eMedicine Specialties > Psychiatry > Addiction

Phencyclidine (PCP)-Related Psychiatric Disorders

Author: Alan D Schmetzer, MD, Professor, Vice-Chair for Education, and Director of Residency Training in General and Addiction Psychiatry, Department of Psychiatry, Indiana University School of Medicine
Coauthor(s): Roland McGrath, MD, Chairman, Professor, Department of Emergency Medicine, Indiana University School of Medicine; David R Diaz, MD, Assistant Professor of Clinical Psychiatry, Indiana University School of Medicine; Attending Psychiatrist, Adult Service, Larue D Carter Memorial Hospital; Attending Psychiatrist, Indiana University Hospital Adult Outpatient Clinic, Indianapolis, Indiana
Contributor Information and Disclosures

Updated: May 31, 2009

Introduction

Background

Phencyclidine (PCP) was originally developed as an anesthetic agent and marketed for a time as Sernylan; however, the agitation that some people developed following phencyclidine-induced anesthesia quickly led to its abandonment for this indication. Unfortunately, it then became a drug of abuse for a small but significant population, mostly younger in age and of a minority ethnicity. Other chemical names for phencyclidine are 1-(phenylcyclidine) piperidine or phenylcyclohexyl piperidine, either of which may have given rise to the PCP acronym.

Phencyclidine was used for a time as an animal anesthetic, but even this use has ceased in the United States. PCP is no longer manufactured in the United States for any legitimate use, so any PCP produced in this country today comes from clandestine labs.

PCP has been studied in animal models1 of schizophrenia2,3 , and, more recently, PCP-like compounds have been investigated for use in treating brain ischemia. PCP is known to produce a syndrome in previously nonpsychiatrically ill humans that is similar to schizophrenia, and it can worsen the psychotic symptoms in people who have a schizophrenic or other psychotic illness. PCP is an N -methyl-D-aspartate (NMDA) antagonist; thus, it blocks the action of glutamate and aspartate, excitatory amino acid CNS neurotransmitters. PCP is also highly anticholinergic in nature.

PCP can be smoked, ingested orally, snorted intranasally, or injected intravenously. Today, the usual route of administration is smoking, often as an additive to marijuana cigarettes. Because it is inexpensive to produce, PCP is sometimes palmed off on unsuspecting street drug buyers as THC (delta-9-tetrahydrocannabinol, the active ingredient in marijuana), LSD (lysergic acid diethylamide), or as some exotic designer hallucinogen.

PCP first came to the attention of emergency department physicians and psychiatric emergency department physicians in California and New York during the 1960s. At that time, it was ingested in pill form (the PeaCePill). During the early 1970s, PCP became available as a white powder, which could also be put into a solution and then insufflated, ingested by mouth, or smoked on tobacco or marijuana or even on mint leaves, parsley, or other leafy materials, usually to cool the otherwise hot and orally irritating smoke. The creation of this powdered form may have led to its increased use from 1972 to the late 1970s. In 1979, the percentage of high school seniors ever having used PCP was 12.8%.

Use of PCP has waxed and waned since, but has never again attained double-digit popularity. Use during the early 1980s slightly increased, followed by another decline. Yet another small increase in use was seen among high school seniors from 1996-2002. The most recent usage figures published by the University of Michigan in their Monitoring the Future study4  noted a rate of 2.1% of high school seniors in 2007 ever having used PCP, and this has not been seen to change in 2008. (For further such statistical information, visit the Monitoring the Future Web site.)

Historically, PCP has gone by many street names, including angel dust, crystal, hog, embalming fluid, ozone, and rocket fuel. In combination with marijuana, street names such as krystal joint (KJ), mintweed, supergrass, and killer weed have been used. When PCP is combined with cocaine, the resultant concoction is sometimes called space base or tragic magic.

Case vignette

Jay, a 20-year-old man, is brought to the emergency department of an inner-city general hospital by the police after he is taken into custody for fighting and then resisting arrest. The arresting officer says that he believes Jay may be hurt, perhaps with a fracture of his right arm, but he has never before seen anyone so violent. The patient is extraordinarily agitated and has to be placed in leather restraints immediately upon being brought in. He does not complain of pain and seems to deny having any when asked. With considerable difficulty, the triage nurse is able to take some of his vital signs: his pulse is elevated at 128 bpm and his blood pressure is high at 150/98.

