Addiction Treatment Blog

The medicine increases the disease.

Virgil (70-19BC), ‘The Aeneid’.

This chapter highlights the important areas of abuse of prescription drugs. Opioids, cocaine, dexamphetamine, anabolic steroids and many of their derivatives are prescription medicines in the UK but these have been the subject of earlier chapters. Similarly, some ‘smart drugs‘ and certain preparations used in association with anabolic steroids are also prescription drugs and are discussed elsewhere in the blog.

Anaesthetics

Many gaseous anaesthetics have been subject to abuse but in practice these all have a low abuse potential because although they may produce pleasurable effects they are not easily available and are inconvenient to use, even for healthcare professionals with access to them. The exception is ketamine abuse which is well-described problem at street level.

Nitrous oxide

Nitrous oxide gas is not a prescription medicine in the UK but is included in this chapter for ease of reference. It is used therapeutically to induce anaesthesia and also as an analgesic. In this setting it is usually mixed with oxygen and is available commercially as Entonox in characteristic blue and white cylinders. Abuse is most likely to involve healthcare personnel who use nitrous oxide in the workplace, e.g. dentists, anaesthetists and theatre staff. However, the gas is also the propellant used in many canisters of pressurised whipped cream. The experienced abuser is able to release the gas into containers, allowing subsequent gas inhalation with minimum cream contamination. Inhalation is usually via a plastic bag, balloon or similar device. Healthcare staff may, of course, use anaesthetic administration equipment. In 1979, a US survey of 524 medical and dental students showed that 16 per cent of those questioned had abused nitrous oxide on at least one occasion.

Acute exposure to nitrous oxide can produce a short-lasting pleasurable intoxication: euphoria, relaxation, feelings of detachment and merriment (hence the alternative name of ‘laughing gas‘). The mechanism behind these central nervous system (CNS) effects is not fully understood but research suggest that it may, to a greater or lesser extent, be the result of an agonist action at central opioid receptors. This could be a direct action on opioid receptors, augmentation of the effects of endogenous opioids of stimulation of their release.

The cognitive impairment produced usually lasts only a few minutes because the gas is rapidly excreted via the lungs. Inhalation of the pure gas without oxygen (i.e. non-Entonox sources) can cause acute hypoxia either via oxygen insufficiency during inhalation or by nitrous oxide displacement of oxygen from alveoli during the excretion of the gas from the body. This latter mechanism – diffusion hypoxia – can be fatal.

As with volatile substance abuse, the results of intoxication are potentially more dangerous than the direct effect of the gas itself because accidents can occur in the disorientated abuser. Nitrous oxide can sometime cause nausea or vomiting; consequently there is a small risk of aspiration of vomit. Unlike many chemicals subject to volatile substance abuse, ’sudden death’ in the same manner as volatile substances. However, some fresh cream aerosol canisters with a nitrous oxide propellant may contain other propellants, such as chlorofluorocarbons, and nitrous oxide itself may produce degrees of hypoxia, as mentioned above. In a review of 11 fatal cases of abuse the cause of death, when it could be determined, was attributed to asphyxiation, fatal accident or aspiration of vomit. Fainting, pneumomediastinum and frostbite have also been reported as acute effects.

Repeated abuse has been associated with the development of a range of severe neurological disorders (mostly myeloneuropathies and neuropathies) and bone marrow depression. These adverse effects are believed to be caused by nitrous oxide accelerating vitamin B12 breakdown. Neurological damage is usually at least partly reversible but recovery is often slow and incomplete. Bone marrow depression is more quickly and completely reversible but has proved a serious complication in acutely ill patients administered long-term, high-dose nitrous oxide for therapeutic reasons. Cases of psychosis have been attributed to long-term use of the gas. Physical dependence may occur following chronic regular use, a delirium-like withdrawal state having been described in one patient but this is probably extremely rare.

