakens the inhibiting effect of GABA on glutamate, may exacerbate a state of heightened excitation. This has been shown in drug addiction studies where the neural excitation that occurs during withdrawal has been associated with impaired GABA transmission (Morrow, Montpied, Lingford-Hughes, Paul, 1990; Petrie et al., 2001).

Of particular interest in understanding disruption in information processing and, thus, learning and memory processes associated with drug addiction, are the two central functions of the hippocampus: 1) its contextualizing function; and 2) its capacity for forming explicit or declarative (consciously accessible) memories. Research shows the hippocampus plays a critical role in providing the amygdala (site where fear conditioning occurs and the structure that evaluates stimuli) with information about the context where emotional learning transpires (LeDoux, 2002; Siegel, 1999), projecting the information to the prefrontal region (where reasoning, abstraction and higher levels of cognitive functioning take place), allowing for increased cortical control over amygdalar excitation and the fear response.

The prefrontal region, specifically, functions to coordinate information across sensory modalities, memory, and emotional circuitry in order to translate the experience into temporal and contextual awareness and, therefore, regulates the significance of the stress experience. However, if there is a disconnect in circuitry between and among these structures—the prefrontal region, hippocampus, and amygdala—as studies have found to occur during intense emotional arousal that impairs hippocampal functioning and shuts the frontal lobe off-line, then implicit or non-declarative (out of conscious awareness) storage of arousal experiences may occur.

Therefore, with hippocampal impairment, forming explicit or declarative (consciously accessible) memories will be inhibited (Squire, 1987, 1992; Squire & Zola-Morgan, 1991; Zola-Morgan & Squire, 1993). Studies show that extreme stress experiences dismpt explicit memory processing as an increase in Cortisol decreases the glucose in hippocampal neurons resulting in heightened sensitivity to the excitatory properties of glutamate. Hippocampal cells in the CA3 region may, then, shrink and die off in reaction to low glucose (energy) levels, causing overall hippocampal volume shrinkage, impaired capacity to form explicit memory, and an inability to properly contextualize sensory-based stimuli, leading to implicit (conditioned automatic learned responses) processing of external experience that affect self regulation capacities (LeDoux, 2002).

Hippocampal impairment, as has been found after repeated alcohol withdrawals (Veatch & Gonzales, 1996), and the subsequent implicit processing of extreme stress experiences, coupled with Spanagel (2003) research that shows increased "glutamatergic excitatory neurotransmission" can lead to drug cravings, indicates that sensoiy-based cue triggers may remain out of "explicit" conscious awareness, and reinforces the importance of multimodal processing approaches, suggesting that CBT is a necessary but perhaps not sufficient treatment method for chronic substance-dependent persons.

More specifically, Morris, Ohman, and Dolan (1998) found that the visual-processing centers in the brain were uniquely affected by amygdala excitation during stress conditioning, showing that visual sensory stimuli were more likely to be stored implicitly, rather than explicitly, during the conditioning process when the amygdala is intensely emotionally aroused. This suggests that multi-modal treatment approaches that focus on access to sensory based, implicitly-stored experiences should include a substantial visual-processing component. Because hippocampal structural changes may be slow to evolve over time, resulting from periods of repeated and chronic exposure to extreme stress conditions, chronic "hard-to-treat" substance-dependent persons who experience such extreme stress over long periods of time may be particularly vulnerable to such structural and functio...

Table of contents

• Cover
• Title
• Copyright
• Contents
• Stress, Trauma, and Substance Use: An Overview
• 1 An Integrated Sensory-Linguistic Approach for Drug Addiction: A Synthesis of the Literature and New Directions for Treatment Research
• 2 Young African-American Male Suicide Prevention and Spirituality
• 3 Acculturative Stress, Violence, and Resilience in the Lives of Mexican-American Youth
• 4 The Prevalence of HIV Among Substance-Abusing African-American Women: A Qualitive Investigation
• 5 Factors Associated with Trauma Symptoms among Runaway/Homeless Adolescents
• 6 "I Came to Prison to Do My Time — Not to Get Raped": Coping Within the Institutional Setting
• 7 Integrating Research and Practice: A Collaborative Model for Addressing Trauma and Addiction
• 8 Subthreshold PTSD: A Comparison of Alcohol, Depression, and Health Problems in Canadian Peacekeepers with Different Levels of Traumatic Stress
• Index