The emergency department physician tries to examine Jay, but Jay is yelling and threatening so continuously that chest and abdominal examinations are practically impossible to perform. The doctor does note vertical nystagmus when Jay looks up at him and also notes that deep tendon reflexes are absent in those locations that can be checked.

Because of the agitation and screaming, the psychiatric resident on call is asked to see the patient as quickly as possible. She arrives in the emergency department some 20 minutes later. At that point, the patient is sobbing uncontrollably and babbling about of his fear of suicide. Trying without success to perform at least a partial cognitive examination, the resident asks her faculty attending to come to the emergency department to see Jay. By the time the attending arrives, the patient is talking calmly, and, when asked about drug use, admits to smoking some “really great pot” earlier that day. Blood and urine samples are quickly ordered, but by the time the phlebotomy team arrives, the patient is trying to remove all of his clothing even while in restraints and is once again cursing and threatening loudly whether anyone is present or not.
 
When a urine drug screen is finally obtained on the inpatient unit in a moment of relative calm, cannabis is present, but so is phencyclidine (PCP). Later that evening, an x-ray also confirms a right wrist fracture about which the patient has yet to complain. Unbeknownst to Jay, his marijuana had been laced with PCP by his drug dealer to “give it a bigger kick.”
 
Jay is a fictional name, but this case vignette is a compilation of dozens of emergency department encounters seen by the lead author with young men and women having a psychotic reaction to PCP.

Pathophysiology

PCP is a sympathomimetic dissociative anesthetic — dissociative means that the user feels that his or her mind is separated from the body. This can be very upsetting to some people, especially first-time users who are not expecting it. PCP is often classified with the hallucinogens, but because it can also act a stimulant or even a CNS depressant, it is sometimes classified separately from all other street drugs. Chemically, it is an arylcycloalkylamine. To this point, at least 20 analogues and metabolites of PCP have been identified within this chemical family.

The current understanding is that PCP acts as a noncompetitive antagonist at the NMDA excitatory amino acid receptor channel complex. The molecule binds to a site within this channel system, thereby physically preventing sodium, calcium, and potassium ions from moving across the cell membrane. This prevention of ion movement results in decreased neuronal firing; however, PCP cannot bind within anion channel unless it is initially opened by glutamate, NMDA, or an NMDA agonist. PCP is absorbed rapidly whether it is smoked, ingested orally, inhaled intranasally, or injected into the veins. PCP hydroxylated metabolites are excreted mainly in the urine.5  

There is some concern that PCP may cause neurotoxicity in humans, but most of the scientific evidence for CNS damage is presently found in studies of mice, rats, and other laboratory animals. Neurotoxicity is currently thought to be due to dioxin contaminants rather than to the phencyclidine molecule directly.

PCP molecule.

PCP molecule.

PCP molecule.

PCP molecule.

 

Olney and colleagues found vacuoles in areas comprised largely of glutaminergic pyramidal neurons in the posterior cingulate and retrosplenial cortex in rats.6  Immunotoxicity has also been reported in mice (reduced humoral immunity and impaired T-cell cytolytic activity), cattle (thymic hypoplasia), and young pigs (decreased total leucocyte counts, reduced gamma globulins, and suppressed IgG) and pregnant mice show an increase in embryo mortality when exposed to PCP, but no increase in birth defects; therefore, PCP can be said to be fetotoxic but not teratogenic in mice. The doses of PCP investigated were often high, so how this evidence might relate to people using lower doses is not known. Interestingly, Olney's results were found using relatively low doses.

Evidence for behavioral toxicity in the human population is clearer, and numerous deaths from suicide, homicide, and accidents related to bizarre behavior have been reported in those intoxicated with PCP. Primary intoxication lasts from 4-6 hours, but behavioral abnormalities may last for as long as several weeks. This lingering presence of behavioral effects is thought to be due to storage of PCP within fatty tissues of the body, PCP being highly lipophilic.

