Cocaine

In Meyler's Side Effects of Drugs (Sixteenth Edition), 2016

Paranoid psychoses

Of 55 individuals with cocaine dependence, 53% reported transient cocaine-induced psychotic symptoms [212]. Paranoid delusions (related to drug use) and auditory hallucinations were often reported. In addition, almost one-third (all of whom also described psychotic symptoms) reported transient behavioral stereotypes.

Paranoid psychosis has also been described in a 64-year-old man who had first begun to use crack cocaine 6 months before. The paranoid symptoms continued for 3 weeks after he stopped using crack. The author suggested that the man's age may have made him particularly sensitive to the psychiatric effects of cocaine [213].

The possible genetic basis of cocaine-induced paranoia has been studied in 45 European Americans with cocaine dependency [214]. Low activity of the enzyme dopamine β-hydroxylase (the enzyme that catalyses the conversion of dopamine to noradrenaline) in the serum or cerebrospinal fluid was positively associated with the occurrence of positive psychotic symptoms in several psychiatric disorders. The activity of dopamine β-hydroxylase is a stable, genetically determined trait that is regulated by genes located at the DBH locus. The haplotype associated with low dopamine β-hydroxylase activity, Del-a, occurred more often in 29 subjects with cocaine-induced paranoia than in 16 without. These findings may have implications for the pharmacological treatment of cocaine dependence.

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Hallucinations, Neural Basis of

R.E. Hoffman , in International Encyclopedia of the Social & Behavioral Sciences, 2001

Tactile or haptic hallucinations: These experiences commonly occur during the delirium tremens stage of severe alcohol withdrawal and consist of formication , i.e., the sensation of insects crawling on the body. Amphetamine or cocaine-induced psychosis can also lead to formication experiences. Phantom limb hallucinations follow arm or leg amputation and consist of the persistent sensation of the lost limb that can include the experience of movement and/or pain. Sensation of altered or duplicated body shapes can

occur in epilepsy, toxic encephalopathy, or with hallucinogenic drugs. When such hallucinations are accompanied by delusions that are fantastic, they are likely to be related to a schizophrenic process (Benson and Gorman 1993).

Hallucinations of bodily sense and movement have also been reported following direct electrical stimulation of the temporal lobe in humans (Ishibashi et al. 1964).

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Brain Stimulation

Jodie Naim-Feil , Abraham Zangen , in Handbook of Clinical Neurology, 2013

Cocaine and cortical excitability

Several studies applied TMS paradigms to index the neurophysiological effects of repeated cocaine administration on cortical excitability. In a preliminary study, Boutros et al. (2001) administered single pulses of TMS over the right and left motor cortex of 10 cocaine-dependent participants (3 weeks postabstinence) and 10 healthy controls. Compared with healthy controls, RMT was significantly increased, bilaterally, in the cocaine-dependent subjects. The authors propose that attenuated cortical excitability may reflect a "compensatory" neuroadaptive response to the effects of repeated cocaine administration, which typically enhances cortical excitability and seizure proneness. It is also possible that continued cocaine use induces cortical damage, which may result in reduced levels of cortical excitability. In a replication study, Boutros et al. (2005) assessed cortical excitability in 19 cocaine-dependent subjects (3 weeks postabstinence) relative to that in 12 healthy controls. Single-pulse TMS was delivered over the motor cortex, and RMT, AMT, and CSP duration were measured. Additionally, participants completed the Cocaine Experience Questionnaire to provide an index of cocaine-induced psychotic symptoms. Consistent with the findings by Boutros et al. (2001), cocaine-dependent subjects exhibited increased RMT in the right hemisphere and increased AMT bilaterally. Prolonged CSP duration was also present in the right hemisphere of patients with cocaine-induced paranoia compared with that in subjects without paranoia. These findings provide evidence of the association between repeated cocaine administration and attenuated cortical excitability. Similar to Boutros et al. (2001), the authors concurred that the alterations in cortical excitability may reflect a compensatory mechanism in response to the excitatory and epileptogenic effects of acute cocaine administration.

