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21.qxd 3/10/08 9:58 AM Page 660<br />

660 Substance use disorders<br />

Course<br />

Recreational use of hallucinogens is very common among<br />

adolescents and young adults; it is typically confined to<br />

occasional use without consequences at parties or social<br />

gatherings. Hallucinogen abuse, that is repeated use<br />

despite significant consequences, is relatively rare. Neither<br />

craving nor, as pointed out earlier, withdrawal occur, and<br />

addiction is not seen.<br />

Etiology<br />

All of the hallucinogens exhibit complex agonist and<br />

antagonist effects at either pre- or post-synaptic serotonin<br />

receptors, and in the case of MDMA there may be destruction<br />

of serotoninergic neurons (McCann et al. 1998;<br />

Ricaurte et al. 1988).<br />

Differential diagnosis<br />

Mild intoxication with phencyclidine may be quite similar<br />

to that seen with hallucinogens, but is suggested by nystagmus,<br />

dysarthria, and ataxia.<br />

Hallucinogen-induced flashbacks, mood changes, and<br />

psychosis are all indicated by the preceding intoxication.<br />

When this history is lacking, disorders noted in the differential<br />

diagnosis for hallucinations, depression, mania, and<br />

psychosis may be considered.<br />

Treatment<br />

‘Bad trips’ may be managed by supportive observation; in<br />

some cases lorazepam may be helpful. Post-intoxication<br />

mood changes, if severe, may require hospitalization for supportive<br />

care until they run their course. Post-intoxication<br />

psychosis may likewise require hospitalization and, if prolonged,<br />

may be treated with an antipsychotic such as olanzapine.<br />

Flashbacks generally do not require treatment but, if<br />

frequent and troubling, consideration may be given to the<br />

use of clonazepam in a dose of 2 mg daily (Lerner et al. 2003).<br />

21.4 PHENCYCLIDINE AND KETAMINE<br />

Phencyclidine and its closely related derivative ketamine are<br />

both arylcyclohexylamines that were developed as ‘dissociative’<br />

anesthetics. The frequent occurrence of post-operative<br />

psychosis with phencyclidine has led to its abandonment in<br />

medical practice; however, ketamine is still used, both as an<br />

anesthetic and as an analgesic. Both drugs are used as intoxicants,<br />

and the use of ketamine in this regard appears to be<br />

on the rise. Phencyclidine is also known as PCP, ‘angel dust’,<br />

‘hog’, and ‘peace pill’, and ketamine may be referred to as<br />

‘K’, ‘special K’, ‘vitamin K’, ‘cat valium’, ‘kat’ or ‘kit-kat’.<br />

Clinical features<br />

Intoxication with phencyclidine may be roughly characterized<br />

as mild, moderate, or severe; ketamine is less potent<br />

than phencyclidine and only rarely produces the severe<br />

and potentially life-threatening intoxication not uncommonly<br />

seen with phencyclidine. Both of these drugs may be<br />

ingested, ‘snorted’ intranasally, smoked, or injected.<br />

Mild intoxication (Javitt and Zukin 1991; Luby et al.<br />

1959; McCarron et al. 1981; Meyer et al. 1959; Pearlson<br />

1981; Weiner et al. 2000) is characterized by euphoria and<br />

a peculiar sense of detachment or dissociation. Patients<br />

may feel as if they are floating, and their bodies may, to<br />

them, appear misshapened. Lability, agitation, or lethargy<br />

may appear, and behavior may become bizarre and unpredictable,<br />

with violence in some cases. Patients may complain<br />

of nausea, vomiting, or vertigo, and examination may<br />

disclose dysarthria, ataxia, nystagmus (which may be rotatory,<br />

horizontal, or vertical), myoclonus, tremor, increased<br />

deep tendon reflexes, decreased pin-prick sensation in the<br />

extremities, and autonomic signs, such as an elevated temperature,<br />

tachycardia, an elevated respiratory rate, elevated<br />

blood pressure, diaphoresis, and flushing; rather than<br />

mydriasis, however, one typically sees miosis.<br />

Moderate intoxication is characterized by a delirium,<br />

which may be accompanied by delusions and visual hallucinations<br />

(Allen and Young 1978). Abnormal movements<br />

may appear, including facial grimacing, posturing, stereotypies,<br />

dystonia, and opisthotonus; grand mal seizures may<br />

also occur (Alldredge et al. 1989). Agitation may be<br />

extreme, and in some cases rhabdomyolysis occurs, with<br />

renal failure.<br />

Severe intoxication is characterized by stupor or coma<br />

(McCarron et al. 1981). In stupor, patients may be quite still<br />

or may evidence random, purposeless movements;<br />

myoclonus is frequent and the deep tendon reflexes are<br />

greatly increased. With even higher doses coma supervenes;<br />

this is a kind of ‘coma vigil’ in which the eyes are open and<br />

the patient appears vigilant, but shows no response to pain<br />

or to anything else. The temperature rises further, as does<br />

the blood pressure, and in some cases a hypertensive<br />

encephalopathy occurs. The electroencephalogram (EEG)<br />

in these cases shows profound generalized slowing.<br />

The duration of intoxication with ketamine, which has<br />

a half-life of about 3 hours, is approximately 4–6 hours.<br />

Phencyclidine intoxication is longer for two reasons. First,<br />

the half-life of phencyclidine is longer, anywhere from 7 to<br />

20 hours. <strong>Second</strong>, phencyclidine is a weak base and hence<br />

is ‘trapped’ in the stomach; phencyclidine is also lipophilic<br />

and is therefore taken up into adipocytes. Thus protected<br />

from hepatic metabolism, phencyclidine may linger for<br />

prolonged periods, and indeed may be detectable in the<br />

blood for weeks or longer after a single dose. Overall,<br />

intoxication with phencyclidine tends to last from half a<br />

day up to many days and, during the overall resolution of<br />

phencyclidine intoxication, the clinical picture may fluctuate<br />

fairly widely.

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