Ketamine

Therapeutically, ketamine is used by the intravenous or intramuscular routes to induce or maintain anaesthesia. It has been known for many years that patients in recovery following ketamine anaesthesia may experience psychotomimetic reactions. These ‘emergence‘ phenomena commonly include feelings of mind-body dissociation (so-called ‘out-of-the-body experiences‘), sensations of floating, severe disorientation, vivid dreams and even delirium. Any of these effects may be subjectively pleasant or unpleasant.

Unlike the other anaesthetic agents described here, illicit supplies of ketamine are available on the street. Commercially ketamine is only available in parenteral formulation, and although it has been abused by injection, it seems to be more popular as an oral intoxicant. Eastman et al. reported in 1992 that an oral formulation might be prepared by evaporation of water from the injection solution, followed by packing into capsules. The drug can also be inhaled into the nose as a dry powder (’snorting‘). Street names for ketamine include ‘K‘, ‘vitamin K‘, ‘super K‘, ‘special K‘, and ‘kit-kat‘. The drug is sometimes detected as an adulterant in other illicit drugs, especially ecstasy, but it is used quite widely in its own right. The prevalence of abuse in Sweden has been such that legislation has been proposed to curtail usage.

Although an anaesthetic agent, ketamine only causes respiratory depression after very high doses. The main danger from abuse arises from the peculiarly altered states of consciousness that it can produce. Individuals may become so divorced from reality that the surrounding environment is perceived completely differently by the abuser. He or she may genuinely experience a ‘different world’. This is called dissociation. In this respect, ketamine intoxication has some similarities to the effects of phencyclidine to which it is structurally related (see Phencyclidine). This, coupled with delusions of paralysis of difficulty in moving and the analgesic effects of ketamine, could obviously result in serious accidents, depending on the location of the abuser. Ketamine has the potential to cause memory impairment, persistent repetitive movements (stereotypies) and can also give rise to ‘flashbacks’.

Other anaesthetics

Historically, anaesthetic ether was subject to abuse in the same way as most volatile liquids have been. Ether is now used as an anaesthetic in the West and supplies are difficult for the potential user to obtain. Some of the simple chlorinated alkanes (e.g. 1,1,1-trichloroethane) abused as solvents today have also been employed as anaesthetics in the past. There are occasional reports of abuse of more modern gaseous anaesthetics, e.g. enflurane, cyclopropane, halothane and fluothane. In each case abuse of these substances was reported in the medical literature because the abuser died as a result. Inhalational anaesthetics such as these are similar to many of the chemicals subject to volatile substance abuse – a well-known cause of sudden death (see Volatile Substance Abuse). Halothane abuse has been cited as a cause of hepatitis, a rare idiosyncratic side-effect when the drug is used as an anaesthetic. Ethyl chloride has also been abused by inhalation; this product is sometimes used as a topical anaesthetic.

Antidepressants

All antidepressants serve to increase the concentration of certain neurotransmitters in the brain: principally dopamine, noradrenaline and serotonin. Illicit drugs such as cocaine and amphetamines also boost the concentrations of these substances in the CNS and this property is known to be important for producing psychotropic effects. It is not surprising therefore that antidepressants themselves have been the subject of abuse. However, the total number of cases reported over the past 30 years is very small. Consequently, it has been argued that patients should not be informed of the abuse potential because the benefits of warning about the tiny risk of abuse are outweighed by the risk of causing non-compliance with a medication that can be life-saving (by preventing suicide). However, other authors feel that the patient should be warned in a non-alarmist way.

Monoamine oxidase inhibitors

Tranylcypromine is the monoamine oxidase inhibitor (MAOI) that has been abused most commonly. It has an amphetamine-like structure and has been abused for its stimulant-like effects. Most reported cases have involved patients with a history of depression who discovered that taking 100 to 300 mg of tranylcypromine per day resolved depression and produced a sense of well-being. Abuse of phenelzine has also been reported at a dosage of 90 to 150 mg per day. As with tranylcypromine, patients reported stimulant effects from these high doses. Some abusers have reported withdrawal reactions upon discontinuation.

Moclobemide, a selective inhibitor of CNS monoamine oxidase A, has been abused to produce euphoria in combination with citalopram or clomipramine. The authors of the report do not provide details of the doses used but do reveal that five individuals involved in this practice died from the serotonin syndrome.

