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21.qxd 3/10/08 9:58 AM Page 657<br />

Course<br />

Recreational use of stimulants is not uncommon, and such<br />

occasional use generally causes few, if any, consequences.<br />

Some patients may develop an abusive pattern of use, however,<br />

and continue to seek intoxication despite suffering<br />

social or legal consequences. Addiction is said to occur when<br />

a craving develops for the stimulant, accompanied by the<br />

phenomena of tolerance and withdrawal; such patients may<br />

use stimulants on a daily basis, in relatively modest doses, or<br />

display a ‘binge’ pattern (Kramer et al. 1967), in which they<br />

use ever-escalating doses until, after a matter of days or<br />

more, they either run out of money or become so debilitated<br />

that they have to stop, after which they suffer through a<br />

withdrawal syndrome before going on yet another binge.<br />

Etiology<br />

It appears that the euphoria seen with stimulants occurs<br />

secondary to dopamine release within the ventral striatum<br />

(Drevets et al. 2001), whereas the autonomic symptomatology<br />

is mediated by enhanced noradrenergic tone<br />

(Nurnberger et al. 1984).<br />

Differential diagnosis<br />

Intoxication with cocaine may be clinically indistinguishable<br />

from stimulant intoxication, and the differential may<br />

rest on history or drug screening.<br />

Lacking a history (as is often the case, given the deceit and<br />

denial seen in many cases), the elation and talkativeness of<br />

the intoxication may suggest mania, and the irritability,<br />

fatigue, and sleep disturbance of withdrawal may suggest<br />

depression. Drug screening is helpful here; however, observation<br />

in a controlled environment will also tell the tale, as<br />

the symptoms resolve over the expected time period.<br />

The stimulant-induced psychosis represents one of the<br />

toxic psychoses, discussed in Section 7.1, and is suggested<br />

by its emergence during an intoxication and its resolution<br />

during enforced abstinence.<br />

Treatment<br />

Intoxication, if mild, may be managed with simple observation.<br />

In severe cases one may utilize an antipsychotic<br />

such as haloperidol, in a dose of approximately 5 mg, either<br />

as the concentrate or parenterally, with repeat doses every<br />

hour or so until the patient is calm, limiting side-effects occur<br />

or a maximum dose of approximate 20 mg is reached.<br />

Stimulant psychosis may be treated with an antipsychotic,<br />

such as haloperidol (5–10 mg) or risperidone<br />

(2–4 mg), with the understanding that the medication<br />

may, given the natural course of the disorder, be eventually<br />

discontinued.<br />

21.2 Cocaine 657<br />

Withdrawal symptomatology, if severe and accompanied<br />

by suicidal ideation, may require hospitalization.<br />

Pharmacologic treatment is generally not indicated.<br />

The overall treatment of stimulant addiction has as its<br />

goal abstinence. Hospitalization is often required to break<br />

the pattern of use, and long-term involvement with groups<br />

such as Cocaine Anonymous or Narcotics Anonymous<br />

may be helpful.<br />

21.2 COCAINE<br />

Several different preparations of cocaine are available illegally.<br />

Cocaine hydrochloride is a white powder that may be<br />

insufflated (‘snorted’) into the nasal passages where it is<br />

absorbed through the nasal mucosa; it is also water soluble<br />

and thus may be dissolved and injected intravenously.<br />

Cocaine hydrochloride is destroyed by heat and is thus not<br />

suitable for smoking; it may, however, be treated with<br />

sodium bicarbonate and then either extracted with ether to<br />

yield a ‘free base’ preparation or warmed to create a ‘rock’<br />

of ‘crack’ cocaine. Both the free base and crack preparations<br />

evaporate with heating and thus may be smoked.<br />

Clinical features<br />

The onset of intoxication varies according to the preparation<br />

used; after snorting, peak levels are reached within<br />

30–60 minutes, whereas after intravenous injection or<br />

smoking, peak levels occur within seconds, creating a<br />

much more intense intoxication. During intoxication<br />

(Kleber and Gawin 1984), patients become euphoric,<br />

hyperalert, talkative, and grandiose. Hyperactivity is common,<br />

and with higher doses agitation may occur<br />

(Fischman et al. 1976). Some patients may experience<br />

visual hallucinations, and these are typically of insects,<br />

which are often referred to as ‘cocaine bugs’; these hallucinations<br />

may be accompanied by tactile hallucinations of<br />

bugs crawling beneath the skin, and some patients may<br />

excoriate themselves in an attempt to ‘get’ them. With mild<br />

intoxication libido increases, and in males there may be<br />

delayed ejaculation; with more severe intoxication, however,<br />

there may be erectile dysfunction. In severe intoxication,<br />

especially after intravenous use or smoking, a<br />

delirium may occur, with confusion, incoherence, lability,<br />

and delusions and hallucinations. Other symptoms and<br />

signs include mydriasis, hypertension, headache, nausea<br />

and vomiting, tachycardia, and arrhythmias or cardiac<br />

arrest (Hsue et al. 2007). Uncommonly, there may be<br />

chorea (‘crack dancing’) (Daras et al. 1994), tics (Pascual-<br />

Leone and Dhuna 1990), myocardial infarction (Virmani<br />

et al. 1988), rhabdomyolysis (Roth et al. 1988), stroke (due<br />

to infarction, intracerebral hemorrhage or subarachnoid<br />

hemorrhage [Klonoff et al. 1989; Lichtenfeld et al. 1986;<br />

Nolte et al. 1996]), and, with chronic, repeated use, a cerebral<br />

vasculitis (Fredericks et al. 1991; Krendel et al. 1990).

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