Psychostimulant Abuse And Psychosis

Psychostimulant abuse and Psychosis

Paola Fuentes Claramonte 20484778N

Psychostimulant abuse and psychosis

Introduction Chronic use of psychostimulant drugs, like cocaine or amphetamines, has been reported to produce several damages in the consumer’s health. Psychiatric problems are a very serious consequence of cocaine abuse which occur approximately in 75% of chronic consumers, although it is not clear wether psychopatology is a consequence of drug abuse or was already there when it started. In fact, individuals who suffer from mental illness seem to be more likely to become drug abusers. Long term abuse of cocaine is related to a great number of psychopathologic problems such as anxiety, irritability, panic attacks, depression, affective disorders, sexual and eating disorders. Moreover, there exists evidence that abuse of substances is associated with greater risk for psychosis in non-psychotic persons. For example, after World War II, there was a large number of diagnosed psychoses that were developed following repetitive administration of amphetamine. The aim of this work is to explore the main characteristics of the psychosis developed after chronic or long abuse of psychostimulants, and the existing models that explain how it occurs. I also would like to examine the similarities and differences of cocaine induced psychosis and those psychotic disorders, like schizophrenia, that appear without substance consumption.

What is stimulant-induced psychosis? Psychotic disorders such as schizophrenia are characterised by a list of symptoms incuding dellusions, hallucinations, disorganised speech and disorganised behavior. These are considered positive symptoms. They also include negative symptoms like catatonia and affective flattening. These symptoms disturb several areas of functioning: work, relationships, self-care... There are different subtypes of schizophrenia. Many patients can be classified in one of these: paranoid, catatonic and disorganised type. Generally, the onset of the disorder occurs in adolescence or early adulthood, but early signals of schizophrenia can be seen even before. In some cases, however, symptoms appear without detected predictors after a long period of stimulant drugs abuse. Then we talk about stimulant-induced psychosis. Cocaine is one of the stimulant drugs that can induce a psychotic disorder. The Diagnostic and Statistical Manual of Mental Disorders (DSM - IV) establishes that a diagnosis of cocaine induced psychosis should be made when psychotic symptoms are in excess of those typically encountered in intoxication or withdrawal. Dellusions or hallucinations may appear during these periods, but

their duration and intensity are significantly lower than those provoked by a psychotic episode. Therefore, stimulant-induced psychosis must be differentiated from those clinical pictures dominated by delirium and confusion that appear after acute administration of high doses of stimulants or during withdrawal. Paranoid schizophrenia is one of the most frequent disorders among cocaine abusers. They typically show paranoid and/or grandiosity dellusions. Hallucinations are often auditory or tactile. Cocaine addicts with psychotic induced disorder usually show agressive behavior consistent with delirious ideation. Within an important percentage of patients this pathology persists for several months and even becomes permanent. Drug-induced psychosis resembling paranoid schizophrenia can also occur with repeated or high-dose use of other psychostimulants, like amphetamine and methanphetamine. Once the psychotic state develops with amphetamine use, recurrence can happen in response to psychological stressors, without further use of amphetamine, making the illness difficult to distinguish from schizophrenia.

Psychosis and behavioral sensitization It is believed that repetitive administration of stimulant drugs leads to chemical alterations in the central nervous system, especially affecting the dopaminergic system. The specific mechanism by which stimulants produce psychosis is not known, but similarities between behavioral sensitization to stimulants, stimulantinduced psychosis, and chronic schizophrenia have been proposed. Behavioral sensitization is the progressive and enduring enhancement of certain stimulant-induced behaviors that develops following repetitive stimulant drug administration. We do not have a clear understanding of the underlying mechanisms of this phenomenon. However, sensitization has been associated with increased stimulant-induced release of dopamine, which also occurs in schizophrenic patients without drug consumption. Similarly, past development of antipsychotic medications was based on their dopamine receptor blocking properties. One hypothesis to explain sensitization suggests that increased dopamine release leads to enhanced behavioral response to stimulant administration. Nevertheless, some researchers have found unchanged or decreased levels of dopamine release in animals showing behavioral sensitization after repetitive stimulant administration. Hence, a causal relationship between change in dopamine release and behavioral sensitization is not firmly established. Therefore, although the ability of stimulant drugs to precipitate or exacerbate psychotic symptoms has been linked to their dopaminergic effects, there are other neural systems that have also been proposed, like the glutamatergic, serotonergic and noradrenergic systems, to be linked with stimulant psychosis, maybe modulating the effects of stimulant drugs on the dopaminergic pathways. For example, several studies suggest a combined action of dopaminergic and