Selective serotonin reuptake inhibitors

Fluoxetine is the foremost selective serotonin reuptake inhibitor (SSRI) used in the world. It has been subject to abuse in three different ways and there is no reason to suppose that any of the other SSRIs are less susceptible:

Amphetamine-like effect

Two cases of fluoxetine abuse have been described in which known street drug abusers discovered that high doses of fluoxetine produced an amphetamine-like stimulant effect. The first of these initially discovered the effect when taking 80 mg of fluoxetine and two cans of beer on an empty stomach. This produced ‘increased energy, talkativeness, mood elevation and slight jitters but she reported that it was unlike ’speed’ because she also felt numb and calm’. The second patient took 80 to 140 mg of fluoxetine per day initially but later increased this to a ‘handful’. He also experienced an amphetamine-like effect and used trazodone and later diazepam to sedate him at night. Both patients’ lives eventually became dominated by the taking of the drug, leading to hospital admission. Neither patient experienced a withdrawal reaction upon discontinuation.

Wilcox described a patient with anorexia who took 120 mg per day on account of the appetite suppressing effects she experienced. at high doses. No psychotropic effects were reported.

Augmentation of the effects of other drugs

Fluoxetine has been used to boost or prolong the actions of amphetamine or ecstasy. Limited animal experiments suggest that fluoxetine can increase the levels of amphetamines in the brain and the duration of action of the amphetamines, perhaps by decreasing the rate of metabolism. Two case reports suggest that when taken together, dexamphetamine and fluoxetine may have significantly greater mood enhancing effects in patients with depression than either drug alone. Theoratically, combining drugs which potentiate the activity of serotonergic systems in the brain will increase the risk of developing the central serotonin syndrome.

Reduction of amphetamine or ecstasy side effects

As discussed in All You Need To Know About Amphetamines and Ecstasy, fluoxetine may have some value in the reduction of amphetamine withdrawal symptoms although the human data are sparse. However, fluoxetine has also been used at street level in an attempt to help users cope with the aftermath of acute ecstasy or amphetamine intoxication. In addition, it has been taken in the belief that it will prevent or reduce long-term amphetamine or ecstasy-induced damage to serotonergic nerves. Animal studies have shown that fluoxetine may prevent excessive loss of brain 5-hydroxytrytamine (5HT) which has been associated with destruction of nerves by these illicit drugs.

Tricyclic antidepressants

There have been several case reports of the abuse of amitriptyline. This is a drug with significant antimuscarinic effects and the abuse potential may derive solely from this pharmacological property. A study in 1978 briefly described 86 patients on a methadone maintenance programme who abused amitriptyline to attain a ‘sedative type of high‘. This effect was reported by the authors to be dose-dependent, although precise details of doses taken were not provided. In one documented case, amitriptyline abuse led to the onset of repeated grand mal convulsions and a diagnosis of epilepsy; these symptoms abated when amitriptyline was withdrawn. The patient took up to 750 mg of amitriptyline per day. In a similar case, the chronic administration of 800 mg of amitriptyline daily led to convulsions and toxicity suggestive of overdose. Another patient took up to 2g per day. The three patients described here were all female and all claimed a calming and/or euphoric effect from high-dose amitriptyline.

Abuse of dothiepin has been reported from Ireland, where this drug is the most popular antidepressant prescribed. A questionnaire of 83 attenders at a Drug Treatment Centre in Dublin revealed that 38 had taken dothiepin for the purpose of abuse. Urine analysis of 99 other attenders showed that 19 had positive tests for tricyclic antidepressants. The total amount taken per day varied from 150 to 600 mg and this was reported to cause euphoria, sedation and various hallucinations (auditory and visual).

Antimuscarinic Drugs

Benzhexol (trihexyphenidyl), orphenadrine, benztropine and procyclidine are examples of antimuscarinic agents that have been abused to produce euphoric, and sometimes hallucinogenic, effects. The usual abusers are psychiatric patients who have been prescribed the drugs to counteract the extrapyramidal side effects of antipsychotic medication. However, the author is aware of two Parkinsonian patients believed to have abused orphenadrine. A large number of cases have been described and several good reviews are available.