Sundaresan et al. (2007) expanded on these studies and administered both single- and paired-pulse TMS over the left motor cortex in 10 cocaine-dependent individuals (3 weeks postabstinence) and in 10 healthy control subjects. Paired-pulse stimulation, long-interval cortical inhibition (LICI) and LICF were administered to provide a more direct investigation of glutamatergic cortical facilitation and GABAergic inhibition. Consistent with Boutros et al. (2001) and Boutros et al. (2005), the authors reported an increased RMT in the cocaine-dependent individuals only. Notably, cocaine-dependent individuals exhibited increased LICF, which reflects increased glutamatergic excitability, but normal LICI. These findings were further supported in a study by Gjini et al. (2012), in which single- and paired-pulse TMS was delivered over the motor cortex of 52 abstinent cocaine-dependent subjects (3 weeks postabstinence) and 42 healthy control subjects. MT, CSP, LICF,, and LICI were measured. Here, again, the cocaine-dependent group was characterized by increased MT and increased LICF, whereas no group differences were observed in LICI. Additionally, the authors revealed a prolonged CSP duration in the cocaine-dependent group, which at high-range stimulus intensity, is mediated by GABA-B receptors and may further reflect motor cortical inhibition. Across both studies, the authors suggest that heightened GLU activity (increased LICF) may relate to the increased vulnerability to develop seizures within a cocaine-dependent population, while reductions in axonal activity (increased RMT), and prolonged CSP duration, could reflect a compensatory adaptation to the epileptogenic effects of repeated cocaine administration (Sundaresan et al., 2007; Gjini et al., 2012). Therefore, these studies highlight the complicated nature of cocaine dependence and the complex interplay between cortical excitability and inhibitory mechanisms in the motor cortex of cocaine-dependent individuals.

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Drug Addiction

John A. RennerJr. MD , E. Nalan Ward MD , in Massachusetts General Hospital Comprehensive Clinical Psychiatry, 2008

COCAINE

Abuse

After alcohol, cocaine is the leading drug of abuse in terms of frequency of ED contacts, general hospital admissions, family violence, and other social problems. 6 The Drug Abuse Warning Network (DAWN) estimates that out of 940,953 illicit drug-related ED visits in 2004, cocaine was involved in nearly 40% of them. 2 Even mature individuals with normal psychological profiles are vulnerable to compulsive cocaine use. Acute users experience intense euphoria often associated with increased sexual desire and with improved sexual function. These acute rewards are often followed by a moderate-to-severe post–cocaine use depression that provides a strong compulsion for further cocaine use. These responses are primarily mediated by disruptions of synaptic dopamine. The initial cocaine response is stimulated by elevated dopamine generated by blockade of the dopamine reuptake transporter (DAT) and the inhibition of the reuptake of synaptic dopamine. Chronic cocaine use leads to down-regulation of dopamine receptors and ultimately depletion of synaptic dopamine, which is thought to be the cause of post–cocaine use depression (Figures 27-1 and 27-3). Like other stimulants, cocaine also disrupts the synthesis and reuptake of serotonin. Other receptors affected include norepinephrine, N-methyl-d-aspartate (NMDA), γ-aminobutyric acid (GABA), and opioid receptors. Plasma cholinesterases rapidly convert cocaine into benzoylecognine (BE), an inactive metabolite that can be detected in the urine for 3 days. When alcohol is taken in conjunction with cocaine, liver esterases produce cocaethylene, an active metabolite that is longer lasting (2- to 4-hour half-life) and more cardiotoxic than is cocaine. The combination of cocaine and marijuana also produces more intense euphoria, higher plasma levels, and more cardiotoxicity than does cocaine alone.