noradrenergic changes underlying psychotic symptoms. Post’s continuum model of cocaine psychosis suggests that early euphoric effects may be present with a high norepinephrine to dopamine ratio, and that this ratio decreases with continued use, leading to psychotogenic effects. A hypothesis relating the behavioral sensitization with the genesis of stimulantinduced psychosis has been proposed. E.H. Ellinwood proposed a gradual evolution of the symptoms following repetitive stimulant drug abuse. Early in stimulant administration, the person shows an intense curiosity, which progresses to intense exploration of the environment if the drug administration continues over the time. This environmental exploration is displayed in repetitive, stereotyped searching, sorting and examining behaviors, that could be characterised as compulsive-like behaviors. Finally, this curious ‘suspiciousness’ of the environment evolves into paranoia and psychotic thought. The addict may then begin to misinterpret stimuli and often to have illusions and hallucinations. When studied on animals, repetitive stimulant administration leads to sensitization of motor behavior and setereotyped movements. Richtand et al. pointed that an anallogy can be stablished between this sensitization and that observed in humans. For example, animals show an increase in stereotyped grooming behaviors after chronic amphetamine administration. Amphetamine addicts suffering from amphetamine induced psychosis often spend hours examining or probing visually accessible parts of the body. Many patients showing this behavior develop delusions of parasitosis and spend many hours examining their skin and digging out imagined parasites. These delusions appear to develop out of early sequences of skin sensations and repetitive ‘grooming responses’. Thus, a parallelism can be drawn between behavioral sensitization in animals and humans, although we must be conscious about its limitations since we cannot reproduce the complex cognition of human psychosis in an animal model. Nevertheless, following the same pattern of grooming sensitization, thinking itself could become repetitious. Perception and attention could manifest sensitization so the subject focuses on minute objects, leading to repetitive examination and disassembling of electric devices, or to the thinking process that directs towards the delusion of parasitosis. A sensitization of the attitude of curiosity and/or suspiciousness that characterizes incipient paranoid schizophrenia or the beginning phase of amphetamine psychosis, combined with behavioral disorganization, increasing arousal and/or fear, may evolve into a paranoid reaction. The pattern followed by this behavioral evolution can be interpreted as a sensitization of the exploration behaviors and more complex cognitive processes. Thus, pathological sensitization of neuronal systems may be an important factor for the onset or relapse of stimulant-induced psychosis and schizophrenia. This sensitization would have an endogen basis in psychotic patients, while stimulant abuse may precipitate it in non-psychotic individuals.

Can stimulant-induced psychosis serve as a model of schizophrenia? As has been said, there are many similarities between stimulant-induced psychosis and schizophrenia developed without drug abuse, making it difficult to differentiate a disorder from the other. This is especially complicated because schizophrenic individuals tend to abuse drugs, so the origin of the disorder is not always clear. When psychosis is present, we may ask if latent or actual schizophrenia is involved. Due to the similarity of the symptoms, it has been proposed that the underlying mechanisms causing both disorders may be the same. The sensitization hypothesis presented above follows this idea. If this was true, then stimulantinduced psychosis could be a useful model of schizophrenia that would permit the investigation of its neurobiological basis as well as the cognitive aspects of the disorder. It would be possible to induce psychosis in animals and study their brains and behavior. The question is if what happens in an addict’s brain after repetitive stimulant administration is the same as what happens in the brain of a schizophrenic without taking drugs. There are some aspects of both disorders that indicate an important similarity between them. One of them is that stimulant administration results in exacerbation of positive symptoms in schizophrenic patients, which is congruent with the general predominance of positive symptoms reported in stimulant psychosis. In addition, both disorders are usually treated with the same antipsychotic medications that attenuate or even eliminate psychotic symptoms. On the other hand, there are some studies that explore the differences between substance-induced psychoses and primary psychotic disorders that co-occur with drug abuse. DSM-IV provides of diagnostic criteria to differentiate the two conditions. Using them, a longitudinal study in New York found that patients with substance-induced psychosis showed a later age of the illness onset, as well as other demographic differencies with the primary psychosis group. Subjects diagnosed as suffering from primary psychotic disorder had more severe psychiatric symptoms associated with less insight. The two groups also showed differences related to hallucinatory behavior (more common in the substance-induced psychosis group), which maybe reflect differences in the underlying mechanisms of psychosis. However, this study does not only reffer to stimulant-induced psychosis, since it included individuals abusing alcohol, cannabis, cocaine, amphetamines and other drugs. Moreover, it was based on behavioral data, so we cannot determine biological differences between the two conditions, which would be very valuable information in the study of substanceinduced psychosis. Following the sensitization hypothesis, there has been proposed that behavioral sensitization in animals, due to repetitive stimulant administration, could be a useful animal model of psychosis (Richtand et al., 2003). However, although it seems to exist a parallelism between the two processes, behavioral sensitization and psychosis development, this animal model would have important limitations. The rodent brain and behavior are more limited than their human counterpart, and there is no direct correspondence between animal behavioral sensitization and human psychiatric disease.

Therefore, the question asked before remains unresponsed. Maybe stimulantinduced psychosis can serve as a model of schizophrenia, but we have to considerate the limitations of this model since the underlying mechanisms of these disorders are not clear yet.

Conclusions I have explored some aspects of stimulant-induced psychosis that I consider relevant for a better understanding of this disorder. It is clear that substance abuse can lead to health problems, some of them relating to mental health. However, it is important to remember that people suffering from mental illness tend to abuse drugs more than the general population, so the origin of the disease may be previous to substance use. This is an important aspect to be considered in diagnosis, since the treatment and prognosis may not be the same. An approximation to the mechanisms that can be on the basis of stimulantinduced psychosis has been proposed as the sensitization hypothesis. But it is only a hypothesis, which needs to be proved in further investigation. Future findings in this field may provide a better comprehension of this disorder, improving the prevention, diagnosis and treatment of these patients.

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