As a group, these drugs are not generally available on the street, although cases of abusers purchasing supplies illegally are occasionally reported. These drugs are nearly always taken orally. Patients abusing their prescribed antimuscarinic drugs may go to great lengths to obtain further quantities. They may, for example, claim to have lost prescribed supplies, pretend resistance to dosage reduction, deny receipt of doses, steal or buy from other patients and even fake extrapyramidal symptoms. Phenothiazines may mask some of the pleasurable effects of antimuscarinic drug abuse: consequently, patients pleasurable effects of antimuscarinic drug abuse: consequently, patients may stop taking regular antipsychotic medication. In addition, there is the risk that some patients will swap these prescribed drugs for other, illicit, drugs of abuse so introducing antimuscarinics onto the local street scene.

For some schizophrenic patients it is difficult to classify this problem as ‘abuse‘ because the effects sought are not euphoria and psychoactive effects but an increased sociability and contentment. However, others simply seek a ‘high’ or entertaining hallucinations.

Large doses of antimuscarinics carry the risk of severe intoxication. The exact presentation of the intoxicated patient depends on the dose taken but some of the symptoms are listed in the table below. These effects usually subside within 24 to 72 hours but the diagnosis can be missed because symptoms may resemble those of a patient’s existing psychiatric illness. Withdrawal symptoms have been described in some chronic abusers and include rebound cholinergic effects, insomnia, headache, myalgia, various forms of gastrointestinal upset and sleep disturbance.

The antimuscarinic properties of certain other medications may, wholly or partly, account for their abuse potential. Examples include amitriptyline (see above) and antihistamines. Plants with antimuscarinic properties will be discussed at a later stage. Opioids, alcohol and cannabis can also produce antimuscarinic-like effects and, perhaps because of this, opioid abusers can be peculiarly sensitive to anti-muscarinic drugs. In the US study of amitriptyline abuse cited above, 25 per cent of 346 participants in a methadone maintenance programme had taken this drug to produce euphoria. The combination seemed to have at least additive effects. Similarly, a case report in 1984 suggested that antimuscarinic intoxication might be potentiated by alcohol.

Potential signs and symptoms of antimuscarinic intoxication

• Dilated pupils,
• Dry mouth and hot, dry skin,
• Tachycardia,
• Incoherence, impaired concentration, confusion, hallucinations, paranoia, anxiety, euphoria, excitement,
• Ataxia, disorientation
• Constipation
• Urinary retention

The main features are summarised in a verse:

Hot as a hare,
Blind as a bat,
Dry as a bone,
Red as a beet,
Mad as a hatter.

Sedatives

Barbiturates

The abuse of barbiturates on the street is now relatively minor problem. Barbiturates, like benzodiazepines (BZDs), are abused for the purposes of producing relaxation and increased sociability – a mild intoxication. Sometimes the oral formulations are injected for much the same reasons as BZDs. Like BZDs, barbiturates can cause physical dependence, and individuals exhibit both tolerance to the drugs’ effects and a withdrawal syndrome upon cessation. Consequently, barbiturates must be withdrawn slowly to the chronic user.

However, barbiturates are more likely than BZDs to cause unpleasant side effects. Even small doses can produce aggression, confusion, depression or anxiety and, unlike BZDs, the drugs are quite likely to depress mental acuity. Barbiturates also commonly precipitate sedation, incoherence and incoordination. These effects all depend on the dose taken. Large doses can cause potentially fatal respiratory depression and this effect is potentiated by alcohol and other CNS depressants such as opioids. In the heyday of barbiturate prescribing for insomnia, this was the usual case of death when barbiturates were taken in overdose. In the absence of pre-existing lung disease, BZDs are unlikely to cause respiratory depression even when enormous doses are taken.

Barbiturates are less easily obtainable on the black market than BZDs and so are more expensive; illicit manufacture is probably very limited.