The signs and the symptoms of acute cocaine intoxication are similar to those of amphetamine abuse. Typical complaints associated with intoxication include anorexia, insomnia, anxiety, hyperactivity, and rapid speech and thought processes ("speeding"). Signs of adrenergic hyperactivity (such as hyperreflexia, tachycardia, diaphoresis, and dilated pupils responsive to light) may also be seen. More severe symptoms (such as hyperpyrexia, hypertension, and cocaine-induced vasospastic events [e.g., stroke or myocardial infarction]) are relatively rare among users, but are fairly common in those seen in hospital EDs. Patients may also manifest stereotyped movements of the mouth, face, or extremities. Snorting may produce rhinitis or sinusitis and, rarely, perforations of the nasal septum. Free-basing (inhalation of cocaine alkaloid vapors) may produce bronchitis. Grand mal seizures are another infrequent complication. Patients also describe "snowlights" (i.e., flashes of light usually seen at the periphery of the visual field). Crack is a highly addictive free-base form of cocaine that is sold in crystals and can be smoked.

The most serious psychiatric problem associated with chronic cocaine use is a cocaine-induced psychosis (manifest by visual and auditory hallucinations and paranoid delusions often associated with violent behavior). Tactile hallucinations (called "coke bugs") involve the perception that something is crawling under the skin. A cocaine psychosis may be indistinguishable from an amphetamine psychosis, but it is usually shorter in duration. High doses of stimulants can also cause a state of excitation and mental confusion known as "stimulant delirium."

Management

Cocaine abuse became common among affluent young people in the early to mid-1980s, but with the availability of packaged smokable cocaine, or crack, in low-cost doses, all classes and racial groups have become potential users. Occasional cocaine use does not require specific treatment except in the case of a life-threatening overdose. Most lethal doses are metabolized within 1 hour. In the interim, intubation and assisted breathing with oxygen may be necessary. Stroke has been reported, and death can be caused by ventricular fibrillation or myocardial infarction. The cardiac status should therefore be monitored closely. High doses of benzodia-zepines are recommended for management of stimulant-induced delirium and agitation. Neuroleptics should be avoided because of the risk of potentially fatal hyperther-mia. Intravenous (IV) diazepam should be used to control convulsions.

Chronic cocaine use produces tolerance, severe psychological dependency, and physiological dependence (marked by irritability, anhedonia, low mood, insomnia or hypersomnia, and anxiety). 7 Dependent users typically follow a cyclical pattern of 2 or 3 days of heavy binge use, followed by a withdrawal "crash." Use is resumed again in 3 to 4 days, depending on the availability of cash and the drug. A gradual reduction in use of the drug is almost never possible. Detoxification is accomplished by the abrupt cessation of all cocaine use, usually through restricted access (e.g., a loss of funds or contacts, or incarceration). Withdrawal symptoms begin to resolve within 7 days; the value of medication treatment for withdrawal symptoms has yet to be confirmed. Drugs that enhance central nervous system (CNS) catecholamine function may reduce craving, although they are of limited clinical benefit and they have not been proven effective in double-blind placebo-controlled trials. There is some indication that amantadine (an indirect dopamine agonist) and propranolol may help individuals with severe withdrawal symptoms. The major complication of withdrawal is a severe depression with suicidal ideation. If this occurs, the patient requires psychiatric hospitalization. The need for inpatient care may be brief, since suicidal ideation usually clears promptly with the cessation of cocaine use. A less severe anhedonic state may persist for 2 to 3 months and is thought to reflect a more persistent state of dopamine depletion.

For the cocaine addict, the compulsion to use is overwhelming. For this reason, a hospitalized, cocaine-dependent patient should be monitored closely and should have a drug screen performed after behavioral change, particularly after departures from the floor or receiving visitors. Urine should be examined for cocaine metabolites and, preferably, for all drugs of abuse.

