Cocaine psychosis

Toxicity 1. Excess NE cardiac arrhythmias, generalized ischemia with possible MI and strokes acute renal and hepatic failures 2. Excess DA major psychosis, cocaine delirium 3. Excess 5HT possible serotonin syndrome 4. All of the above convulsion, hyperpyrexia, and death... 

Ciraulo DA, Rotrosen J, Leiderman D, et al Nefazodone induced alterations of cocaine craving and use in dysphoric cocaine users. Drug Alcohol Depend 60 S38, 2000 Connell PH Amphetamine Psychosis (Maudsley Monographs No 5). London, Oxford University Press, 1938... 

McDougle CJ, Price LH, Palumbo JM, et al Dopaminergic responsivity during cocaine abstinence a pilot smdy. Psychiatry Res 43 77-85, 1992 McDougle CJ, Black JE, Malison RT, et al Noradrenergic dysregulation during discontinuation of cocaine use in addicts. Arch Gen Psychiatry 51 713-719,1994 Misra L, Kofoed L Risperidone treatment of methamphetamine psychosis (letter). Am J Psychiatry 154 1170, 1997... 

Somoza EC, Winhusen TM, Bridge TP, et al An open-label pilot study of methylpheni-date in the treatment of cocaine-dependent patients with adult attention deficit/ hyperactivity disorder. J Addict Dis 23 77—92, 2004 Sora 1, Wichems C, Takahashi N, et al Cocaine reward models conditioned place preference can be established in dopamine- and in serotonin-transporter knockout mice. Proc Natl Acad Sci U S A 95 7699-7704, 1998 Soral, Hall FS, Andrews AM, etal Molecular mechanisms of cocaine reward combined dopamine and serotonin transporter knockouts eliminate cocaine place preference. Proc Nad Acad Sci U S A 98 5300-5305, 2001 Spear J, Alderton D Psychosis associated with prescribed dexamphetamine use 0etter). 

The treatment goals for acute intoxication of ethanol, cocaine/amphetamines, and opioids include (1) management of psychological manifestations of intoxication, such as aggression, hostility, or psychosis, and (2) management of medical manifestations of intoxication such as respiratory depression, hyperthermia, hypertension, cardiac arrhythmias, or stroke. 

Cocaine or stimulant intoxication may require administration of a small dose of a short-acting benzodiazepine (e.g., lorazepam 1 to 2 mg) for agitation or severe anxiety. Antipsychotics (e.g., haloperidol 2 to 5 mg) should be used only if psychosis is present. If hyperthermia is present, initiate cooling measures. 

Staley J., Wetli C., Ruttenber A., DeamW., Mash D. Altered dopaminergic synaptic markers in cocaine psychosis and sudden death. Natl. Inst. Drug Abuse Res. Monogr. 153 491, 1995. 

Satel, S.L., Seibyl, J.P., and Charney, D.S. Prolonged cocaine psychosis implies underlying major psychopathology. J. Clin. Psychiatry. 52 8, 1991. 

Wetli, C.V. and Fishbain, D.A. Cocaine-induced psychosis and sudden death in recreational cocaine users. J. Forensic. Sci. 30 873, 1985. 

Staley, J.K., Wetli, C.V., Ruttenber, A.J., Heam, W.L., Kung, H.F., and Mash, D.C. Dopamine transporter and receptor autoradiography in cocaine psychosis and sudden death. Biol. Psychiatry. 37 656, 1995. 

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). 

Chronic cocaine use can cause a syndrome of insomnia, hallucinations, delusions, and apathy. This syndrome develops around the time when the euphoria turns to a paranoid psychosis, which resembles paranoid schizophrenia. Further, after cessation of cocaine use, the hallucinations may stop, but the delusions can persist. Still, the incidence of a persistent cocaine-induced psychosis appears to be rare. One study found only 4 out of 298 chronic cocaine users receiving a diagnosis of psychotic disorder (Rounsaville et al. 1991). This incidence is approximately the... 

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. 

In addition to the acute ingestion of these hallucinogenic drugs, the chronic use of alcohol, amphetamines, or cocaine can lead to paranoia that in many respects resembles the psychosis of schizophrenia. In these cases, the psychotic symptoms may persist long after the substance use has been stopped. 

Amphetamine used at high doses can provoke a toxic syndrome ( amphetamine psychosis ) in healthy subjects that shows certain similarities to schizophrenic psychoses. Like cocaine, high-dose amphetamine is known to trigger a massive release of dopamine and noradrenaline from presynaptic sites and thus to produce a temporary excess supply of both neurotransmitters at the respective synapses. 

Curran C, Byrappa N McBride A (2004). Stimulant psychosis systematic review. British Journal of Psychiatry, 185, 196-204 Dallery J, Silverman K, Chutuape MA, Bigelow GE Stitzer ML (2001). Voucher-based reinforcement of opiate plus cocaine abstinence in treatment-resistant methadone patients effects of reinforcer magnitude. Experimental and Clinical Psychopharmacology, 9, 317-25... 

As noted above, large doses of amphetamine, cocaine, and other sympathomimetics can cause acute paranoid reactions, either spontaneously in abusers or experimentally in normal volunteers. An injection of a large amphetamine dose, for example, often produces a paranoid psychosis within hours. Frequent smaller doses over several days can also produce a paranoid psychotic reaction. An episode s duration usually parallels the length of time the drug remains in the body. 

The classification of NMDA antagonists as nonaddictive drugs was based on early assessments, which, in the case of PCP, have recently been questioned. In fact, animal research shows that PCP can increase mesolimbic dopamine concentrations and has some reinforcing properties in rodents. Concurrent effects on both thalamocortical and mesolimbic systems also exist for other addictive drugs. Psychosis-like symptoms can be observed with cannabinoids, amphetamines, and cocaine, which may reflect their effects on thalamocortical structures. For example, cannabinoids, in addition to their documented effects on the mesolimbic dopamine system, also enhance excitation in cortical circuits through presynaptic inhibition of GABA release. 

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