Benzodiazepines

There are two different aspects to the subject of benzodiazepine (BZD) ‘abuse’.

1. Overprescribing and/or inappropriate prescribing of hypnotic and anxiolytic BZDs has resulted in large numbers of patients becoming dependent upon them.
2. Abuse of BZDs occurs on the street often by intravenous injection of formulations designed for oral administration.

Whereas the first of these two groups are patients who have been prescribed BZDs for a medical indication, the second group is largely composed of known abusers of a range of illicit substances. For ease of discussion, these might be termed ‘BZD-dependents’ and ‘BZD abusers’ respectively.

Benzodiazepine dependents

In 1995 there were nearly 13.9 million prescriptions for benzodiazepines in England. This compares over 35 million in 1979, suggesting that doctors are gradually acting to combat the problem of BZD dependence. The table below suggests straightforward ways in which this change needs to progress. BZDs are very useful and, on the whole, safe drugs but prescribing practice still needs to be more rational in many cases. GPs and hospital doctors are jointly responsible for starting patients on benzodiazepines, failing to review treatment regularly and not stopping treatment when it is no longer required. However, as Hallstrom has argued, it can be very difficult to specify why patients should not take these drugs chronically. He suggests that the main reasons are as follows.

• Benzodiazepines are often prescribed to blot out psychological stresses and so do not enable the affected individual to learn how to adapt to stress and thereby mature.
• Patients and doctors can be tempted into thinking there is a ‘pill for every ill’ and rely too much on pharmacological approaches to treatment when other approaches might be more appropriate.
• A large proportion of prescriptions are made out by male doctors for female patients. If women have an unequal role in society this is the cause of their stress, then BZDs are not the answer. However, feminists might feel that ‘They are given transquillisers by the establishment to stop them complaining too much’.
• The long-term efficacy of BZDs is unproven.
• Side effects, although sometimes difficult to identify, include memory loss and psychomotor incoordination. Benzodiazepines impair driving ability.
• Dependence is not a problem in itself as long as supplies of benzodiazepines continue; the sudden cessation of drug in the dependent individual is the problem (i.e. withdrawal, see below).

Most health authorities or Trusts have produced guidelines on BZD prescribing and withdrawal. It is important that new patients are warned of the risk of dependence and steps taken to prevent it happening. Where practicable, existing dependents should be withdrawn slowly, usually following conversion to oral diazepam which has a very long half-life and this renders withdrawal easier. The symptoms of withdrawal must be explained to the patient, as these are often very similar to the original complaint for which BZDs were prescribed. Cessation of long-term BZDs is associated with a withdrawal syndrome in many, but not all, patients. The symptoms are varied but include anxiety, irritability, depression, dysphoria, decreased concentration, insomnia, malaise, muscle twitching, tremors, depersonalisation, perceptual distortions and headaches. Symptoms usually peak at about two weeks after stopping chronic BZDs abruptly.

Benzodiazepine Abusers

The main drug involved is temazepam. Although sometimes taken orally, it is common for abusers to inject one of the oral preparations intravenously. The doses used can be very large. One study cited 3600 mg as the maximum encountered, with 600 mg as the average. Liquid-filled capsules were withdrawn in 1990 but abusers still inject the contents of gel-filled capsules after liquefying the contents or inject tablets after crushing and suspending in water. Often quite elaborate preparation is required. This procedure can clearly have a range of deleterious consequences which are discussed in more depth in Adverse Consequences of Drug Injection. In the case of temazepam, the effects are exacerbated by the irritant nature of the drug.

Temazepam liquid is low concentration formulation designed for oral administration. It is very viscous. Parenteral administration would require injection of very large quantities of thick, sticky liquid, which is obviously difficult. Consequently, a switch to prescribing of liquid formulations has been advocated as a means of reducing temazepam simply encourage the preferential abuse of the other BZDs which are available in tablet form.