Once compulsive cocaine use has begun, it is almost impossible for the user to return to a pattern of occasional, controlled use. Such individuals are also likely to develop problems with alcohol and other drugs. For that reason, the goal of treatment should be abstinence from cocaine and all other drugs. All cocaine abusers should be referred for individual or group counseling, and participation in 12-step self-help programs should be strongly recommended. Manual-guided cognitive-behavioral therapy (CBT) has been efficacious in the treatment of cocaine dependence. 8 Twelve-step facilitation and CBT appear to be helpful, particularly in individuals with more severe dependence and in those with co-morbid disorders. 9 Family members or significant others should be referred separately to Al-Anon because they will gain insights that may help them eliminate systemic support for the patient's drug use. There is no Food and Drug Administration (FDA)–approved pharmacotherapy for cocaine dependence. Trials with desipramine, fluoxetine, bupropion, amantadine, and carbamazepine have had inconsistent results. Positive responses have been reported in trials with topiramate, baclofen, and modafinil, but these drugs require further investigation. Several trials with disulfiram have shown benefit, with reduced craving and use, and a reported increase in the aversive effects of cocaine should the patient relapse. These reactions are thought to be mediated by the inhibitory effect of disulfiram on dopamine beta-hydroxylase. This action will elevate depleted plasma dopamine levels in chronic users and will produce abnormally high dopamine levels if cocaine is ingested; this results in a dysphoric experience for most users.

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Toxicology Emergencies

Steven W. Salyer PA‐C , ... Roy JohnsonIII, in Essential Emergency Medicine, 2007

Clinical Presentation and Examination

Cocaine is a potent sympathomimetic agent. Manifestations of use involve the CNS and autonomic nervous system. Initial symptoms are euphoria, restlessness, and excitement. Pupils are dilated; blood pressure, respiratory rate, and pulse are increased. Patients may become restless as symptoms progress to diaphoresis, tremors, and the tactile and visual pseudohallucinations of "cocaine bugs" and "snow lights." Cocaine psychosis may occur; this resembles paranoid schizophrenia.

Progression from the initial agitation to seizures, status epilepticus, hyperthermia, ventricular arrhythmias, and rapid cardiopulmonary collapse and death can occur within minutes to half an hour after cocaine use. Most users experience only euphoria and self‐limited mild to moderate CNS stimulation, but many acute and chronic complications of cocaine use can occur and should be recognized and treated.

Cardiovascular complications include acute MI, arrhythmias, aortic dissection, dilated cardiomyopathy, myocarditis, and endocarditis. Acute MI is a well‐known complication of cocaine use but is relatively rare. Although cocaine accounts for up to 25% of acute MIs in patients aged 18–45 years, the actual rate of MI in patients presenting with chest pain after cocaine use is only 6%. Patients with cocaine‐related MI can have typical or atypical chest pain, most are male, 75% smoke, and ECGs can appear normal. Symptoms can occur immediately after use to more than 24 hours later. MI, as with most cocaine complications, can occur with first time or chronic use, with any route of use, and with small doses. Many patients with cocaine‐induced MI have no coronary disease revealed on cardiac cauterization. Mechanisms for cocaine‐associated MI are believed to be increased myocardial oxygen demand, vasospasm of the coronary arteries, enhanced thrombogenesis, and accelerated atherosclerosis seen in cocaine users. A wide variety of atrial and ventricular arrhythmias have been seen and are attributed to the increase in circulating catecholamines, cocaine's direct quinidine‐like effects on the myocardium, QT prolongation, and multiple other problems that occur in this setting such as myocardial ischemia, hypotension, hypoxia, and seizures.

Strokes can occur, both ischemic and hemorrhagic. Patients may present with headache, focal signs and symptoms, or seizures. The possibility of an intracranial event should be considered in any cocaine user who presents with headache, altered level of consciousness, seizures, or persistent agitation. Other neurological complications include seizures, altered mental status, migraine like headaches, movement disorders, and cerebral vasculitis.

