Withdrawal symptoms cocaine

Modified and reprinted with permission from American Psychiatric Association. Diagnostic and Statistical Manual of Mental Disorders, 4th ed.r text revision. Washington, DC American Psychiatric Association, 2000 Sofuoglu M, Dudish-Poulsen S, Poling J, et al. The effect of individual cocaine withdrawal symptoms on outcomes in cocaine users. Addict Behav 2005,30 1 125-1134 and Patten SB, Barbui C. Drug-induced depression a systematic review to inform clinical practice. Psychoth Psychosom 2004 73 207-215. 

Extern, Irl L., David A. Gross, and Mark S. Gold. 1989. "Bromocriptine Treatment of Cocaine Withdrawal Symptoms." American Journal of Psychiatry 146 403. 

Modafinil (Fig. 18.12) is also a non-amfetamine with psychostimulant properties, used for the treatment of narcolepsy, ADHD, obstruaive sleep apnea/hypopnea syndrome and may show potential for the treatment of cocaine withdrawal symptoms. Inspection of the structural representation indicates that modafinil contains a diphe-nylmethyl moiety and hence is dissimilar from an... 

Because chronic cocaine use appears to reduce the efficiency of central dopamine neurotransmission, a number of dopaminergic compounds, including amantadine, bromocriptine, mazindol, and methylphenidate, have been examined as treatments for cocaine abuse. It is thought that these relatively slow-onset dopaminergic agents, with low or relatively low abuse potential, would correct the dopamine dysregulation and alleviate withdrawal symptoms following chronic stimulant use. 

The treatment goals for withdrawal from ethanol, cocaine/ amphetamines, and opioids include (1) a determination if pharmacologic treatment of withdrawal symptoms is necessary, (2) management of medical manifestations of withdrawal such as hypertension, seizures, arthralgias, and nausea, and (3) referral to the appropriate program for substance abuse treatment. 

Collectively, evidence strongly suggests that alterations in monoamine systems and their targets mediate the acute effects of cocaine, and that changes in these systems mirror the addiction, cravings, and withdrawal symptoms. 

Animals self-administer cathinone in a pattern common to abuses of monoamine stimulants such as cocaine (Woolverton and Johanson 1984). Cathinone can induce a conditioned place preference in rats (Schechter 1991). Withdrawal symptoms of khat include lethargy, depression, nightmares, and mild tremor (Kalix 1994). /V-methylated cathinone (methcathinone) is more potent, and has become available on the illegal market. It was subsequently scheduled as a controlled substance (Glennon et al. 1995). 

Substance-Induced Anxiety Disorder. Numerous medicines and drugs of abuse can produce panic attacks. Panic attacks can be triggered by central nervous system stimulants such as cocaine, methamphetamine, caffeine, over-the-counter herbal stimulants such as ephedra, or any of the medications commonly used to treat narcolepsy and ADHD, including psychostimulants and modafinil. Thyroid supplementation with thyroxine (Synthroid) or triiodothyronine (Cytomel) can rarely produce panic attacks. Abrupt withdrawal from central nervous system depressants such as alcohol, barbiturates, and benzodiazepines can cause panic attacks as well. This can be especially problematic with short-acting benzodiazepines such as alprazolam (Xanax), which is an effective treatment for panic disorder but which has been associated with between dose withdrawal symptoms. 

It is beheved that phenomena such as sensitization, tolerance and drug-dependence might also involve synaptic plasticity. In fact, numerous studies indicate that NMDA receptor antagonists block sensitization to amphetamine and cocaine as well as tolerance and dependence to ethanol and opioids in animal models (Trujillo and Akil 1991 Pasternak and Inturrisi 1995 Trujillo and Akil 1995 Mao 1999). Recent studies indicate that the uncompetitive NMDA receptor antagonists dextromethorphan, memantine and neramexane not only prevent the development of morphine tolerance, but also reverse estabhshed tolerance in the continuing presence of this opioid, prevent the expression of withdrawal symptoms in rats (Popik and Skolnick 1996 Popik and Danysz 1997 Popik and Kozela 1999 Houghton et al. 2001) and attenuate the expres-... 

It is known, however, that drugs are readily available in many prisons, and the rate of adverse incidents and the time and effort spent in detecting smuggling of drugs in has been enough to persuade some authorities that at least the basics of treatment should be available. The most routine option has become to provide a detoxification for opiate misusers, with for instance lofexidine or dihydrocodeine, and also benzodiazepines will often be issued if there is a history of abuse of these and it is intended to avoid the possibility of fits with a short withdrawal course. The adverse incidents in custody and prisons have included some deaths in users of crack cocaine, with physical explanations postulated but no very satisfactory treatment for cocaine withdrawal indicated. Prison services have typically been wary of methadone, and in favouring lofexidine use it was encouraging that a randomized double-blind trial carried out by prison specialists found lofexidine to be as effective as methadone in relief of withdrawal symptoms (Howells et al. 2002). 

Desipramine is a tricyclic antidepressant that has been tested in several double-blind trials among cocaine addicts. Like cocaine, desipramine inhibits monoamine neurotransmitter reuptake, but its principal effects are on norepinephrine reuptake. It was hypothesized that desipramine could relieve some of the withdrawal symptoms of cocaine dependence and reduce the desire for cocaine during the vulnerable period following cessation of cocaine. This drug showed efficacy early in the epidemic in a group of patients who were primarily white collar intranasal cocaine users. The majority of subsequent studies of desipramine-using, more severely ill cocaine addicts have been negative. 

---