Supplies of temazepam are obtained by purchase on the black market or from legitimate receivers of BZD prescriptions. Theft from health centres and pharmacies may also play a part. Some abusers obtain prescriptions by deception, claiming temporary resident status or giving false names. Illicit manufacture has not been reported. In Liverpool the prevalence of temazepam use in 1994 was estimated at 44 per cent of attendees at a drug dependency unit. In a UK questionnaire survey of those attending drug clinics in seven UK cities, 89 per cent of 208 respondents had abused benzodiazepines and 50 per cent had injected them. The table below lists some of the reasons for BZD abuse.

Apart from the problems detailed above, abuse of temazepam clearly could cause sedation in potentially dangerous circumstances. The high doses may be associated with ‘blackouts’, risk-taking behaviour and personality disorders (e.g. paranoia, violent behaviour) and BZD withdrawal symptoms may sometimes occur in the chronic abuser when regular administration is interrupted.

The prevalence of temazepam abuse in the UK encouraged the government to reclassify the drug as a Schedule 3 Controlled Drug in 1996. This made unlawful possession a crime punishable by up to two years imprisonment and/or an unlimited fine. However, legal restrictions of this nature may only focus abusers’ attentions onto other BZDs not controlled by this legislation. The seven-city survey mentioned above found that although temazepam was most popular, 75 per cent of respondents had abused diazepam tablets, 52 per cent had used nitrazepam tablets and 35 per cent lorazepam.

Avoiding benzodiazepine dependence or abuse – guidance on prescribing

Benzodiazepine dependents

• Use BZDs only for anxiety or insomnia that seriously disrupts the patient’s lifestyle not for minor complaints.
• There are non-drug alternative treatment strategies for both conditions that should be considered, e.g. elimination of underlying causes, lifestyle changes, counselling
• Warn the patient of tolerance, dependence potential and the difficulty of withdrawal if treatment is prolonged
• Limit the supply of medication provided, e.g. for insomnia 7 doses, for anxiety 14 days
• Write ‘when required’ on the prescription and make sure the patient understands that daily dosing is usually not mandatory for beneficial effects. Generally, intermittent use (by this method or by prescribing occasional short courses) is more likely to be efficacious and is less likely to cause dependence in the long-term
• Use the smallest dose possible
• Regularly review the need for medication and discontinue as soon as possible
• Withdraw dependents from BZDs slowly

Benzodiazepine abusers

• Avoid prescribing to those with a history of drug abuse
• Do not prescribe BZDs to temporary residents and be cautious concerning supply to new patients of a practice
• Remember that non-abusers may sell their medication to abusers, so review all BZD prescriptions regularly and limit quantities prescribed
• Document known history of BZD abuse so that any other doctor will be aware of the problem
• Where street abuse is suspected, refuse to supply; alternatively supply elixir which is much more difficult to abuse

Reasons for benzodiazepine abuse ‘on the street’

• ‘Rush’ or ‘buzz’ after rapid injection
• CNS depressant properties, e.g. sedative, relaxant, anxiolytic, confidence-boosting and disinhibitive effects
• Increase in the intensity and duration of the effect of heroin when the two are used concurrently. Street heroin may be very impure and over-’cut’ with bulking agents. Use of temazepam is claimed partially to counteract this
• Suppression of opioid withdrawal symptoms

Chlormethiazole

Chlormethiazole abuse has been described. A study in 1979 provided details on 17 abusers. All but four of these were alcoholics, ex-alcoholics or heavy drinkers of alcohol. Data on dosage are only provided for three patients and each took up to 10 g chlormethiazole daily when available. Seven patients were identified by urine screening alone, so few data are available on these, but the remaining ten patients all showed drug-seeking behaviour of one kind or another – mostly by manipulating extra supplies from GPs. Symptoms of withdrawal were described in two patients in whom dosage reduction was attempted; these were similar to those seen with other sedatives.

The intravenous injection of the contents of chlormethiazole capsules is unlikely to be attractive because the drug is dissolved in lipid. The lipid would break into small globules in plasma from which the drug would diffuse very slowly. There would not be a rapid rise in plasma concentrations of chlormethiazole which would be the effect sought. The lipid vehicle could also theoretically occlude small blood vessels, causing damage to tissues downstream of intravenous injection sites.