The behavioral and physiologic effects depend on dose, with lower blood levels in the range of 20-30 ng/mL usually causing sedation, irritability, hyperactivity, impaired attention, and mood elevation. As serum levels rise above 30 ng/mL, ataxia, psychosis, analgesia, paresthesia, and mood lability may occur. The range in which paranoia and aggressive behaviors are most likely to occur is 30-100 ng/mL. When serum levels are higher than 100 ng/mL, patients become stuporous, hyper-reflexive, and hypertensive, and, ultimately, they may experience seizures, coma7 , and death. Note that serum levels with PCP are relatively unreliable, so treatment-related decisions always should be based on the specific patient's clinical status.

In terms of metabolism, PCP has a large volume of distribution due to its lipid solubility. This is the reason for the relative lack of correlation between serum or urine values and clinical manifestations. It is metabolized primarily in the liver, with renal elimination of the resulting hydroxylase metabolites; hence, urinary acidification fails to have much effect in speeding detoxification. In addition, alkalinization is the recommended treatment for the myoglobinuria that can accompany PCP intoxication, so acidification is both irrational and in conflict with current treatment recommendations.

Frequency

United States

Abuse of PCP began in the 1960s and peaked in the late 1970s. In 1978, the National Annual High School Senior and Young Adult Survey found that 12.8% of high school seniors had used PCP. Actually, more may have used PCP without realizing it; a 1975 survey showed that 91% of the street substances sold as THC, LSD, or some other hallucinogen such as mescaline actually contained PCP. Overall, abuse of this substance has decreased in the United States, and a 2007 survey found that only 2.1% of high school seniors had ever knowingly used PCP.4 PCP use reportedly remained steady in 2008. In the United States, quite a lot of regional variability in the abuse of PCP exists, with some of the highest areas of use being Washington, DC; Newark, NJ; Philadelphia, Pa; Baltimore, Md; and Dallas, Tex.

International

International use of PCP is also regional. The use of all drugs in Canada, including PCP, is similar to use in the United States, except that the relative percentages are usually smaller there. Mexico has an unusually large number of available indigenous hallucinogens, such as peyote cacti, Psilocybe mushrooms, and psychedelic morning glory seeds (ololiuqui); therefore, artificial hallucinogens are not as much in demand there. In the rest of the world, various preferred substances of abuse are regionally determined. PCP use has never been as much of a problem worldwide as it was in the United States in the 1960s and 1970s.

Mortality/Morbidity

Death from PCP is usually caused by one of the following: overdose (serum levels >100 ng/mL), suicide while under the influence of the drug, or accidental death due to bizarre behavior during intoxication or withdrawal. Those intoxicated with PCP have also been reported to be more likely to be violent, up to and including the commission of homicides.

Nonlethal physical injuries are an additional possible complication because PCP has anesthetic properties and greatly decreases pain perception such that individuals under its influence may not realize how badly they are injured, and thus may greatly aggravate what are originally more minor physical injuries.

Race

PCP seems to have been abused more often by members of inner-city minority groups than by members of the middle class majority population. The reasons for this are not clear.

Sex

In terms of sexual distribution, PCP is more likely to be knowingly abused by males, but this is true of many substances that are abused.

Age

PCP is a drug primarily abused by adolescents and young adults. Older users tend to have started using when they were young.

Clinical

History

If a patient can tell the physician reliably what he or she has used, it is obviously of help. Asking specifically about PCP can produce better information some of the time; however, since PCP is sold under other names, the history may be inaccurate. If any family or friends are present, they may also be of help in obtaining history, but, again, no one may know for certain if a substance is a causative factor for symptoms or what it may have been.

Physical

The Mental Status Examination is the most important area of abnormality in PCP intoxication. A great deal of variability frequently occurs in the mental status findings with these patients, and, at times, their results may appear normal or nearly normal, while a few (about 20) minutes later, obvious psychosis and possible evidence of dangerousness to self and/or others will appear. Therefore, one must carefully document the hallucinations, delusions, and mood-related issues (such as suicidal and homicidal thinking) that are present with reference to the time of the examination and comment on any changes noted during the examination.

