Addiction Treatment Blog

Over the past two decades there appears to have been a shift within health care from an expectation that patients with medical problems should entrust themselves passively to the care of physicians to an expectation that they should co-operate in their own care and indeed have some responsibility for the outcome of medical procedures they undergo. The changes are reflected in the terms we used; the word patient, which means someone who endures, is being replaced by terms such as client or consumer, which suggest a more active and discriminating participant in the medical process.

Nowhere is this shift more clear than when it comes to the question of what is known as informed consent. Informed consent was not an issue in medical practice 20 years ago. Today it forms a central issue in a number of ethical codes from the Nuremberg Code to the Helsinki Code as well as Codes originating from the Food and Drugs Administration (FDA) in the United States and the US Department of Health. Read more…

Separation Liability

Liability for drug induced injuries did not become an issue of general concern until quite recently. However, a number of drug-induced problems from thalidomide in the 1960s to Opren and diethylstilbestrol in the 1970s have caused widespread public disquiet and led to increasing awareness of issues to do with liability. In psychiatry, concern in the UK focuses on the question of benzodiazepine prescribing, while in the US the paramount issue concerns the occurrence of tardive dyskinesia in individuals taking neuroleptics. The question has become an emotive one with some commentators who survey the problem referring to the appalling frequency of drug-induced injury, while others comment on its astonishing tray (1). Whatever the absolute frequencies, contrary probably to public belief, the evidence suggests that the larger the pharmaceutical company, the better its practice regarding drug safety is likely to be (2).

Drug-induced problems may stem from toxic effects of a drug, or toxic effects caused by an impure additive, or from allergic reactions to the drug or its additive. Problems may also stem from over prescribing. For instance, in the case of someone who dies from a resistant bacterial infection, a relative could claim that the subject’s death arose in part from the excessive prescription of antibiotics that in its own right brings about the production of resistant infections. In the case of neuroleptics, problems may be brought about by the overuse of these drugs but this overuse, far from being solely promoted by drug companies stems in part from the current politics of mental health – deaths have stemmed from rapid tranquillisation often by harassed staff in psychiatric units. Read more…

Mania is for practical purposes the mirror image of depression. Approximately 50% of people affected present with an elated, euphoric mood. They may be grandiose in their attitudes and beliefs uninhibited in their behaviour. However, the remainder may be irritable and tetchy rather than elated and euphoric and paranoid rather than grandiose. Common to both groups is an increased level of activity, so that hyperactivity is perhaps the most consistent diagnostic feature of mania. In addition, there is typically an increase in appetite and a decrease in time spent asleep.

In 1853, Falret and Baillarger independently described a bipolar disorder, in which affected individuals cycled between periods of elation, or mania, and depression. This was variously called folie circulaire or folie à deux periodes. It forms the basis for what is now recognised as manic-depressive disorder. In 1896, Emil Kraepelin divided the major psychiatric illnesses into manic-depressive illness and schizophrenia. The former was primarily a disorder of mood, the latter a disturbance of cognitive functions. The former usually followed an episodic course with individuals recovering to normal between episodes. The latter was more likely to become a chronic illness with a majority of affected individuals not every fully recovering. These distinctions have broadly speaking held to this day. Read more…

Coping with stress can be hard at times.

The term ‘affective disorder‘ is sometimes taken to encompass both the mood and anxiety disorders. In this blog, it will be restricted to the former. Two disorders will be considered, depression and mania. Depression will be covered first followed by a consideration of mania and then the question of prophylaxis of recurrent episodes of a bipolar disorder, be they depressive or manic.

It is perhaps more difficult to specify exactly what antidepressants do than it is for any other drug that acts on the brain. In the following articles, I will employ an ulcer model of depression in an attempt to clarify the issues. This model, however, simplifies both ulcers and depression and this should be borne in mind. In clear cut cases of depression, an ulcer model performs passably. But in less clear-cut cases, the difficulty in pinpointing what it is that antidepressants do re-emerges.