Other Drugs

Many other prescription medicines have been abused. Often there are only a very small number of cases reported in the literature. Some of these are described below.

Antibiotics

One report highlighted a case of tetracycline and penicillin abuse in association with alcohol. The combination was said to produce euphoria but this is most likely to have been a placebo effect.

Carbamazepine

Two cases have been described of the abuse of carbamazepine by alcoholics. The authors stated that they were aware of other cases. At least one of the two patients took the drug with alcohol. The dose taken was between 1000 and 1500 mg, which was reported to cause euphoria and light-headedness. One patient, who abused the drug for at least four months, eventually developed carbamazepine toxicity.

Clonidine

Two cases have been described of clonidine abuse and dependence in patients taking methadone as maintenance therapy. The average daily dose was 1 to 2 mg per day but one patient had taken up to 15 mg on a single day. The reasons for abusing clonidine were given as: an ability to boost the effects of methadone; to reduce symptoms associated with insufficient methadone; for sedation. Each patient was aware of others maintained on methadone who abused clonidine. Side effects of clonidine that might be seen in the abuser include low blood pressure, depression, tiredness, rhinorrhoea and sweating. In the cases described above, both patients experienced a withdrawal reaction upon discontinuation, although the symptoms of this were completely different in each case.

Diuretics

Abuse of diuretics has been attempted as a misguided method of quick weight loss.

Levodopa

Five patients taking levodopa plus carbidopa (Sinemet) for Parkinson’s disease were reported to have derived psychotropic effects from taking the preparation. All of those involved were male and younger than the average sufferer from this condition (46 to 60 years of age). Patients reported effects such as the feelings of optimism, increased mental power, a sense of well-being, increased sexual energy and animation. However, relatives noticed a range of unpleasant personality changes including paranoia and aggression. Larger doses than prescribed were taken for this purpose – up to 2500 mg of levodopa per day – despite patients experiencing severe dystonias and other movement-related side-effects of levodopa at this dosage. When the drug was discontinued, both the adverse effects and psychothropic effects disappeared but these were often replaced by depression, craving for the drug, drug-seeking behaviour and covert administration. In each case Parkinsonian symptoms were later controlled with lower doses of levodopa.

Oestrogens

Although no cases of abuse have been described per se, oestrogens are psychoactive. It has been proposed that women talking this group of drugs for therapeutic reasons could exhibit tolerance and dependence during prolonged administration after the menopause.

Salbutamol

Abuse of salbutamol has been reported. In most cases the individuals involved were children. Infants and children may be more susceptible to the psychotropic effects of salbutamol. A study in 21 psychiatrically normal adults revealed no evidence of mood-elevating or dependence-producing properties. However, even in adults therapeutic doses can, very rarely, cause visual hallucination. Brennan reported a variety of anectodes connected with salbutamol abuse, including a non-asthmatic schoolboy who used salbutamol Rotacaps because they ‘made him feel good’. This is unusual because most cases of salbutamol abuse involve the use of aerosol devices. Intoxication with salbutamol and other available medications by the inhalation of large amounts of aerosol inhalers is likely to be caused by the chlorofluorocarbon propellant (ie a form of volatile substance abuse). The eight patients described in four published papers were all from 4 to 17 years old and in many cases a whole inhaler (200 puffs) or more was used each day. Edwards and Holgate described abuse in a 24 year old man who used up to 90 puffs of salbutamol aerosol per day and exhibited drug-seeking behaviour to ensure that he had a constant supply of inhalers. However, no psychotropic effects were reported by the patient who had a history of psychiatric illness. The patient seems more likely to have suffered from an obsessive-compulsive disorder.

Addicted to Prescription Drugs?

The Causeway Retreat, Europe’s finest addiction treatment rehab clinic is ‘the’ place for you to be. Based on a unique 400 acre private island, The Causeway Retreat offers the state-of-the-art treatment for addiction problems and our number one priority is to keep the our clients’ confidential information privately. To find out more by talking to a clinical nurse specialist, give us a call on 0207 100 7260 or fill the form below to receive the latest version of our brochure.