  • Individuals intoxicated with PCP frequently seem to feel a need to undress, whether due to their elevated temperature or for some delusion-related impulse. 
  • These patients may look highly distressed, often crying and upset and citing their suicidal and homicidal urges as related to this discomfort. 
  • Affective lability also occurs, with a wide range from normal or near-normal mood to rage, dysphoria and depression, or anxiety. 
  • Orientation and other mental status measures of mentation are also important to document because PCP produces a drug-induced delirium as well as the psychosis.
  • Concentration should be poor, so serial 7 calculations or spelling the word "world" backward, or even forward, will usually be difficult for such patients.
  • Judgment is impaired with impulsivity being commonly observed, as well as a seeming lack of normal fear. 
  • Insight is highly variable from moment to moment and cannot be relied upon to remain stable over any period of time.

The physical examination may be difficult because these patients are usually not very cooperative, but, if possible, look for decreased deep tendon reflexes and nystagmus (particularly vertical but it may also be of the horizontal or rotatory variety). Videos of various forms of nystagmus may be found online on the Journal of Neurology, Neurosurgery, and Psychiatry Web site.8

Other evidence of loss of muscle coordination may also be present, and examinations such as finger-to-nose or heel-to-shin testing, if possible, may show abnormalities. Typical anticholinergic findings are common because PCP is a highly anticholinergic substance. Elevations in vital signs are also often present for this reason, with tests of blood pressure, pulse, and temperature likely to yield higher-than-normal findings. Keep in mind that PCP is related to anesthetics, and the findings will be similar to those observed as people descend into dose-related anesthesia.

Physical examination findings of PCP-intoxicated individuals vary in accordance with the serum level of the drug:

  • Lower blood levels (20-30 ng/mL) cause a picture of sedation, irritability, hyperactivity, impaired attention, and mood elevation.
  • As the level rises above 30 ng/mL, physical examination shows progressive levels of ataxia, paresthesias, and psychosis.
  • At 100 ng/mL, stimulant effects are noted most, with hypertension and hyperreflexia becoming more pronounced.
  • At more than 100 ng/mL, stupor and seizures can occur. In this range, overdose-related death is possible.

Causes

  • Risk factors for use of PCP include the following:
    • Male sex (72%)
    • African American (54%) or Hispanic ethnicity
    • Young adult age range (62% of people treated for PCP overdose are in the second decade of life)
  • Obviously, to ingest PCP, one must have access to this illicit substance, but it is fairly inexpensive and simple to synthesize and is thus relatively easy to obtain.
  • Sometimes, people who are intoxicated on PCP do not know that PCP is the drug they have received. Rather, the buyer of the drug is often told that he or she is getting something more exotic, such as THC or a designer drug.

More on Phencyclidine (PCP)-Related Psychiatric Disorders

Overview: Phencyclidine (PCP)-Related Psychiatric Disorders
Differential Diagnoses & Workup: Phencyclidine (PCP)-Related Psychiatric Disorders
Treatment & Medication: Phencyclidine (PCP)-Related Psychiatric Disorders
Follow-up: Phencyclidine (PCP)-Related Psychiatric Disorders
Multimedia: Phencyclidine (PCP)-Related Psychiatric Disorders
References
Further Reading

References

  1. Enomoto T, Noda Y, Mouri A, Shin EJ, Wang D, Murai R. Long-lasting impairment of associative learning is correlated with a dysfunction of N-methyl-D-aspartate-extracellular signaling-regulated kinase signaling in mice after withdrawal from repeated administration of phencyclidine. Mol Pharmacol. Dec 2005;68(6):1765-74. [Medline].

  2. Hajszan T, Leranth C, Roth RH. Subchronic phencyclidine treatment decreases the number of dendritic spine synapses in the rat prefrontal cortex. Biol Psychiatry. Sep 15 2006;60(6):639-44. [Medline].

  3. Kehrer C, Maziashvili N, Dugladze T, Gloveli T. Altered Excitatory-Inhibitory Balance in the NMDA-Hypofunction Model of Schizophrenia. Front Mol Neurosci. 2008;1:6. [Medline].