Pulmonary complications are more often seen with the use of crack or freebase. These include spontaneous pneumothorax, pneumomediastinum, inhalation injuries and burns to the respiratory tract, "crack lung" (a form of hypersensitivity pneumonitis), and hemoptysis. Asthma exacerbations, pulmonary edema, pulmonary emboli, pulmonary artery hypertrophy, and cor pulmonale can be seen with other forms of cocaine use as well.

Rhabdomyolysis is a well‐recognized cocaine complication. It occurs with all forms of use, even in the absence of seizures, hypotension, crush injuries, or other precipitating factors.

Hyperthermia is always present with severe cocaine toxicity. GI effects include ischemic injury and infarction in almost every organ, bowel perforation, and perforated ulcers. Renal infarctions, idiopathic thrombocytopenic purpura, and diabetic ketoacidosis can occur. Obstetrical complications of cocaine include placental abruption, spontaneous abortions, and premature births. In addition, IV cocaine users will have all the complications of IV drug abuse, ranging from endocarditis to AIDS.

Body packer and body stuffer are terms used to describe a person who ingests cocaine in an attempt to conceal the drug. Body packers are smugglers who ingest many cocaine‐filled bags in an attempt to transport the drug through customs. The packets are well wrapped, usually with multiple layers of latex, and often followed by an antimotility agent. However, rupture of even one packet can be fatal because of the large amount of cocaine per packet. Body stuffers are those who hastily down several packets to hide the evidence, usually during a traffic stop or drug bust. Stuffers ingest fewer packets, but the packets are not wrapped well for ingestion and the risk of rupture or leak into the GI tract is greater.

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Schizophrenia

Juri D. Kropotov , in Quantitative EEG, Event-Related Potentials and Neurotherapy, 2009

IV DOPAMINE HYPOTHESIS OF SCHIZOPHRENIA

A Excess of Striatal Dopamine Receptors

Relative hyperfunction of the subcortical dopamine systems has been suggested to be one of the key pathophysiologic mechanisms in schizophrenic psychosis. In spite of the fact that research in this field was rather contradictive, dopamine hypothesis of schizophrenia still remains the most popular one. It continues to receive a strong empirical support.

The empirical evidence obtained so far can be summarized as follows. First, recent studies on a variety of animal models of psychosis such as sensitization of animal behavior by amphetamine show that those animals were associated with a marked behavioral supersensitivity to dopamine and a marked rise in the number of dopamine D2 receptors in the brain. Second, in humans psychostimulants such as amphetamine and cocaine increase levels of dopamine in the brain and, after prolonged use, cause psychosis (named as amphetamine or cocaine psychosis) that is virtually indistinguishable from the positive symptoms associated with schizophrenia. Third, antipsychotic drugs block D2 dopamine receptors and reduce positive psychotic symptoms.

A recent positron emission tomography (PET) study of a Finnish group from University of Turku gives an additional evidence to the dopamine hypothesis of schizophrenia (Hirvonen et al., 2005). Using the carbon 11 labeled racropride (a substance with affinity to D2 receptors) they studied mono and heterozygotic twins with and without history of schizophrenia. They found that unaffected monozygotic co-twins had increased caudate D2 density compared with unaffected dizygotic co-twins and healthy control twins. Higher D2 receptor binding in the caudate nucleus was associated with a poor performance on cognitive tasks related to schizophrenia vulnerability in the whole sample. The authors concluded that the caudate dopamine D2 receptor upregulation is related to genetic risk for schizophrenia.

B Neural Net Model

According to our theory of action selection within the basal ganglia thalamo-cortical circuits (see Chapter 18) the striatum serves as a map of actions in which representations of different actions are mapped into separate locations. The selection of the relevant representation of action is performed within the striatum by means of long distance lateral inhibition according to "winner takes all" principle. In line with the model, the representation of an action is selected if its activation exceeds some threshold (Fig. 18.2). The threshold of activation of striatal neurons 14 is set by the mediator dopamine. The effect of dopamine is defined by density of dopamine receptors at the postsynaptic membrane of striatal neurons.