Another way to consider the issues is by considering what the terms ‘mood’ and ‘emotion’ mean. These are notoriously difficult to define, but one way the problem has been approached is to define them in relation to each other – to compare, for instance, the relation of mood to emotions with the relation between climate and weather, or the relation between the pedal and the keys of the piano. Read more…

Schizophrenia can be dangerous to yourself and others around you if treated incorrectly.

In any consideration of the dopamine hypothesis of schizophrenia, one of the arguments invariably put forward is that psychostimulant drugs, in particular the amphetamines, lead to a mental disorder characterised by prominent paranoid feelings, or outright paranoid delusions. This many authorities have suggested, is a state that is very similar to some schizophrenic states. As the psychostimulants increase brain dopamine levels or neurotransmission, schizophrenia must therefore involve increased dopamine functioning and accordingly dopamine antagonists are its appropriate treatment.

However, the picture in real life is considerably more ambiguous. In the first place there has long been a substantial amount of evidence that up to a third of individuals with ‘schizophrenia‘ actually do well on psychostimulants. Read more…

Anticholinergics

The anticholinergics are a group of drugs, examples of which are given in the table below, which antagonise the action of the neurotransmitter acetylcholine (Ach) at one of its receptors – the muscarinic receptor.

These drugs were initially used to treat Parkinson’s disease. They have since largely been superseded by the use of L-dopa. As most neuroleptics commonly cause parkinsonian symptoms, the anticholinergics have been used routinely to alleviate side effects, where the effect of L-dopa would be blocked by the neuroleptics themselves.

It has been suggested that they have been used too routinely. In many instances it has been common practice to prescribe an anticholinergic agent along with a neuroleptic, when the neuroleptic is first given – that is even before side effects have appeared. The rationale for this has been that the emergence of side effects may compromise an individual’s willingness to continue with medication. The more cynical view is that an early prescription of an anticholinergic drug means that hospital staff or general practitioner will not be called out of hours by a distressed patient, who has just been paralysed by a dystonic reaction or had some other side effect. This of course ensures that they both get a night’s sleep. Read more…

As with most of the drugs, Neuroleptics may have some serious side effects.

Neuroleptics all bind to dopamine receptors. Almost all bind to at least one other receptor as well but not all of them bind to the same other receptor. People also differ. The combination of these two principles means that the side effects of a neuroleptic may differ from one individual to another.

The side effects listed seem fearsome. But most are readily reversible by reducing the dose, changing or halting the drug or using an antidote.

Treatment, however, may involve a trade-off. In practice, it seems that many individuals are prepared to tolerate the interference with daily living that some of the side effects listed may cause, in exchange for peace of mind. The reason for listing these side effects in full is not to deter prescribers from prescribing or takers from taking but rather to involve the taker in making the trade-off rather than having it imposed insensitively on them, and to give prescribers some feel for the nature of that trade-off. Read more…

History of the Neuroleptics

There is considerable controversy over who discovered the neuroleptics, one that is highly relevant to the question of just what these drugs do. Chlorpromazine was first synthesised in 1950, with the intention of producing centrally acting antihistamine for the control of cardiorespiratory sock or collapse. It was first used widely in humans in 1952, along with other agents, as part of an anaesthetic cocktail, when its effects were noted by a chlorpromazine – they were neither sedated in the usual way with anaesthetic agents or analgesic, but rather appeared to become indifferent. This he described as an ataractic effect. A notable point here is that the effect must have come on within an hour or so after having had the drug – and it came on in normal subjects.

In 1952, Jean Delay and Pierre Deniker reported that chlorpromazine was of benefit in controlling states of manic and psychotic agitation. Around the time of its launch in 1954, there was no suggestion that chlorpromazine was likely in any way to be specific to schizophrenia. That came later. In the mid-1950s, chlorpromazine was being reported as being useful for almost every psychiatric condition (hence its trade name Largactil – Large Action).

Laborit has always claimed priority in the discovery of chlorpromazine. Delay and Deniker and others have disputed this. To some extent taking sides in the dispute depends on whether you see the neuroleptics as being in some way curative of psychotic illness or as producing an anti-agitation effect – an effect that is produced equally in all takers who are agitated, whether or not they have a psychological problem. Laborit’s descriptions are in line with the approach that is adopted in this article, which is that neuroleptics act by inducing a state of psychic indifference – in everyone who has them, and that they do this within a short period of time. Delay and Deniker’s approach is the approach that later led to the notion that neuroleptics were anti-schizophrenic.