  4. Johnston LD, O'Malley PM, Bachman JG, Schulenberg JE. Monitoring the Future, National Results on Adolescent Drug Use. Overview of Key Findings. Monitoring the Future. Available at http://www.monitoringthefuture.org/pubs/monographs/overview2008.pdf. Accessed April 9, 2009.

  5. Wong LK, Biemann K. Metabolites of phencyclidine. Clin Toxicol. 1976;9(4):583-91. [Medline].

  6. Olney JW, Labruyere J, Price MT. Pathological changes induced in cerebrocortical neurons by phencyclidine and related drugs. Science. June 1989;244:1360-1362. [Medline].

  7. Corales RL, Maull KI, Becker DP. Phencyclidine abuse mimicking head injury. JAMA. Jun 13 1980;243(22):2323-4. [Medline].

  8. Serra A, Leigh RJ. Diagnostic value of nystagmus: spontaneous and induced ocular oscillations. J Neurol Neurosurg Psychiatry. Dec 2002;73(6):615-8. [Medline][Full Text].

  9. Barton CH, Sterling ML, Vaziri ND. Rhabdomyolysis and acute renal failure associated with phencyclidine intoxication. Arch Intern Med. 1980;140:568-569. [Medline][Full Text].

  10. Prochaska JO and DiClemente CC. Transtheoretical therapy: Toward a more integrative model of change. Psychotherapy: Theory, Research and Practice. 1982;19:276-288.

  11. Tennant FS Jr, Rawson RA, McCann M. Withdrawal from chronic phencyclidine (PCP) dependence with desipramine. Am J Psychiatry. Jun 1981;138(6):845-7. [Medline].

  12. Pestaner JP, Southall PE. Sudden death during arrest and phencyclidine intoxication. Am J Forensic Med Pathol. Jun 2003;24(2):119-22. [Medline].

  13. Aniline O, Allen RE, Pitts FN Jr. The urban epidemic of phencyclidine use: laboratory evidence from a public psychiatric hospital inpatient service. Biol Psychiatry. Oct 1980;15(5):813-7. [Medline].

  14. Camilleri JG. The use of phencyclidine (Cl-395) in obstetric procedures: a preliminary communication. Anesthesia. 2007;17(4):422-426. [Full Text].

  15. Crider R. Phencyclidine: changing abuse patterns. NIDA Res Monogr. 1986;64:163-73. [Medline].

  16. Davis BL. The PCP epidemic: a critical review. Int J Addict. Oct 1982;17(7):1137-55. [Medline].

  17. Gorelick DA, Balster RL. Phencyclidine (PCP). In: Kupfer DJ, Bloom FE. Psychopharmacology - the fourth generation of progress. 4. Philadelphia, PA: Lippincott Williams & Wilkins; 2002:[Full Text].

  18. Jodo E, Suzuki Y, Katayama KY, Takeuchi S, Niwa SI, Kayama Y. Activation of medial prefrontal cortex by phencyclidine is mediated via a hippocampal-prefrontal pathway. Cerebral Cortex. 2005;15(5):663-669.

  19. Johnston LD, O'Malley PM, Bachman JG, Schulenberg JE. Various stimulant drugs show continuing declines among teens in 2008, most illicit drugs hold steady. University of Michigan News Service, Ann Arbor, MI. Available at http://www.monitoringthefuture.org. Accessed 02/04/2009.

  20. Koek W, Woods JH. Correlations between phencyclidine-like activity and N-methyl-D-aspartate antagonism: behavioral evidence. In: Sigma and Phencyclidine-like Compounds as Molecular Probes in Biology. Ann Arbor, Mich: NPP Books; 1988.

  21. Lehrmann E, Colantuoni C, Deep-Soboslay A, Becker KG, Lowe R, Huestis MA, et al. Transcriptional changes common to human cocaine, cannabis, and phencyclidine abuse. PLoS ONE [serial online]. 1(1):e114. Available at http://www.plosone.org/article/fecthArticle.action?articleURI=info:do.

  22. Lundberg GD, Gupta RC, Montgomery SH. Phencyclidine: patterns seen in street drug analysis. Clin Toxicol. 1976;9(4):503-11. [Medline].