Figure 18.2. Impaired action selection in the striatum of schizophrenic patients. (a) Parallel basal ganglia thalamo-cortical loops with the dopaminergic modulatory input from the substantia nigra to the striatum. (b) Two overlapped representations of potential actions overlapped in the cortex, but segregated at the striatal level. Excess of modulatory dopaminergic activation from the substantia nigra due to the excess of density of postsynaptic dopamine receptors in schizophrenia leads to a condition in which the irrelevant action (depicted as a lower amplitude bell shape) is selected together with the relevant action (giving the largest input to the striatum) – the state called as "split of consciousness." DA – dopamine, D-receptors – postsynaptic striatal receptors to DA, antipsychotic drug – a schematic representation of a molecular of an antipsychotic drug that blocks the D-receptors and lessen symptoms of schizophrenia. (c) The schematic relationship between the affinity to D2 receptors of antipsychotic drug (the ability to block D2 receptors) versus reduction of psychotic symptoms.

In healthy subjects the threshold is high enough so that only currently important actions are selected while others are suppressed. The selected action is performed and comes into consciousness. In schizophrenic patients the density of D-receptors is high and consequently the threshold is low. The low threshold enables selection of several actions simultaneously. The selected actions compete with each other and create "the split of consciousness" 15 . Blocking D2-receptors by antipsychotic drugs increases the threshold for action selection and restrains psychosis. Note that the ability of a drug to lessen symptoms of psychosis strongly correlates with the affinity of the drug molecules to the D-receptors, that is, with the ability of the drug to block the D-receptors (Fig. 18.2c). The amount of cortical resources allocated by the brain to execution of the selected action is reflected in the P3b component of ERPs. If the resources are split among competing actions the P3b component decreases. This explains why schizophrenic patients exhibit lower amplitudes of P3b component in comparison to healthy controls.

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Drugs, Moral and Legal Issues

W.M. Bush , in Encyclopedia of Applied Ethics (Second Edition), 2012

Effects of drug use as a ground for moral distinction

Both the 'good' effects of drug use that consumers seek and the harmful effects that they virtually never do are consequences of drug use. The term 'drug use' simply describes a human action without attributing any consequences to it. The moral quality of the action of drug use must therefore be considered in light of its intended and actual consequences and, notably, its harms that are not sought. The harms associated with the action that can vary with a combination of many personal and environmental factors can be classified in various ways. Pharmacological side effects vary greatly. Heroin, particularly when used with other drugs, can lead to overdoses. Cocaine carries the risk of psychosis. These are harms to the user himself or herself. Other possible harms also carry risks to others. Heavy use of methamphetamine as well as cocaine can produce uncontrolled, violent behavior. Alcohol is also associated with much violence. Cannabis and other drugs can impair driving ability.

Many harms are dependent on the circumstances in which the drugs are procured or used. Injecting drug users run the risk of abscesses and blood-borne diseases contracted as a result of unsterile syringes and injecting practices. Illicitly obtained drugs are commonly mixed, and these additives may be harmful. Users come in contact with a criminal peer group in order to procure their drug.

Some harms are temporary. They may be short term, such as intoxication or nausea from hallucinogens, or reversible over a longer period after use ceases, such as decreased motivation associated with protracted cannabis smoking and cocaine psychosis. Some harms are permanent, such as acquired brain injury from an overdose or liver damage from benzodiazepines. (Paracetamol can also cause liver damage.)

Some harms, such as intoxication, arise directly from the drug use. Others, such as impoverishment, fracturing of family relationships, and reduced productivity, are remote harms, avoidable in different circumstances.

