The relationship between psychological dependence and the time course of a drug's action is Psychological dependence develops quickly when a drug gets to the brain rapidly, such as through IV or inhalation. Physical dependence occurs when the drug leaves the system quicker than the body can adapt.
Full Answer
May 03, 2003 · In addition, for some individuals, there appears to be a reciprocating and complex relationship between anxiety and dependence on other substances. 59-68 Individuals dependent on other nonbenzodiazepine medications, such as analgesics, as well as alcohol, nicotine, and illicit, drugs, are often reported to have concomitant anxiety disorders. The extent to which …
Among those seeking treatment for alcohol dependence, an estimated 20 to 67 percent had experienced depression and 6 to 8 percent had experienced a bipolar disorder at some time in their lives (Brady, Myrick, and Sonne, 1998). In samples of cocaine-dependent individuals, the corresponding estimates have ranged between 30 and 40 percent and ...
Sep 10, 2004 · Abstract. Neuroscientific approaches to drug addiction traditionally have been based on the premise that addiction is a process that results from brain changes that in turn result from chronic administration of drugs of abuse. An alternative approach views drug addiction as a behavioral disorder in which drugs function as preeminent reinforcers.
From a psychological and neurological perspective, addiction is a disorder of altered cognition. The brain regions and processes that underlie addiction overlap extensively with those that are involved in essential cognitive functions, including learning, memory, attention, reasoning, and impulse control. Drugs alter normal brain structure and function in these regions, producing …
A substance-abusing patient who exhibits symptoms of a mood disorder may be suffering from acute intoxication or withdrawal, substance-induced mood disorder, preexisting affective disorder, or a combination of these conditions . The potential for diagnostic uncertainty and confusion is high, but a methodical approach can point clinicians in the right direction.
One reason for the differences in reported prevalence rates is the complexity of diagnostic issues at the interface of mood disorders and SUDs. For example, because abstinence from drugs can temporarily depress mood, a patient who is evaluated while in withdrawal may be misdiagnosed as suffering from a mood disorder. Clinicians may reach different conclusions, depending on when they conduct assessments relative to the patient’s entry into treatment.
In the ECA Study, the lifetime prevalence rate for any non-SUD mental disorder was estimated to be 22.5 percent, compared with 13.5 percent for alcohol abuse/dependence and 6.1 percent for other drug abuse/dependence (Regier et al., 1990). Among individuals with a mood disorder, 32 percent had a co-occurring SUD. Of individuals with lifetime major depression, 16.5 percent had an alcohol use disorder and 18 percent had a drug use disorder. SUDs were particularly common among individuals with bipolar disorder—56 percent had a lifetime SUD.
Chronic/less severe form of bipolar disorder; 2-year duration, with multiple periods of hypomania/depression
Mood disorders, including depression and bipolar disorders, are the most common psychiatric comorbidities among patients with substance use disorders. Treating patients’ co-occurring mood disorders may reduce their substance craving and taking and enhance their overall outcomes. A methodical, staged screening and assessment can ease the diagnostic challenge of distinguishing symptoms of affective disorders from manifestations of substance intoxication and withdrawal. Treatment should maximize the use of psychotherapeutic interventions and give first consideration to medications proven effective in the context of co-occurring substance abuse. Expanded communication and collaboration between substance abuse and mental health providers is crucial to improving outcomes for patients with these complex, difficult co-occurring disorders.
During abstinence pending diagnostic assessment, patients with symptoms indicating possible mood disorders generally need support and supervision. Some require observation in an inpatient setting, either due to symptoms of withdrawal that require treatment in a controlled environment or because of psychiatric symptoms such as suicidality or mania. When patients show severe symptoms of depression, mania, or hypomania, immediate treatment rather than continued waiting may be necessary to relieve suffering and facilitate treatment engagement.
Some portion of the reported high co-occurrence of SUD and mood disorders may represent confounding of mood disorders and transient symptoms related to acute abuse and withdrawal. Drug abuse symptoms can mimic symptoms of both depression and mania. Acute alcohol and stimulant intoxication can produce symptoms of mania or hypomania, and substance withdrawal often manifests as symptoms of dysphoria and depression. Chronic use of central nervous system (CNS) stimulants, such as cocaine and amphetamines, may produce symptoms that are typical of bipolar spectrum disorders, such as euphoria, increased energy, decreased appetite, grandiosity, and paranoia. Conversely, withdrawal from CNS stimulants (especially cocaine) can give rise to anhedonia (inability to feel pleasure), apathy, depressed mood, and suicidal ideation. Chronic use of CNS depressants (e.g., alcohol, benzodiazepines, barbiturates, and opiates) can lead to depressive symptoms such as poor concentration, anhedonia, and problems sleeping, while withdrawal from these drugs can result in anxiety and agitation. The more subtle affective disorders such as dysthymia and cyclothymia are particularly difficult to differentiate from symptoms of SUD.
