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Toxic psychosis

Several "sigma opiates," which differ structurally from PCP, are known to induce a PCP-like toxic psychosis, and to displace PCP from rat brain membranes (Zukin 1982 Hampton et al. 1982 ... [Pg.56]

In adult patients, the manifestations of PCP use can be grouped into nine clinical patterns of intoxication. Four of these are called major patterns because they may be associated with severe toxicity and often necessitate hospitalization. Patients with major patterns are usually unpredictable symptoms wax and wane, and the patient may abruptly change from one pattern of intoxication to another. Five other symptom complexes are designated as minor patterns since toxicity is usually mild and of short duration. Major Patterns consist of coma, catatonic syndrome, toxic psychosis, and acute brain syndrome. Minor Patterns are lethargy, bizarre behavior, violent behavior, agitation, and euphoria (McCarron et al. 1981b). [Pg.225]

Toxic Psychosis. Any patient who is not catatonic but has hallucinations, delusions, paranoid ideation, or other psychiatric manifestations is classified as having toxic psychosis. These patients are often difficult to differentiate from those with acute agitated psychosis, and about 25 percent appear manic. [Pg.226]

In some areas, PCP may be a leading precipitant of psychiatric emergencies. Routine blood samples from 145 consecutive admissions to the Los Angeles County Hospital psychiatric emergency room during a 48-hr period in June, 1979 showed 63 samples positive for PCP. A wide variety of psychiatric clinical pictures were found in these patients, including mania, depression, and schizophrenia. Three patients also had symptoms of a toxic psychosis (50). [Pg.144]

Toxic psychosis Several monoamine stimulants including cocaine are known to produce a temporary or even a lasting psychotic state after heavy use. Reviews of numerous clinical case reports have shown amphetamine to produce a chronic psychotic state, sometimes persisting for months after cessation. There appears to be a sensitization effect in this regard, because after recovery, psychotic states may recur with minimal use of amphetamine or alcohol. When compared to schizophrenic patients, people with amphetamine-induced psychosis demonstrate fewer negative symptoms (Boutros and Bowers 1996). [Pg.138]

As would be expected, khat overuse produces symptoms similar to those of other monoamine stimulants, such as cocaine or amphetamine, including signs of sympathetic overarousal. In the extreme this can involve a toxic psychosis. Disorders more frequently associated with chronic khat use in males are headaches, anorexia, insomnia, constipation, and respiratory illnesses (Kennedy et al. 1983). Females report higher incidences of acute gastritis, jaundice, bronchitis and hepatic diseases. Also, cathinone has toxic reproductive effects in humans and experimental animals (Islam et al. 1990). It decreases sperm count and motility, and increases the number of abnormal sperm cells. It also decreases plasma testosterone in rats. [Pg.143]

Steroid psychosis Steroid psychosis is characterized by a delirious or toxic psychosis with clouded sensorium. Other symptoms may include euphoria, insomnia, mood swings, personality changes, and severe depression. The onset of symptoms usually occurs within 15 to 30 days. Predisposing factors include doses greater than prednisone 40 mg equivalent, female predominance, and, possibly, a family history of psychiatric illness. [Pg.264]

CNS When used to treat extrapyramidal reactions resulting from phenothiazines in psychiatric patients, antiparkinson agents may exacerbate mental symptoms and precipitate a toxic psychosis. [Pg.1300]

CNS CNS effects including convulsions, increased intracranial pressure, and toxic psychosis have been reported with nalidixic acid therapy. Convulsive seizures have been reported with other drugs in this class. Quinolones also may cause CNS stimulation, which may lead to confusion, hallucinations, light-headedness, restlessness, and tremor. Therefore, use nalidixic acid with caution in patients with known or suspected CNS disorders (eg, cerebral arteriosclerosis, epilepsy) or other factors that predispose to seizures. If these reactions occur in patients receiving... [Pg.1549]

Symptoms Convulsions, increased intracranial pressure, metabolic acidosis, or toxic psychosis may occur in patients taking more than the recommended dosage. Lethargy, nausea, and vomiting, also may occur after overdosage. [Pg.1552]

Seizures Increased intracranial pressure, convulsions, and toxic psychosis have occurred. CNS stimulation also may occur and may lead to tremor, restlessness, lightheadedness, confusion, dizziness, depression, hallucinations, and rarely, suicidal thoughts or acts. [Pg.1573]

Hallucinogens LSD (lysergide) Psilocybin, psilocin DMT, mescaline DOM, STP + Distortion of perception, mood, and thought -H-M- Neurotoxicity Flashbacks Toxic psychosis... [Pg.409]

Chronic stimulant abuse alters the personality of the abuser. These and related changes are the result of neurotoxicity and are not characterized as either acute drug effects or withdrawal signs. Individuals have delusions of being pursued or persecuted and therefore become suspicious and paranoid. They become self-occupied and hostile toward others. Long-term abuse can produce toxic psychosis that closely resembles schizophrenia and must be treated with neuroleptic drugs (haloperidol, chlorpromazine). This psychosis can develop even within 1 to 2 weeks if the person is on a run of very high doses of stimulants. [Pg.411]

C. Abuse of stimulants can produce toxic psychosis that closely resembles schizophrenia. An agent such as haloperidol or a phenothiazine will provide im-... [Pg.420]