  23. McCarron MM, Schulze BW, Thompson GA. Acute phencyclidine intoxication: clinical patterns, complications, and treatment. Ann Emerg Med. Jun 1981;10(6):290-7. [Medline].

  24. Meyer JS, Greifsenstein F, Devault M. A new drug causing symptoms of sensory deprivation. J Nerv Ment Dis. 1959;129:29-40.

  25. Narendran R, Frankle WG, Keefe R, Gil R, Martinez D, Slifstein M. Altered prefrontal dopaminergic function in chronic recreational ketamine users. Am J Psychiatry. Dec 2005;162(12):2352-9. [Medline].

  26. Penschuck S, Flagstad P, Didriksen M, Leist M, Michael-Titus AT. Decrease in parvalbum in-expressing neurons in the hippocampus and increased phencyclidine-induced locomotor activity in the rat methylazoxymethanol (MAM) model of schizophrenia. Eur J Neurosci. 2005;23(1):279-284.

  27. Petersen RC, Stillman RC. Phencyclidine: an overview. NIDA Res Monogr. Aug 1978;(21):1-17. [Medline].

  28. Phillips WA, Silverstein SM. Convergence of biological and psychological perspectives on cognitive coordination in schizophrenia. Behav Brain Sci. Feb 2003;26(1):65-82; discussion 82-137. [Medline].

  29. Pichot JT, Schmetzer AD. Phencyclidine Bibliography. AAAP - Resource Site for the PGY-5 Curriculum Project - Bibliography. Available at http://www.aaap.org/pgy5/10.10.01pencyclidine.html. Accessed 02/21/2009.

  30. Self D. Drug dependence and addiction: neural substrates. Am J Psychiatry. Feb 2004;161(2):223. [Medline].

  31. Sena SF, Kazimi S, Wu AH. False-positive phencyclidine immunoassay results caused by venlafaxine and O-desmethylvenlafaxine. Clin Chem. 2002;48(4):676-7. [Medline].

  32. Shi WX, Zhang XX. Dendritic glutamate-induced bursting in the prefrontal cortex: further characterization and effects of phencyclidine. J Pharmacol Exp Therapeutics. 2003;305(2):680-687.

  33. Shulgin AT, Mac Lean DE. Illicit synthesis of phencyclidine (PCP) and several of its analogs. Clin Toxicol. 1976;9(4):553-60. [Medline].

  34. Stefani MR, Moghaddam B. Systemic and prefrontal cortical NMDA receptor blockade differentially affect discrimination learning and set-shift ability in rats. Behav Neurosci. Apr 2005;119(2):420-8. [Medline].

  35. Stockard JJ, Werner SS, Aalbers JA, Chiappa KH. Electroencephalographic findings in phencyclidine intoxication. Arch Neurol. Mar 1976;33(3):200-3. [Medline].

  36. Weiss CJ, Millman RB. Hallucinogens, phencyclidine, marijuana, inhalants. In: Clinical Textbook of Addictive Disorders. New York, NY: Guilford Press; 1991.

  37. West WB, Lou A, Perchersky K, Chadich ME, Appel JB. Antagonism of a PCP drug discrimination by hallucinogens and related drugs. Neuropsychopharmacology. 2000;22(6):618-625. [Full Text].

  38. Wong LK, Biemann K. Metabolites of phencyclidine in humans. Biological Mass Spectrometry. April 2005;2(4):204-205.

  39. Yago KB, Pitts FN Jr, Burgoyne RW. The urban epidemic of phencyclidine (PCP) use: clinical and laboratory evidence from a public psychiatric hospital emergency service. J Clin Psychiatry. May 1981;42(5):193-6. [Medline].

  40. Ziedonis D, Wyatt S. Psychotic disorders. In: Principles of Addiction Medicine. 2nd ed. Chevy Chase, Md: American Society of Addiction Medicine; 1998.

  41. Zukin SR, Zukin RS. Phencyclidine. In: Substance Abuse: A Comprehensive Textbook. Baltimore, Md: Williams & Wilkins; 1992.