Neuroscientific approaches to drug addiction traditionally have been based on the premise that addiction is a process that results from brain changes that in turn result from chronic administration of drugs of abuse. An alternative approach views drug addiction as a behavioral disorder in which drugs function as preeminent reinforcers.
Neuroscientific approaches to drug addiction traditionally have been based on the premise that addiction is a process that results from brain changes that in turn result from chronic administration of drugs of abuse. An alternative approach views drug addiction as a behavioral disorder in which drugs function as preeminent reinforcers. Although there is a fundamental discrepancy between these two approaches, the emerging neuroscience of reinforcement and choice behavior eventually may shed light on the brain mechanisms involved in excessive drug use. Behavioral scientists could assist in this understanding by devoting more attention to the assessment of differences in the reinforcing strength of drugs and by attempting to develop and validate behavioral models of addiction.
Neuroscience, because it searches for relationships between brain function and behavior, is in an especially appropriate position to study the neural correlates of the behavior of drug abuse, and neuroscientists have contributed a tremendous amount to our understanding of the effects of drugs of abuse on the brain and nervous system. This article will address some of the neuroscience research on the problem of drug abuse, but will touch only on limited aspects of what is a massive area of scientific inquiry.
The first section on brain reward circuitry is included because this is the neuroanatomical basis for virtually all hypotheses and research on the neuroscience of drug abuse. The next section describes some recent research from a few of the many neuroscientists who have concentrated their efforts on drug addiction.
Sensitization has only the fact that it is produced by repeated administration of a drug, and is maintained for several weeks or months following drug withdrawal, to recommend it as a model of addiction. This drug-induced increase in locomotion lacks even face validity as an indicator of compulsive drug taking or loss of control of drug-taking behavior. Conditioned place preference probably measures a different process from either reinforcement or sensitization (Bardo & Bevins, 2000), but there is no evidence that this is related to addiction. Reinstatement has good face validity, but has not been shown to have predictive validity as a model of relapse (Katz & Higgins, 2003).
It is in the various parts of this reward circuit anatomy and its connection with motor circuitry where neuroscientists look for brain changes that reflect reinforced behavior.
This research group has studied the importance of glutamate, the excitatory neurotransmitter that is released by the neural connections that travel from the prefrontal cortex and amygdala to the nucleus accumbens and ventral tegmental area, in mediating the neuronal plasticity involved in drug addiction.
The relationship between psychological dependence and the time course of a drug's action is Psychological dependence develops quickly when a drug gets to the brain rapidly, such as through IV or inhalation. Physical dependence occurs when the drug leaves the system quicker than the body can adapt. One way to alleviate this is to decrease ...
Physical dependence occurs when the drug leaves the system quicker than the body can adapt. One way to alleviate this is to decrease the dose slowly and over time. Short duration drugs leave the body quicker and are more likely to have physical dependency. THIS SET IS OFTEN IN FOLDERS WITH... Chapter 6: Stimulants.
receptors near GABA...when they bind to their receptor site, they enhance the normally inhibitory effects of GABA on its receptors. This is called a GABA receptor complex.
Anxiety, impaired concentration and memory, insomnia, nightmares, muscle cramps, increased sensitivity to touch and to light, and more. Severe withdrawal symptoms occur after abrupt withdrawal from chronic use of larger doses and may include delirium tremens, delusions, convulsions (may lead to death), and severe depression.
depression of respiration rate, can lead to death
From a psychological and neurological perspective, addiction is a disorder of altered cognition. The brain regions and processes that underlie addiction overlap extensively with those ...
Individuals in the second stage of the addictive process present additional clinical features, including withdrawal symptoms during early abstinence, persistent vulnerability to relapse, and alterations in decisionmaking and other cognitive processes. Although modification of the dopaminergic reward system remains important at this stage, it probably is not sufficient to maintain these complex and long-lasting changes. Kalivas and Volkow (2005)summarize evidence implicating drug-induced alterations in signals carried by the neurotransmitter glutamate from the brain area that is primarily associated with judgment—the prefrontal cortex—to the NAc. Le Moal and Koob (2007)emphasize changes in brain stress circuits and negative reinforcement (i.e., effects that motivate drug taking by causing discomfort during abstinence, such as the onset of withdrawal symptoms). Thus, whereas early drug use fosters maladaptive drug-stimulus associations that contribute to drug seeking and use, later stages disrupt cognitive and other processes that are important for successful abstinence.
