What Is Craving? Models and Implications for Treatment - alcohol craving

Alcohol Research & Health, Fall, 1999 by Raymond F. Anton

Even people who have remained abstinent for many months or years, however, can relapse to alcohol abuse. These people often report an intense urge or desire for alcohol as well as thoughts of drinking that can either appear suddenly or increase over a period of time. This craving for alcohol that occurs later in recovery likely is caused by a long-term recollection of "what it was like to drink." Situations in which alcohol previously was experienced as pleasurable or in which alcohol previously served to relieve stress may activate this memory. The conditioning models of craving and relapse attempt to explain these situations in the terms of classical stimulus-response relationships. According to those models, environmental events or changes in internal emotional states trigger a series of neurochemical reactions that through past experience have been programmed to activate various brain systems, thereby leading to the experience of craving.

Many alcoholism treatment approaches attempt to intervene in this conditioning process and thereby prevent relapse resulting from craving elicited during late recovery. For example, cognitive-behavioral therapy strives to provide the patient with cognitive strategies to manage craving or craving-inducing situations. Treatment approaches based on social networks (e.g., Alcoholics Anonymous) attempt to distract the client from craving and enhance his or her resistance mechanisms against the phenomenon (e.g., by encouraging members to call their sponsors if they experience craving). Finally, "anticraving" medications, which prevent the brain from initiating or amplifying the craving-related neuro-chemical processes, are beginning to be used in clinics.

BRAIN NETWORKS ASSOCIATED WITH CRAVING

Advances in neuroscience, particularly in brain-imaging technology, are bringing researchers' understanding of craving to a new level by beginning to link the psychology of craving to certain brain structures. These analyses have led to the development of a neuroanatomical model that attempts to correlate some of the characteristics of AOD craving with specific neural systems (see figure 2 below). Although this model is based on both clinical experience and laboratory data, it should be considered speculative until further confirmation has been obtained. Nevertheless, the model can allow researchers to test concepts and hypotheses and to link subjective experiences such as craving to physical brain structures.

Alcohol (like all other drugs of abuse) activates a brain area called the nucleus accumbens, which is thought to be the brain's reward center. Neurons located in the nucleus accumbens extend to both the amygdala and the frontal cortex areas. The amygdala, which is highly connected to brain regions that control emotions (i.e., the limbic system), plays a role in the modulation of stress and mood. The frontal cortex areas integrate incoming sensory information, such as sights, smells, and sounds. One of those areas is the dorsal lateral prefrontal cortex (DLPC), where the memories for the rewarding aspects of AOD use and their salience may be located (Kalivas et al. 1998). Accordingly, situations that are coupled with alcohol use could be "remembered" with increased salience, because the DLPC is activated both by the sensory information associated with these situations and by the information coming from those parts of the brain that control emotion and reward (i.e., the amygdala and the nucleus accumbens). Bec ause the DLPC also sends information back to the nucleus accumbens, researchers have hypothesized that in recovering alcoholics, sensory information associated with alcohol-paired situations stimulates the DLPC, which, in turn, stimulates the nucleus accumbens and induces greater neural activity in that brain region (Kalivas et. al. 1998).