Further Reading

Gorelick DA, Balster RL. Phencyclidine (PCP). Back to Psychopharmacology - The Fourth Generation of Progress

Pinchot JT, Schmetzer AD. Phencyclidine bibliography, for AAAP - Resource Site for the PGY-5 Curriculum Project, July 2001

Books and book chapters on PCP:

Hafen B, Frandsen K. Phencyclidine - Angel Dust: By any name not fit for human consumption. Hazelden Foundation, 1980.

Carroll M. The dangerous angel. In: Snyder SH, ed. The Encyclopedia of Psychoactive Drugs. Chelsea House Publishers, 1985, ISBN: 087754753X

Ogelsby EW, Faber S, Faber S. Angel Dust - What everyone should know about PCP. Charing Cross Publishing Company, 1982, ISBN: 0890740666

Keywords

phencyclidine-related psychiatric disorders, PCP, angel dust, crystal, hog, krystal joint, KJ, mintweed, rocket fuel, delta-9-tetrahydrocannabinol, THC, N -methyl-D-aspartate, NMDA, lysergic acid diethylamide, LSD, substance-induced psychosis, 1-(phenylcyclidine) piperidine

Contributor Information and Disclosures

Author

Alan D Schmetzer, MD, Professor, Vice-Chair for Education, and Director of Residency Training in General and Addiction Psychiatry, Department of Psychiatry, Indiana University School of Medicine
Alan D Schmetzer, MD is a member of the following medical societies: American Academy of Addiction Psychiatry, American Academy of Clinical Psychiatrists, American Academy of Psychiatry and the Law, American College of Physician Executives, American Medical Association, American Neuropsychiatric Association, American Psychiatric Association, and Association for Convulsive Therapy
Disclosure: Nothing to disclose.

Coauthor(s)

Roland McGrath, MD, Chairman, Professor, Department of Emergency Medicine, Indiana University School of Medicine
Roland McGrath, MD is a member of the following medical societies: American Academy of Emergency Medicine, American College of Emergency Physicians, and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.

David R Diaz, MD, Assistant Professor of Clinical Psychiatry, Indiana University School of Medicine; Attending Psychiatrist, Adult Service, Larue D Carter Memorial Hospital; Attending Psychiatrist, Indiana University Hospital Adult Outpatient Clinic, Indianapolis, Indiana
David R Diaz, MD is a member of the following medical societies: American Psychiatric Association, Indiana Psychiatric Society, Indiana State Medical Association, and Indianapolis Medical Society
Disclosure: Johnson and Johnson Ownership interest Other

Medical Editor

Barry I Liskow, MD, Professor of Psychiatry, Vice Chairman, Psychiatry Department, Director, Psychiatric Residency Program, University of Kansas School of Medicine; Director, Psychiatric Outpatient Clinic, The University of Kansas Medical Center
Barry I Liskow, MD is a member of the following medical societies: American Academy of Clinical Psychiatrists, American Academy of Psychiatrists in Alcoholism and Addictions, American Medical Association, American Psychiatric Association, and Research Society on Alcoholism
Disclosure: Nothing to disclose.

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Iqbal Ahmed, MBBS, Professor, Department of Psychiatry, John A Burns School of Medicine, University of Hawaii
Iqbal Ahmed, MBBS is a member of the following medical societies: Academy of Psychosomatic Medicine, American Association for Geriatric Psychiatry, American Neuropsychiatric Association, and American Psychiatric Association
Disclosure: Nothing to disclose.

CME Editor

Harold H Harsch, MD, Program Director of Geropsychiatry, Department of Geriatrics/Gerontology, Associate Professor, Department of Psychiatry and Department of Medicine, Froedtert Hospital, Medical College of Wisconsin
Harold H Harsch, MD is a member of the following medical societies: American Psychiatric Association
Disclosure: lilly Honoraria Speaking and teaching; Forest Labs Honoraria Speaking and teaching; AstraZeneca Honoraria Speaking and teaching; Pfizer Grant/research funds Speaking and teaching; Northstar Grant/research funds Research; Novartis Grant/research funds research; Pfizer  Speaking and teaching; Sanofi-avetis Grant/research funds research; Otsuke Grant/research funds reseach; GlaxoSmithKline Grant/research funds research

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Stephen Soreff, MD is a member of the following medical societies: American College of Mental Health Administration and American Psychosomatic Society
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