The multistage model of addiction attributes addicted individuals’ strong responses to drug cues to a learning process that inculcates powerful drug-stimulus associations (e.g., Robinson and Berridge, 2000). In this view, the individual taking a drug perceives his or her present surroundings as highly significant (salient) and makes exceptionally strong mental connections between features of those surroundings and the intense pleasure of the drug. Subsequently, when he or she re-encounters those features, the powerful associations reassert themselves, consciously or subconsciously, and are experienced as prompts for drug seeking and drug taking. Consistent with this account, exposing addicted individuals to cues that they associate with substance abuse elicits, along with physiological responses and drug cravings, changes in the activity levels of brain regions involved in learning and memory (i.e., striatum, amygdala, orbitofrontal cortex, hippocampus, thalamus, and left insula) (Franklin et al., 2007; Volkow et al., 2006).
The full extent of drugs’ impacts on cognition is not yet known, but research indicates that addicted individuals have alterations in brain regions including the striatum, prefrontal cortex, amygdala, and hippocampus (Jones and Bonci, 2005; Kalivas and Volkow, 2005; Kelley, 2004; Le Moal and Koob, 2007). These same regions underlie declarative memory—the memories that define an individual, without which it would be difficult to generate and maintain a concept of self (Cahill and McGaugh, 1998; Eichenbaum, 2000; Kelley, 2004; Setlow, 1997). Drugs’ capacity to act upon the substrates of declarative memory suggests that their impact on cognition is potentially extremely far-reaching.
Finally, understanding how prenatal exposure to drugs of abuse changes neural development should be a high priority, as prenatal exposure increases the new generation’s susceptibility to addiction and other problems. LEARNING IN THE MIND AND BRAIN.
In a 2005 review, Steven Hyman stated the current neurological conception of drug abuse concisely: Characterizing addiction as a disease of “pathological learning,” he wrote, “[A]ddiction represents a pathological usurpation of the neural mechanisms of learning and memory that under normal circumstances serve to shape survival behaviors related to the pursuit of rewards and the cues that predict them.”
The brain regions and neural processes that underlie addiction overlap extensively with those that support cognitive functions, including learning, memory, and reasoning. Drug activity in these regions and processes during early stages of abuse foster strong maladaptive associations between drug use and environmental stimuli that may underlie future cravings and drug-seeking behaviors. With continued drug use, cognitive deficits ensue that exacerbate the difficulty of establishing sustained abstinence. The developing brain is particularly susceptible to the effects of drugs of abuse; prenatal, childhood, and adolescent exposures produce long-lasting changes in cognition. Patients with mental illness are at high risk for substance abuse, and the adverse impact on cognition may be particularly deleterious in combination with cognitive problems related to their mental disorders.
The biological weakening of decision-making areas in the brain suggests why addicts pursue and consume drugs even in the face of negative consequences or the knowledge of positive outcomes that might come from quitting the drugs.
Addiction comes about through the brain’s normal pathways of pleasure. It is known that addiction changes the circuitry of the brain in ways that make it increasingly difficult for people to regulate the allure of an intense chemical rush of reward. In response to repeated use of a highly pleasurable experience—drugs, ...
Under the unrestrained influence of dopamine, the brain becomes highly efficient in wanting the drug; it focuses attention on anything drug-related and prunes away nerve connections that respond to other inputs.
Neuroscience research supports the idea that addiction is a habit that becomes quickly and deeply entrenched and self-perpetuating, rapidly rewiring the circuitry of the brain because it is aided and abetted by the power of dopamine.
Because substances of abuse act directly on the reward center of the brain to deliver their high—this involves speedy and intense release of the neurotransmitter dopamine—addiction can be seen as a shortcut to reward, one that, over time, can have a high cost to physical and mental health. Nevertheless, the outsize sensation ...
Under the influence of dopamine, that repetition changes the wiring of the brain in ways to increase the drug-wanting and decrease the ability to regulate the drug usage.
The disease model of addiction, which arose in the 1950s to counteract the view of addiction as a moral failing, is based on the observation that addiction involves biological changes in the brain. The brain alterations change the way the brain works—notably in the dopamine system—to create the craving, the progressive inability to exert control, ...
The goal of psychotherapy is (check all that apply) a. the same as biological therapies which is to relieve peoples c. to help people overcome their problems. d. to treat a person's psychological disorder. a. the same as biological therapies which is to relieve peoples suffering.
a. learned and can be unlearned. The goal of cognitive therapies is to change a person's behaviors and feelings by changing their: (check all that apply) a. thoughts. b. cognitions. c. behaviors. d. feelings. a. thoughts. b. cognitions. The goal of a cognitive therapist is to change a client's behavior by.