Two points to stress from this discussion are (1) that illicit drugs vary greatly in the harm they cause, including the severity of harm, and (2) that the use of some legal substances is productive of harms comparable to illicit drugs, making it difficult to use harm as a ground for moral judgment of illicit drugs without reaching a similar conclusion regarding use of those other substances. Indeed, studies have ranked the misuse of some legal substances as more harmful than some illegal ones. An assessment of 20 substances published in The Lancet ranked alcohol as the fifth most harmful and tobacco ninth, above cannabis at 11th place. Ecstasy ranked 18th. The ranking took physical harm, dependence, and social harm into account.

Addictiveness is a characteristic common to nearly all illicit drugs and is the foremost reason given for their status as such. Three points must be made. First, addictiveness of different illicit drugs varies. Simply trying a drug does not produce dependence, as is shown by the highly addictive substance tobacco. Cocaine is extremely addictive. Addiction to benzodiazepines could be expected to develop within 4–6 weeks of regular use. Cannabis and Ecstasy are not particularly addictive, with psychological dependence indicated by the need for the drug in order to unwind or party being a far greater risk than physiological dependence. Such dependence is reasonably common among tea and coffee drinkers. (Caffeine is listed in The ICD-10 Classification of Mental and Behavioural Disorders: Clinical Descriptions and Diagnostic Guidelines (ICD-10).)

Second, many of the characteristics of addiction are shared by activities that do not involve drugs, including gambling, sex, eating, and even work. Third, addiction does not involve complete loss of control. The extent of compulsion to engage in the addictive activity varies with personal and environmental factors as well as the drug. This is reflected in the looseness of the relevant definitions of 'dependence syndrome' in ICD-10 and of 'substance dependence' in the Diagnostic and Statistical Manual of Mental Disorders, fourth edition (DSM-IV) that require the manifestation at some time over a year of just three out of a list of six or seven symptoms that, with the exception of tolerance and withdrawal, are all behavioral or cognitive patterns. Many people who, for example, have access to sufficient funds to support their habit find it relatively easy to live otherwise responsible lives.

Finally, many of the harms associated with drug addiction flow from their illicit status rather than their pharmacological consequences. Their illicit status is responsible for the adulteration of drugs, hurried injection in unsanitary environments out of fear of being arrested, and other stresses of the law enforcement process. These add immensely to the harm of drug use. In other words, although the drugs cause certain harms in the sense that these harms would not occur in the absence of consumption, consumption alone does not do so. Other factors combine with the consumption to bring about those harms.

Husak warns that what addiction is and, insofar as it is a genuine phenomenon, what causes addiction are questions that are subject to competing psychological, social, and biological models. Subject to the foregoing observations and this warning, the risk of harm entailed by drug use, whether to oneself or to others, provides the strongest basis for judging that use is morally unacceptable. We now turn to relevant ethical principles bearing on this possible conclusion.

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Substance-induced psychosis and cognitive functioning: A systematic review

Kristina M. Gicas , ... Farzaneh Mashhadi , in Psychiatry Research, 2022

3.4 Other stimulant-induced psychosis

In a young all-male sample of patients with amphetamine-induced psychosis, there were no cognitive differences in the domains of intellectual functioning, psychomotor speed, visuospatial functioning, and memory when compared to patient groups with schizophrenia and bipolar, respectively (Ostadghafour et al., 2014 ). Similarly, in a mostly male sample of precariously housed persons with cocaine-induced psychosis, this group did not differ from persons with cocaine dependence and no psychosis on premorbid functioning, verbal learning and memory, inhibition, sustained attention, mental flexibility, or decision-making ( Willi et al., 2017). Using the same sample of precariously housed adults, another study examined persons with stimulant-induced psychosis and concurrent stimulant dependence (methamphetamine or cocaine) compared to a group of persons with schizophrenia plus concurrent stimulant dependence and a group of persons with schizophrenia and no concurrent stimulant dependence (Alexander et al., 2019). The stimulant-induced psychosis group did not differ from the two schizophrenia groups on any cognitive measures of premorbid functioning, verbal learning and memory, inhibition, sustained attention, mental flexibility, or decision-making.

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