Displacement of GABA from its receptors by ciprofloxacin results in increased levels of the neu-roexcitatory transmitter and acute CNS toxicity. The neuroexcitation can range from irritability, confusion, and agitation to seizures and toxic psychosis. Ciprofloxacin has no interaction with alcohol. A disulfiramlike reaction (flushing, nausea, vomiting, and profuse sweating) is associated with alcohol and metronidazole. Avoid alcohol and metronidazole coadministration. [Pg.525]

Severe paradoxical reactions, marked by hallucinations, tremor, seizures, and toxic psychosis, may occur. [Pg.131]

Chronic alcohol drinkers, when forced to reduce or discontinue alcohol, experience a withdrawal syndrome, which indicates the existence of physical dependence. Alcohol withdrawal symptoms classically consist of hyperexcitability in mild cases and seizures, toxic psychosis, and delirium tremens in severe ones. The dose, rate, and duration of alcohol consumption determine the intensity of the withdrawal syndrome. When consumption has been very high, merely reducing the rate of consumption may lead to signs of withdrawal. [Pg.496]

Amantadine has a number of undesirable central nervous system effects, all of which can be reversed by stopping the drug. These include restlessness, depression, irritability, insomnia, agitation, excitement, hallucinations, and confusion. Overdosage may produce an acute toxic psychosis. With doses several times higher than recommended, convulsions have occurred. [Pg.611]

The psychomotor stimulants, cocaine and D-amphetamine, are considered together because they share a similar psychopharmacological profile.19 20 Low to moderate doses of both drugs given acutely to nontolerant, nonanxious subjects produce increases in positive mood (euphoria), energy, and alertness. Experienced cocaine users were unable to distinguish between intravenous (IV) cocaine and D-amphetamine,21 and cross-tolerance between cocaine and D-amphetamine with respect to their anorectic effect has been demonstrated.22 Additionally, the toxic psychosis observed after days or weeks of continued use of both psychostimulants is very similar. The fully developed toxic syndrome, characterized by vivid auditory and visual hallucinations, paranoid delusions, and... [Pg.66]

Research studies on human performance have typically involved the administration of cocaine and d-amphetamine in single doses that do not produce toxic psychosis. In the studies reviewed, d-amphetamine was administered orally (PO). Given that the performance effects of D-amphetamine have been studied for more than 60 years and its widespread use during World War II,24 it is not surprising that much is known about the effects of D-amphetamine on vigilance and attention. However, the effect of psychostimulants on higher-order cognitive processes has not been widely studied. [Pg.67]

Some experts have reported that children taking Ritalin experience a change in the cognitive and intellectual processes. Parents and teachers have noticed that some children answer questions in more compliant or narrow ways, which could suggest that their creative thinking is restricted. The results of the studies on these effects are not consistent. In some cases, children on Ritalin become withdrawn, too focused, zombie-like, somber, and quiet, and spend increasing amounts of time alone. Ritalin can also cause toxic psychosis, a syndrome that includes symptoms of hallucinations, delirium, and sometimes violent behavior. Usually, this... [Pg.20]

Severe OP-poisoning is evidenced by the rapid onset of unconsciousness, local or generalized seizures, incontinence and other manifestations of a cholinergic crisis. Further indications of severe intoxication may include a slow heartbeat, tearing, toxic psychosis... [Pg.385]

Other than in sensitive individuals, the aromatic nitro compounds are only moderately irritating to the skin, but very toxic to the liver, kidneys and nervous system. The basic mechanism of toxicity is stimulation of oxidative metabolism in cell mitochondria through interference with the normal coupling of carbohydrate oxidation to phosphorylation (ADP to AT ). The increased oxidative metabolism leads to pyrexia, tachycardia, dehydration and the ultimate depletion of fat stores. The most severe toxicity occurs when workers are concurrently exposed to hot, humid environments. Pyrexia and direct action on the brain cause cerebral edema, clinically evidenced by toxic psychosis and, at times, convulsions. Degenerative changes occur in the liver parenchyma, and renal tubules, and clinical signs of renal injury appear (albuminuria, hematuria, pyuria, increased BUN). [Pg.402]

Many different classes of drugs can produce hallucinations when given in toxic doses (e.g. the anticholinergics, such as atropine and scopolamine), but such symptoms are generally associated with confusion and lack of sensory clarity. As such, hallucinations are a component of a toxic psychosis. [Pg.405]

Alcohol should be avoided during furazolidone and metronidazole therapy. Toxic psychosis has been seen in patients under treatment with furazolidone. Metronidazole should be used with caution when coadministering with warfarin, phenytoin, lithium, omeprazole, and phenobarbital. The coadministration of pentamidine with drugs toxic to the kidney should be avoided. [Pg.337]


See other pages where Toxic psychosis is mentioned: [Pg.97]    [Pg.841]    [Pg.130]    [Pg.885]    [Pg.1157]    [Pg.1715]    [Pg.407]    [Pg.521]    [Pg.452]    [Pg.115]    [Pg.172]    [Pg.35]    [Pg.373]    [Pg.427]    [Pg.133]    [Pg.16]    [Pg.98]   
See also in sourсe #XX -- [ Pg.97 ]

See also in sourсe #XX -- [ Pg.248 ]




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