Within a few years of their use, it became  clear that the new group of drugs produced extrapyramidal side effects. As further compounds came on stream, it seemed that only those that produced extrapyramidal effects brought about benefits in the psychoses. This led to two things. One was that the drugs as a group came to be called neuroleptics by Delay, a term which literally means ‘nerve seizing‘. The second effect was that, for 30 years, little effort was put into finding ‘antipsychotic‘ agents that would not produce extrapyramidal effects – atypical neuroleptics as such agents are now called. It is only in recent years with the rediscovery of clozapine – a drug almost devoid of extrapyramidal effects – that the picture is changing.

Are Neuroleptics Anti-Schizophrenic?

It is commonly believed that neuroleptics drugs are anti-schizophrenic.

The evidence that neuroleptics are anti-schizophrenic comes from a series of research projects which have shown that subjects who take them after discharge from hospital are much less likely to be readmitted than those who do not.

The dopamine hypothesis of schizophrenia has been developed based on this kind of evidence. Briefly, this hypothesis states that as all neuroleptics block the dopamine system in the brain, and as they are beneficial in schizophrenia, therefore there must be something wrong with the dopamine system in the brains of individuals with schizophrenia. A major research enterprise has developed around attempts to test this hypothesis. From a sociological point if view, there have been two consequences of this. One is that many current researchers have had a vested interest in believing that neuroleptics are anti-schizophrenic. Another has been given the ‘known’ abnormalities in the dopamine system in schizophrenia, the fact that the drugs work on the dopamine system means that they are anti-schizophrenic.

For those who take the approach that neuroleptics do reverse the core disturbance in schizophrenia, the usual response to patients not getting better has been to give more of the drugs, and the idea that an individual might not take their drugs is viewed very seriously. In addition, the idea of paying much heed to what the takers of the drugs have to say about whether they are helpful or not seemed irrelevant – after all, these drugs are curative of an illness, a cardinal manifestation of which is supposedly lack of judgement.

The view taken throughout this chapter is that neuroleptics are not specifically anti-schizophrenic but that they are useful for anyone who is agitated, rather than just for people who have schizophrenia. The evidence for this comes from daily practice. Anyone who is agitated will usually be prescribed neuroleptics, whether or not they have schizophrenia. They may have depression, mania or just be agitated. Read more…

Traditionally, three psychoses or major categories of psychiatric illness have been described. These are schizophrenia, manic-depressive psychosis and a third group, variously termed the paranoid, reactive or sensitive psychoses, which more recently have been called the delusional disorders.

This seeming diagnostic precision, however, masks a situation in which, since World War II, there has been a tendency to label all serious psychiatric conditions as schizophrenia. Accordingly, the pharmacological management of the psychoses, in practice, reduces to the management of schizophrenia. It has also reduced in the past 30 years, to the clinical employment of a group of drugs called the neuroleptics, which have been supposed to be in some way specifically therapeutic for schizophrenia. Read more…

The number of children contemplating suicide has increased by fourteen per cent over the past year.

Up to fifteen to twenty per cent of unresponsive manic depressives kill themselves. When the condition is poorly controlled through incorrect medication, or combinations of them, and in harrowing life circumstances, suicide can happen, and it is vital to encourage sufferers to keep as much contact with carers as they can and, if possible, so that when things start to go wrong there is help to prevent these crises.

Statistics

Around 4500 people kill themselves in England and Wales each year (one in 100 deaths), while at least ten times that number of people attempt suicide.

In almost all cultures, the suicide rate rises with age, with the highest rates in the UK for those over seventy-five. In recent years, suicide has also increased in young man, and it is now the second leading cause of death in the fifteen to twenty-four age group, after accidents.

Certain factors are known to be associated with increased risk, including drug and alcohol misuse, unemployment, social isolation and family breakdown. People with diagnosed mental health problem are at  particular risk. Indeed, up to ninety per cent of suicide victims have been reported to have been suffering from a psychiatric disorder at the time of their death. Read more…